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Answers and Critiques 'lhis patient's presentation does not indicate a specific I tr CONT carcliac structural or functionirl c;tuse that rvould make ejection murmur, are commonly present, as more than 50'/. of patients with coarctation also have a bicuspid aortic valve. transthoracic echocardiography (Option D) usefirl at this The ECG demonstrates left ventricular hypertrophy, and a point. 'l'ransthor:rcic echocardiography is the mainstay <tf typical chest radiograph shows abnormal aortic contour and noni nvasive clrdior,ascular imagi ng for structural abnonnal rib notching. ities. The patient's presclttation potentiirlly indicates other A small patent ductus arteriosus (PDA) (Option C) gen- causes of the chest pain that are l)etter evaluated u,ith coro erally causes no cardiovascular symptoms. A continuous nary C'f angiography'. murmur heard beneath the left clavicle that envelops the S, is typical. Occasionally, no murmur is heard, and the IEY POIilT diagnosis is made by echocardiography. The ECG and chest . Coronary CT angiography, by allowing visualization radiograph are normal in a patient with a small PDA. ofcoronary and other thoracic pathologr, plays an important role in the evaluation of acute chest pain XEY POITIS UI e A small ventricular septal defect presents with a loud 6' in the emergency department. (often palpable) holosystolic murmur located at the t Bibliography left sternal border that obliterates the Sr. U Rybicki FJ, Udelson JE, Peacock WF, et al. 20ts ACR/ACC/AHA/AATS/ACEp/ o Ventricular septal defect closure is not indicated for ?, ASNC/NASCI/SAEM/SCCT/SCMR/SCPC/SNMMI/STR/STS appropriate utilization of cardiovascular imaging in emergency department patients patients with a small left-to-right shunt and no cham tu with chest pain: a joint document of the American College of Radiolog, vt ber enlargement or valve disease, but periodic clinical Appropriateness Criteria Committee and the American College of 0, Cardiologz Appropriate Use Criteria Task Force. J Am Coll Cardiol. 20161 evaluation and imaging are recommended. 3 a 67 :853 79. IPMID: 26809772] doi:10.1016/j.jacc.2015.09.011

'lhis patient's presentation does not indicate a specific I tr CONT carcliac structural or functionirl c;tuse that rvould make ejection murmur, are commonly present, as more than 50'/. of patients with coarctation also have a bicuspid aortic valve. transthoracic echocardiography (Option D) usefirl at this The ECG demonstrates left ventricular hypertrophy, and a point. 'l'ransthor:rcic echocardiography is the mainstay <tf typical chest radiograph shows abnormal aortic contour and noni nvasive clrdior,ascular imagi ng for structural abnonnal rib notching. ities. The patient's presclttation potentiirlly indicates other A small patent ductus arteriosus (PDA) (Option C) gen- causes of the chest pain that are l)etter evaluated u,ith coro erally causes no cardiovascular symptoms. A continuous nary C'f angiography'. murmur heard beneath the left clavicle that envelops the S, is typical. Occasionally, no murmur is heard, and the IEY POIilT diagnosis is made by echocardiography. The ECG and chest . Coronary CT angiography, by allowing visualization radiograph are normal in a patient with a small PDA. ofcoronary and other thoracic pathologr, plays an important role in the evaluation of acute chest pain XEY POITIS UI e A small ventricular septal defect presents with a loud 6' in the emergency department. (often palpable) holosystolic murmur located at the t Bibliography left sternal border that obliterates the Sr. U Rybicki FJ, Udelson JE, Peacock WF, et al. 20ts ACR/ACC/AHA/AATS/ACEp/ o Ventricular septal defect closure is not indicated for ?, ASNC/NASCI/SAEM/SCCT/SCMR/SCPC/SNMMI/STR/STS appropriate utilization of cardiovascular imaging in emergency department patients patients with a small left-to-right shunt and no cham tu with chest pain: a joint document of the American College of Radiolog, vt ber enlargement or valve disease, but periodic clinical Appropriateness Criteria Committee and the American College of 0, Cardiologz Appropriate Use Criteria Task Force. J Am Coll Cardiol. 20161 evaluation and imaging are recommended. 3 a 67 :853 79. IPMID: 26809772] doi:10.1016/j.jacc.2015.09.011 Bibliography Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC guideline for the Item 5 Answer: D management of adults with congenital heart disease: a report of the American College of Cardiolos,/American Heart Association Task Force Educational Objective: Diagnose ventricular septal on Clinical Practice Guidelines. J Am Coll Cardiol. 2Ol9:73:e9l-e192. IPMID' 301212391 doi:10.1016/j.jacc.2018.08.1029 defect.

Bibliography Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC guideline for the Item 5 Answer: D management of adults with congenital heart disease: a report of the American College of Cardiolos,/American Heart Association Task Force Educational Objective: Diagnose ventricular septal on Clinical Practice Guidelines. J Am Coll Cardiol. 2Ol9:73:e9l-e192. IPMID' 301212391 doi:10.1016/j.jacc.2018.08.1029 defect. The most likely diagnosis in this patient is a small (restrictive) ventricular septal defect (VSD) (Option D). The presentation Item 6 Answer: h of an isolated VSD depends on the VSD size and pulmonary Ed ucationa I Objective: Treat complex multivessel vascular resistance. Small VSDs are usually asymptomatic. A coronary artery disease. palpable systolic murmur (thrill) is often noted at the left ster nal border, accompanied by a loud holosystolic murmur that The most appropriate management is coronary artery bypass obliterates the Sr, as observed in this patient. Small VSDs do grafting (CABG) (Option A). This patient has complex mul not cause left heart enlargement or pulmonary hlpertension, tivessel coronary artery disease (CAD) involving the left and the ECG and chest radiograph reveal norrnal flndings. main coronary artery distal bifurcation, proximal left cir VSD closure is not indicated for patients with a small left-to cumflex artery and proximal left anterior descending and right shunt and no chamber enlargement or valve disease, but flrst diagonal artery bifurcation. CABG, especially with use periodic clinical evaluation and imaging are recommended. of arterial (internal mammary artery) conduits, is indicated Patients with small VSDs do not require activity restrictions. in patients with multivessel CAD and no contraindications, An adult with an atrial septal defect (ASD) (Option because it is associated with enhanced survival compared A) most often presents with dyspnea, atrial arrhythmias, with medical therapy alone. CABG also results in decreased or right heart enlargement. Physical examination findings recurrence of angina, lower rates of myocardial infarction, include elevation in venous pressure, a right ventricular and fewer repeat revascularization procedures compared Iift, flxed splitting of the Sr, a pulmonary midsystolic flow with percutaneous coronary intervention or medical ther murmur, and, when there is a large shunt, a tricuspid dia apy alone in these patients. stolic flow rumble. The ECG demonstrates right axis devi Guideline-directed medical therapy (Option B) is essen ation and incomplete right bundle branch block, and the tial for improved prognosis before and after surgical or per chest radiograph generally demonstrates features of right cutaneous revascularization. Aspirin, B blockade, and statin heart enlargement and enlarged pulmonary arteries with therapy, along with ACE inhibition in patients with systolic increased pulmonary blood flow. left ventricular (LV) dysfunction, such as this patient, are Typical physical examination flndings in aortic coarcta indicated for secondary prevention of major adverse vas- tion (Option B) include upper extremity hypertension, radial cular events. However, anti ischemic and cardioprotective artery-to-femoral artery pulse and blood pressure differ medical therapy would be inferior to revascularization in entials, and a systolic murmur over the left chest related to improving survival in this patient with complex CAD involv obstruction from the coarctation. In addition, findings of ing the left main coronary artery and a large area of poten- bicuspid aortic valve, including ejection click and systolic tially ischemic myocardium.

The most likely diagnosis in this patient is a small (restrictive) ventricular septal defect (VSD) (Option D). The presentation Item 6 Answer: h of an isolated VSD depends on the VSD size and pulmonary Ed ucationa I Objective: Treat complex multivessel vascular resistance. Small VSDs are usually asymptomatic. A coronary artery disease. palpable systolic murmur (thrill) is often noted at the left ster nal border, accompanied by a loud holosystolic murmur that The most appropriate management is coronary artery bypass obliterates the Sr, as observed in this patient. Small VSDs do grafting (CABG) (Option A). This patient has complex mul not cause left heart enlargement or pulmonary hlpertension, tivessel coronary artery disease (CAD) involving the left and the ECG and chest radiograph reveal norrnal flndings. main coronary artery distal bifurcation, proximal left cir VSD closure is not indicated for patients with a small left-to cumflex artery and proximal left anterior descending and right shunt and no chamber enlargement or valve disease, but flrst diagonal artery bifurcation. CABG, especially with use periodic clinical evaluation and imaging are recommended. of arterial (internal mammary artery) conduits, is indicated Patients with small VSDs do not require activity restrictions. in patients with multivessel CAD and no contraindications, An adult with an atrial septal defect (ASD) (Option because it is associated with enhanced survival compared A) most often presents with dyspnea, atrial arrhythmias, with medical therapy alone. CABG also results in decreased or right heart enlargement. Physical examination findings recurrence of angina, lower rates of myocardial infarction, include elevation in venous pressure, a right ventricular and fewer repeat revascularization procedures compared Iift, flxed splitting of the Sr, a pulmonary midsystolic flow with percutaneous coronary intervention or medical ther murmur, and, when there is a large shunt, a tricuspid dia apy alone in these patients. stolic flow rumble. The ECG demonstrates right axis devi Guideline-directed medical therapy (Option B) is essen ation and incomplete right bundle branch block, and the tial for improved prognosis before and after surgical or per chest radiograph generally demonstrates features of right cutaneous revascularization. Aspirin, B blockade, and statin heart enlargement and enlarged pulmonary arteries with therapy, along with ACE inhibition in patients with systolic increased pulmonary blood flow. left ventricular (LV) dysfunction, such as this patient, are Typical physical examination flndings in aortic coarcta indicated for secondary prevention of major adverse vas- tion (Option B) include upper extremity hypertension, radial cular events. However, anti ischemic and cardioprotective artery-to-femoral artery pulse and blood pressure differ medical therapy would be inferior to revascularization in entials, and a systolic murmur over the left chest related to improving survival in this patient with complex CAD involv obstruction from the coarctation. In addition, findings of ing the left main coronary artery and a large area of poten- bicuspid aortic valve, including ejection click and systolic tially ischemic myocardium. 157

Answers and Critiques Myocardial viability testing (Option C) uses imaging Exercise echocardiography (Option B) is useful fbr diag to detect potentially reversible states of ischemic ventric nosing coronary artery disease and evaluating valvular heart ular dysfunction. Myocardial viability is associated with disease. tt is not indicated for this patient with no anginal improved survival and ventricular recovery following revas symptoms and near normal left ventricular (LV) systolic cularization in patients with LV dysfunction; horvever, per function. fbrming viability testing befbre revascularization has not Right and left heart catheterization (Option C) may been shown to predict or enhance outcomes and is not demonstrate hemodynamic features consistent with restric indicated in this patient. tive physiologr but would not diagnose the underlying cause Drug eluting stent based percutaneous coronary of this patient's symptoms without concomitant endomyo intervention (Option D) is a reasonable option in patients cardial biopsy. Endomyocardial biopsy may be uselul if the with symptomatic CAD. including those with unprotected diagnosis of an infiltrative cardiomyopathy is unclear, but left main CAD (without bypass to the left coronary circu given the risks of this inrasive test, it would not be indicated D lation). However, in patients with complex CAD including as the initial test ol choice. la multiple bifurcations and/or long lesions who are not at Fabry disease is a lysosomal storage disorder that aflects (D increased surgical risk, CABG is the preferred revascular the heart, with marked diltuse LV hypertrophy. The ECG = usually demonstrates marked LV hypertrophy with prom UI ization strateg/. q, inent ST T abnormalities, rather than the low voltage seen I(EY POIl{I CL in this patient. Neuropathy in Fabry disease often presents n . In patients with multivessel coronary artery disease, as burning dysesthesia. not carpal tunnel syndrome. Onset coronary artery bypass grafting is associated with of Fabry disease occurs in childhood, and the diagnosis is .,El enhanced survival compared with medical therapy established through genetic testing or an abnormal serum .D t^ alone. o. galactosidase level (Option D).

Myocardial viability testing (Option C) uses imaging Exercise echocardiography (Option B) is useful fbr diag to detect potentially reversible states of ischemic ventric nosing coronary artery disease and evaluating valvular heart ular dysfunction. Myocardial viability is associated with disease. tt is not indicated for this patient with no anginal improved survival and ventricular recovery following revas symptoms and near normal left ventricular (LV) systolic cularization in patients with LV dysfunction; horvever, per function. fbrming viability testing befbre revascularization has not Right and left heart catheterization (Option C) may been shown to predict or enhance outcomes and is not demonstrate hemodynamic features consistent with restric indicated in this patient. tive physiologr but would not diagnose the underlying cause Drug eluting stent based percutaneous coronary of this patient's symptoms without concomitant endomyo intervention (Option D) is a reasonable option in patients cardial biopsy. Endomyocardial biopsy may be uselul if the with symptomatic CAD. including those with unprotected diagnosis of an infiltrative cardiomyopathy is unclear, but left main CAD (without bypass to the left coronary circu given the risks of this inrasive test, it would not be indicated D lation). However, in patients with complex CAD including as the initial test ol choice. la multiple bifurcations and/or long lesions who are not at Fabry disease is a lysosomal storage disorder that aflects (D increased surgical risk, CABG is the preferred revascular the heart, with marked diltuse LV hypertrophy. The ECG = usually demonstrates marked LV hypertrophy with prom UI ization strateg/. q, inent ST T abnormalities, rather than the low voltage seen I(EY POIl{I CL in this patient. Neuropathy in Fabry disease often presents n . In patients with multivessel coronary artery disease, as burning dysesthesia. not carpal tunnel syndrome. Onset coronary artery bypass grafting is associated with of Fabry disease occurs in childhood, and the diagnosis is .,El enhanced survival compared with medical therapy established through genetic testing or an abnormal serum .D t^ alone. o. galactosidase level (Option D). f,tY POTilTS Bibliography RltCI MR. CAIhOOTT JII. DChNTCT GJ, Ct AI. ACCIA,\TS/AIIA/ASEIASNC/SCAI o Cardiac magnetic resonance imaging with gadolin SCCT'STS 2017 appropriate Llse critcria for coronan rerascullriz:tion in ium is highly sensitive and specific for cardiac amy patients s,ith stablc ischemic hearl disease: a report of the Americar-r College of Cardiokrgr Appr)priate Use Criteril'lask Force, Americf,n Association fi)r loidosis, but it does not distinguish between AL 'lhoracic Surgery American Heart Associittion, Anlerican Societ-n.' ot (immunoglobulin light-chain) amyloidosis and I:chocardiographl: Americirn Societ) of Nuclear Cardiokrs: Societ)' ti)r Cardiovlscular Angiography and Interventions. Society of Cardiovascullr transthyretin amyloidosis. Computed Tomogrrrphy: and Societ-v ol Thoracic Surget)ns. J Am Coll Cardi(r. ')017 $9)212 22.11. IPMtD' 2829166i]l doi:10.1016 j.jacc.20l7.02.0Ol r In patients with cardiac magnetic resonance imaging findings consistent with cardiac amyloidosis, an abnormal 99m-technetium pyrophosphate scan Item 7 Answer: A would confirm transthyretin amyloidosis without the Educational Objective Diagnose infi ltrative cardiac need fbr a biopsy. disease. Bibliography Cardiac magnetic resonance (CMR) imaging with gadolin Ruberg l;l-. Grogrn M. Hanna \{. et rl.'lransth}retin iim}'loid cardiomy)p, ium contrast (Option A) is the most appropriate test to thy: J;\CC state of the trt revieu: J Am Coll Cardiol. 2019:73:2872 9l perform next. The patient's history and physical exam IPMID: :]l l7l094l doi:10. l0l6/j.jacc.2019.01.003

f,tY POTilTS Bibliography RltCI MR. CAIhOOTT JII. DChNTCT GJ, Ct AI. ACCIA,\TS/AIIA/ASEIASNC/SCAI o Cardiac magnetic resonance imaging with gadolin SCCT'STS 2017 appropriate Llse critcria for coronan rerascullriz:tion in ium is highly sensitive and specific for cardiac amy patients s,ith stablc ischemic hearl disease: a report of the Americar-r College of Cardiokrgr Appr)priate Use Criteril'lask Force, Americf,n Association fi)r loidosis, but it does not distinguish between AL 'lhoracic Surgery American Heart Associittion, Anlerican Societ-n.' ot (immunoglobulin light-chain) amyloidosis and I:chocardiographl: Americirn Societ) of Nuclear Cardiokrs: Societ)' ti)r Cardiovlscular Angiography and Interventions. Society of Cardiovascullr transthyretin amyloidosis. Computed Tomogrrrphy: and Societ-v ol Thoracic Surget)ns. J Am Coll Cardi(r. ')017 $9)212 22.11. IPMtD' 2829166i]l doi:10.1016 j.jacc.20l7.02.0Ol r In patients with cardiac magnetic resonance imaging findings consistent with cardiac amyloidosis, an abnormal 99m-technetium pyrophosphate scan Item 7 Answer: A would confirm transthyretin amyloidosis without the Educational Objective Diagnose infi ltrative cardiac need fbr a biopsy. disease. Bibliography Cardiac magnetic resonance (CMR) imaging with gadolin Ruberg l;l-. Grogrn M. Hanna \{. et rl.'lransth}retin iim}'loid cardiomy)p, ium contrast (Option A) is the most appropriate test to thy: J;\CC state of the trt revieu: J Am Coll Cardiol. 2019:73:2872 9l perform next. The patient's history and physical exam IPMID: :]l l7l094l doi:10. l0l6/j.jacc.2019.01.003 ination are consistent with heart failure, and the elevated B type natriuretic peptide level supports this. Signilicantly Item 8 Answer: D increased wall thickness is present on the echocardiogram. Educational Objective: Treat a patient with symptom- with discordantly low voltage on the ECG. These findings atic severe aortic stenosis with transcatheter aortic valve suggest an inflltrative cardiomyopathy and, in combination implantation. with the patient's history of carpal tunnel syndrome, suggest possible transthyretin amyloid (ATTR) amyloidosis. ATTR The most appropriate next step in treatment is transcath amyloidosis is much more common in men. and the patho eter aortic valve implantation (TAVI) (Option D). Aortic logic V1221 mutation in the TTR gene is present in 3'l, to 3.5',1, valve replacement is a life prolonging procedure in patients of Black persons. If cardiac amyloidosis is present in this with severe aortic stenosis. The indications for aortic valve patient, CIvIR imaging with gadolinium contrast would likely replacement in severe aortic stenosis are (1) the presence of show diffuse late mid myocardial gadolinium enhancement symptoms, (2) left ventricular systolic dysfunction (ejection in a noncoronary distribution. CMR imaging with gadolin fiaction <50'X,) in an asymptomatic patient. or (3) a con ium is highly sensitive and speciflc fbr cardiac amyloidosis, comitant cardiac surgical procedure for other indications. but it does not distinguish between AL (immunoglobulin Flxertional dyspnea. syncope, and angina are the most com light chain) amyloidosis and ATTR amyloidosis. An abnor mon presenting symptoms that result in aortic valve inter- mal 99m technetium pyrophosphate scan would conflrm vention. Aortic valve replacement can be performed with ATTR amyloidosis without the need fbr a biopsy. surgical aortic valve replacement (SAVR) or via transcatheter

ination are consistent with heart failure, and the elevated B type natriuretic peptide level supports this. Signilicantly Item 8 Answer: D increased wall thickness is present on the echocardiogram. Educational Objective: Treat a patient with symptom- with discordantly low voltage on the ECG. These findings atic severe aortic stenosis with transcatheter aortic valve suggest an inflltrative cardiomyopathy and, in combination implantation. with the patient's history of carpal tunnel syndrome, suggest possible transthyretin amyloid (ATTR) amyloidosis. ATTR The most appropriate next step in treatment is transcath amyloidosis is much more common in men. and the patho eter aortic valve implantation (TAVI) (Option D). Aortic logic V1221 mutation in the TTR gene is present in 3'l, to 3.5',1, valve replacement is a life prolonging procedure in patients of Black persons. If cardiac amyloidosis is present in this with severe aortic stenosis. The indications for aortic valve patient, CIvIR imaging with gadolinium contrast would likely replacement in severe aortic stenosis are (1) the presence of show diffuse late mid myocardial gadolinium enhancement symptoms, (2) left ventricular systolic dysfunction (ejection in a noncoronary distribution. CMR imaging with gadolin fiaction <50'X,) in an asymptomatic patient. or (3) a con ium is highly sensitive and speciflc fbr cardiac amyloidosis, comitant cardiac surgical procedure for other indications. but it does not distinguish between AL (immunoglobulin Flxertional dyspnea. syncope, and angina are the most com light chain) amyloidosis and ATTR amyloidosis. An abnor mon presenting symptoms that result in aortic valve inter- mal 99m technetium pyrophosphate scan would conflrm vention. Aortic valve replacement can be performed with ATTR amyloidosis without the need fbr a biopsy. surgical aortic valve replacement (SAVR) or via transcatheter 158

Answers and Critiques approach (TAVI). TAVI is reconrmended in preference to ventricular frlnction, an ICD is 'uvarranted before dischargc. SAVR for symptomatic patients with severe aortic stenosis barring a clear. acute contrailldication (e.g., active bacterc who are older than 80 years or fbr younger patients with a mia). [CDs are ir-rdicated and eflective in the sefting of second life expectancy less than l0 years. 'IAVI is also recommended lry prevention of sudden cardiac death, even if the causc is lbr symptomatic patients ol any age with severe aortic ste- not confirmed (unless it is very clear that the cause is acutely nosis and a high or prohibitive surgical risk if predicted reversibie and correctable). l{owever, her presentation is not postprocedure survival is more thar.r 12 months with an unusual fbr arrlrythmogenic right ver-rtricular cardion.ryopathy acceptable quality of iife. For symptomatic patients aged (AltVC). an inherited "r,tear and tear" disorder that primarily 65 to B0 years, either SAVR or TAVI is appropriate following itfibcts the right ventricle but nta1, be seen in the left. Ventric shared decision making. ular arrhythmias are often tl.re initial presentation. and somc Balloon aortic valvuloplasty (Option A) was previously rlre very clrarnatic (as in tl-ris case); they are also lery likely to used to treat symptomatic severe aortic stenosis by tempo recur. Cardiac magnetic resoltzlnce imaging lr,ould be helplul rarily increasing the aortic valve area in patients who were to ,ssess m),,ocardial inliltration, ideally before ICD placement. t (u not surgical candidates. With the advent of the less invasive A nrajor facet of her treatnlent will be exertional limitation, TAVI, balloon valvuloplasty is now rarely used. EF of ten a major challenge lor patients who are athletes. Although the patient is at prohibitive surgical risk and Arniodarone (Option A) is a multichannel antiarrhythmic would not likely be approved for SAVR, she would likely be a agent that ma1, be necessary in patiellts with ARVC and re{rac' \, candidate for TAVI. Thus, simply continuing medical therapy tory ventricular arrhl.thrnias. [-lower,er, this patient has 1at tcr =, .E (Option B) would be inappropriate, given the mortality and htle a trial ol exerlional limitation andior a p blocker (e.g., {^ quality of-life benefit associated with TAVI. r.netoprolol). and she is quite )our1g to commit to amiodarone c, The patient's comorbid conditions*atrial fibrillation, as Iirst line therapy Furthennorc. amiodarone is not nearly as vt = E stage G3a chronic kidney disease, COPD, and hypertension e {lective as is :rn ICD ir, preventing sudden cardiac death. make her a poor candidate lor SAVR (Option C). Her high Genetic testing (Option B) n.ray be helpful to under surgical risk is further quantified by her Society ofThoracic star.rcl this patient's disease risl< and severity, and results muy Surgeons adult cardiac surgery risk score. have implications fbr ITer future children and other family nrcnrbers. Ift.lwever, genetic testing is not required for diag IEY POtXTS r.rosis or ICD placement, irnd it should not be undertaken o Transcatheter aortic valve implantation is recom- i,r,,ithout prior genetic counseling. 'lherefore. it is not nec mended in preference to surgical aortic valve replace essary befbre discharge, ls it is unlikely to affect immediatc ment for symptomatic patients with severe aortic ste- decision rn:rking regarding ICI) placement. nosis who are older than 80 years or younger patients Lisinopril (Option D) may be helpful fbr patients n'ith with a life expectancy less than 10 years. ne'ut lcfl rrentricular d1'sfurT ction and has been recommended . Transcatheter aortic valve implantation is recom- in patients r,r,ith ARVC n,ith right ventricular dysfunctior.rr mended for symptomatic patients of any age with holtever. it has no current role in this patient. Furthermore, severe aortic stenosis and a high or prohibitive surgi it is not irs imperative bcfbre discharge as is an lCD. cal risk if predicted postprocedure survival is more XEY POIilI than 12 months with an acceptable quality of life. . Patients with zustained ventricular arrhy'thmias (>30 seconds) or cardiac arrest without a revenible cause Bibliography have a class 1 recommendation for secondary prevention Otto CM. Nishimura RA. Bonon' RO. et rl. 2020 ACC AI IA guideline frrr thc manirgement of patients with \'rlvular heart disease: a report of the with implantable cardioverter-defibrillator placement. American College of Cardiolog Anlerican Heart Association Joint (i)mmittee on Clinical Practice Guidelines. Circulation. 2o21:111]:e72 e227. IPMID: 33332150] doi:10.1161 (11R.0000000000000923 Bibliography Al Khatib SM. Stevenson WG. Ackernrrn l\4J. et al. 2017 AHAIACCIHRS guicleline for management of patients with ventricular affhythmias and the prevention ofsudden cardiirc deilth: r report ofthe American College

approach (TAVI). TAVI is reconrmended in preference to ventricular frlnction, an ICD is 'uvarranted before dischargc. SAVR for symptomatic patients with severe aortic stenosis barring a clear. acute contrailldication (e.g., active bacterc who are older than 80 years or fbr younger patients with a mia). [CDs are ir-rdicated and eflective in the sefting of second life expectancy less than l0 years. 'IAVI is also recommended lry prevention of sudden cardiac death, even if the causc is lbr symptomatic patients ol any age with severe aortic ste- not confirmed (unless it is very clear that the cause is acutely nosis and a high or prohibitive surgical risk if predicted reversibie and correctable). l{owever, her presentation is not postprocedure survival is more thar.r 12 months with an unusual fbr arrlrythmogenic right ver-rtricular cardion.ryopathy acceptable quality of iife. For symptomatic patients aged (AltVC). an inherited "r,tear and tear" disorder that primarily 65 to B0 years, either SAVR or TAVI is appropriate following itfibcts the right ventricle but nta1, be seen in the left. Ventric shared decision making. ular arrhythmias are often tl.re initial presentation. and somc Balloon aortic valvuloplasty (Option A) was previously rlre very clrarnatic (as in tl-ris case); they are also lery likely to used to treat symptomatic severe aortic stenosis by tempo recur. Cardiac magnetic resoltzlnce imaging lr,ould be helplul rarily increasing the aortic valve area in patients who were to ,ssess m),,ocardial inliltration, ideally before ICD placement. t (u not surgical candidates. With the advent of the less invasive A nrajor facet of her treatnlent will be exertional limitation, TAVI, balloon valvuloplasty is now rarely used. EF of ten a major challenge lor patients who are athletes. Although the patient is at prohibitive surgical risk and Arniodarone (Option A) is a multichannel antiarrhythmic would not likely be approved for SAVR, she would likely be a agent that ma1, be necessary in patiellts with ARVC and re{rac' \, candidate for TAVI. Thus, simply continuing medical therapy tory ventricular arrhl.thrnias. [-lower,er, this patient has 1at tcr =, .E (Option B) would be inappropriate, given the mortality and htle a trial ol exerlional limitation andior a p blocker (e.g., {^ quality of-life benefit associated with TAVI. r.netoprolol). and she is quite )our1g to commit to amiodarone c, The patient's comorbid conditions*atrial fibrillation, as Iirst line therapy Furthennorc. amiodarone is not nearly as vt = E stage G3a chronic kidney disease, COPD, and hypertension e {lective as is :rn ICD ir, preventing sudden cardiac death. make her a poor candidate lor SAVR (Option C). Her high Genetic testing (Option B) n.ray be helpful to under surgical risk is further quantified by her Society ofThoracic star.rcl this patient's disease risl< and severity, and results muy Surgeons adult cardiac surgery risk score. have implications fbr ITer future children and other family nrcnrbers. Ift.lwever, genetic testing is not required for diag IEY POtXTS r.rosis or ICD placement, irnd it should not be undertaken o Transcatheter aortic valve implantation is recom- i,r,,ithout prior genetic counseling. 'lherefore. it is not nec mended in preference to surgical aortic valve replace essary befbre discharge, ls it is unlikely to affect immediatc ment for symptomatic patients with severe aortic ste- decision rn:rking regarding ICI) placement. nosis who are older than 80 years or younger patients Lisinopril (Option D) may be helpful fbr patients n'ith with a life expectancy less than 10 years. ne'ut lcfl rrentricular d1'sfurT ction and has been recommended . Transcatheter aortic valve implantation is recom- in patients r,r,ith ARVC n,ith right ventricular dysfunctior.rr mended for symptomatic patients of any age with holtever. it has no current role in this patient. Furthermore, severe aortic stenosis and a high or prohibitive surgi it is not irs imperative bcfbre discharge as is an lCD. cal risk if predicted postprocedure survival is more XEY POIilI than 12 months with an acceptable quality of life. . Patients with zustained ventricular arrhy'thmias (>30 seconds) or cardiac arrest without a revenible cause Bibliography have a class 1 recommendation for secondary prevention Otto CM. Nishimura RA. Bonon' RO. et rl. 2020 ACC AI IA guideline frrr thc manirgement of patients with \'rlvular heart disease: a report of the with implantable cardioverter-defibrillator placement. American College of Cardiolog Anlerican Heart Association Joint (i)mmittee on Clinical Practice Guidelines. Circulation. 2o21:111]:e72 e227. IPMID: 33332150] doi:10.1161 (11R.0000000000000923 Bibliography Al Khatib SM. Stevenson WG. Ackernrrn l\4J. et al. 2017 AHAIACCIHRS guicleline for management of patients with ventricular affhythmias and the prevention ofsudden cardiirc deilth: r report ofthe American College tr Item 9 Answer: C Educational Objective: Provide secondary prevention of of Cirrdiologr/American Hean Association Trsk Force on Clinical Practice Cuidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2018r72: c9l e220. [PN4ID: 290972961 doi:10.1016ij.jacc.2017.10.054 sudden cardiac death using an implantable cardioverter- defibrillator. Item 10 Answer: B Jhc rnost appropriate aclclitional nranagenrent before dis Educational Objective: Treat a patient with diabetes cl.rarge is implantable cardiovefter defibrillator (lCD) place mellitus and heart failure with a sodium-glucose cotrans- n.rcr-rt (Option C) in this athletc r,r'ho presented lvith rescuecl porter 2 inhibitor. sudden cardiac death. P:rtients $'ith sustained r,entricular arrhythmitrs (>30 secor-rcls) <tr carcliac arrest \\rithollt a revers The most appropriate additional treatment is empagliflozin ible cause have a class I recommendation for secondary (Option B). Sodium-glucose cotransporter 2 (SGLI2) inhibi prevention with ICD placement. Despite her nornral left tors have been studied in patients with diabetes mellitus and

tr Item 9 Answer: C Educational Objective: Provide secondary prevention of of Cirrdiologr/American Hean Association Trsk Force on Clinical Practice Cuidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2018r72: c9l e220. [PN4ID: 290972961 doi:10.1016ij.jacc.2017.10.054 sudden cardiac death using an implantable cardioverter- defibrillator. Item 10 Answer: B Jhc rnost appropriate aclclitional nranagenrent before dis Educational Objective: Treat a patient with diabetes cl.rarge is implantable cardiovefter defibrillator (lCD) place mellitus and heart failure with a sodium-glucose cotrans- n.rcr-rt (Option C) in this athletc r,r'ho presented lvith rescuecl porter 2 inhibitor. sudden cardiac death. P:rtients $'ith sustained r,entricular arrhythmitrs (>30 secor-rcls) <tr carcliac arrest \\rithollt a revers The most appropriate additional treatment is empagliflozin ible cause have a class I recommendation for secondary (Option B). Sodium-glucose cotransporter 2 (SGLI2) inhibi prevention with ICD placement. Despite her nornral left tors have been studied in patients with diabetes mellitus and 159

Answers and Critiques in patients with heart failure with or without diabetes. For EAST AFNET 4 randomized clinical trial, which evaluated a patients with diabetes, studies have shown a reduction in rhythm control strates/ versus usual care (typically includ cardiovascular events, including heart lailure-related mor ing rate control) in patients with a recent diagnosis (within tality and hospitalizations, with use of these agents. SGLI2 12 months) of atrial flbrillation and coexisting cardiovas- inhibitors (empagliflozin, canagliflozin, and dapagliflozin) cular conditions. The inclusion criteria were age older than seem to reduce the risk for heart failure hospitalization and 75 years or previous transient ischemic attack or stroke, or cardiovascular death by 1.9"/,' and death from any cause by two of the following: age older than 65 years, female sex, 2.3'7,, independent of glucose control. The mechanisms of heart failure, hypertension, diabetes mellitus, severe coro this reduction are unclear but are thought to be independent nary artery disease, chronic kidney disease, and left ventric of increased diuresis due to glucose excretion. The American ular hypertrophy. The trial demonstrated improved clinical Diabetes Association Standards of Medical Care in Diabetes. outcomes. including a reduction in the primary composite endorsed by the American College of Cardiologr, recom- end point of cardiovascular death, stroke, or hospitaliza mends initiating an SGLT2 inhibitor with proven cardiovas- tion for heart failure or acute coronary syndrome, among U} cular beneflt to reduce the risk for worsening heart failure patients randomly assigned to an early rhythm control o and cardiovascular death in patients with type 2 diabetes strates/, including asymptomatic patients. The intervention = included either antiarrhy'thmic drugs or catheter ablation, ut and established heart failure with reduced ejection fraction. q, Digoxin (Option A) reduces the risk for heart failure but importantly, it included aggressive concomitant medical EL hospitalization but does not reduce mortality. It is occasion therapy (e.g., oral anticoagulation when indicated, hyper- a.l ally used in patients r.r,ith heart failure symptoms refractory tension treatment) in both the intervention and the control to optimal therapy, but because of its associated toxiciry groups. Based on the trial results, this patient is mostly likely 4t (D digoxin is not recommended as routine therapy in most to beneflt from early rhythm control for atrial flbrillation. UI patients with heart failure. This patient is appropriately receiving stroke prevention Loop diuretics, such as furosemide (Option C), are the therapy with a direct oral anticoagulant (DOAC), and he has primary diuretic therapy for volume overload in heart failure had no recurrent stroke or signiflcant bleeding episodes on because of increased potency compared with other diuretics. the current therapy. Therefore, left atrial appendage occlu- However, this patient has no clinical evidence of volume sion (Option A) is not indicated. overload. and furosemide is not indicated. Among the common indications for permanent pace- Guidelines recommend the addition of isosorbide maker implantation (Option B) are symptomatic bradycar dinitrate-hydralazine (Option D) in Black patients who dia without reversible cause; permanent atrial flbrillation remain s),,rnptomatic on maximal doses of a p blocker; ACE with symptomatic bradycardia; alternating bundle branch inhibitor, angiotensin receptor blocker (ARB), or valsartan- block; and complete heart block, high-degree atrioventric sacubitril; and aldosterone antagonist. In patients who are ular (AV) block, or Mobitz type 2 second-degree AV block, intolerant of ACE inhibitor or ARB therapy, especially those irrespective of symptoms. This patient has no indications for with chronic kidney disease, isosorbide dinitrate hydralazine pacemaker implantation. may be considered as a therapeutic option. Oral anticoagulation in patients with atrial flbrillation can be accomplished with a vitamin K antagonist (warfarin) I(EY POIl{T or DOAC, such as rivaroxaban. Rivaroxaban is noninferior to o A sodium-glucose cotransporter 2 inhibitor is recom warfarin in the prevention of stroke or systemic embolism mended to reduce risk for worsening heart failure and and is associated with less intracranial and fatal bleeding. cardiovascular death in patients with type 2 diabetes The 2019 American College of Cardiologz/American Heart mellitus and established heart failure with reduced Association atrial flbrillation guideline recommends DOACs ejection fraction. in preference to warfarin in DOAC eligible patients. Thus, there is no suggestion that switching to warlarin (Option D) Bibliography would improve outcomes in this patient. Dunlay SM, Givertz MM, Aguilar D, et al; American Heart Association Heart Offering no additional therapy (Option E) would be Failure and Transplantation Committee of the Council on Clinical Cardiologz. Type 2 diabetes mellitus and heart failure, a scientific state- inappropriate because early rhythm control is associated ment from the American Heart Association and Heart Failure Society of with improved clinical outcomes in patients such as this one. America. I Card Fail. 2019;25:584 619. IPMID: 31174952] doi:10.1016/j. cardfai1.2019.05.007 XEY POIilI . In patients with recently diagnosed atrial fibrillation Item 11 Answer: C and concomitant cardiovascular conditions, early Educational Objective: Manage atrial fibrillation with rhl.thm control (antiarrhyhmic drugs or ablation) early rhythm control. reduces the primary composite end point of cardio- vascular death, stroke, or hospitalization for heart Rhythm control (Option C) is the most appropriate treat failure or acute coronary syndrome compared with ment for this patient who presents with paroxysmal atrial usual care. flbrillation. This patient is reflective of those included in the

in patients with heart failure with or without diabetes. For EAST AFNET 4 randomized clinical trial, which evaluated a patients with diabetes, studies have shown a reduction in rhythm control strates/ versus usual care (typically includ cardiovascular events, including heart lailure-related mor ing rate control) in patients with a recent diagnosis (within tality and hospitalizations, with use of these agents. SGLI2 12 months) of atrial flbrillation and coexisting cardiovas- inhibitors (empagliflozin, canagliflozin, and dapagliflozin) cular conditions. The inclusion criteria were age older than seem to reduce the risk for heart failure hospitalization and 75 years or previous transient ischemic attack or stroke, or cardiovascular death by 1.9"/,' and death from any cause by two of the following: age older than 65 years, female sex, 2.3'7,, independent of glucose control. The mechanisms of heart failure, hypertension, diabetes mellitus, severe coro this reduction are unclear but are thought to be independent nary artery disease, chronic kidney disease, and left ventric of increased diuresis due to glucose excretion. The American ular hypertrophy. The trial demonstrated improved clinical Diabetes Association Standards of Medical Care in Diabetes. outcomes. including a reduction in the primary composite endorsed by the American College of Cardiologr, recom- end point of cardiovascular death, stroke, or hospitaliza mends initiating an SGLT2 inhibitor with proven cardiovas- tion for heart failure or acute coronary syndrome, among U} cular beneflt to reduce the risk for worsening heart failure patients randomly assigned to an early rhythm control o and cardiovascular death in patients with type 2 diabetes strates/, including asymptomatic patients. The intervention = included either antiarrhy'thmic drugs or catheter ablation, ut and established heart failure with reduced ejection fraction. q, Digoxin (Option A) reduces the risk for heart failure but importantly, it included aggressive concomitant medical EL hospitalization but does not reduce mortality. It is occasion therapy (e.g., oral anticoagulation when indicated, hyper- a.l ally used in patients r.r,ith heart failure symptoms refractory tension treatment) in both the intervention and the control to optimal therapy, but because of its associated toxiciry groups. Based on the trial results, this patient is mostly likely 4t (D digoxin is not recommended as routine therapy in most to beneflt from early rhythm control for atrial flbrillation. UI patients with heart failure. This patient is appropriately receiving stroke prevention Loop diuretics, such as furosemide (Option C), are the therapy with a direct oral anticoagulant (DOAC), and he has primary diuretic therapy for volume overload in heart failure had no recurrent stroke or signiflcant bleeding episodes on because of increased potency compared with other diuretics. the current therapy. Therefore, left atrial appendage occlu- However, this patient has no clinical evidence of volume sion (Option A) is not indicated. overload. and furosemide is not indicated. Among the common indications for permanent pace- Guidelines recommend the addition of isosorbide maker implantation (Option B) are symptomatic bradycar dinitrate-hydralazine (Option D) in Black patients who dia without reversible cause; permanent atrial flbrillation remain s),,rnptomatic on maximal doses of a p blocker; ACE with symptomatic bradycardia; alternating bundle branch inhibitor, angiotensin receptor blocker (ARB), or valsartan- block; and complete heart block, high-degree atrioventric sacubitril; and aldosterone antagonist. In patients who are ular (AV) block, or Mobitz type 2 second-degree AV block, intolerant of ACE inhibitor or ARB therapy, especially those irrespective of symptoms. This patient has no indications for with chronic kidney disease, isosorbide dinitrate hydralazine pacemaker implantation. may be considered as a therapeutic option. Oral anticoagulation in patients with atrial flbrillation can be accomplished with a vitamin K antagonist (warfarin) I(EY POIl{T or DOAC, such as rivaroxaban. Rivaroxaban is noninferior to o A sodium-glucose cotransporter 2 inhibitor is recom warfarin in the prevention of stroke or systemic embolism mended to reduce risk for worsening heart failure and and is associated with less intracranial and fatal bleeding. cardiovascular death in patients with type 2 diabetes The 2019 American College of Cardiologz/American Heart mellitus and established heart failure with reduced Association atrial flbrillation guideline recommends DOACs ejection fraction. in preference to warfarin in DOAC eligible patients. Thus, there is no suggestion that switching to warlarin (Option D) Bibliography would improve outcomes in this patient. Dunlay SM, Givertz MM, Aguilar D, et al; American Heart Association Heart Offering no additional therapy (Option E) would be Failure and Transplantation Committee of the Council on Clinical Cardiologz. Type 2 diabetes mellitus and heart failure, a scientific state- inappropriate because early rhythm control is associated ment from the American Heart Association and Heart Failure Society of with improved clinical outcomes in patients such as this one. America. I Card Fail. 2019;25:584 619. IPMID: 31174952] doi:10.1016/j. cardfai1.2019.05.007 XEY POIilI . In patients with recently diagnosed atrial fibrillation Item 11 Answer: C and concomitant cardiovascular conditions, early Educational Objective: Manage atrial fibrillation with rhl.thm control (antiarrhyhmic drugs or ablation) early rhythm control. reduces the primary composite end point of cardio- vascular death, stroke, or hospitalization for heart Rhythm control (Option C) is the most appropriate treat failure or acute coronary syndrome compared with ment for this patient who presents with paroxysmal atrial usual care. flbrillation. This patient is reflective of those included in the 160

Answers and Critiques Bibliography Bibliography Kirchhof B Camm AJ, Goette A, et al; EAST AFNET ,t Trial Investigators. Katz D, Gavin MC. Stable ischemic heart disease. Ann Intern Med. 2019;171: Early rhythm-control therapy in patients with atrial fibrillation. N Engl J ITC17 ITC32. IPMtD: 31382288] doi:10.7326lAITC2019O806O Med. 2020;383:1305 1316. [PMID: 328653751 doi:10.los6/NEJMoa20l9422

Bibliography Bibliography Kirchhof B Camm AJ, Goette A, et al; EAST AFNET ,t Trial Investigators. Katz D, Gavin MC. Stable ischemic heart disease. Ann Intern Med. 2019;171: Early rhythm-control therapy in patients with atrial fibrillation. N Engl J ITC17 ITC32. IPMtD: 31382288] doi:10.7326lAITC2019O806O Med. 2020;383:1305 1316. [PMID: 328653751 doi:10.los6/NEJMoa20l9422 Item 12 Ansurer: A Educational Objective: Treat stable angina pectoris in Item 13 Answer: C Educational Objective: Diagnose peripartum tr cardiomyopathy. an aspirin-intolerant patient. 'lhe most likely diagnosis is lteripartunt cardionryoprrtltl, Clopidogrel (Option A) is the most appropriate cardiopro (Option C). Peripartum clrdiomyoprrthl, is newly notecl tective medication for this patient. The patient's chest pain lcft vcntricular s1'stolic dysfunction n'ith onset in the. symptoms, which occur with exertion and subside with rest, trot.tths after delivery or toward thc end of pregnancf in are consistent with typical angina. Therefore, he has a high tt the absence of another identifiable ciruse. Paticnts usuirlly (l, pretest likelihood ofcoronary artery disease and is a candi- present u'ith feltures of heart failure. Trcltnrent u'itl.r ET date for secondary preventive therapy. All patients with sta- stndard medical therap),'. including B blockers. digoxin. ble ischemic heart disease should receive guideline directed (J hyclralazine, nitrates, ancl tliuretics, is appropriate. AOIi therapies consisting of risk factor modiflcation with regular inhibitors. xngiotelrsin receptor blockers. anrl alclostenrnc physical exercise, attention to diet, weight loss, and smoking =, rntagor.lists sl-toulcl be i.trtrided until ittter delive rt'becuusc .E cessation, as well as cardioprotective therapy to improve tt of teratogenicity. (l, prognosis and antianginal medication as needed to improve Pulrnonarr enrbolisnr (PIr) (Option A) nr:r1, occur post functional capacity. The Antithrombotic Trialists' Collabora vl = prrtunr. particularly in patierlts requiring prokrnged becl tion collaborative meta analysis of nearly 3000 patients with rest. Patierlts with l)1,) tiequently present with dysprrea. ilow stable ischemic heart disease found an association between cver, this patient's elevatect \renous prcssure. pnlmonary aspirin use and reduced risk for serious vascular events, c<rngestion. and global recluctior-r in lelt ver-rtricular function including a 46% decrease in the risk for unstable angina and suggest heart tailurc; in aclclition, thc nornral right herrt a 53% risk reduction in the need for coronary angioplasty. size ancl {irnctiorr noted by echocarcliography lrgue :rgainst Therefore, in the absence of contraindications, antiplatelet henroclvnirmicalll significlnt PIJ. therapy in the form of low dose aspirin (75 162 mg/d) is Thc patient's presentirtioll does trot sup;urrt a clilg indicated indeflnitely for secondary prevention to reduce rrosis of irscending irortic clissection (Option B). I'he risk the risk for myocardial infarction and cardiovascular death. firr aortic clissection is incrcased in tl.re peri itnd p<tst In patients who have an intolerance or allergz to aspirin, partur-lr pcriods. [)atients usttally ]r:tve sudclerr orlset chcst clopidogrel therapy is considered an acceptable alternative. irncl bacl< plin and often clescribe a tcuring cluality. Ph_vsi Aspirin desensitization is another approach. cill exalrinirtion of'ten denlorlstrates right Ief t dift'erentirtl This patient has experienced an adverse reaction to pulse ancl blood pressure. I'.cl.tocarcliography iu ascetrtlitrg aspirin. Aspirin desensitization can be performed safely aortic clissection usually dcnronstrates aortic tiilatiltiott. under medical supervision in patients who require initiation rrnd thc clissectior-t tlap rnrrv be visualized. Lctl ventric of aspirin (for example, those who require dual antiplatelet tular funclior.r is usualll' trrlnnal in petienls witlr aortic therapy after percutaneous coronary intervention). How clissect iou. ever, in a patient with aspirin allergr or sensitivity, lowering Spontirneous coronar)' rrtery clissection (Option D) is the aspirin dose (Option B) will not improve tolerance. the most comnlon cause ot'pregnarlcy associlted tnYoctlr Prasugrel (Option C) and ticagrelor (Option D) are newer, dial inlrrrction irncl riccurs ntost contrnol.rly during the filst more potent, and more costly antiplatelet agents with potential nrontl-r postpartnrn. Patients usually ltresent r,r'ith symptotrrs for increased bleeding events, and their use as monotherapy of chesl piiin. and nryocarcliitl ischentic changes ltre expectcci has not been studied in the context of secondary prevention orr the [i(](1. Regionirl wall nrotion abnormirlitics are iclen fbr patients with stable ischemic heart disease; they are not tified by echocirrctiography in patients lvitlt sllotttanctltts suggested for this indication in current guidelines. coronary ilrtery dissectioll.

Item 12 Ansurer: A Educational Objective: Treat stable angina pectoris in Item 13 Answer: C Educational Objective: Diagnose peripartum tr cardiomyopathy. an aspirin-intolerant patient. 'lhe most likely diagnosis is lteripartunt cardionryoprrtltl, Clopidogrel (Option A) is the most appropriate cardiopro (Option C). Peripartum clrdiomyoprrthl, is newly notecl tective medication for this patient. The patient's chest pain lcft vcntricular s1'stolic dysfunction n'ith onset in the. symptoms, which occur with exertion and subside with rest, trot.tths after delivery or toward thc end of pregnancf in are consistent with typical angina. Therefore, he has a high tt the absence of another identifiable ciruse. Paticnts usuirlly (l, pretest likelihood ofcoronary artery disease and is a candi- present u'ith feltures of heart failure. Trcltnrent u'itl.r ET date for secondary preventive therapy. All patients with sta- stndard medical therap),'. including B blockers. digoxin. ble ischemic heart disease should receive guideline directed (J hyclralazine, nitrates, ancl tliuretics, is appropriate. AOIi therapies consisting of risk factor modiflcation with regular inhibitors. xngiotelrsin receptor blockers. anrl alclostenrnc physical exercise, attention to diet, weight loss, and smoking =, rntagor.lists sl-toulcl be i.trtrided until ittter delive rt'becuusc .E cessation, as well as cardioprotective therapy to improve tt of teratogenicity. (l, prognosis and antianginal medication as needed to improve Pulrnonarr enrbolisnr (PIr) (Option A) nr:r1, occur post functional capacity. The Antithrombotic Trialists' Collabora vl = prrtunr. particularly in patierlts requiring prokrnged becl tion collaborative meta analysis of nearly 3000 patients with rest. Patierlts with l)1,) tiequently present with dysprrea. ilow stable ischemic heart disease found an association between cver, this patient's elevatect \renous prcssure. pnlmonary aspirin use and reduced risk for serious vascular events, c<rngestion. and global recluctior-r in lelt ver-rtricular function including a 46% decrease in the risk for unstable angina and suggest heart tailurc; in aclclition, thc nornral right herrt a 53% risk reduction in the need for coronary angioplasty. size ancl {irnctiorr noted by echocarcliography lrgue :rgainst Therefore, in the absence of contraindications, antiplatelet henroclvnirmicalll significlnt PIJ. therapy in the form of low dose aspirin (75 162 mg/d) is Thc patient's presentirtioll does trot sup;urrt a clilg indicated indeflnitely for secondary prevention to reduce rrosis of irscending irortic clissection (Option B). I'he risk the risk for myocardial infarction and cardiovascular death. firr aortic clissection is incrcased in tl.re peri itnd p<tst In patients who have an intolerance or allergz to aspirin, partur-lr pcriods. [)atients usttally ]r:tve sudclerr orlset chcst clopidogrel therapy is considered an acceptable alternative. irncl bacl< plin and often clescribe a tcuring cluality. Ph_vsi Aspirin desensitization is another approach. cill exalrinirtion of'ten denlorlstrates right Ief t dift'erentirtl This patient has experienced an adverse reaction to pulse ancl blood pressure. I'.cl.tocarcliography iu ascetrtlitrg aspirin. Aspirin desensitization can be performed safely aortic clissection usually dcnronstrates aortic tiilatiltiott. under medical supervision in patients who require initiation rrnd thc clissectior-t tlap rnrrv be visualized. Lctl ventric of aspirin (for example, those who require dual antiplatelet tular funclior.r is usualll' trrlnnal in petienls witlr aortic therapy after percutaneous coronary intervention). How clissect iou. ever, in a patient with aspirin allergr or sensitivity, lowering Spontirneous coronar)' rrtery clissection (Option D) is the aspirin dose (Option B) will not improve tolerance. the most comnlon cause ot'pregnarlcy associlted tnYoctlr Prasugrel (Option C) and ticagrelor (Option D) are newer, dial inlrrrction irncl riccurs ntost contrnol.rly during the filst more potent, and more costly antiplatelet agents with potential nrontl-r postpartnrn. Patients usually ltresent r,r'ith symptotrrs for increased bleeding events, and their use as monotherapy of chesl piiin. and nryocarcliitl ischentic changes ltre expectcci has not been studied in the context of secondary prevention orr the [i(](1. Regionirl wall nrotion abnormirlitics are iclen fbr patients with stable ischemic heart disease; they are not tified by echocirrctiography in patients lvitlt sllotttanctltts suggested for this indication in current guidelines. coronary ilrtery dissectioll. XEY POIl{TS I(EY POIl{T . All patients with stable ischemic heart disease should . Peripartum cardiomyopathy is left ventricular systolic receive guideline directed therapies consisting of life- dysfunction with onset toward the end of pregnancy style modification, cardioprotective therapy, and or in the months after delivery in the absence of antianginal medication. another identifiable cause; patients often present with o Patients with stable ischemic heart disease should features of heart failure.

XEY POIl{TS I(EY POIl{T . All patients with stable ischemic heart disease should . Peripartum cardiomyopathy is left ventricular systolic receive guideline directed therapies consisting of life- dysfunction with onset toward the end of pregnancy style modification, cardioprotective therapy, and or in the months after delivery in the absence of antianginal medication. another identifiable cause; patients often present with o Patients with stable ischemic heart disease should features of heart failure. receive antiplatelet therapy (low-dose aspirin or clo- pidogrel in aspirin-intolerant patients) for secondary Bibliography prevention of cardiovascular events. Douglass EJ, Blauwet LA. Peripartum cardiomyopathy. Cardiol Clin.2o21; 39:ll9 42. IPMID: 332228081 doi:10.1016/j.cc1.2020.09.008 161

Answers and Critiques Item 14 u,ith acute heart failurc in the setting of volume overload, tr Answer: C Educational Objective: Diagnose cardiac angiosarcoma. and he h.rs several signs of an increascd intrirvascular volume. ir.rcluding eler,ated central vetrous pressure and peripheral The most likel_v diagnosis is cardiac angiosarconta (Option C). eclema. h.r this setting, the initial IV dose of a diuretic should lhis rare rnalignant canliac tuntor often presellts u'ith symp be 1 to 2.5 times the patient's total daily oral dosei if the patient toms o{ clyspnca and chest pair.r. A cardiac angiosarcomrr is unresponsir,e to the initial IV dose. it should be increased by generally arises in the right hcirrt. most commonll'the right 50')1, to 100')i,. Adding a thiazicle diuretic may also be consid atrium. and tl-ris paticnt's finclings of a right atrial mass ered, but these agents are usually associated rvith an increased in'r'olving the lateral atrial uall u'ith tamponade and bloody incidence of l.rl ponatremia. pcricardial fluid are fypical. Metastasis to the iungs, lir,er, lnotropes, such as tnilrinone (OptionA), do not improve l1-rnphatic system. bone. and adrenal glands is cotnmotrll' outcolnes in pirtients admitted r,r,'ith acute decompensatcd present at the time of diagnosis. Pcricardiocentesis urith heart tailure or incrcase urine outpttt. Inotropes may be D cytologic examination o{'tl-re fluid is ollen negative ltrr malig considered in patients with low-output heart failure (lolt' UI nanc\,. and tissuc biopsy is frequer.rtly required tbr diaguosis. pulse pressure. cool extremities. presence ol S,) to improve Surgical resection and adjuvant chemotheralry or rircliother cardiac output but should n<tt be usecl in the routine therapy o = l^ apy should be considered. but sun'ival rates are lort even filr of patients adrnitted with heart failure. o, patients in whom surgery is t'easib1e. IV vasodilator therapy: such as nitroglycerin (Option B)' CL Atrial myxomas (Option A) occur most commonly' is occasionally addecl in patients hospitalized w'ith acute n u'ithin the iell atriurn and u'ith association to the intcr l.reart Iailure ancl might be considered for this patient. With atrial fossa, although they may present in ttther locations. reduction of systenric rascular resistance. stroke volume lrtr including the right atrillm. Thel' t1'picalll' cituse collstitu can oftcr.r be in.rproveci, $'ith resulting patient improve .D (a tional synlptonrs of fever, rvcight loss, and fatigue; embolic ment. l{owever, diuretic therapy is the principal treatment phenomena; or synlptoms related to obstructiot-t. Pericardiitl fbr patients rvith dccompensated l.reart failure and {luid e{fusion with tamponade r'r,ould be au exceptiouirlly rare overloaci. prc'sentltion of atrial myxoma. According to the 2019 American College of Cardiology The CT scan short's only a single, srnail pulmonarl expert consensus decision pathrt'a1,' otr risk assessment. nodule. All pulmor.rary rtodules har,e potential for associatecl lxanagement, and clir-rical trajectory of patients hospital- malignant risk. but giver.r this patient's nonstnoking status ized u'ith heart tailure. patients r,r'ith herrt failure with a and the nodulc's small size, it is unlikely trt be a prim;rry wet antl r,,,,ann profile who are receiving p blocker ther malignanc-v car,rsir-rg prolbund cardilc metastasis (Option B). irpy on admission should cttntintte the p blocker unless Papillnry flbroelastorna (Option D) usually occurs on blood pressure is lo',v. If hcart failure rernains refractory the surfhce ol the aortic and rnitral val'nes atld is cotntnol1ly to diuretics, the dose should be halved. Discontinuit.tg discor,ered in the eighth decade of life. Papillary fibroelas metoprolol (Option C) rright be appropriate if this patient toma typically does not cause symptoms but may be asso is resistant to high closes of lV diuretics: regardless. the ciated r,vith strtlke, trirnsient ischen.ric attack. al1d. rarel): best initial step for this patient nould be to increase the IV coronary embol iz.ation with inf arction. Ott cchocarcliogram. furosenride dose. these turnors oflen have a heterogencous globular shape or XIY POIilT a mobile liorrd like appearance. This patient's presentation is not characteristic of fibroelastoma. . For hospitalized patients with acute decompensated heart failure, the initial dose of an intravenous (lV) XEY POIXI diuretic should be 1 to 2.5 times the patient's total o Cardiac angiosarcomas are rare malignant cardiac daily oral dose; if the patient is unresponsive, the IV tumors that typically arise within the right atrium dose should be increased by 50% to 100%. and are commonly associated with sanguinous peri- cardial effusion. Bibliography Felker GM. Ellison DH, Mullens W, et al. Diuretic therapy for patients with Bibliography heart tailure: JACC state of the art revier.n J Am Coll Cardiol. 2020r 75:1178-1195. IPMID: 32164892] doi:10.1016ij.jacc.2019.12.059 Look Hong NJ, Pandalai PK, Hornick lL, et al. Cardiac angiosarcoma manage ment and outcomes: 20 year single institution experience. Ann Surg Oncol. 2012:19 :2707 I 5. [PM ID: 224767521 doi : 10. 12.15 I sl} 134 O12 - 2331 2 Item 16 Answer: C Educational Objective: Treat complicated type B aortic tr Item 15 tr Ed ucationa I Objective Answer: D : Treat acute decompensated dissection.

Item 14 u,ith acute heart failurc in the setting of volume overload, tr Answer: C Educational Objective: Diagnose cardiac angiosarcoma. and he h.rs several signs of an increascd intrirvascular volume. ir.rcluding eler,ated central vetrous pressure and peripheral The most likel_v diagnosis is cardiac angiosarconta (Option C). eclema. h.r this setting, the initial IV dose of a diuretic should lhis rare rnalignant canliac tuntor often presellts u'ith symp be 1 to 2.5 times the patient's total daily oral dosei if the patient toms o{ clyspnca and chest pair.r. A cardiac angiosarcomrr is unresponsir,e to the initial IV dose. it should be increased by generally arises in the right hcirrt. most commonll'the right 50')1, to 100')i,. Adding a thiazicle diuretic may also be consid atrium. and tl-ris paticnt's finclings of a right atrial mass ered, but these agents are usually associated rvith an increased in'r'olving the lateral atrial uall u'ith tamponade and bloody incidence of l.rl ponatremia. pcricardial fluid are fypical. Metastasis to the iungs, lir,er, lnotropes, such as tnilrinone (OptionA), do not improve l1-rnphatic system. bone. and adrenal glands is cotnmotrll' outcolnes in pirtients admitted r,r,'ith acute decompensatcd present at the time of diagnosis. Pcricardiocentesis urith heart tailure or incrcase urine outpttt. Inotropes may be D cytologic examination o{'tl-re fluid is ollen negative ltrr malig considered in patients with low-output heart failure (lolt' UI nanc\,. and tissuc biopsy is frequer.rtly required tbr diaguosis. pulse pressure. cool extremities. presence ol S,) to improve Surgical resection and adjuvant chemotheralry or rircliother cardiac output but should n<tt be usecl in the routine therapy o = l^ apy should be considered. but sun'ival rates are lort even filr of patients adrnitted with heart failure. o, patients in whom surgery is t'easib1e. IV vasodilator therapy: such as nitroglycerin (Option B)' CL Atrial myxomas (Option A) occur most commonly' is occasionally addecl in patients hospitalized w'ith acute n u'ithin the iell atriurn and u'ith association to the intcr l.reart Iailure ancl might be considered for this patient. With atrial fossa, although they may present in ttther locations. reduction of systenric rascular resistance. stroke volume lrtr including the right atrillm. Thel' t1'picalll' cituse collstitu can oftcr.r be in.rproveci, $'ith resulting patient improve .D (a tional synlptonrs of fever, rvcight loss, and fatigue; embolic ment. l{owever, diuretic therapy is the principal treatment phenomena; or synlptoms related to obstructiot-t. Pericardiitl fbr patients rvith dccompensated l.reart failure and {luid e{fusion with tamponade r'r,ould be au exceptiouirlly rare overloaci. prc'sentltion of atrial myxoma. According to the 2019 American College of Cardiology The CT scan short's only a single, srnail pulmonarl expert consensus decision pathrt'a1,' otr risk assessment. nodule. All pulmor.rary rtodules har,e potential for associatecl lxanagement, and clir-rical trajectory of patients hospital- malignant risk. but giver.r this patient's nonstnoking status ized u'ith heart tailure. patients r,r'ith herrt failure with a and the nodulc's small size, it is unlikely trt be a prim;rry wet antl r,,,,ann profile who are receiving p blocker ther malignanc-v car,rsir-rg prolbund cardilc metastasis (Option B). irpy on admission should cttntintte the p blocker unless Papillnry flbroelastorna (Option D) usually occurs on blood pressure is lo',v. If hcart failure rernains refractory the surfhce ol the aortic and rnitral val'nes atld is cotntnol1ly to diuretics, the dose should be halved. Discontinuit.tg discor,ered in the eighth decade of life. Papillary fibroelas metoprolol (Option C) rright be appropriate if this patient toma typically does not cause symptoms but may be asso is resistant to high closes of lV diuretics: regardless. the ciated r,vith strtlke, trirnsient ischen.ric attack. al1d. rarel): best initial step for this patient nould be to increase the IV coronary embol iz.ation with inf arction. Ott cchocarcliogram. furosenride dose. these turnors oflen have a heterogencous globular shape or XIY POIilT a mobile liorrd like appearance. This patient's presentation is not characteristic of fibroelastoma. . For hospitalized patients with acute decompensated heart failure, the initial dose of an intravenous (lV) XEY POIXI diuretic should be 1 to 2.5 times the patient's total o Cardiac angiosarcomas are rare malignant cardiac daily oral dose; if the patient is unresponsive, the IV tumors that typically arise within the right atrium dose should be increased by 50% to 100%. and are commonly associated with sanguinous peri- cardial effusion. Bibliography Felker GM. Ellison DH, Mullens W, et al. Diuretic therapy for patients with Bibliography heart tailure: JACC state of the art revier.n J Am Coll Cardiol. 2020r 75:1178-1195. IPMID: 32164892] doi:10.1016ij.jacc.2019.12.059 Look Hong NJ, Pandalai PK, Hornick lL, et al. Cardiac angiosarcoma manage ment and outcomes: 20 year single institution experience. Ann Surg Oncol. 2012:19 :2707 I 5. [PM ID: 224767521 doi : 10. 12.15 I sl} 134 O12 - 2331 2 Item 16 Answer: C Educational Objective: Treat complicated type B aortic tr Item 15 tr Ed ucationa I Objective Answer: D : Treat acute decompensated dissection. The most appropriate management fbr this patient is elner heart failure with optimal diuretic dosing. gency endovascular repair of the descending aorta (Option C). -lhe '11'pe B aortic clissection involves the descendir.rg thoracic most appn)priate treatment is to increase the dose of intrl venous (lV) lurosemide (Option D). This patient pr-esentcd aorta. typically just distal to the left subclavian artery, and

The most appropriate management fbr this patient is elner heart failure with optimal diuretic dosing. gency endovascular repair of the descending aorta (Option C). -lhe '11'pe B aortic clissection involves the descendir.rg thoracic most appn)priate treatment is to increase the dose of intrl venous (lV) lurosemide (Option D). This patient pr-esentcd aorta. typically just distal to the left subclavian artery, and 162

Answers and Critiques tr CONT. may extend into the abdominal aorta and lower extremity arteries; it does not involve the ascending aorta. Patients with uncomplicatcd type B aortic syndromes nray be treated failure or exertional limitations. No additional evaluation is necessary because this patient's PVCs are asymptomatic and not accompanied by other signs or symptoms of cardiopul- u,ith medical therapy initiallyr hortever, aortic repair is monary disease. Ambulatory ECG monitoring lor assess indicated when type B aortic dissection is complicated by ment of PVC burden may be performed, but in an asymp- limb or end organ ischemia. persistent severe hypertension, tomatic patient, results are unlikely to affect management. persistent pain, irropagation of the dissection, enlargement Asymptomatic PVCs, even at higher burden, are common in of the descending aorta, and/'or rupture of the aorta. This the general population and may vary dramatically through patient has propagation ol a type B aortic dissection, as out the day and/or from day to day They may be influenced evidenced by new onset abdominal pain (representing mes by stress, alcohol or cafleine intake, sleep disturbances, and enteric ischemia) ar.rd the developmer.rt of limb ischemia. comorbid conditions, such as thyroid disorders or anemia. Patients with type B aortic dissection sl.rould be preferen ln the absence of a significant comorbid condition and/or tially managed u,ith thoracic endovascular aortic repair. symptoms, reassurance is appropriate. Among patients with a (l, lt,ith the primary goal ol sealing both proximal and distal a consistently very high burden of PVCs (>15'2, 20'X,) that are Et- segments of dissection. Surgicai repair of the descending asymptomatic, periodic echocardiographic monitoring for aorta is associated with high morbidity and mortality. PVC induced cardiomyopathy may be considered, but there !, Enalaprilat (Option A) is an intravenous ACE inhibitor is no consensus on this surveillance. E that is useful mainly in hyperlensi'"e emergencies associated Cardiac magnetic resonance imaging (Option A) of the IE with high plasma renin activity, such as sclenrdernta renal cri chest is recommended for cardiac sarcoidosis, which may vt (l, sis. It is a difficult drug to titrate, with slor,v onset of action and present with ventricular arrhythmias. Howevet this patient unpredictable blood pressure response. 'lhis patient needs has no flndings that suggest sarcoidosis (such as pulmonary vl = urgent repair of the aorta. not the additior.r oi enalaprilat. disease or ECG flndings demonstrating conduction disease The acute management of aortic dissection focuses [abnormal PR, QRS, QT intervals]). Thus, it would be prema on reducing blood pressure and shear stress. Rapid,acting ture and of low yield to screen for cardiac sarcoidosis in this p blockers, such as esmolol. are initiatec'l kr reduce heafi rate asymptomatic patient. to less than 60,rrnin; alter the acute phase of treatment, an This patient has no exertional symptoms or signs con oral p blocker such as rneloprolol mzry replace intravenous sistent with coronary ischemia. Exercise ECG (Option B) is esmolol (Option D). If blood pressure rc'mains elevated, not needed, and intervention on any positive findings is of intravenous nitroprusside (Option B) is usccl to lower the debatable net clinical beneflt. blood pressure to thc lonrest tolerable limit lvithout impair In the absence of high-risk features (syncope, family ing kidney firnction or cerebral perf'usion, typically between history of premature sudden cardiac death, structural heart 100 to 120 nrm lJg. However, this patient has clear evidence disease), medical therapy is often unnecessary. However, ol'complicated type B aortic dissection, ancl urgenl repair of PVCs require treatment when symptoms are bothersome or the aorta is indicated. frequent (>10% of all beats or 10,000 PVCs per day). First line therapy for these patients is a B-blocker, such as metop TEV POIilIS rolol (Option C), or calcium channel blocker. o Complicated type B aortic dissection is characterized by limb or end-organ ischemia, persistent severe f,EY POIXT hypertension, persistent pain, propagation ofthe dis- . For patients with asymptomatic premature ventricu- section, enlargement ofthe descending aorta, and/or lar contractions, reassurance is appropriate; medical rupture of the aorta. therapy is unnecessary in the absence of high-risk . Complicated type B aortic dissection is an indication features (syncope, family history of premature sudden

tr CONT. may extend into the abdominal aorta and lower extremity arteries; it does not involve the ascending aorta. Patients with uncomplicatcd type B aortic syndromes nray be treated failure or exertional limitations. No additional evaluation is necessary because this patient's PVCs are asymptomatic and not accompanied by other signs or symptoms of cardiopul- u,ith medical therapy initiallyr hortever, aortic repair is monary disease. Ambulatory ECG monitoring lor assess indicated when type B aortic dissection is complicated by ment of PVC burden may be performed, but in an asymp- limb or end organ ischemia. persistent severe hypertension, tomatic patient, results are unlikely to affect management. persistent pain, irropagation of the dissection, enlargement Asymptomatic PVCs, even at higher burden, are common in of the descending aorta, and/'or rupture of the aorta. This the general population and may vary dramatically through patient has propagation ol a type B aortic dissection, as out the day and/or from day to day They may be influenced evidenced by new onset abdominal pain (representing mes by stress, alcohol or cafleine intake, sleep disturbances, and enteric ischemia) ar.rd the developmer.rt of limb ischemia. comorbid conditions, such as thyroid disorders or anemia. Patients with type B aortic dissection sl.rould be preferen ln the absence of a significant comorbid condition and/or tially managed u,ith thoracic endovascular aortic repair. symptoms, reassurance is appropriate. Among patients with a (l, lt,ith the primary goal ol sealing both proximal and distal a consistently very high burden of PVCs (>15'2, 20'X,) that are Et- segments of dissection. Surgicai repair of the descending asymptomatic, periodic echocardiographic monitoring for aorta is associated with high morbidity and mortality. PVC induced cardiomyopathy may be considered, but there !, Enalaprilat (Option A) is an intravenous ACE inhibitor is no consensus on this surveillance. E that is useful mainly in hyperlensi'"e emergencies associated Cardiac magnetic resonance imaging (Option A) of the IE with high plasma renin activity, such as sclenrdernta renal cri chest is recommended for cardiac sarcoidosis, which may vt (l, sis. It is a difficult drug to titrate, with slor,v onset of action and present with ventricular arrhythmias. Howevet this patient unpredictable blood pressure response. 'lhis patient needs has no flndings that suggest sarcoidosis (such as pulmonary vl = urgent repair of the aorta. not the additior.r oi enalaprilat. disease or ECG flndings demonstrating conduction disease The acute management of aortic dissection focuses [abnormal PR, QRS, QT intervals]). Thus, it would be prema on reducing blood pressure and shear stress. Rapid,acting ture and of low yield to screen for cardiac sarcoidosis in this p blockers, such as esmolol. are initiatec'l kr reduce heafi rate asymptomatic patient. to less than 60,rrnin; alter the acute phase of treatment, an This patient has no exertional symptoms or signs con oral p blocker such as rneloprolol mzry replace intravenous sistent with coronary ischemia. Exercise ECG (Option B) is esmolol (Option D). If blood pressure rc'mains elevated, not needed, and intervention on any positive findings is of intravenous nitroprusside (Option B) is usccl to lower the debatable net clinical beneflt. blood pressure to thc lonrest tolerable limit lvithout impair In the absence of high-risk features (syncope, family ing kidney firnction or cerebral perf'usion, typically between history of premature sudden cardiac death, structural heart 100 to 120 nrm lJg. However, this patient has clear evidence disease), medical therapy is often unnecessary. However, ol'complicated type B aortic dissection, ancl urgenl repair of PVCs require treatment when symptoms are bothersome or the aorta is indicated. frequent (>10% of all beats or 10,000 PVCs per day). First line therapy for these patients is a B-blocker, such as metop TEV POIilIS rolol (Option C), or calcium channel blocker. o Complicated type B aortic dissection is characterized by limb or end-organ ischemia, persistent severe f,EY POIXT hypertension, persistent pain, propagation ofthe dis- . For patients with asymptomatic premature ventricu- section, enlargement ofthe descending aorta, and/or lar contractions, reassurance is appropriate; medical rupture of the aorta. therapy is unnecessary in the absence of high-risk . Complicated type B aortic dissection is an indication features (syncope, family history of premature sudden for immediate vascular intervention. cardiac death, structural heart disease).

tr CONT. may extend into the abdominal aorta and lower extremity arteries; it does not involve the ascending aorta. Patients with uncomplicatcd type B aortic syndromes nray be treated failure or exertional limitations. No additional evaluation is necessary because this patient's PVCs are asymptomatic and not accompanied by other signs or symptoms of cardiopul- u,ith medical therapy initiallyr hortever, aortic repair is monary disease. Ambulatory ECG monitoring lor assess indicated when type B aortic dissection is complicated by ment of PVC burden may be performed, but in an asymp- limb or end organ ischemia. persistent severe hypertension, tomatic patient, results are unlikely to affect management. persistent pain, irropagation of the dissection, enlargement Asymptomatic PVCs, even at higher burden, are common in of the descending aorta, and/'or rupture of the aorta. This the general population and may vary dramatically through patient has propagation ol a type B aortic dissection, as out the day and/or from day to day They may be influenced evidenced by new onset abdominal pain (representing mes by stress, alcohol or cafleine intake, sleep disturbances, and enteric ischemia) ar.rd the developmer.rt of limb ischemia. comorbid conditions, such as thyroid disorders or anemia. Patients with type B aortic dissection sl.rould be preferen ln the absence of a significant comorbid condition and/or tially managed u,ith thoracic endovascular aortic repair. symptoms, reassurance is appropriate. Among patients with a (l, lt,ith the primary goal ol sealing both proximal and distal a consistently very high burden of PVCs (>15'2, 20'X,) that are Et- segments of dissection. Surgicai repair of the descending asymptomatic, periodic echocardiographic monitoring for aorta is associated with high morbidity and mortality. PVC induced cardiomyopathy may be considered, but there !, Enalaprilat (Option A) is an intravenous ACE inhibitor is no consensus on this surveillance. E that is useful mainly in hyperlensi'"e emergencies associated Cardiac magnetic resonance imaging (Option A) of the IE with high plasma renin activity, such as sclenrdernta renal cri chest is recommended for cardiac sarcoidosis, which may vt (l, sis. It is a difficult drug to titrate, with slor,v onset of action and present with ventricular arrhythmias. Howevet this patient unpredictable blood pressure response. 'lhis patient needs has no flndings that suggest sarcoidosis (such as pulmonary vl = urgent repair of the aorta. not the additior.r oi enalaprilat. disease or ECG flndings demonstrating conduction disease The acute management of aortic dissection focuses [abnormal PR, QRS, QT intervals]). Thus, it would be prema on reducing blood pressure and shear stress. Rapid,acting ture and of low yield to screen for cardiac sarcoidosis in this p blockers, such as esmolol. are initiatec'l kr reduce heafi rate asymptomatic patient. to less than 60,rrnin; alter the acute phase of treatment, an This patient has no exertional symptoms or signs con oral p blocker such as rneloprolol mzry replace intravenous sistent with coronary ischemia. Exercise ECG (Option B) is esmolol (Option D). If blood pressure rc'mains elevated, not needed, and intervention on any positive findings is of intravenous nitroprusside (Option B) is usccl to lower the debatable net clinical beneflt. blood pressure to thc lonrest tolerable limit lvithout impair In the absence of high-risk features (syncope, family ing kidney firnction or cerebral perf'usion, typically between history of premature sudden cardiac death, structural heart 100 to 120 nrm lJg. However, this patient has clear evidence disease), medical therapy is often unnecessary. However, ol'complicated type B aortic dissection, ancl urgenl repair of PVCs require treatment when symptoms are bothersome or the aorta is indicated. frequent (>10% of all beats or 10,000 PVCs per day). First line therapy for these patients is a B-blocker, such as metop TEV POIilIS rolol (Option C), or calcium channel blocker. o Complicated type B aortic dissection is characterized by limb or end-organ ischemia, persistent severe f,EY POIXT hypertension, persistent pain, propagation ofthe dis- . For patients with asymptomatic premature ventricu- section, enlargement ofthe descending aorta, and/or lar contractions, reassurance is appropriate; medical rupture of the aorta. therapy is unnecessary in the absence of high-risk . Complicated type B aortic dissection is an indication features (syncope, family history of premature sudden for immediate vascular intervention. cardiac death, structural heart disease). Bibliography Bibliography Al Khatib SM, Stevenson WG, Ackerman MJ. et al. 2017 AIIA/ACC/HRS tsouli M, Patterson BO, Loundou AD, et al. Endovascular versus open repair guideline for management of patients with ventricular rrrhythmias and for chronic type B dissection treatment: a meta analysis. Ann Thorac the prevention ofsudden cardiac death: a report of the American College Surg. 2019;107:1.559 1 570. [PMID: 30481.51 6l doi : 10. i016/j.athoracsur. ofCardiologr/American I Ieart Association Task Force on Clinical Practice 201 8_lo.o45 Cuidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2018;72:e91 e220. f PMID: 290972961 doi: 0. 01 6 /j.iacc.2017.10.054 1 1

Bibliography Bibliography Al Khatib SM, Stevenson WG, Ackerman MJ. et al. 2017 AIIA/ACC/HRS tsouli M, Patterson BO, Loundou AD, et al. Endovascular versus open repair guideline for management of patients with ventricular rrrhythmias and for chronic type B dissection treatment: a meta analysis. Ann Thorac the prevention ofsudden cardiac death: a report of the American College Surg. 2019;107:1.559 1 570. [PMID: 30481.51 6l doi : 10. i016/j.athoracsur. ofCardiologr/American I Ieart Association Task Force on Clinical Practice 201 8_lo.o45 Cuidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2018;72:e91 e220. f PMID: 290972961 doi: 0. 01 6 /j.iacc.2017.10.054 1 1 Item 17 Answer: D Educational Objective: Manage asymptomatic prema- Item 18 Answer: C ture ventricular contractions. Educational Objective: Evaluate possible infective endocarditis with transesophageal echocardiography. Reassurance (Option D) is the most appropriate management for this patient with asymptomatic premature ventricular The most appropriate management is tr:rnsesophageal contractions (PVCs). He has no signs or symptoms of heart echocardiography (TEE) (Option C). The patient's history 163

Answers and Critiques tr CONT. of intermittent f'evers and dyspnea is concerning lbr infec tive endocarditis (lE). possibly due to dir,erticulitis relatcd episodes of transient bacterernia. Ol note. an1-onc with disease (ASCVD) (Option C). Cardiovascular risk scores can be used to assess a patient's future risk for major cardiovascu- lar events and to identi$r preventive interventions. The Amer- a bioprosthetic valve is at high risk fbr endocarditis with ican College of Cardiologr (ACC)/American Heart Association any significant episode of bacteremia. This patient has a (AHA) Pooled Cohort Equations can be used to calculate risk. bioprosthetic valve. symptoms of inf'ection, and a possible The ACC/AHA guidelines recommend that adults aged 40 to source of bacteremia. According to current guidelines. in 75 years without diabetes mellitus and with an LDL cho- patients'uvith suspected IE. transthoracic echocardiographl' lesterol level of 70 to 189 mg/dl (1.81 4.89 mmol/L) should ('l"lE) is recommended to idcntify vegetations. character undergo risk assessment with the Pooled Cohort Equations ize the hemodynarnic scverity ol valvular lesior.rs, assess to classiff 1o-year risk as low (<5%), borderline (5'2, to <7.5'1,), ventricular function and pulnronary pressures, and cletect intermediate (>7.5'7, to <2o'/,), or high (>20'1,). All current complications. In all patients witl-r knor,r,n or suspected IE ASCVD primary prevention guidelines recommend calcula and nondiagnostic TTE results, or il complications have tion ofthe 1o-year ASCVD risk. vl developed or are clinically suspected or if intracardiac According to the ACC/AHA guidelines, high intensity .D device leads are present, TFIFI is recommended. statin therapy (Option A) is indicated for primary preven- = vt Cardiac CT (Option A) is less:rccurate than TTE ancl TEE tion in patients with an LDL cholesterol level of 190 mg/dl o, fbr iclentifying t alvular vegetation iind valvular perfbrations. (4.92 mmollL) or higher and those with diabetes and CL However, in patients in rt'hom the anatomy cannot be clearll' multiple ASCVD risk factors. This patient meets neither a.| clelineated by echocardiographl, in the setting of'suspected criterion. High-intensity statin therapy would also be parirvalvular ir-rfections. PE'l Cf imaging is reasonable and indicated for patients with an LDL cholesterol level of lt superior to cardiac CT alone. This patient has no indicatlon 7O mgldL to 189 mg/dl (1.81-4.89 mmol/L) and a 10-year (D tl fbr cardiac CT. risk of20% or greater. This patient's calculated 10-year risk Although cardiac magnctic resonance imaging (Option B) is 0.4%. All current ASCVD primary prevention guidelines is useful in the diagnosis of'many conditions, it is not the agree that this patient does not require high intensity appropriate or gold standarcl test lbr diagnosing tlJ. statin therapy. ln patients with suspectecl IE. TTE is recornrnended For primary prevention of ASCVD, the ACC/AHA to identify vegetations, charlcterize the hernocll namic cholesterol guideline recommends ezetimibe (Option B) in severity of valvular lcsions, assess ventricular function ancl patients with an initial LDL cholesterol level of 190 mg/dl puln.ronary pressures. and cletect complications. Given the (+.gz mmol/L) or higher who do not achieve a 50'2, reduction suspicion fbr prosthetic virlve endocarditis. a potentially in LDL cholesterol while taking maximally tolerated statin letl.ral condition, not pursuing firrther testing (Option D) is therapy or who have an LDL cholesterol level of 100 mg/dl inappropriate. (z.sq mmol/L) or higher. All guidelines are in consensus that this patient would not require combination cholesterol KEY POIXTS lowering therapy. . In patients with suspected infective endocarditis, Fasting and nonfasting total cholesterol and HDL transthoracic echocardiography is recommended as cholesterol levels have fairly similar prognostic value and the initial imaging choice in most clinical situations. association with cardiovascular outcomes. Fasting samples o In all patients with known or suspected infective are preferred in adults with an initial nonfasting triglyceride endocarditis and nondiagnostic transthoracic echo- level of 400 mgldL (4.s2 mmol/L) or higher or with a fam cardiographic results, or if complications have devel- ily history of premature ASCVD or genetic hyperlipidemia. oped or are clinically suspected or if intracardiac A fasting lipid profile (Option D) is unnecessary for this patient. device leads are present, transesophageal echocardi- ography is recommended. XEY POIXIS o Cardiovascular risk scores can be used to assess a Bibliography patient's future risk for major cardiovascular events Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: a report of the and to identify preventive interventions. American College of Cardiologz/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2O21;143:e72 . The American College of Cardiologr/American Heart e227. [PMID: 333321501 doi:10.1161/CIR.0000000000000923 Association Pooled Cohort Equations are commonly used to calculate the 10-year risk for atherosclerotic cardiovascular disease. Item 19 Answer: C : Evaluate lo-year atherosclerotic Ed u cati ona I O bjective Bibliography cardiovascular disease risk. Amett DK, Blumenthal RS, Alberr MA, er al. 2019 ACClAHA guideline on the primary prevention of cardiovascular disease: executive summary: a report of the American College of Cardiologz/American [{eart Association The most appropriate next step in management is to calculate Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2019: this patient's 1O-year risk for atherosclerotic cardiovascular 74:7376-1414. IPMID: 30894319J doi:10.1016/j.jacc.2019.03.009

tr CONT. of intermittent f'evers and dyspnea is concerning lbr infec tive endocarditis (lE). possibly due to dir,erticulitis relatcd episodes of transient bacterernia. Ol note. an1-onc with disease (ASCVD) (Option C). Cardiovascular risk scores can be used to assess a patient's future risk for major cardiovascu- lar events and to identi$r preventive interventions. The Amer- a bioprosthetic valve is at high risk fbr endocarditis with ican College of Cardiologr (ACC)/American Heart Association any significant episode of bacteremia. This patient has a (AHA) Pooled Cohort Equations can be used to calculate risk. bioprosthetic valve. symptoms of inf'ection, and a possible The ACC/AHA guidelines recommend that adults aged 40 to source of bacteremia. According to current guidelines. in 75 years without diabetes mellitus and with an LDL cho- patients'uvith suspected IE. transthoracic echocardiographl' lesterol level of 70 to 189 mg/dl (1.81 4.89 mmol/L) should ('l"lE) is recommended to idcntify vegetations. character undergo risk assessment with the Pooled Cohort Equations ize the hemodynarnic scverity ol valvular lesior.rs, assess to classiff 1o-year risk as low (<5%), borderline (5'2, to <7.5'1,), ventricular function and pulnronary pressures, and cletect intermediate (>7.5'7, to <2o'/,), or high (>20'1,). All current complications. In all patients witl-r knor,r,n or suspected IE ASCVD primary prevention guidelines recommend calcula and nondiagnostic TTE results, or il complications have tion ofthe 1o-year ASCVD risk. vl developed or are clinically suspected or if intracardiac According to the ACC/AHA guidelines, high intensity .D device leads are present, TFIFI is recommended. statin therapy (Option A) is indicated for primary preven- = vt Cardiac CT (Option A) is less:rccurate than TTE ancl TEE tion in patients with an LDL cholesterol level of 190 mg/dl o, fbr iclentifying t alvular vegetation iind valvular perfbrations. (4.92 mmollL) or higher and those with diabetes and CL However, in patients in rt'hom the anatomy cannot be clearll' multiple ASCVD risk factors. This patient meets neither a.| clelineated by echocardiographl, in the setting of'suspected criterion. High-intensity statin therapy would also be parirvalvular ir-rfections. PE'l Cf imaging is reasonable and indicated for patients with an LDL cholesterol level of lt superior to cardiac CT alone. This patient has no indicatlon 7O mgldL to 189 mg/dl (1.81-4.89 mmol/L) and a 10-year (D tl fbr cardiac CT. risk of20% or greater. This patient's calculated 10-year risk Although cardiac magnctic resonance imaging (Option B) is 0.4%. All current ASCVD primary prevention guidelines is useful in the diagnosis of'many conditions, it is not the agree that this patient does not require high intensity appropriate or gold standarcl test lbr diagnosing tlJ. statin therapy. ln patients with suspectecl IE. TTE is recornrnended For primary prevention of ASCVD, the ACC/AHA to identify vegetations, charlcterize the hernocll namic cholesterol guideline recommends ezetimibe (Option B) in severity of valvular lcsions, assess ventricular function ancl patients with an initial LDL cholesterol level of 190 mg/dl puln.ronary pressures. and cletect complications. Given the (+.gz mmol/L) or higher who do not achieve a 50'2, reduction suspicion fbr prosthetic virlve endocarditis. a potentially in LDL cholesterol while taking maximally tolerated statin letl.ral condition, not pursuing firrther testing (Option D) is therapy or who have an LDL cholesterol level of 100 mg/dl inappropriate. (z.sq mmol/L) or higher. All guidelines are in consensus that this patient would not require combination cholesterol KEY POIXTS lowering therapy. . In patients with suspected infective endocarditis, Fasting and nonfasting total cholesterol and HDL transthoracic echocardiography is recommended as cholesterol levels have fairly similar prognostic value and the initial imaging choice in most clinical situations. association with cardiovascular outcomes. Fasting samples o In all patients with known or suspected infective are preferred in adults with an initial nonfasting triglyceride endocarditis and nondiagnostic transthoracic echo- level of 400 mgldL (4.s2 mmol/L) or higher or with a fam cardiographic results, or if complications have devel- ily history of premature ASCVD or genetic hyperlipidemia. oped or are clinically suspected or if intracardiac A fasting lipid profile (Option D) is unnecessary for this patient. device leads are present, transesophageal echocardi- ography is recommended. XEY POIXIS o Cardiovascular risk scores can be used to assess a Bibliography patient's future risk for major cardiovascular events Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: a report of the and to identify preventive interventions. American College of Cardiologz/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2O21;143:e72 . The American College of Cardiologr/American Heart e227. [PMID: 333321501 doi:10.1161/CIR.0000000000000923 Association Pooled Cohort Equations are commonly used to calculate the 10-year risk for atherosclerotic cardiovascular disease. Item 19 Answer: C : Evaluate lo-year atherosclerotic Ed u cati ona I O bjective Bibliography cardiovascular disease risk. Amett DK, Blumenthal RS, Alberr MA, er al. 2019 ACClAHA guideline on the primary prevention of cardiovascular disease: executive summary: a report of the American College of Cardiologz/American [{eart Association The most appropriate next step in management is to calculate Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2019: this patient's 1O-year risk for atherosclerotic cardiovascular 74:7376-1414. IPMID: 30894319J doi:10.1016/j.jacc.2019.03.009 164

Answers and Critiques tr Item 20 Answer: A Educational Objective: Treat non ST-elevation acute l(tV P0lXTl (antinued) . Early loading with either clopidogrel or ticagrelor in coronary syndrome in a low-risk patient. addition to aspirin is recommended in patients with Ckrpidogrcl (Option A) is the most appropriate additionat acute coronary syndrome regardless ofeither an early nlxnagement titr this patieltt with proltable unstable angina. invasive strates/ or ischemia-guided strategr. a lirrnr clf non ST-elevati<;n acutc coroltary s_vnclrome (NS'lll ACS). F.:rrl1, clopidogrel loacling has been recom Bibliography mencled in lrirtients r,l,ith ACS regarclless of reperlr-rsion or Anderson JL, Morrow DA. Acute myocardial infarction. N Engl J Med. 2017 May 25;376:2053 64. IPMID: 28538121] doi: 10.1056/NEJMral606915 revascularization strategy. In patients prcsenting with signs and symptor.ns suggestive <tf NS'I'E ACS, risk assesstnent is indicated to select the trcatment stratct+,. Severirl risk cri Item 21 Answer: D tcria and scorcs are available. 'lhe 'l'lN4l risk score includes UI Educational Objective: Reduce cardiovascular risk in a et scvcn indepencler.rt predictors fbr cieath, nonfatal ntyocar clial infarction. or ischenria requiring revascularization at patient with peripheral artery disease with very low-dose ET

tr Item 20 Answer: A Educational Objective: Treat non ST-elevation acute l(tV P0lXTl (antinued) . Early loading with either clopidogrel or ticagrelor in coronary syndrome in a low-risk patient. addition to aspirin is recommended in patients with Ckrpidogrcl (Option A) is the most appropriate additionat acute coronary syndrome regardless ofeither an early nlxnagement titr this patieltt with proltable unstable angina. invasive strates/ or ischemia-guided strategr. a lirrnr clf non ST-elevati<;n acutc coroltary s_vnclrome (NS'lll ACS). F.:rrl1, clopidogrel loacling has been recom Bibliography mencled in lrirtients r,l,ith ACS regarclless of reperlr-rsion or Anderson JL, Morrow DA. Acute myocardial infarction. N Engl J Med. 2017 May 25;376:2053 64. IPMID: 28538121] doi: 10.1056/NEJMral606915 revascularization strategy. In patients prcsenting with signs and symptor.ns suggestive <tf NS'I'E ACS, risk assesstnent is indicated to select the trcatment stratct+,. Severirl risk cri Item 21 Answer: D tcria and scorcs are available. 'lhe 'l'lN4l risk score includes UI Educational Objective: Reduce cardiovascular risk in a et scvcn indepencler.rt predictors fbr cieath, nonfatal ntyocar clial infarction. or ischenria requiring revascularization at patient with peripheral artery disease with very low-dose ET 1.1 ctays. r,r,ith I poir.rt assigned fbr each ol these preclictors: rivaroxaban therapy. lr, agc 6.5 years or older, three rlr lnore coronaly artery disease .E, The most appropriate treatment to reduce cardiovascular (CAI)) risk facturrs (cholestcrol, lamily hiskiry hypcrtcnsion, risk in this patient is to initiate very low-dose rivaroxaban .E cliabctes mellilus. smoking). pr-eviously documented CAI) (Option D). In a randomized trial, the addition of very low- vt (irrrgiographic stenosis >50'l;,). aspiriu use in the past 7 days. {, dose rivaroxaban (2.5 mg twice daily) to aspirin (81 mg daily) tu() or lrorc ischemic episocles in thc ptst 2.1 l.rours. S'i' seg, was shown to reduce the occurrence ofcardiovascular death. t = nrent deviation on ECC. and elevatccl cardiac biomarkers myocardial infarction, or stroke in patients with peripheral (crcltine kinase MB or tropollin).'lhis pirtient presellts \ rith artery disease (PAD). The absolute risk reduction, when com- lbatures corlsisterlt u,ith possible ACS but has a'l'lMl sc<lre ol pared with aspirin alone, was 2"1, in 7470 patients enrolled I uncl is clinicalll stable. [.ow risk p:rticnts undergo noninr,a with either lower extremity PAD or carotid stenosis. Major sivc stress testing with lcf t vcntricular tirnction ilssesslrent bleeding, primarily gastrointestinal bleeding, was increased belirre hospitll clischarge. Clrdiac cathctcrization is reserved by 1% in patients assigned to aspirin plus rivaroxaban. Thus, firr patier.rts with active or iutermittent ischemia, including low dose rivaroxaban should be avoided in patients with PAD those lr,ith arrgina despite nredical therirpl, or evi(lence ot' who have a higher risk for bleeding. It should be noted that ischernia on stress testing, and patients iit very higl.r clinical use of rivaroxaban in patients with PAD is at odds with the risk based on risk score. 'll.rc ischernia guicled approach is 2016 American Heart Association/American College of Cardi- rtppropriate lirr lur,r risk patients (TIMI score <2). pirrticu ologz (AHA/ACC) PAD guideline, which recommends against hrll lou' risk u,ornen. r,rlto mlry have r,r,orse outconles with anticoagulation to reduce the risk for cardiovascular events an carly invasive appro:rch. in patients with PAD due to lack of beneflt and increased risk Nitrates are used prinraril-y to lrrnage angina symptorns for harm from major bleeding events, including intracranial in ACS. Sublingual nitrates should be adlllinistere(l at pre bleeding. The studies that informed the AHA/ACC recom- sentation to relieve chest pailt. Fbr pltients u,-ith persistent mendation used warfarin as the anticoagulant. chesl pain despite p blocl<ade, intravcnous nitroglycerin Cilostazol (Option A), a phosphodiesterase inhibitor (Option B) can irlleviate symptoms, plrticularly in those with antiplatelet and vasodilator activity, has been asso \\'ith hvpertcnsion. 'lhis prtient does not have chest pain, ciated with improvements in pain-free walking distance and nitroglycerin infusion is not neecled. and overall walking distance in patients with claudication. If r-rsecl, intravenous gl_Vcoprotein Ilbillla inhibitors. Cilostazol should be considered in this patient in addition to such as tirolibln (Option C). are gencrirlly reservccl fbr use supervised exercise therapy; however, it will not reduce this during percutancous intcrventior-r: they' should be aclntinis patient's cardiovascular risk. terccl only in thc catheterizirtion l:rboratorv becausc o[ the No study has demonstrated the beneflt of intensi$zing lack olbenefit iurcl increase in bleeding with upfiont aclmin lipid management, such as with the initiation of ezetimibe istrultion in the ernergency clcpartment. (Option B), when the LDL cholesterol level is below 70 mg/dl Urgent inr.'asive treatnlent (rvithin 2 hours) (Option D) is (r.sr mmol/L). reconrmenclecl ftrr patients rt'ith NSTE r\CS rd-ro hlve herno Revascularization, such as with peripheral artery dynamic instabilityl ref'ractoly chest pirin, heart f:rilure, or bypass surgery (Option C), improves symptoms, increases vcnlricular arrhythmias. 'lhis patient cloes not have an ir,di functional capacity, and improves wound healing (when cation Itrr Llrgent coronilrl, angiographl,. applicable) in patients with intermittent claudication or I(EY POIilIS critical limb ischemia when standard measures, such as exercise training, cilostazol, and/or wound treatment, are . In patients with low risk non-ST-elevation acute inadequate. Peripheral artery bypass surgery is not appro coronary syndrome, an ischemia guided strates/ is priate for this patient without life limiting symptoms and appropriate. (Continued) would not reduce his cardiovascular risk.

1.1 ctays. r,r,ith I poir.rt assigned fbr each ol these preclictors: rivaroxaban therapy. lr, agc 6.5 years or older, three rlr lnore coronaly artery disease .E, The most appropriate treatment to reduce cardiovascular (CAI)) risk facturrs (cholestcrol, lamily hiskiry hypcrtcnsion, risk in this patient is to initiate very low-dose rivaroxaban .E cliabctes mellilus. smoking). pr-eviously documented CAI) (Option D). In a randomized trial, the addition of very low- vt (irrrgiographic stenosis >50'l;,). aspiriu use in the past 7 days. {, dose rivaroxaban (2.5 mg twice daily) to aspirin (81 mg daily) tu() or lrorc ischemic episocles in thc ptst 2.1 l.rours. S'i' seg, was shown to reduce the occurrence ofcardiovascular death. t = nrent deviation on ECC. and elevatccl cardiac biomarkers myocardial infarction, or stroke in patients with peripheral (crcltine kinase MB or tropollin).'lhis pirtient presellts \ rith artery disease (PAD). The absolute risk reduction, when com- lbatures corlsisterlt u,ith possible ACS but has a'l'lMl sc<lre ol pared with aspirin alone, was 2"1, in 7470 patients enrolled I uncl is clinicalll stable. [.ow risk p:rticnts undergo noninr,a with either lower extremity PAD or carotid stenosis. Major sivc stress testing with lcf t vcntricular tirnction ilssesslrent bleeding, primarily gastrointestinal bleeding, was increased belirre hospitll clischarge. Clrdiac cathctcrization is reserved by 1% in patients assigned to aspirin plus rivaroxaban. Thus, firr patier.rts with active or iutermittent ischemia, including low dose rivaroxaban should be avoided in patients with PAD those lr,ith arrgina despite nredical therirpl, or evi(lence ot' who have a higher risk for bleeding. It should be noted that ischernia on stress testing, and patients iit very higl.r clinical use of rivaroxaban in patients with PAD is at odds with the risk based on risk score. 'll.rc ischernia guicled approach is 2016 American Heart Association/American College of Cardi- rtppropriate lirr lur,r risk patients (TIMI score <2). pirrticu ologz (AHA/ACC) PAD guideline, which recommends against hrll lou' risk u,ornen. r,rlto mlry have r,r,orse outconles with anticoagulation to reduce the risk for cardiovascular events an carly invasive appro:rch. in patients with PAD due to lack of beneflt and increased risk Nitrates are used prinraril-y to lrrnage angina symptorns for harm from major bleeding events, including intracranial in ACS. Sublingual nitrates should be adlllinistere(l at pre bleeding. The studies that informed the AHA/ACC recom- sentation to relieve chest pailt. Fbr pltients u,-ith persistent mendation used warfarin as the anticoagulant. chesl pain despite p blocl<ade, intravcnous nitroglycerin Cilostazol (Option A), a phosphodiesterase inhibitor (Option B) can irlleviate symptoms, plrticularly in those with antiplatelet and vasodilator activity, has been asso \\'ith hvpertcnsion. 'lhis prtient does not have chest pain, ciated with improvements in pain-free walking distance and nitroglycerin infusion is not neecled. and overall walking distance in patients with claudication. If r-rsecl, intravenous gl_Vcoprotein Ilbillla inhibitors. Cilostazol should be considered in this patient in addition to such as tirolibln (Option C). are gencrirlly reservccl fbr use supervised exercise therapy; however, it will not reduce this during percutancous intcrventior-r: they' should be aclntinis patient's cardiovascular risk. terccl only in thc catheterizirtion l:rboratorv becausc o[ the No study has demonstrated the beneflt of intensi$zing lack olbenefit iurcl increase in bleeding with upfiont aclmin lipid management, such as with the initiation of ezetimibe istrultion in the ernergency clcpartment. (Option B), when the LDL cholesterol level is below 70 mg/dl Urgent inr.'asive treatnlent (rvithin 2 hours) (Option D) is (r.sr mmol/L). reconrmenclecl ftrr patients rt'ith NSTE r\CS rd-ro hlve herno Revascularization, such as with peripheral artery dynamic instabilityl ref'ractoly chest pirin, heart f:rilure, or bypass surgery (Option C), improves symptoms, increases vcnlricular arrhythmias. 'lhis patient cloes not have an ir,di functional capacity, and improves wound healing (when cation Itrr Llrgent coronilrl, angiographl,. applicable) in patients with intermittent claudication or I(EY POIilIS critical limb ischemia when standard measures, such as exercise training, cilostazol, and/or wound treatment, are . In patients with low risk non-ST-elevation acute inadequate. Peripheral artery bypass surgery is not appro coronary syndrome, an ischemia guided strates/ is priate for this patient without life limiting symptoms and appropriate. (Continued) would not reduce his cardiovascular risk. 165

Answers and Critiques In the EUCLID study of patients with symptomatic PAD, functional capacity and qualily of life. LVAD placement is ticagrelor (Option E) was not associated with improved currently indicated in patients with ejection lraction less prevention of cardio'vascular death, myocardial infarction, than 25'., and poor exercise tolerance (Ne'o' York Heart or ischemic stroke when compared with clopidogrel; it does Association functional class IV) despite maximally toler- not have a role in the management of patients with PAD for ated therapy, with either a high predicted 1 or 2-year cardiovascular risk reduction. mortality or inotrope dependency, who still want aggressive restorative care. Because this patient qualifles for trans TEY POITIS plantation. which is currently associated with better long- . In patients with peripheral artery disease, antithrom- term survival, that would be a better choice. Some patients botic therapy with very low-dose rivaroxaban plus receive an LVAD before transplantation if they have acute aspirin reduces the occurrence of cardiovascular decompensation. death, myocardial infarction, or stroke by 2'7, and Tolvaptan (Option D) is a vasopressin receptor blocker increases the risk for major bleeding by 1'7,. that is currently approved for the treatment of hypervolemic UI o No study has demonstrated the benefit of intensifliing and euvolemic hyponatremia with a serum sodium level E less than 125 mEq/L (125 mmol/L). It must be initiated in the .D lipid management when the LDL cholesterol level is UI below 70 mg/dl (1.81 mmol/L). hospital setting and cannot be used for more than 30 days. q, Although this patient has hyponatremia, his serum sodium EL level is greater than 125 mEq/L (12s mmol/L) and he is not n Bibliography hospitalized; thus, tolvaptan is not indicated. There is no Anand SS. Bosch J, Eikelboom lW, et alr COMPASS lnvestigators. Riraroxaban It with or without aspirin in patients s,ith stable peripheral or carotid evidence that tolvaptan improves chronic heart failure or E artery disease: an intemational. randomised. double blind. placebo clinical outcomes. .D controlled trial. Lancet. 2018r391 :219 229. [PMID: 291328801 doi:10.1016 t^ s0140 6736(17)32,109 i XEY POI ]TT . Patients with persistent severe heart failure symptoms despite maximal medical therapy are candidates for Item 22 Answer: B advanced treatment; acceptable candidates for cardiac Educational Objective: Evaluate a patient with transplantation are generally younger than 65 to 70 years advanced heart failure for heart transplantation. with no medical contraindications and have good Heart transplantation (Option B) is appropriate for this social support and adherence. patient with advanced heart failure who has signs and symp toms of a poor prognosis over the next year. He has hypona- Bibliography tremia and worsening kidney function, has had recurrent Guglin M. Zucker MJ. Borlaug BA. et al: ACC Heart Failure and Transplant l\,,lember Section and I-eadership Council. Ilvalultion fbr heart transplanta hospitalizations for heart failure, and has a reduction in tion and L\AD implantation: JACC Council Perspectives. I Am Coll (lardiol. his functional capacity. All of these signs point to a poor '2020 :7 5 :1171 1.187. I PM I I): 32216916] doi : 10. I 0l 6 i.jacc.2020.01.031

In the EUCLID study of patients with symptomatic PAD, functional capacity and qualily of life. LVAD placement is ticagrelor (Option E) was not associated with improved currently indicated in patients with ejection lraction less prevention of cardio'vascular death, myocardial infarction, than 25'., and poor exercise tolerance (Ne'o' York Heart or ischemic stroke when compared with clopidogrel; it does Association functional class IV) despite maximally toler- not have a role in the management of patients with PAD for ated therapy, with either a high predicted 1 or 2-year cardiovascular risk reduction. mortality or inotrope dependency, who still want aggressive restorative care. Because this patient qualifles for trans TEY POITIS plantation. which is currently associated with better long- . In patients with peripheral artery disease, antithrom- term survival, that would be a better choice. Some patients botic therapy with very low-dose rivaroxaban plus receive an LVAD before transplantation if they have acute aspirin reduces the occurrence of cardiovascular decompensation. death, myocardial infarction, or stroke by 2'7, and Tolvaptan (Option D) is a vasopressin receptor blocker increases the risk for major bleeding by 1'7,. that is currently approved for the treatment of hypervolemic UI o No study has demonstrated the benefit of intensifliing and euvolemic hyponatremia with a serum sodium level E less than 125 mEq/L (125 mmol/L). It must be initiated in the .D lipid management when the LDL cholesterol level is UI below 70 mg/dl (1.81 mmol/L). hospital setting and cannot be used for more than 30 days. q, Although this patient has hyponatremia, his serum sodium EL level is greater than 125 mEq/L (12s mmol/L) and he is not n Bibliography hospitalized; thus, tolvaptan is not indicated. There is no Anand SS. Bosch J, Eikelboom lW, et alr COMPASS lnvestigators. Riraroxaban It with or without aspirin in patients s,ith stable peripheral or carotid evidence that tolvaptan improves chronic heart failure or E artery disease: an intemational. randomised. double blind. placebo clinical outcomes. .D controlled trial. Lancet. 2018r391 :219 229. [PMID: 291328801 doi:10.1016 t^ s0140 6736(17)32,109 i XEY POI ]TT . Patients with persistent severe heart failure symptoms despite maximal medical therapy are candidates for Item 22 Answer: B advanced treatment; acceptable candidates for cardiac Educational Objective: Evaluate a patient with transplantation are generally younger than 65 to 70 years advanced heart failure for heart transplantation. with no medical contraindications and have good Heart transplantation (Option B) is appropriate for this social support and adherence. patient with advanced heart failure who has signs and symp toms of a poor prognosis over the next year. He has hypona- Bibliography tremia and worsening kidney function, has had recurrent Guglin M. Zucker MJ. Borlaug BA. et al: ACC Heart Failure and Transplant l\,,lember Section and I-eadership Council. Ilvalultion fbr heart transplanta hospitalizations for heart failure, and has a reduction in tion and L\AD implantation: JACC Council Perspectives. I Am Coll (lardiol. his functional capacity. All of these signs point to a poor '2020 :7 5 :1171 1.187. I PM I I): 32216916] doi : 10. I 0l 6 i.jacc.2020.01.031 survival over the next year. Patients with persistent severe heart failure symptoms despite maximal medical therapy are candidates for advanced treatment. Clinical outcomes Item 23 Answer: B in patients with advanced heart failure undergoing heart Educational Objective: Diagnose hypertrophic cardio- transplantation are excellent. The 1 year survival is around myopathy on physical examination. 907,, and median survival is almost 12 years. Acceptable candidates for transplantation are generally younger than The most likely diagnosis is hypertrophic cardiomyopathy 65 to 70 years with no medical contraindications (e.g., dia (HCM) (Option B). The murmur of HCM is typically a rap- betes mellitus with end organ complications, malignan idly peaking crescendo decrescendo murmur heard best cies within 5 years, kidney dysfunction, or other chronic along the left lower sternal border. Dynamic maneuvers, illnesses that will decrease survival) and have good social such as Valsalva maneuver or squatting and standing. may support and adherence. be useful in making the diagnosis. During the strain phase Digoxin (Option A) has been shown to reduce readmis- of Valsalva maneuver, decreased ventricular preload wors sions in patients with heart failure; however. this drug has ens the degree of left ventricular outflow tract obstruction, a very small therapeutic window. In this patient with poor increasing the intensity of the murmur (positive likelihood kidney function and older age. digoxin would be a risky drug ratio, 14). Squatting increases both preload and afterload, because of the potential for an increase in adverse events. resulting in a decrease in dynamic left ventricular outflow If this patient were older or had comorbid conditions tract obstruction and in the intensify of the murmur (pos- that would not make him a transplant candidate, he might itive likelihood ratio, 7.6). The murmur of HCM typically be a candidate for left ventricular assist device (I.VAD) place does not radiate to the carotid arteries. as it does in aortic ment (Option C). With newer continuous-flow devices, stenosis, and the carotid upstroke is more commonly brisk patients have l-year survival approximating that of car- and two phased (bifid), reflecting ejection, obstruction, and diac transplant recipients and substantial improvements in a later phase of ejection.

survival over the next year. Patients with persistent severe heart failure symptoms despite maximal medical therapy are candidates for advanced treatment. Clinical outcomes Item 23 Answer: B in patients with advanced heart failure undergoing heart Educational Objective: Diagnose hypertrophic cardio- transplantation are excellent. The 1 year survival is around myopathy on physical examination. 907,, and median survival is almost 12 years. Acceptable candidates for transplantation are generally younger than The most likely diagnosis is hypertrophic cardiomyopathy 65 to 70 years with no medical contraindications (e.g., dia (HCM) (Option B). The murmur of HCM is typically a rap- betes mellitus with end organ complications, malignan idly peaking crescendo decrescendo murmur heard best cies within 5 years, kidney dysfunction, or other chronic along the left lower sternal border. Dynamic maneuvers, illnesses that will decrease survival) and have good social such as Valsalva maneuver or squatting and standing. may support and adherence. be useful in making the diagnosis. During the strain phase Digoxin (Option A) has been shown to reduce readmis- of Valsalva maneuver, decreased ventricular preload wors sions in patients with heart failure; however. this drug has ens the degree of left ventricular outflow tract obstruction, a very small therapeutic window. In this patient with poor increasing the intensity of the murmur (positive likelihood kidney function and older age. digoxin would be a risky drug ratio, 14). Squatting increases both preload and afterload, because of the potential for an increase in adverse events. resulting in a decrease in dynamic left ventricular outflow If this patient were older or had comorbid conditions tract obstruction and in the intensify of the murmur (pos- that would not make him a transplant candidate, he might itive likelihood ratio, 7.6). The murmur of HCM typically be a candidate for left ventricular assist device (I.VAD) place does not radiate to the carotid arteries. as it does in aortic ment (Option C). With newer continuous-flow devices, stenosis, and the carotid upstroke is more commonly brisk patients have l-year survival approximating that of car- and two phased (bifid), reflecting ejection, obstruction, and diac transplant recipients and substantial improvements in a later phase of ejection. 166

Answers and Critiques Bicuspid aortic stenosis (Option A) may be associated use ol illicit substances (rnctharrphetamines. cocaine) or with an early systolic ejection sound (click) that heralds prescription drugs (5 lluorourircil, bromocriptine). EC(l the murmur. This is heard more commonly while the valve abnormalities may be nonspecific or mimic ST elevation leaflets remain pliable, before valvular calciflcation pro- myocardial inlarction patterns. It is a diagnosis ol'exclu gresses. The murmur radiates to the carotid arteries, and sion and oflen involves coronary ar.rgiography to exclucle when signiflcant stenosis is present, the carotid upstroke is fixed disease. Administratit)n ol nitrates or calcium channel low amplitude and delayed (parvus et tardus). The murmur's blocl<ers during cardiac catheterization may show coronary intensity decreases during Valsalva maneuver, with little dilatation, r,vhich may inclicate a vasospastic vessel. change during squatting. 'lhis patient is in the r,r,ir.rdolv of time fbr an initial pr-e A restrictive membranous ventricular septal defect sentatiur of periparturr cardiomyopathl' (Option C). r,vhich (Option C) is not typically associated with symptoms of' is charircterized by' increasing dyspnea and heart failure dyspnea. In this condition, a harsh pansystolic murmur is sylxptoms as opposed to chest pain. the absence ot phy'sical present at the left lower sternal border. lt does not markedly Iindir.rgs of volume overload mal<es peripaftum cardiomy<-rp tt (l, change with dynamic maneuvers. athy unlikely. ET Sinus of Valsalva aneurysm (Option D) of the right or Spontaneous coronary artery dissection (SCAI)) noncoronary cusp may rupture into the right heart and (Option D) is a common cause of cl.resl pain among youniler (, is associated with acute dyspnea and decompensation. \{omcn during the peripartum period. SCAD involves devel ?, Because pressure within the aorta is always higher than in oplnent of a nontraumatic ancl noniatrogenic intramtiral E .! the right heart, the loud murmur is heard in both systole and hernatoma. u'ith or rvithout ir.rtinral clissection \ rith lunti UI q, diastole (continuous murmur). nal communication. lhe enlarging hematoma ir-r the fhlse Iumen compresses the true lunren ol the coronary artcr)' l,I = XEY POIXIS ar.rd il con.rbined u'ith obstrr.rcting dissection, leads to chest . The murmur of hlpertrophic cardiomyopathy is typi- pain, ischemia. and,or inlarction. Indicative findings on cally a rapidly peaking crescendo-decrescendo murmur coronary angiography including rnultiple radiolucent heard best along the Ieft lower sternal border. lunrens and perilurninal contrast staining, are absent in . Dynamic maneuvers, such as Valsalva maneuver or this patient. squatting and standing, may be useful in diagnosing t(EY POtllr hypertrophic cardiomyopathy. o In women with typical angina symptoms, nonob- structive coronary stenoses are present on coronary Bibliography angiography in more than 50% of cases, and micro- Ommen SR. Mital S. Burke MA. et al. 2020 AIiA,'ACC guideline for the diag nosis and treatment of patients with hypertrophic cardiomyopathy: a vascular dysfunction is thought to be a predominant report ofthe American College ol Cardi0krgl/American Ileart Association cause of symptoms in these patients. Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2020; 76:e159-e240. IPMID: 33229116] doi: I0.1016ij.jacc.2020.08.045 Bibliography 'l'irmis Holland JE, Jneid FI, Reynolds llR, et al; American Heart Association

Bicuspid aortic stenosis (Option A) may be associated use ol illicit substances (rnctharrphetamines. cocaine) or with an early systolic ejection sound (click) that heralds prescription drugs (5 lluorourircil, bromocriptine). EC(l the murmur. This is heard more commonly while the valve abnormalities may be nonspecific or mimic ST elevation leaflets remain pliable, before valvular calciflcation pro- myocardial inlarction patterns. It is a diagnosis ol'exclu gresses. The murmur radiates to the carotid arteries, and sion and oflen involves coronary ar.rgiography to exclucle when signiflcant stenosis is present, the carotid upstroke is fixed disease. Administratit)n ol nitrates or calcium channel low amplitude and delayed (parvus et tardus). The murmur's blocl<ers during cardiac catheterization may show coronary intensity decreases during Valsalva maneuver, with little dilatation, r,vhich may inclicate a vasospastic vessel. change during squatting. 'lhis patient is in the r,r,ir.rdolv of time fbr an initial pr-e A restrictive membranous ventricular septal defect sentatiur of periparturr cardiomyopathl' (Option C). r,vhich (Option C) is not typically associated with symptoms of' is charircterized by' increasing dyspnea and heart failure dyspnea. In this condition, a harsh pansystolic murmur is sylxptoms as opposed to chest pain. the absence ot phy'sical present at the left lower sternal border. lt does not markedly Iindir.rgs of volume overload mal<es peripaftum cardiomy<-rp tt (l, change with dynamic maneuvers. athy unlikely. ET Sinus of Valsalva aneurysm (Option D) of the right or Spontaneous coronary artery dissection (SCAI)) noncoronary cusp may rupture into the right heart and (Option D) is a common cause of cl.resl pain among youniler (, is associated with acute dyspnea and decompensation. \{omcn during the peripartum period. SCAD involves devel ?, Because pressure within the aorta is always higher than in oplnent of a nontraumatic ancl noniatrogenic intramtiral E .! the right heart, the loud murmur is heard in both systole and hernatoma. u'ith or rvithout ir.rtinral clissection \ rith lunti UI q, diastole (continuous murmur). nal communication. lhe enlarging hematoma ir-r the fhlse Iumen compresses the true lunren ol the coronary artcr)' l,I = XEY POIXIS ar.rd il con.rbined u'ith obstrr.rcting dissection, leads to chest . The murmur of hlpertrophic cardiomyopathy is typi- pain, ischemia. and,or inlarction. Indicative findings on cally a rapidly peaking crescendo-decrescendo murmur coronary angiography including rnultiple radiolucent heard best along the Ieft lower sternal border. lunrens and perilurninal contrast staining, are absent in . Dynamic maneuvers, such as Valsalva maneuver or this patient. squatting and standing, may be useful in diagnosing t(EY POtllr hypertrophic cardiomyopathy. o In women with typical angina symptoms, nonob- structive coronary stenoses are present on coronary Bibliography angiography in more than 50% of cases, and micro- Ommen SR. Mital S. Burke MA. et al. 2020 AIiA,'ACC guideline for the diag nosis and treatment of patients with hypertrophic cardiomyopathy: a vascular dysfunction is thought to be a predominant report ofthe American College ol Cardi0krgl/American Ileart Association cause of symptoms in these patients. Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2020; 76:e159-e240. IPMID: 33229116] doi: I0.1016ij.jacc.2020.08.045 Bibliography 'l'irmis Holland JE, Jneid FI, Reynolds llR, et al; American Heart Association tr Item24 Answer: B Ed u cational Objective: Diagnose microvascular dys- Interventional Cardiovascular Care Committee of the Council on Clinical Cardiologr; Council on Cardiovascular and Stroke Nursing; Council on Fipidemiolory and Preventir)n; lnd (iruncil on Quality of Care and function as the cause of chest pain in a young woman. C)utcomes Research. Contenrporary diagnosis and management 01' patients with myocardial inlarction in the absence ofobstructive coronary 'l he r.nost likely cause oi'this patient's chest pirin is microvirs artery disease: a scientific statement fnrm the American Heart Association. cular cl1'slunction (Option B). In rvorlen r,r'ith typical angina Circulation. 2019;139:e891 e908. IPMID: 309138931 doi:10.1161rCIR. 0000000000000670 s!'1r1pton1s. nonobstructi'n'e cororlrir].' stenoses are present on col-onarl angiography in more than 50'll, of cases. lir-rd rnicrovascLrlar clysiunction (cr.rdothcliunr dependent or Item 25 Answer: C enclothelium independent) is thought to be a predominant Educational Objective: Diagnose atrioventricular nodal cluse of symptclms in these patients. Although the epicarclial reentrant tachycardia. coronirry :rrteries are easily visualizecl via coronary angi ography, the coronary rnicrocirculltion (r,essels <0.5 mm This patient's presentation is typical for atrioventricu in cliameter) is not e*sil1,' visualizccl yet accounts lor approx lar nodal reentrant tachycardia (AVNRT) (Option C), the inrltely 70')1, of the coronary rcsistance ir.r the absence ot most common form of supraventricular tachycardia (SVT). obstructive coronary artery discasc. Inrpaired microcircu SVTs are rapid heart rhythms that arise from the atrium lirtion can be determined b1' several provoc:rtive tests in the or require conduction through the atrioventricular node. carcl iac catheterization laboratory Clinical disorders of coro SVTs usually occur in the absence of structural heart dis narl microvascular dl,sliurctior.r have largely ireen describecl ease, although echocardiography should be performed to in pirtiellts presenting'"vith stablc angin:t. exclude underlying cardiac dysfunction or structural defects. (irronary lasospasnl (Option A) is sudden coronilry Patients often have repeated episodes of tachycardia and artery constriction occurring spontancously or fbllowing may report palpitations, a sensation of pounding in the

tr Item24 Answer: B Ed u cational Objective: Diagnose microvascular dys- Interventional Cardiovascular Care Committee of the Council on Clinical Cardiologr; Council on Cardiovascular and Stroke Nursing; Council on Fipidemiolory and Preventir)n; lnd (iruncil on Quality of Care and function as the cause of chest pain in a young woman. C)utcomes Research. Contenrporary diagnosis and management 01' patients with myocardial inlarction in the absence ofobstructive coronary 'l he r.nost likely cause oi'this patient's chest pirin is microvirs artery disease: a scientific statement fnrm the American Heart Association. cular cl1'slunction (Option B). In rvorlen r,r'ith typical angina Circulation. 2019;139:e891 e908. IPMID: 309138931 doi:10.1161rCIR. 0000000000000670 s!'1r1pton1s. nonobstructi'n'e cororlrir].' stenoses are present on col-onarl angiography in more than 50'll, of cases. lir-rd rnicrovascLrlar clysiunction (cr.rdothcliunr dependent or Item 25 Answer: C enclothelium independent) is thought to be a predominant Educational Objective: Diagnose atrioventricular nodal cluse of symptclms in these patients. Although the epicarclial reentrant tachycardia. coronirry :rrteries are easily visualizecl via coronary angi ography, the coronary rnicrocirculltion (r,essels <0.5 mm This patient's presentation is typical for atrioventricu in cliameter) is not e*sil1,' visualizccl yet accounts lor approx lar nodal reentrant tachycardia (AVNRT) (Option C), the inrltely 70')1, of the coronary rcsistance ir.r the absence ot most common form of supraventricular tachycardia (SVT). obstructive coronary artery discasc. Inrpaired microcircu SVTs are rapid heart rhythms that arise from the atrium lirtion can be determined b1' several provoc:rtive tests in the or require conduction through the atrioventricular node. carcl iac catheterization laboratory Clinical disorders of coro SVTs usually occur in the absence of structural heart dis narl microvascular dl,sliurctior.r have largely ireen describecl ease, although echocardiography should be performed to in pirtiellts presenting'"vith stablc angin:t. exclude underlying cardiac dysfunction or structural defects. (irronary lasospasnl (Option A) is sudden coronilry Patients often have repeated episodes of tachycardia and artery constriction occurring spontancously or fbllowing may report palpitations, a sensation of pounding in the 167

Answers and Critiques neck, fatigue, light headedness, chest discomfort, dyspnea, Item 26 Answer: D presyncope, and, Iess commonly, syncope. AVNRT accounts Educational Objective: Treat severe secondary mitral for approximately two thirds of all cases of SW. It frequently regurgitation with guideline-directed medical therapy. occurs in women and is often terminated by performing vagal maneuvers, as with this patient. The ECG typically No change in therapy (Option D) is the most appropriate demonstrates a narrow QRS complex. AVNRT is character management. This patient's echocardiogram is consistent ized by a short RP interval with a retrograde P wave (orrouus) with severe secondary mitral regurgitation (MR). Left ven inscribed very close to the QRS complex, which is best seen tricular systolic dysfunction is the most common cause of in lead V, (appearing as a pseudo r'wave). In the emergency chronic secondary MR. Consequently, guideline-directed department, adenosine is commonly used for acute termi medical therapy (GDMT) is loundational in improving nation. Cardioversion is rarely required. Ultimately, catheter symptoms in patients such as this one. GDMT includes a ablation may be curative and is often flrst-line therapy, but p-blocker, an ACE inhibitor or angiotensin receptor blocker, AVNRT also can be managed conservatively at the patient's and an aldosterone antagonist. Loop diuretics are used as UI discretion. needed. GDMT improves symptoms and prolongs life in patients with heart failure and probably does so when heart = ID failure is complicated by chronic secondary MR. Current UI o, guidelines recommend GDMT as flrst line therapy (class IL 1 recommendation) because it can reduce left ventricular f..l volumes (reverse remodeling) in many patients and, in so doing, reduces severity ofsecondary MR. 4r Cardiac magnetic resonance imaging (Option A) or o UI transesophageal echocardiography may be pursued if trans- thoracic echocardiography is insufficient to determine either the exact severity or the mechanism of mitral regurgitation. Atrial flbrillation (Option A) is a narrow-complex Howevel in this case, the severity and mechanism of MR are tachycardia primarily deflned by the absence of regular P not in question. waves and presence of an irregular ventricular response. GDMT also includes consideration of cardiac reqmchroni- The patient's ECG has a regular tachycardia with evidence zation therapy (CRI) (Option B) in appropriate patients. Among of retrograde P waves, which is not consistent with atrial patients with a left ventricular ejection fraction (LVEF) of 35'U, flbrillation. or less and sinus rhythm, CRT is indicated in those with left Atrial tachycardia (Option B) is an automatic SVT that bundle branch block, New York Heart Association functional is less common than AVNRT, is less likely to start abruptly, class II to ambulatory class lV heart failure ry.rnptoms, and a and is not usually terminated with vagal maneuvers. The QRS duration of 150 ms or longer despite GDMT. In addition, in ECG more commonly shows discrete atrial activity, with an patients with an L\EF of 35'7, or less and a QRS duration of 120 abnormal P wave axis, and the rate is usually slower than to 149 ms, CRI may be useful. This patient now has New York that seen in this patient. Heart Association functional class I symptoms with an LVEF Ventricular tachycardia (Option D) is a wide- greater than 35% and therefore does not qualifiz for CRL complex tachycardia. In contrast, this patient presents In patients with chronic severe secondary MR related with a narrow complex tachycardia. Among patients to left ventricular systolic dysfunction who have persistent with a structurally normal heart and no cardiac history, symptoms while receiving optimal GDMT, transcatheter edge ventricular tachycardia would be much less common to edge repair (TEER) is a reasonable option (class 2a recom than AVNRT. mendation), according to current guidelines. Surgical mitral t(EY P0t 1{r5 valve repair (Option C) is also reasonable if the patient is . Atrioventricular nodal reentrant tachycardia, the most undergoing concomitant coronary artery bypass graft surgery. common form of supraventricular tachycardia, Bpi Surgery also may be considered if the patient has unfavorable cally has a narrow QRS complex; it often can be ter- anatomy for TEER. However, this patient should undergo a minated by performing vagal maneuvers. trial of GDMT before mitral valve repair is considered. o Atrioventricular nodal reentrant tachycardia is char- r(Ev P0lrTs acterized electrocardiographically by a short RP inter- . Left ventricular systolic dysfunction is the most com- val with a retrograde P wave inscribed very close to mon cause of chronic secondary mitral regurgitation. the QRS complex, which is best seen in lead V,, appearing as a pseudo r'wave. . Guideline-directed medical therapy is recommended as first-line therapy for patients with heart failure and sec- Bibliography ondary mitral regurgitation because it can reduce left Kotadia ID, Williams SE, O'Neill M. Supraventricular tachycardia: an over ventricular volumes in many patients and, in so doing, view of diagnosis and management. Clin Med (Lond). 2020;20:43 7. reduces severity of secondary mitral regurgitation. IPM I D: 319417311 doi:10.7861/clinmed.cme.20.1.3

neck, fatigue, light headedness, chest discomfort, dyspnea, Item 26 Answer: D presyncope, and, Iess commonly, syncope. AVNRT accounts Educational Objective: Treat severe secondary mitral for approximately two thirds of all cases of SW. It frequently regurgitation with guideline-directed medical therapy. occurs in women and is often terminated by performing vagal maneuvers, as with this patient. The ECG typically No change in therapy (Option D) is the most appropriate demonstrates a narrow QRS complex. AVNRT is character management. This patient's echocardiogram is consistent ized by a short RP interval with a retrograde P wave (orrouus) with severe secondary mitral regurgitation (MR). Left ven inscribed very close to the QRS complex, which is best seen tricular systolic dysfunction is the most common cause of in lead V, (appearing as a pseudo r'wave). In the emergency chronic secondary MR. Consequently, guideline-directed department, adenosine is commonly used for acute termi medical therapy (GDMT) is loundational in improving nation. Cardioversion is rarely required. Ultimately, catheter symptoms in patients such as this one. GDMT includes a ablation may be curative and is often flrst-line therapy, but p-blocker, an ACE inhibitor or angiotensin receptor blocker, AVNRT also can be managed conservatively at the patient's and an aldosterone antagonist. Loop diuretics are used as UI discretion. needed. GDMT improves symptoms and prolongs life in patients with heart failure and probably does so when heart = ID failure is complicated by chronic secondary MR. Current UI o, guidelines recommend GDMT as flrst line therapy (class IL 1 recommendation) because it can reduce left ventricular f..l volumes (reverse remodeling) in many patients and, in so doing, reduces severity ofsecondary MR. 4r Cardiac magnetic resonance imaging (Option A) or o UI transesophageal echocardiography may be pursued if trans- thoracic echocardiography is insufficient to determine either the exact severity or the mechanism of mitral regurgitation. Atrial flbrillation (Option A) is a narrow-complex Howevel in this case, the severity and mechanism of MR are tachycardia primarily deflned by the absence of regular P not in question. waves and presence of an irregular ventricular response. GDMT also includes consideration of cardiac reqmchroni- The patient's ECG has a regular tachycardia with evidence zation therapy (CRI) (Option B) in appropriate patients. Among of retrograde P waves, which is not consistent with atrial patients with a left ventricular ejection fraction (LVEF) of 35'U, flbrillation. or less and sinus rhythm, CRT is indicated in those with left Atrial tachycardia (Option B) is an automatic SVT that bundle branch block, New York Heart Association functional is less common than AVNRT, is less likely to start abruptly, class II to ambulatory class lV heart failure ry.rnptoms, and a and is not usually terminated with vagal maneuvers. The QRS duration of 150 ms or longer despite GDMT. In addition, in ECG more commonly shows discrete atrial activity, with an patients with an L\EF of 35'7, or less and a QRS duration of 120 abnormal P wave axis, and the rate is usually slower than to 149 ms, CRI may be useful. This patient now has New York that seen in this patient. Heart Association functional class I symptoms with an LVEF Ventricular tachycardia (Option D) is a wide- greater than 35% and therefore does not qualifiz for CRL complex tachycardia. In contrast, this patient presents In patients with chronic severe secondary MR related with a narrow complex tachycardia. Among patients to left ventricular systolic dysfunction who have persistent with a structurally normal heart and no cardiac history, symptoms while receiving optimal GDMT, transcatheter edge ventricular tachycardia would be much less common to edge repair (TEER) is a reasonable option (class 2a recom than AVNRT. mendation), according to current guidelines. Surgical mitral t(EY P0t 1{r5 valve repair (Option C) is also reasonable if the patient is . Atrioventricular nodal reentrant tachycardia, the most undergoing concomitant coronary artery bypass graft surgery. common form of supraventricular tachycardia, Bpi Surgery also may be considered if the patient has unfavorable cally has a narrow QRS complex; it often can be ter- anatomy for TEER. However, this patient should undergo a minated by performing vagal maneuvers. trial of GDMT before mitral valve repair is considered. o Atrioventricular nodal reentrant tachycardia is char- r(Ev P0lrTs acterized electrocardiographically by a short RP inter- . Left ventricular systolic dysfunction is the most com- val with a retrograde P wave inscribed very close to mon cause of chronic secondary mitral regurgitation. the QRS complex, which is best seen in lead V,, appearing as a pseudo r'wave. . Guideline-directed medical therapy is recommended as first-line therapy for patients with heart failure and sec- Bibliography ondary mitral regurgitation because it can reduce left Kotadia ID, Williams SE, O'Neill M. Supraventricular tachycardia: an over ventricular volumes in many patients and, in so doing, view of diagnosis and management. Clin Med (Lond). 2020;20:43 7. reduces severity of secondary mitral regurgitation. IPM I D: 319417311 doi:10.7861/clinmed.cme.20.1.3 168

Answers and Critiques Bibliography xEY P0lxTS (oilinued) tsonow RO, O'Gara PT, Adams DH. et al. 2020 Focused update ofthe 20U ACC expert consensus decision pathway on the management of mitral . Patent ductus arteriosus closure is indicated in regurgitation: a report ofthe American &rllege ofCardiolory Solution Set patients with left-sided cardiac chamber enlargement Oversight Committee. J Am Coll (lardiol. 2020;75:2236-2270. IPMID: 320680841 doi:10.1016/i.jacc.202O.02.0Os even in the absence of symptoms, as long as pulmonary artery systolic pressure is less than 50% systemic.

Bibliography xEY P0lxTS (oilinued) tsonow RO, O'Gara PT, Adams DH. et al. 2020 Focused update ofthe 20U ACC expert consensus decision pathway on the management of mitral . Patent ductus arteriosus closure is indicated in regurgitation: a report ofthe American &rllege ofCardiolory Solution Set patients with left-sided cardiac chamber enlargement Oversight Committee. J Am Coll (lardiol. 2020;75:2236-2270. IPMID: 320680841 doi:10.1016/i.jacc.202O.02.0Os even in the absence of symptoms, as long as pulmonary artery systolic pressure is less than 50% systemic. Item 27 Answer: C Bibliography Educational Objective: Treat patent ductus arteriosus. Stout KK, Daniels Cl, Aboulhosn JA, et al. 2018 AHA/ACC guideline for the management of adults with congenital heart disease: a report of the American College of Cardiolory/American Heart Association Task Force The most appropriate management is patent ductus arteri- on Clinical Practice Guidelines. J Am Coll Cardiol. 2Ol9;73:e81 e192. osus (PDA) device closure (Option C). A PDA is a persistent IPMID: 30121239] doi:10.1016/j.jacc.2018.08.1029 f'etal connection between the aorta and the left pulmo UI nary artery that leads to volume overload of the left-sided o, chambers, manifested by left atrial and left ventricular Item 28 Answer: A ET enlargement. The typical murmur of a PDA is a continuous Educational Objective: Diagnose peripheral artery dis- "machinery" murmur that envelops the Sr, making it inau ease in a patient with normal ankle-brachial index values. rJ dible; the murmur is heard beneath the left clavicle. A tiny E' PDA is generally asymptomatic and inaudible. Closure of the The most appropriate next step is exercise ankle brachial IE UI PDA is indicated in patients with left sided cardiac chamber index (ABI) testing (Option A). This patient has limb symp- o enlargement as long as pulmonary artery systolic pressure toms consistent with peripheral artery disease (PAD). Gen U! is less than 50% systemic, even in the absence of symptoms. erally, patients with claudication have an ABI of 0.40 to 0.90, = E Closure may be considered in patients with some degree whereas patients with ischemic rest pain, ulceration, or of pulmonary hypertension in selected cases (pulmonary gangrene have an ABI less than 0.40. A resting ABI greater artery pressure 50"/,'-66"1' systemic). Percutaneous closure than 1.40 indicates the presence of noncompressible, cal is usually performed; referral to a congenital cardiac center cifled arteries in the lower extremities and is considered fbr consideration of closure options is recommended. PDA uninterpretable. Between 79"1' and 317, of patients with typi closure should be avoided in patients with irreversible pul- cal claudication symptoms have a normal or borderline ABI. monary vascular disease. PDA closure in patients with severe Because this patient with classic claudication symptoms pulmonary hypertension (pulmonary artery systolic pres and faint pulses has a nondiagnostic ABI, further testing is sure >66'l,, systemic) is associated with greater risk compared indicated. Exercise ABI testing is useful in patients with ABI with PDA closure in those without pulmonary hypertension values between 0.91 and 1.40 and high pretest probability of and is not associated with improved survival. In patients PAD. It requires ABI measurements at rest and after treadmill with pulmonary hypertension, the existence of right-to-left walking or plantar flexion exercises. A post-exercise ankle ductal shunting may be necessary to maintain cardiac out- pressure drop of 30 mm Hg or more or signiflcant decline in put, and closure may result in clinical worsening. the ABI suggests PAD. Cardiac magnetic resonance imaging (Option A) will Invasive angiography (Option B) is often reserved for further delineate cardiac chamber size and function and patients with an indication for revascularization, usually demonstrate the dimension and length of the PDA. However, either intermittent claudication or chronic limb-threatening adequate data are available from the echocardiogram to con- ischemia. Likewise, noninvasive anatomic imaging studies, firm that PDA closure is indicated. including arterial duplex ultrasonography, CT angiography, lndomethacin (Option B), an inhibitor of prostaglandin and magnetic resonance angiography (Option C), are used synthesis, is used to promote closure of a PDA in preterm to plan for endovascular or surgical revascularization. This infants. However, indomethacin has no impact on closure patient with typical limb symptoms, normal resting ABI rates in full-term infants and older patients with a PDA and values, and no contraindication to exercise should undergo is not indicated in this patient. noninvasive physiologic testing, such as exercise ABI, to Serial echocardiographic monitoring (Option D) is not conflrm the diagnosis of PAD before anatomic assessment recommended in patients with a PDA and left to right shunt is considered.

Item 27 Answer: C Bibliography Educational Objective: Treat patent ductus arteriosus. Stout KK, Daniels Cl, Aboulhosn JA, et al. 2018 AHA/ACC guideline for the management of adults with congenital heart disease: a report of the American College of Cardiolory/American Heart Association Task Force The most appropriate management is patent ductus arteri- on Clinical Practice Guidelines. J Am Coll Cardiol. 2Ol9;73:e81 e192. osus (PDA) device closure (Option C). A PDA is a persistent IPMID: 30121239] doi:10.1016/j.jacc.2018.08.1029 f'etal connection between the aorta and the left pulmo UI nary artery that leads to volume overload of the left-sided o, chambers, manifested by left atrial and left ventricular Item 28 Answer: A ET enlargement. The typical murmur of a PDA is a continuous Educational Objective: Diagnose peripheral artery dis- "machinery" murmur that envelops the Sr, making it inau ease in a patient with normal ankle-brachial index values. rJ dible; the murmur is heard beneath the left clavicle. A tiny E' PDA is generally asymptomatic and inaudible. Closure of the The most appropriate next step is exercise ankle brachial IE UI PDA is indicated in patients with left sided cardiac chamber index (ABI) testing (Option A). This patient has limb symp- o enlargement as long as pulmonary artery systolic pressure toms consistent with peripheral artery disease (PAD). Gen U! is less than 50% systemic, even in the absence of symptoms. erally, patients with claudication have an ABI of 0.40 to 0.90, = E Closure may be considered in patients with some degree whereas patients with ischemic rest pain, ulceration, or of pulmonary hypertension in selected cases (pulmonary gangrene have an ABI less than 0.40. A resting ABI greater artery pressure 50"/,'-66"1' systemic). Percutaneous closure than 1.40 indicates the presence of noncompressible, cal is usually performed; referral to a congenital cardiac center cifled arteries in the lower extremities and is considered fbr consideration of closure options is recommended. PDA uninterpretable. Between 79"1' and 317, of patients with typi closure should be avoided in patients with irreversible pul- cal claudication symptoms have a normal or borderline ABI. monary vascular disease. PDA closure in patients with severe Because this patient with classic claudication symptoms pulmonary hypertension (pulmonary artery systolic pres and faint pulses has a nondiagnostic ABI, further testing is sure >66'l,, systemic) is associated with greater risk compared indicated. Exercise ABI testing is useful in patients with ABI with PDA closure in those without pulmonary hypertension values between 0.91 and 1.40 and high pretest probability of and is not associated with improved survival. In patients PAD. It requires ABI measurements at rest and after treadmill with pulmonary hypertension, the existence of right-to-left walking or plantar flexion exercises. A post-exercise ankle ductal shunting may be necessary to maintain cardiac out- pressure drop of 30 mm Hg or more or signiflcant decline in put, and closure may result in clinical worsening. the ABI suggests PAD. Cardiac magnetic resonance imaging (Option A) will Invasive angiography (Option B) is often reserved for further delineate cardiac chamber size and function and patients with an indication for revascularization, usually demonstrate the dimension and length of the PDA. However, either intermittent claudication or chronic limb-threatening adequate data are available from the echocardiogram to con- ischemia. Likewise, noninvasive anatomic imaging studies, firm that PDA closure is indicated. including arterial duplex ultrasonography, CT angiography, lndomethacin (Option B), an inhibitor of prostaglandin and magnetic resonance angiography (Option C), are used synthesis, is used to promote closure of a PDA in preterm to plan for endovascular or surgical revascularization. This infants. However, indomethacin has no impact on closure patient with typical limb symptoms, normal resting ABI rates in full-term infants and older patients with a PDA and values, and no contraindication to exercise should undergo is not indicated in this patient. noninvasive physiologic testing, such as exercise ABI, to Serial echocardiographic monitoring (Option D) is not conflrm the diagnosis of PAD before anatomic assessment recommended in patients with a PDA and left to right shunt is considered. large enough to have caused left heart enlargement. Device Segmental blood pressure measurements (Option D) closure should be pursued in this patient before irreversible of the lower extremities are typically performed in patients pulmonary hypertension develops. with abnormal resting ABI values to localize diseased ves sels or segments. This procedure involves pulse volume t( EY P0 r 1{TS recordings (measurement of the magnitude and contour . The typical murmur of a patent ductus arteriosus is a of blood pulse volume in the lower extremities) and blood continuous "machinery" murmur that envelops the pressure measurements at several locations in the lower 52, making it inaudible; the murmur is heard beneath extremities. In this patient, the resting ABI was normal; the left clavicle. thus, the indication for segmental blood pressure mea (Continued) surement is unclear.

large enough to have caused left heart enlargement. Device Segmental blood pressure measurements (Option D) closure should be pursued in this patient before irreversible of the lower extremities are typically performed in patients pulmonary hypertension develops. with abnormal resting ABI values to localize diseased ves sels or segments. This procedure involves pulse volume t( EY P0 r 1{TS recordings (measurement of the magnitude and contour . The typical murmur of a patent ductus arteriosus is a of blood pulse volume in the lower extremities) and blood continuous "machinery" murmur that envelops the pressure measurements at several locations in the lower 52, making it inaudible; the murmur is heard beneath extremities. In this patient, the resting ABI was normal; the left clavicle. thus, the indication for segmental blood pressure mea (Continued) surement is unclear. 169

Answers and Critiques KEY POII{It dyspnea. This patient has no need for supplemental oxygen . Betvveen 19'l. and 31'l. of patients with typical claudi therapy. cation symptoms have a normal or borderline ankle- l( EY PO I t{rS brachial index. . The preferred method of treating ST elevation myo . Exercise ankle brachial index (ABI) testing is useful to cardial infarction is primary percutaneous coronary evaluate for peripheral artery disease in patients with intervention. normal ABI values (>0.90 and <1.40) and high pretest . Approximately 50% of patients with ST elevation probability. myocardial infarction (STEMI) have other obstructive lesions remote from the area of infarction ("noncul- Bibliography prit" lesions); studies have shown the benefit of non Mehta A, Sperling LS, Wells BJ. Postexercise ankle brachial inde-x testing. JAMA. 2020;324:796 7. IPMID: lZtZtOOt] doi:10.1001/jama.2020.1016.1 culprit lesion revascularization within 4 to 6 weeks following STEMI. = UI E .D Item 29 Answer: C Bibtiography Ut o, Educational Objective: Treat multivessel coronary Mehta SR. Wbod DA. Storey RFL er al; COMPLETE Trial Sreering Commitree irnd lnvestigators. Complete revascularization with multivessel PCI fbr o- artery disease in a patient with an ST-elevation myocardial m1'ocardial infarction. N Engl J Med. 2019:381:1.111 21. [PN{ID, yqlSlSSl n infarction. doi:10.'l 0561 NEIM oa1917775

cation symptoms have a normal or borderline ankle- l( EY PO I t{rS brachial index. . The preferred method of treating ST elevation myo . Exercise ankle brachial index (ABI) testing is useful to cardial infarction is primary percutaneous coronary evaluate for peripheral artery disease in patients with intervention. normal ABI values (>0.90 and <1.40) and high pretest . Approximately 50% of patients with ST elevation probability. myocardial infarction (STEMI) have other obstructive lesions remote from the area of infarction ("noncul- Bibliography prit" lesions); studies have shown the benefit of non Mehta A, Sperling LS, Wells BJ. Postexercise ankle brachial inde-x testing. JAMA. 2020;324:796 7. IPMID: lZtZtOOt] doi:10.1001/jama.2020.1016.1 culprit lesion revascularization within 4 to 6 weeks following STEMI. = UI E .D Item 29 Answer: C Bibtiography Ut o, Educational Objective: Treat multivessel coronary Mehta SR. Wbod DA. Storey RFL er al; COMPLETE Trial Sreering Commitree irnd lnvestigators. Complete revascularization with multivessel PCI fbr o- artery disease in a patient with an ST-elevation myocardial m1'ocardial infarction. N Engl J Med. 2019:381:1.111 21. [PN{ID, yqlSlSSl n infarction. doi:10.'l 0561 NEIM oa1917775 4t The most appropriate management is right coronary artery .D revascularization (Option C). This patient presents with an Item 30 Answer: C tn anterior ST-elevation myocardial infarction (STEMI). Prompt Educational Objective: Evaluate palpitations with a reperfusion with primary percutaneous coronary interven- l2-lead resting ECG. tion (PCI) is indicated. Because rates of achieving vessel patency are higher and more reliable with primary PCI than The most appropriate initial test for this patient with pal with thrombolysis, primary PCI is the pref'erred method of pitations is l2-lead resting ECG (Option C). The initial test treating STEMI. In addition to the left anterior descending in patients with a history of palpitations, presyncope, or artery culprit lesion, the patient has obstruction to the mid syncope when an arrhythmia is suspected should be 12 lead right coronary artery. Approximately 50'/o of patients with resting ECG. The ECG may show evidence of preexcitation, STEMI have other obstructive lesions remote from the area of ectopic rhythms, atrioventricular block, or intraventricular infarction ("nonculprit" lesions). Several studies have shown conduction delay, which can provide insight into the cause the beneflt of nonculprit lesion revascularization within 4 of the symptoms. Other conditions that might be suspected to 6 weeks following STEMI. Although optimal timing of from the 12 lead resting ECG include hypertrophic cardio nonculprit PCI has not been Iirmly established, prospective myopathy (marked left ventricular hypertrophy and deep studies have shown the safety and beneflt of immediate mul septal Q waves in leads I, aVL, and V, through Vu) or previous tivessel revascularization. myocardial infarction (Q waves), each suggesting the possi There is no indication for initiation ofpotent antiplatelet bility of ventricular tachycardia. Ventricular tachycardia also therapy, such as intravenous glycoprotein IIb/llla inhibition might be suspected if the ECG demonstrated a prolonged (Option A), following successful primary PCI in the absence QT interval. The need for further testing is determined by of thrombotic complications, because the hemorrhagic risk the ECG findings and suspicion of structural or functional outweighs potential reduction in thrombosis in patients heart disease. treated appropriately with oral dual antiplatelet therapy. Findings on the 12-lead resting ECG that indicate pos Low risk patients with non-ST elevation acute coro sible ischemia as the cause of the symptoms might lead nary syndrome can be managed with an ischemia guided to exercise ECG (Option A) as the next step. This patient's strategy. These patients will undergo noninvasive stress differential diagnosis is still broad, as he has no history or testing before hospital discharge. Cardiac catheterization is physical examination findings that suggest a heightened risk reserved for patients rvith active or intermittent ischemia, for premature coronary artery disease; exercise ECG is not including those with angina despite medical therapy or evi indicated as the initial diagnostic test. dence of ischemia on stress testing. This patient with STEMI A 30 day event monitor (Option B) is useful for infre has undergone revascularization of a culprit lesion and will quent symptoms that are thought to be related to an arrhyth undergo revascularization of a nonculprit lesion; predis mia. Use of an event monitor is ideal when symptoms last charge exercise ECG (Option B) will serve no useful purpose. longer than 1 to 2 minutes so that patients can activate the Supplemental oxygen (Option D) in the setting of nor- monitor in time for the symptoms to be recorded. These mal oxygen saturation is associated with increased mortality monitors can be carried around and then held to the chest in patients with acute coronary syndrome. The American when symptoms occur or attached to the chest via elec- Heart Association recommends oxygen therapy for oxygen trodes. However, even if the 12-lead resting ECG were nor saturation less than 90'l. or in the presence ofheart failure or mal, this patient has frequent symptoms, occurring daily. In

4t The most appropriate management is right coronary artery .D revascularization (Option C). This patient presents with an Item 30 Answer: C tn anterior ST-elevation myocardial infarction (STEMI). Prompt Educational Objective: Evaluate palpitations with a reperfusion with primary percutaneous coronary interven- l2-lead resting ECG. tion (PCI) is indicated. Because rates of achieving vessel patency are higher and more reliable with primary PCI than The most appropriate initial test for this patient with pal with thrombolysis, primary PCI is the pref'erred method of pitations is l2-lead resting ECG (Option C). The initial test treating STEMI. In addition to the left anterior descending in patients with a history of palpitations, presyncope, or artery culprit lesion, the patient has obstruction to the mid syncope when an arrhythmia is suspected should be 12 lead right coronary artery. Approximately 50'/o of patients with resting ECG. The ECG may show evidence of preexcitation, STEMI have other obstructive lesions remote from the area of ectopic rhythms, atrioventricular block, or intraventricular infarction ("nonculprit" lesions). Several studies have shown conduction delay, which can provide insight into the cause the beneflt of nonculprit lesion revascularization within 4 of the symptoms. Other conditions that might be suspected to 6 weeks following STEMI. Although optimal timing of from the 12 lead resting ECG include hypertrophic cardio nonculprit PCI has not been Iirmly established, prospective myopathy (marked left ventricular hypertrophy and deep studies have shown the safety and beneflt of immediate mul septal Q waves in leads I, aVL, and V, through Vu) or previous tivessel revascularization. myocardial infarction (Q waves), each suggesting the possi There is no indication for initiation ofpotent antiplatelet bility of ventricular tachycardia. Ventricular tachycardia also therapy, such as intravenous glycoprotein IIb/llla inhibition might be suspected if the ECG demonstrated a prolonged (Option A), following successful primary PCI in the absence QT interval. The need for further testing is determined by of thrombotic complications, because the hemorrhagic risk the ECG findings and suspicion of structural or functional outweighs potential reduction in thrombosis in patients heart disease. treated appropriately with oral dual antiplatelet therapy. Findings on the 12-lead resting ECG that indicate pos Low risk patients with non-ST elevation acute coro sible ischemia as the cause of the symptoms might lead nary syndrome can be managed with an ischemia guided to exercise ECG (Option A) as the next step. This patient's strategy. These patients will undergo noninvasive stress differential diagnosis is still broad, as he has no history or testing before hospital discharge. Cardiac catheterization is physical examination findings that suggest a heightened risk reserved for patients rvith active or intermittent ischemia, for premature coronary artery disease; exercise ECG is not including those with angina despite medical therapy or evi indicated as the initial diagnostic test. dence of ischemia on stress testing. This patient with STEMI A 30 day event monitor (Option B) is useful for infre has undergone revascularization of a culprit lesion and will quent symptoms that are thought to be related to an arrhyth undergo revascularization of a nonculprit lesion; predis mia. Use of an event monitor is ideal when symptoms last charge exercise ECG (Option B) will serve no useful purpose. longer than 1 to 2 minutes so that patients can activate the Supplemental oxygen (Option D) in the setting of nor- monitor in time for the symptoms to be recorded. These mal oxygen saturation is associated with increased mortality monitors can be carried around and then held to the chest in patients with acute coronary syndrome. The American when symptoms occur or attached to the chest via elec- Heart Association recommends oxygen therapy for oxygen trodes. However, even if the 12-lead resting ECG were nor saturation less than 90'l. or in the presence ofheart failure or mal, this patient has frequent symptoms, occurring daily. In 170

Answers and Critiques this situation, a 24-hour ambulatory ECG monitor would be with an ACE inhibitor increases the risk for angioedema; a more suitable diagnostic test than an event monitor. therefore, these agents should not be used together. In fact, A 24 hour ambulatory IjCG monitor (Option D) is ACE inhibitors must be discontinued at least 36 hours before indicated for patients with daily symptoms after a resting staft ing valsartan sacubitril. 12 lead ECG is obtained. This continuous monitor captures I(EY POIXI every heartbeat for 24 hours (or up to 30 days) and allows the patient to log symptoms during the course of the study. . In Black patients with New York Heart Association func It may be that this patient will require 24 hour ambula tional class III to IV slmptoms, isosorbide dinitrate tory ECG monitoring, but the initial test remains 12 lead hydralazine used in combination with an ACE inhibitor, resting ECG. B-blockea and aldosterone antagonist has been shov,rn to reduce mortality compared with placebo. I(EY POITT . The initial test in patients with a history of palpitations, Bibliography vl (l, presyncope, or syncope is l2-lead resting ECG. (larnethon MR, Pu l, Howard G, et ll; American Head Association Council on Iipiclemiologr and Prevention; Council on Cardiovascular Disease in CT the Young; Council on Cardiovascular and Stroke Nursing; Council on Bibliography Clinical Cardiolo$/; Council on Functional Genomics and Translational (J Weinstock C, Wagner II. Snuckel M, et al. Ilvidence based approach to pal Biolog,: and Stroke Council. Cardiovlscuhr health in African Americans: pitations. Med Clin North Am. 2021r105:93 106. IPMID: 3324652.51 a scientific statement fiom the American Heart Association. Circulation. =, E doi: 10. 101 6rj.mcna.2020.09.00.1 2017:136:e393 e,l23. IPMII): 29061565] doi:10.1161/CIR.0000000 .E 00000053.1 ta o UI Item 31 Answer: B Item 32 Answer: B = g Educational Objective: Treat heart failure with reduced Educational Objective: Treat typical atrial flutter with ejection fraction in a Black patient. catheter ablation.

this situation, a 24-hour ambulatory ECG monitor would be with an ACE inhibitor increases the risk for angioedema; a more suitable diagnostic test than an event monitor. therefore, these agents should not be used together. In fact, A 24 hour ambulatory IjCG monitor (Option D) is ACE inhibitors must be discontinued at least 36 hours before indicated for patients with daily symptoms after a resting staft ing valsartan sacubitril. 12 lead ECG is obtained. This continuous monitor captures I(EY POIXI every heartbeat for 24 hours (or up to 30 days) and allows the patient to log symptoms during the course of the study. . In Black patients with New York Heart Association func It may be that this patient will require 24 hour ambula tional class III to IV slmptoms, isosorbide dinitrate tory ECG monitoring, but the initial test remains 12 lead hydralazine used in combination with an ACE inhibitor, resting ECG. B-blockea and aldosterone antagonist has been shov,rn to reduce mortality compared with placebo. I(EY POITT . The initial test in patients with a history of palpitations, Bibliography vl (l, presyncope, or syncope is l2-lead resting ECG. (larnethon MR, Pu l, Howard G, et ll; American Head Association Council on Iipiclemiologr and Prevention; Council on Cardiovascular Disease in CT the Young; Council on Cardiovascular and Stroke Nursing; Council on Bibliography Clinical Cardiolo$/; Council on Functional Genomics and Translational (J Weinstock C, Wagner II. Snuckel M, et al. Ilvidence based approach to pal Biolog,: and Stroke Council. Cardiovlscuhr health in African Americans: pitations. Med Clin North Am. 2021r105:93 106. IPMID: 3324652.51 a scientific statement fiom the American Heart Association. Circulation. =, E doi: 10. 101 6rj.mcna.2020.09.00.1 2017:136:e393 e,l23. IPMII): 29061565] doi:10.1161/CIR.0000000 .E 00000053.1 ta o UI Item 31 Answer: B Item 32 Answer: B = g Educational Objective: Treat heart failure with reduced Educational Objective: Treat typical atrial flutter with ejection fraction in a Black patient. catheter ablation. The most appropriate treatment is isosorbide dinitrate Catheter ablation (Option B) is the most appropriate addi hydralazine (Option B). This young Black woman has peri tional treatment for this patient with typical atrial flutter. partum cardiomyopathy, New York Heart Association func- Atrial flutter is an organized macro reentrant tachycardia tional class III symptoms, and heart failure. At baseline, she with discrete regular atrial activity on ECG, usually with an is receiving appropriate guideline directed medical ther- atrial rate of 250/min to 300/min. This patient has an atrial apy (GDMT). Despite this, she has elevated blood pressure rate of 300/min with 2:1 block, resulting in a ventricular rate and heart failure symptoms. In Black patients receiving of 150/min. Typical atrial flutter is characterized electrocar GDMT, isosorbide dinitrate hydralazine has been shown diographically by a sawtooth pattern with inverted flutter to improve survival by 43"1,, reduce flrst hospitalizations by waves in leads II, III, and aVF and positive flutter waves in 3ll'/,, and improve quality of litb. lead V,. Tachycardia induced heart failure (HF) may be the Digoxin (Option A) has been shown to reduce hospital initial presentation of poorly controlled atrial flutter among admissions in patients with heart failure, with no effect on patients who are otherwise asymptomatic, and unrecog mortality. Compared with isosorbide dinitrate-hydralazine, nized, prolonged tachycardia may lead to HFl, This form of which shows a mortality benefit, digoxin would not be the cardiomyopathy is often reversible with control of heart rate best next agent to add to this patient's regimen. and/or rhythm. In typical atrial flutter, catheter ablation may In patients with type 2 diabetes mellitus and established be curative for most patients and is appropriate first line heart tailure with reduced ejection fraction, a sodium therapy for this patient. Acute cardioversion was a reasonable glucose cotransporter 2 (SGLI2) inhibitor with proven ben choice for this patient to achieve acute improvement in clini efit in this patient population is recommended to reduce cal status. However, it is extremely likely that atrial flutter will risk for worsening heart failure and cardiovascular death. recur, which makes this patient at very high risk for recurrent ln patients with diabetes and established atherosclerotic HF and underscores the need for definitive treatment. cardiovascular disease (ASCVD) or several ASCVD risk fac- A rhythm control strate$/ is favored in atrial flutter tors, either an SGLT2 inhibitor or a glucagon like peptide because rate control may be difficult to achieve and often I receptor agonist, such as liraglutide (Option C), is recom requires high doses of more than one drug. However, drug mended to reduce both cardiovascular and all cause mor therapy (Options A, C, D) may be complicated, toxic, and tatity. Liraglutide is not indicated tbr this patient who has often unsuccessful. p Blockers are unlikely to prevent or heart failure in the absence ofASCVD risk factors and does treat a recurrence. Catheter ablation is the deflnitive treat not have diabetes. ment for typical atrial flutter, owing to a very high success Adding an ACE inhibitor, such as lisinopril (Option D), to rate (>95'/.) and low complication rate. this patient's medication regimen is not appropriate because Because the risk for recurrence is high and this patient she is already taking valsartan-sacubitril, which in random poorly tolerates the rapid ventricular rate, observation with ized trials was shown to improve survival compared with the out additional treatment (Option E) is insufficient for this ACE inhibitor enalapril. In addition, using valsartan sacubitril patient. Catheter ablation is the most appropriate treatment.

The most appropriate treatment is isosorbide dinitrate Catheter ablation (Option B) is the most appropriate addi hydralazine (Option B). This young Black woman has peri tional treatment for this patient with typical atrial flutter. partum cardiomyopathy, New York Heart Association func- Atrial flutter is an organized macro reentrant tachycardia tional class III symptoms, and heart failure. At baseline, she with discrete regular atrial activity on ECG, usually with an is receiving appropriate guideline directed medical ther- atrial rate of 250/min to 300/min. This patient has an atrial apy (GDMT). Despite this, she has elevated blood pressure rate of 300/min with 2:1 block, resulting in a ventricular rate and heart failure symptoms. In Black patients receiving of 150/min. Typical atrial flutter is characterized electrocar GDMT, isosorbide dinitrate hydralazine has been shown diographically by a sawtooth pattern with inverted flutter to improve survival by 43"1,, reduce flrst hospitalizations by waves in leads II, III, and aVF and positive flutter waves in 3ll'/,, and improve quality of litb. lead V,. Tachycardia induced heart failure (HF) may be the Digoxin (Option A) has been shown to reduce hospital initial presentation of poorly controlled atrial flutter among admissions in patients with heart failure, with no effect on patients who are otherwise asymptomatic, and unrecog mortality. Compared with isosorbide dinitrate-hydralazine, nized, prolonged tachycardia may lead to HFl, This form of which shows a mortality benefit, digoxin would not be the cardiomyopathy is often reversible with control of heart rate best next agent to add to this patient's regimen. and/or rhythm. In typical atrial flutter, catheter ablation may In patients with type 2 diabetes mellitus and established be curative for most patients and is appropriate first line heart tailure with reduced ejection fraction, a sodium therapy for this patient. Acute cardioversion was a reasonable glucose cotransporter 2 (SGLI2) inhibitor with proven ben choice for this patient to achieve acute improvement in clini efit in this patient population is recommended to reduce cal status. However, it is extremely likely that atrial flutter will risk for worsening heart failure and cardiovascular death. recur, which makes this patient at very high risk for recurrent ln patients with diabetes and established atherosclerotic HF and underscores the need for definitive treatment. cardiovascular disease (ASCVD) or several ASCVD risk fac- A rhythm control strate$/ is favored in atrial flutter tors, either an SGLT2 inhibitor or a glucagon like peptide because rate control may be difficult to achieve and often I receptor agonist, such as liraglutide (Option C), is recom requires high doses of more than one drug. However, drug mended to reduce both cardiovascular and all cause mor therapy (Options A, C, D) may be complicated, toxic, and tatity. Liraglutide is not indicated tbr this patient who has often unsuccessful. p Blockers are unlikely to prevent or heart failure in the absence ofASCVD risk factors and does treat a recurrence. Catheter ablation is the deflnitive treat not have diabetes. ment for typical atrial flutter, owing to a very high success Adding an ACE inhibitor, such as lisinopril (Option D), to rate (>95'/.) and low complication rate. this patient's medication regimen is not appropriate because Because the risk for recurrence is high and this patient she is already taking valsartan-sacubitril, which in random poorly tolerates the rapid ventricular rate, observation with ized trials was shown to improve survival compared with the out additional treatment (Option E) is insufficient for this ACE inhibitor enalapril. In addition, using valsartan sacubitril patient. Catheter ablation is the most appropriate treatment. 171

Answers and Critiques I(EY PO I ilI I(EY POITT . Catheter ablation is an appropriate treatment for . Guideline-directed medical therapy for peripheral patients with atrial flutter. artery disease includes exercise; an antiplatelet agent; and aggressive management of atherosclerotic risk Bibliography factors, including smoking, hypertension, diabetes Page RL, loglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the mellitus, and dyslipidemia. management of adult patients with supraventricular tachycardia: execu tive summary: a report of the American College of Cardiolory/American Heart Association Task Force on Clinical Practice Guidelines and the Bibliography Heart Rhythm Societll Heart Rhythm. 2016r13:e92-135. IPMID: Gerhard-Herman MD. Gornik HL, Barrett C, et dl. 2016 AHATACC guideline 264090971 doi:10.1016,i. hrrhm.2O15. 09.018 on the management of patients with lower extremity peripheral artery disease: executive summary: a report of the American College of Cardiolory/American Heart Association Task Force on Clinical Practice Item 33 Answer: D Cuidelines. J Am Coll Cardiol. 2017;69:1.165-1508. [PMID: 27851991] D doi:10.1016/j.jacc.2016.11.008 (t Educational Objective: Treat peripheral artery disease with guideline-directed medical therapy. (D = UI This patient requires no additional treatment (Option D). Item 34 Answer: C o, Patients with peripheral artery disease (PAD) are less Iikely CL Educational Objective: Monitor a patient with bicuspid n to receive guideline-directed medical therapy than are aortic valve and aortopathy with surveillance echocardi- patients with other forms of cardiovascular disease, includ- ography. .,cr ing coronary artery disease. Antiplatelet therapy with aspi- .D rin alone (75 325 mg/d) or clopidogrel alone (75 mg/d) is The most appropriate management is serial echocardio u] recommended to reduce myocardial infarction (MI), stroke, graphic imaging (Option C). Bicuspid valvulopathy is often and vascular death in patients with symptomatic PAD. Treat accompanied by aortic abnormalities, including aneurysm, ment with a statin is indicated for all patients with PAD. dissection, or coarctation. In patients with a bicuspid aortic Antihypertensive therapy should be administered to patients valve, the ascending aorta and aortic arch should be exam with hypertension and PAD to reduce the risk for MI, stroke, ined for aortopathy with cardiac magnetic resonance (CMR) heart failure, and cardiovascular death. Patients with PAD imaging, echocardiography, or cardiac CT. In patients with who smoke cigarettes or use other forms of tobacco should a bicuspid aortic valve and aortic sinuses or an ascending be advised at every visit to quit. Although not guideline rec- aorta 4.0 cm or Iarger in diameter, lifelong serial evalua ommended, the combination of low-dose rivaroxaban plus tion of the size and morphologr of the aortic sinuses and low-dose aspirin in patients with PAD may reduce cardio ascending aorta by echocardiography, CMR imaging, or CT vascular death, MI, or stroke compared with aspirin alone. angiography is reasonable. This otherwise healthy patient This patient is receiving appropriate management for PAD, with mild aortic regurgitation and an ascending aortic root and no additional treatment is recommended at this time. diameter below the threshold for repair should undergo Cilostazol (Option A) is recommended for patients repeat echocardiography for surveillance. with PAD and intermittent claudication to improve symp- Management of bicuspid aortic valve disease is deter toms and maximal walking distance; however, cilostazol mined by the predominant lesion type (stenosis or regur- has no impact on mortaliry MI, or stroke. Furthermore, this gitation) and its severity. In patients with a bicuspid valve patient is symptom-free and therefore has no indication for undergoing surgery for severe aortic stenosis or regurgi cilostazol. tation, surgical repair of the ascending aorta (Option A) is Evolocumab (Option B) is a proprotein convertase advised when the aortic diameter is greater than 4.5 cm. In subtilisin/kexin type 9 (PCSK9) inhibitor. Treatment with the absence of surgical indications for a stenotic or regur PCSK9 inhibitors produces a 50'2, to 60'2, reduction in LDL gitant aortic valve, surgical repair of the ascending aorta or cholesterol. The American College of Cardiologr and Ameri aortic sinuses is advised when the aortic diameter is greater can Heart Association guidelines suggest an LDL cholesterol than 5.5 cm or when the diameter is greater than 5.0 cm in a target of less than 70 mg/dl (1.8 mmol/L) for patients at very patient with additional risk factors for dissection (family his- high risk for future atherosclerotic cardiovascular events. tory rate of progression >0.5 cm/year). This asymptomatic However, this patient has an LDL cholesterol level of 50 mg/dl patient does not have an indication for surgical intervention. (t.3 mmol/L) while being treated with rosuvastatin; treat- In patients with a bicuspid aortic valve, CMR imaging ment with evolocumab is not indicated. (Option B), angiography, or CT angiography is indicated if Ticagrelor (Option C) currently does not have an indi- morphologz of the aortic sinuses, sinotubular junction, or cation for use in patients with PAD. In the EUCLID study of ascending aorta cannot be assessed accurately or fully by 13,885 patients with lower extremity PAD, monotherapy with echocardiography. This patient has no indication for CMR ticagrelor had very similar effectiveness and safety outcomes imaging. to clopidogrel. The use of ticagrelor in this setting, when No medical therapies slow aortic dilatation in patients added to aspirin, has not been shown to decrease cardiovas- with bicuspid aortopathy. Blood pressure should be con- cular risk. trolled in patients with concomitant hypertension by using

I(EY PO I ilI I(EY POITT . Catheter ablation is an appropriate treatment for . Guideline-directed medical therapy for peripheral patients with atrial flutter. artery disease includes exercise; an antiplatelet agent; and aggressive management of atherosclerotic risk Bibliography factors, including smoking, hypertension, diabetes Page RL, loglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the mellitus, and dyslipidemia. management of adult patients with supraventricular tachycardia: execu tive summary: a report of the American College of Cardiolory/American Heart Association Task Force on Clinical Practice Guidelines and the Bibliography Heart Rhythm Societll Heart Rhythm. 2016r13:e92-135. IPMID: Gerhard-Herman MD. Gornik HL, Barrett C, et dl. 2016 AHATACC guideline 264090971 doi:10.1016,i. hrrhm.2O15. 09.018 on the management of patients with lower extremity peripheral artery disease: executive summary: a report of the American College of Cardiolory/American Heart Association Task Force on Clinical Practice Item 33 Answer: D Cuidelines. J Am Coll Cardiol. 2017;69:1.165-1508. [PMID: 27851991] D doi:10.1016/j.jacc.2016.11.008 (t Educational Objective: Treat peripheral artery disease with guideline-directed medical therapy. (D = UI This patient requires no additional treatment (Option D). Item 34 Answer: C o, Patients with peripheral artery disease (PAD) are less Iikely CL Educational Objective: Monitor a patient with bicuspid n to receive guideline-directed medical therapy than are aortic valve and aortopathy with surveillance echocardi- patients with other forms of cardiovascular disease, includ- ography. .,cr ing coronary artery disease. Antiplatelet therapy with aspi- .D rin alone (75 325 mg/d) or clopidogrel alone (75 mg/d) is The most appropriate management is serial echocardio u] recommended to reduce myocardial infarction (MI), stroke, graphic imaging (Option C). Bicuspid valvulopathy is often and vascular death in patients with symptomatic PAD. Treat accompanied by aortic abnormalities, including aneurysm, ment with a statin is indicated for all patients with PAD. dissection, or coarctation. In patients with a bicuspid aortic Antihypertensive therapy should be administered to patients valve, the ascending aorta and aortic arch should be exam with hypertension and PAD to reduce the risk for MI, stroke, ined for aortopathy with cardiac magnetic resonance (CMR) heart failure, and cardiovascular death. Patients with PAD imaging, echocardiography, or cardiac CT. In patients with who smoke cigarettes or use other forms of tobacco should a bicuspid aortic valve and aortic sinuses or an ascending be advised at every visit to quit. Although not guideline rec- aorta 4.0 cm or Iarger in diameter, lifelong serial evalua ommended, the combination of low-dose rivaroxaban plus tion of the size and morphologr of the aortic sinuses and low-dose aspirin in patients with PAD may reduce cardio ascending aorta by echocardiography, CMR imaging, or CT vascular death, MI, or stroke compared with aspirin alone. angiography is reasonable. This otherwise healthy patient This patient is receiving appropriate management for PAD, with mild aortic regurgitation and an ascending aortic root and no additional treatment is recommended at this time. diameter below the threshold for repair should undergo Cilostazol (Option A) is recommended for patients repeat echocardiography for surveillance. with PAD and intermittent claudication to improve symp- Management of bicuspid aortic valve disease is deter toms and maximal walking distance; however, cilostazol mined by the predominant lesion type (stenosis or regur- has no impact on mortaliry MI, or stroke. Furthermore, this gitation) and its severity. In patients with a bicuspid valve patient is symptom-free and therefore has no indication for undergoing surgery for severe aortic stenosis or regurgi cilostazol. tation, surgical repair of the ascending aorta (Option A) is Evolocumab (Option B) is a proprotein convertase advised when the aortic diameter is greater than 4.5 cm. In subtilisin/kexin type 9 (PCSK9) inhibitor. Treatment with the absence of surgical indications for a stenotic or regur PCSK9 inhibitors produces a 50'2, to 60'2, reduction in LDL gitant aortic valve, surgical repair of the ascending aorta or cholesterol. The American College of Cardiologr and Ameri aortic sinuses is advised when the aortic diameter is greater can Heart Association guidelines suggest an LDL cholesterol than 5.5 cm or when the diameter is greater than 5.0 cm in a target of less than 70 mg/dl (1.8 mmol/L) for patients at very patient with additional risk factors for dissection (family his- high risk for future atherosclerotic cardiovascular events. tory rate of progression >0.5 cm/year). This asymptomatic However, this patient has an LDL cholesterol level of 50 mg/dl patient does not have an indication for surgical intervention. (t.3 mmol/L) while being treated with rosuvastatin; treat- In patients with a bicuspid aortic valve, CMR imaging ment with evolocumab is not indicated. (Option B), angiography, or CT angiography is indicated if Ticagrelor (Option C) currently does not have an indi- morphologz of the aortic sinuses, sinotubular junction, or cation for use in patients with PAD. In the EUCLID study of ascending aorta cannot be assessed accurately or fully by 13,885 patients with lower extremity PAD, monotherapy with echocardiography. This patient has no indication for CMR ticagrelor had very similar effectiveness and safety outcomes imaging. to clopidogrel. The use of ticagrelor in this setting, when No medical therapies slow aortic dilatation in patients added to aspirin, has not been shown to decrease cardiovas- with bicuspid aortopathy. Blood pressure should be con- cular risk. trolled in patients with concomitant hypertension by using 172

Answers and Critiques standard drug therapy, including thiazide diuretics, calcium early and sustained relief of signs and symptoms of inflam channel blockers, ACE inhibitors, or angiotensin receptor mation and signiflcant reduction in the risk for recurrent blockers. Angiotensin receptor blockers, such as losartan pericarditis. (Option D), slow the rate of progressive aortic root dilation Intravenous immune globulin (Option B) has been used in patients with Marfan aortopathy, even in the absence with some success to treat pericarditis that recurs despite of hypertension, but are not eflective in bicuspid aortopa- combination therapy including prednisone. For this patient, thy and are not indicated in this patient in the absence of glucocorticoid treatment should precede consideration of hypertension. intravenous immune globulin. Ibuprofen monotherapy without colchicine (Option C) TEY POIilIS may be considered to treat an initial episode of acute peri- . Management of bicuspid aortic valve disease follows carditis, but it is unlikely to be eflective in patients with the recommendations for the predominant valve recurrent pericarditis. lesion type (aortic stenosis or regurgitation) and its |a KEY POIIII Qt severity. . In patients with a bicuspid aortic valve and aortic . In patients with recurrent pericarditis initially treated lr with both colchicine and an NSAID, the addition of a sinuses or an ascending aorta 4.0 cm or larger in L' glucocorticoid should be considered. diameter, lifelong serial imaging is reasonable. =, r! Bibliography vt Bibliography o, Adler Y, Charron R Imazio M, et al; ESC Scientific Document Group. 2015 Otto CM, Nishimura RA. Bonow RO, et al. 2020 ACC/AHA guideline for the ESC guidelines for the diagnosis and management ofpericardial diseases: ttl management of patients with valvular heart disease: a report of the The Task Force for the Diagnosis and Management ofPericardial Diseases = E American College of CardiolorylAmerican Heart Association loint of the European Society of Cardiologl (ESC) Endorsed by: The European Committee on Clinical Practice Cuidelines. Circulation. 2o2l:143:e72 Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2015;36: e227. IPMID: 33332150] doi:10.1161/CIR.0000000000000923 2927-64. IPMID: 26320112] doi:10.1093/eurhearti/ehv318

standard drug therapy, including thiazide diuretics, calcium early and sustained relief of signs and symptoms of inflam channel blockers, ACE inhibitors, or angiotensin receptor mation and signiflcant reduction in the risk for recurrent blockers. Angiotensin receptor blockers, such as losartan pericarditis. (Option D), slow the rate of progressive aortic root dilation Intravenous immune globulin (Option B) has been used in patients with Marfan aortopathy, even in the absence with some success to treat pericarditis that recurs despite of hypertension, but are not eflective in bicuspid aortopa- combination therapy including prednisone. For this patient, thy and are not indicated in this patient in the absence of glucocorticoid treatment should precede consideration of hypertension. intravenous immune globulin. Ibuprofen monotherapy without colchicine (Option C) TEY POIilIS may be considered to treat an initial episode of acute peri- . Management of bicuspid aortic valve disease follows carditis, but it is unlikely to be eflective in patients with the recommendations for the predominant valve recurrent pericarditis. lesion type (aortic stenosis or regurgitation) and its |a KEY POIIII Qt severity. . In patients with a bicuspid aortic valve and aortic . In patients with recurrent pericarditis initially treated lr with both colchicine and an NSAID, the addition of a sinuses or an ascending aorta 4.0 cm or larger in L' glucocorticoid should be considered. diameter, lifelong serial imaging is reasonable. =, r! Bibliography vt Bibliography o, Adler Y, Charron R Imazio M, et al; ESC Scientific Document Group. 2015 Otto CM, Nishimura RA. Bonow RO, et al. 2020 ACC/AHA guideline for the ESC guidelines for the diagnosis and management ofpericardial diseases: ttl management of patients with valvular heart disease: a report of the The Task Force for the Diagnosis and Management ofPericardial Diseases = E American College of CardiolorylAmerican Heart Association loint of the European Society of Cardiologl (ESC) Endorsed by: The European Committee on Clinical Practice Cuidelines. Circulation. 2o2l:143:e72 Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2015;36: e227. IPMID: 33332150] doi:10.1161/CIR.0000000000000923 2927-64. IPMID: 26320112] doi:10.1093/eurhearti/ehv318 Item 35 Answer: D Educational Obiective: Treat recurrent pericarditis. Item 36 Answer: D Educational Objective: Treat a patient with extended The most appropriate treatment is triple therapy with an dual antiplatelet therapy following percutaneous NSAID, such as ibuprofen; colchicine; and a glucocorti- intervention. coid, such as prednisone (Option D). This patient meets the deflnition of recurrent idiopathic pericarditis, having a Dual antiplatelet therapy (DAPT) beyond l year (Option D) documented flrst episode of acute pericarditis flollowed by is reasonable for this patient with acute coronary syndrome a recurrent episode after a symptom-free interval of 4 to (ACS) to reduce the risk for repeat myocardial infarction. 6 weeks. This patient had a favorable response to initial treat DAPT with aspirin and P2Yr2 inhibition is recommended ment with an NSAID and colchicine, followed by recurrent for I year after ACS presentation with ST-elevation myo- symptoms after tapering standard therapy on two difl'erent cardial infarction (STEMI) or non STEMI. Clopidogrel or occasions. Recurrence occurs in 15'2, to 30'/. of pericarditis ticagrelor is typically indicated as the P2Y,, inhibitor, cases, and the recurrence rate is higher when initial therapy regardless of revascularization status, and prasugrel is does not include colchicine. In patients initially treated only reserved for patients treated with percutaneous coronary with NSAIDs, it would be reasonable to use the combi intervention. Whereas lifelong aspirin therapy is recom nation of NSAIDs and colchicine to treat a recurrence. In mended as secondary prevention after discontinuation of patients initially treated with both colchicine and NSAIDs, the P2Y,, inhibitor, guidelines indicate that it is reasonable the addition of a low to moderate dose of prednisone is to extend DAPT beyond 12 months (up to 36 months) in reasonable to achieve better control of symptoms. When patients who have successfully tolerated 12 months of DAPT patients re-present with pain but without other evidence and remain at high risk for recurrent vascular events (e.9., of pericarditis, cardiac CT or MRI and measurement of those with depressed left ventricular systolic function, C-reactive protein level may infbrm the decision of whether saphenous vein graft stenting, or diabetes mellitus), for to add glucocorticoids. Infectious diseases, including tuber whom the beneflt exceeds the increased bleeding risk. A culosis, must be excluded before starting a glucocorticoid. personalized approach is appropriate when considering Glucocorticoids are not recommended as flrst line therapy whether to extend DAPT, with readily available risk scores, fbr acute pericarditis. such as the DAPT bleeding risk score, which provides com The interleukin 1 receptor antagonist anakinra posite risk beneflt assessment for patients considered for (Option A) has shown benefit in small trials for treatment of DAPT extension. colchicine-resistant, glucocorticoid dependent recurrent Low-dose aspirin is the preferred single antiplatelet pericarditis, but it is not, at present, FDA approved for this agent beyond 1 year after ACS because of its low cost, effec use. Consideration should be given to initiating rilonacept, tiveness, and lower risk for bleeding compared with P2Yr2 an FDA approved interleukin 1 trap that demonstrated inhibitors. Clopidogrel is a reasonable substitute for aspirin

Item 35 Answer: D Educational Obiective: Treat recurrent pericarditis. Item 36 Answer: D Educational Objective: Treat a patient with extended The most appropriate treatment is triple therapy with an dual antiplatelet therapy following percutaneous NSAID, such as ibuprofen; colchicine; and a glucocorti- intervention. coid, such as prednisone (Option D). This patient meets the deflnition of recurrent idiopathic pericarditis, having a Dual antiplatelet therapy (DAPT) beyond l year (Option D) documented flrst episode of acute pericarditis flollowed by is reasonable for this patient with acute coronary syndrome a recurrent episode after a symptom-free interval of 4 to (ACS) to reduce the risk for repeat myocardial infarction. 6 weeks. This patient had a favorable response to initial treat DAPT with aspirin and P2Yr2 inhibition is recommended ment with an NSAID and colchicine, followed by recurrent for I year after ACS presentation with ST-elevation myo- symptoms after tapering standard therapy on two difl'erent cardial infarction (STEMI) or non STEMI. Clopidogrel or occasions. Recurrence occurs in 15'2, to 30'/. of pericarditis ticagrelor is typically indicated as the P2Y,, inhibitor, cases, and the recurrence rate is higher when initial therapy regardless of revascularization status, and prasugrel is does not include colchicine. In patients initially treated only reserved for patients treated with percutaneous coronary with NSAIDs, it would be reasonable to use the combi intervention. Whereas lifelong aspirin therapy is recom nation of NSAIDs and colchicine to treat a recurrence. In mended as secondary prevention after discontinuation of patients initially treated with both colchicine and NSAIDs, the P2Y,, inhibitor, guidelines indicate that it is reasonable the addition of a low to moderate dose of prednisone is to extend DAPT beyond 12 months (up to 36 months) in reasonable to achieve better control of symptoms. When patients who have successfully tolerated 12 months of DAPT patients re-present with pain but without other evidence and remain at high risk for recurrent vascular events (e.9., of pericarditis, cardiac CT or MRI and measurement of those with depressed left ventricular systolic function, C-reactive protein level may infbrm the decision of whether saphenous vein graft stenting, or diabetes mellitus), for to add glucocorticoids. Infectious diseases, including tuber whom the beneflt exceeds the increased bleeding risk. A culosis, must be excluded before starting a glucocorticoid. personalized approach is appropriate when considering Glucocorticoids are not recommended as flrst line therapy whether to extend DAPT, with readily available risk scores, fbr acute pericarditis. such as the DAPT bleeding risk score, which provides com The interleukin 1 receptor antagonist anakinra posite risk beneflt assessment for patients considered for (Option A) has shown benefit in small trials for treatment of DAPT extension. colchicine-resistant, glucocorticoid dependent recurrent Low-dose aspirin is the preferred single antiplatelet pericarditis, but it is not, at present, FDA approved for this agent beyond 1 year after ACS because of its low cost, effec use. Consideration should be given to initiating rilonacept, tiveness, and lower risk for bleeding compared with P2Yr2 an FDA approved interleukin 1 trap that demonstrated inhibitors. Clopidogrel is a reasonable substitute for aspirin 173

) : Answers and Critiques i in patients with aspirin sensitivity or intolerance, or those and support the diagnosis of'VT. Wide complex tachycardias with a history of upper gastrointestinal bleeding. There is no that are positive in lead aVR, have a QRS morpholory that is indication to stop aspirin (Option A) in this patient. concordant (all predominantly positive or negative) in the Stopping both aspirin and clopidogrel (Option B) is not precordial leads, have QRS morphologr other than typi' ;

in patients with aspirin sensitivity or intolerance, or those and support the diagnosis of'VT. Wide complex tachycardias with a history of upper gastrointestinal bleeding. There is no that are positive in lead aVR, have a QRS morpholory that is indication to stop aspirin (Option A) in this patient. concordant (all predominantly positive or negative) in the Stopping both aspirin and clopidogrel (Option B) is not precordial leads, have QRS morphologr other than typi' ; indicated. This patient needs an antiplatelet agent consisting cal right or left bundle branch block, and exhibit extreme of aspirin, clopidogrel, or both to reduce the risk for stent axis deviation ("northwest" axis) are usually VT. Fusion \ thrombosis and myocardial infarction, stroke, and other beats (suprar,entricular and ventricular impulses coinciding I cardiovascular events. to produce a hybrid complex) (orrou's in the ECG shown Evidence from the COMPASS (Rivaroxaban for the belou') and capture beats (a sinus conducted beat producing i Prevention of Major Cardiovascular Events in Coronary or a normal QRS) are all highly suggestive of VT. Of importance, i i Peripheral Artery Disease) trial demonstrated that aspirin the fact that the patient is awake. alert. and interactive and, (too mg/d) plus rivaroxaban (2.s mg twice daily), a direct or has a measurable bloocl pressure does not exclude VT. : factor Xa inhibitor, was associated with improved major lf the origin of a wide-complex tachycardia cannot be j ur adverse cardiovascular and limb end points compared with determined, VT should be assumed until expert consultation E (D aspirin plus placebo in patients with coronary artery dis can be obtained. This patient with structural heart disease :

indicated. This patient needs an antiplatelet agent consisting cal right or left bundle branch block, and exhibit extreme of aspirin, clopidogrel, or both to reduce the risk for stent axis deviation ("northwest" axis) are usually VT. Fusion \ thrombosis and myocardial infarction, stroke, and other beats (suprar,entricular and ventricular impulses coinciding I cardiovascular events. to produce a hybrid complex) (orrou's in the ECG shown Evidence from the COMPASS (Rivaroxaban for the belou') and capture beats (a sinus conducted beat producing i Prevention of Major Cardiovascular Events in Coronary or a normal QRS) are all highly suggestive of VT. Of importance, i i Peripheral Artery Disease) trial demonstrated that aspirin the fact that the patient is awake. alert. and interactive and, (too mg/d) plus rivaroxaban (2.s mg twice daily), a direct or has a measurable bloocl pressure does not exclude VT. : factor Xa inhibitor, was associated with improved major lf the origin of a wide-complex tachycardia cannot be j ur adverse cardiovascular and limb end points compared with determined, VT should be assumed until expert consultation E (D aspirin plus placebo in patients with coronary artery dis can be obtained. This patient with structural heart disease : ut o, ease and peripheral artery disease (PAD). This patient does (in the form of ischemic hearl disease) has ECG findings l not have PAD, and aspirin plus rivaroxaban (Option C) is characteristic of VT. It is monomorphic VT because consecu - r

ut o, ease and peripheral artery disease (PAD). This patient does (in the form of ischemic hearl disease) has ECG findings l not have PAD, and aspirin plus rivaroxaban (Option C) is characteristic of VT. It is monomorphic VT because consecu - r CL not indicated. a't tive beats have a uniform and stable QRS morpholog,l : Antidromic atrioventricular reciprocating tachy'cardia is XEY POITI .Et a preexcited tachycardia (Option B) that is characterized by o Extending dual antiplatelet therapy (DA[T) beyond a u,ide. slurred QRS complex resulting from conduction orer .D u) 12 months is reasonable in patients who have success- the bypass tract and activation ol the ventricle r,r.ithout use of fully tolerated 12 months of DAPT and remain at high the specialized conduction system. lt may be lery difficult to risk for recurrent vascular events ifthe benefit exceeds distingrish from VT on a single ECG tracing. Houever, this the risk for increased bleeding. tachycardia tends to occur in younger people, and it is not i

CL not indicated. a't tive beats have a uniform and stable QRS morpholog,l : Antidromic atrioventricular reciprocating tachy'cardia is XEY POITI .Et a preexcited tachycardia (Option B) that is characterized by o Extending dual antiplatelet therapy (DA[T) beyond a u,ide. slurred QRS complex resulting from conduction orer .D u) 12 months is reasonable in patients who have success- the bypass tract and activation ol the ventricle r,r.ithout use of fully tolerated 12 months of DAPT and remain at high the specialized conduction system. lt may be lery difficult to risk for recurrent vascular events ifthe benefit exceeds distingrish from VT on a single ECG tracing. Houever, this the risk for increased bleeding. tachycardia tends to occur in younger people, and it is not i associated with cannon o waves, lusion beats, or capture beats. \ Bibliography Antidromic atrioventricular reciprocating tachycardia is much l.evine GN. Bates ER, Bittl JA, et al. 2016 ACC/AHA guideline focused update less likely than VT in this patient with structural heart disease. on duration ofdual antiplatelet therapy in patients with coronary artery disease: a report of the American College of Cardiolosr/American Heart SW associated with a bundle branch block or a nonspe \ l Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. cific intraventricular conduction delay (Option C) will present 2O16;68:1082-115. IPMID: 27036918] doi:10.1016/j.jacc.2016.03.513 as a n ide-complex tachlrcardia (SVf u,ith aberranry). However, 1

associated with cannon o waves, lusion beats, or capture beats. \ Bibliography Antidromic atrioventricular reciprocating tachycardia is much l.evine GN. Bates ER, Bittl JA, et al. 2016 ACC/AHA guideline focused update less likely than VT in this patient with structural heart disease. on duration ofdual antiplatelet therapy in patients with coronary artery disease: a report of the American College of Cardiolosr/American Heart SW associated with a bundle branch block or a nonspe \ l Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. cific intraventricular conduction delay (Option C) will present 2O16;68:1082-115. IPMID: 27036918] doi:10.1016/j.jacc.2016.03.513 as a n ide-complex tachlrcardia (SVf u,ith aberranry). However, 1 the same reasons that make antidromic atrioventricular recip- tr Item 37 Answer: A Educational Objective: Diagnose ventricular tachycardia. rocating tachycardia unlikely apply to S\T with aberrancy. Torsades de pointes (Option D) is a polymorphic VT with ventricular rates from l60rmin to 250imin. The tor l

tr Item 37 Answer: A Educational Objective: Diagnose ventricular tachycardia. rocating tachycardia unlikely apply to S\T with aberrancy. Torsades de pointes (Option D) is a polymorphic VT with ventricular rates from l60rmin to 250imin. The tor l The most likely diagnosis fbr this wide-complex tachycardia sades de pointes pattern is associated with QT intervai pro , is ventricular tachycardia (VT) (Option A). A wide-complex longation and is characterized by changing ofthe QRS axis ! j tachycardia is any tachycardia with a QRS complex of 120 ms by 180 degrees every few beats. This pattern is not present, or longer. Differential diagnoses include suprar,entricular and torsades de pointes is ar.r unlikely diagnosis. '1 tachycardia (SVT) with aberrancy, preexcited tachycardia TEY POIXI (antidromic tachycardia), ventricular paced rhythm, and :

tachycardia (SVT) with aberrancy, preexcited tachycardia TEY POIXI (antidromic tachycardia), ventricular paced rhythm, and : VT. In adult patients with structural heart disease, 95'71, of . In adult patients with structural heart disease, 95% of l wide-complex tachycardias are VT. Several important clin wide-complex tachycardias are ventricular tachycardia. ical and ECG features can distinguish VT from other condi : Bibliography \ tions. The presence of irregular jugular venous pulsations Kxtritsis DG, Brugada J. Differential diagnosis ol wide QRS tachycardias. of greater amplitude than normai venous waves (cannon Arrhythm Electrophysiol Rev 2020;9: 155 160. [PMID: 33240511] doi;10. waves) signal the presence of atrioventricuiar dissociation 15420 /aer.2O2O.2O n n IIEM 37 174 i t I

Answers and Item 38 Answer: A Bibliography Educational Objective: Treat a patient with heart failure Murphy Sf lbrahim NE, Ja:n:uzzi JL Jr. Heart failure u,ith recluced ejection fraction:areview.JAN4A.202O;324:,188 S0.1.IPMTD:32749493]doi:10.1001i with aldosterone antagonist therapy jama.2020.10262 The most appropriate treatment is to add eplerenone (Option A) to this patient's regimen. He is clinically stable with New Item 39 Answer: C York Heart Association functional class III heart failure Educational Objective: Reduce cardiovascular risk with symptoms, and the goal of treatment at this point is to opti smoking cessation. mize medical therapy to improve his chances of maintaining clinical stability and reducing morlality. Aldosterone antag Smoking cessation counseling and varenicline (Option C) is onist therapy (spironolactone or eplerenone) is inclicated in the most appropriate management for this patient. lbbacco all patients with symptomatic hearl failure with reduced use is the leading preventable cause ofdisease, disability, and

The most appropriate treatment is to add eplerenone (Option A) to this patient's regimen. He is clinically stable with New Item 39 Answer: C York Heart Association functional class III heart failure Educational Objective: Reduce cardiovascular risk with symptoms, and the goal of treatment at this point is to opti smoking cessation. mize medical therapy to improve his chances of maintaining clinical stability and reducing morlality. Aldosterone antag Smoking cessation counseling and varenicline (Option C) is onist therapy (spironolactone or eplerenone) is inclicated in the most appropriate management for this patient. lbbacco all patients with symptomatic hearl failure with reduced use is the leading preventable cause ofdisease, disability, and ejection fraction and normal kidney function (estimated glo death in the United States. Almost one third of cardiovascular disease deaths are attributable to smoking and exposure to |a merular filtration rate >30 mL/min/1.73 m2), as these agents (lr have been shown to improve suruival in this population. secondhand smoke. Even low Ievels of smoking increase risks ET Eplerenone is a more selective aldosterone antagonist than for acute myocardial infarction; thus, reducing the number of spironolactone; it is associated with fewer endocrine side cigarettes per day does not eliminate risk completely. Smok tJ effects and reduced incidence of gynecomastia (17, vs. 10,/,,). ing cessation substantially reduces cardiovascular risk within !t 2 years, with risk returning to the level of a nonsmoker after IE Therefore, although this patient had gynecomastia when tt approximately 15 years. Smoking status should be assessed taking spironolactone, it is reasonable to try epierenone as c, an alternative aldosterone antagonist. at every visit, and cessation counseling and pharmacologic F ta therapy should be oflered to active smokers. Of all the rec g Ivabradine (Option B) has been shown to reduce heart ommended pharmacologic agents approved for smoking failure admissions in patients u,'ith symptomatic heart cessation, varenicline is the most ellective monotherapy Com- failure with reduced ejection fraction (ejection fiaction bination pharmacologic therapy is probably more eflbctive. <35%) who are in sinus rhythm with a heart rate of at least Psychosocial factors, including depression, anger, and TOlmin and taking maximally tolerated doses of a p blocker. anxiety, are associated with worse cardiovascular outcomes. Ivabradine works by slowing the sinus node and decreasing Depression has been linked to a higher risk for cardiovas heart rate. For patients with atrial flbrillation, however, the cular events. Psychosocial stressors also aflect the course of drug is not helpful. treatment and adherence to healthy lifestyles after a cardio- Guideline directed medical therapy for heart failure vascular event. Although it is impoftant to detect and treat includes B-blocker therapy for al1 patients, regardless of these disorders ifpresent, there is no evidence that detection heart failure stage. The benefits of p blocker therapy do and treatment (Option A) affect cardiovascular risk itself. not seem to be a class effect, and one of the three agents The U.S. Preventive Services Task Force recommends shown to have a mortality beneflt (bisoprolol, carvedilol, and 1ow dose aspirin (Option B) for the primary prevention metoprolol succinate) should be used. Changing from can/e of atherosclerotic cardiovascular disease (ASCVD) and col dilol to metoprolol succinate (Option C) might be of benefit orectal cancer in adults aged 50 to 59 years with a 10 year if the patient were nonadherent with a twice daily drug, but ASCVD risk of 10'% or greater who do not have an increased other-wise, there is no demonstrated beneflt from switching risk fbr bleeding, have a life expectancy of at least 10 years, from one to another. and are willing to take iow dose aspirin daily for at least Valsartan sacubitril is an angiotensin receptor neprilysin 10 years. The American College of Cardiologr/American inhibitor that improves survival and symptoms in patients Heart Association guideline recommends that aspirin be with heart failure with reduced ejection fraction when com used infrequently in the routine primary prevention of pared with ACE inhibitor therapy Guidelines recommend ASCVD because of lack of net beneflt. replacing an ACE inhibitor or angiotensin receptor blocker The National Diabetes Prevention Progranr found that (ARB) with valsartan sacubitril in patients who are tolerating in persons at high risk for diabetes, interventions such as therapy with these agents, or initiating therapy with valsaftan changes in diet, exercise, and weight loss (Option D) of 57, sacubitril instead of an ACE inhibitor or ARB for patients to 7% reduced the risk for developing diabetes by 5B'X, but did with new onset heart failure. However. valsartan-sacubitril is not reduce CVD events. contraindicated in patients with a history of angioedema with either ACE inhibitor or ARB therapy Therefore, this patient KIY POIflTS should not be switched to valsadan sacubitril (Option D). . Smoking cessation substantially reduces cardiovascular K EY PO I]tT risk within 2 years, with risk returning to the level of a o Aldosterone antagonist therapy (spironolactone, nonsmoker after approximately 15 years.

ejection fraction and normal kidney function (estimated glo death in the United States. Almost one third of cardiovascular disease deaths are attributable to smoking and exposure to |a merular filtration rate >30 mL/min/1.73 m2), as these agents (lr have been shown to improve suruival in this population. secondhand smoke. Even low Ievels of smoking increase risks ET Eplerenone is a more selective aldosterone antagonist than for acute myocardial infarction; thus, reducing the number of spironolactone; it is associated with fewer endocrine side cigarettes per day does not eliminate risk completely. Smok tJ effects and reduced incidence of gynecomastia (17, vs. 10,/,,). ing cessation substantially reduces cardiovascular risk within !t 2 years, with risk returning to the level of a nonsmoker after IE Therefore, although this patient had gynecomastia when tt approximately 15 years. Smoking status should be assessed taking spironolactone, it is reasonable to try epierenone as c, an alternative aldosterone antagonist. at every visit, and cessation counseling and pharmacologic F ta therapy should be oflered to active smokers. Of all the rec g Ivabradine (Option B) has been shown to reduce heart ommended pharmacologic agents approved for smoking failure admissions in patients u,'ith symptomatic heart cessation, varenicline is the most ellective monotherapy Com- failure with reduced ejection fraction (ejection fiaction bination pharmacologic therapy is probably more eflbctive. <35%) who are in sinus rhythm with a heart rate of at least Psychosocial factors, including depression, anger, and TOlmin and taking maximally tolerated doses of a p blocker. anxiety, are associated with worse cardiovascular outcomes. Ivabradine works by slowing the sinus node and decreasing Depression has been linked to a higher risk for cardiovas heart rate. For patients with atrial flbrillation, however, the cular events. Psychosocial stressors also aflect the course of drug is not helpful. treatment and adherence to healthy lifestyles after a cardio- Guideline directed medical therapy for heart failure vascular event. Although it is impoftant to detect and treat includes B-blocker therapy for al1 patients, regardless of these disorders ifpresent, there is no evidence that detection heart failure stage. The benefits of p blocker therapy do and treatment (Option A) affect cardiovascular risk itself. not seem to be a class effect, and one of the three agents The U.S. Preventive Services Task Force recommends shown to have a mortality beneflt (bisoprolol, carvedilol, and 1ow dose aspirin (Option B) for the primary prevention metoprolol succinate) should be used. Changing from can/e of atherosclerotic cardiovascular disease (ASCVD) and col dilol to metoprolol succinate (Option C) might be of benefit orectal cancer in adults aged 50 to 59 years with a 10 year if the patient were nonadherent with a twice daily drug, but ASCVD risk of 10'% or greater who do not have an increased other-wise, there is no demonstrated beneflt from switching risk fbr bleeding, have a life expectancy of at least 10 years, from one to another. and are willing to take iow dose aspirin daily for at least Valsartan sacubitril is an angiotensin receptor neprilysin 10 years. The American College of Cardiologr/American inhibitor that improves survival and symptoms in patients Heart Association guideline recommends that aspirin be with heart failure with reduced ejection fraction when com used infrequently in the routine primary prevention of pared with ACE inhibitor therapy Guidelines recommend ASCVD because of lack of net beneflt. replacing an ACE inhibitor or angiotensin receptor blocker The National Diabetes Prevention Progranr found that (ARB) with valsartan sacubitril in patients who are tolerating in persons at high risk for diabetes, interventions such as therapy with these agents, or initiating therapy with valsaftan changes in diet, exercise, and weight loss (Option D) of 57, sacubitril instead of an ACE inhibitor or ARB for patients to 7% reduced the risk for developing diabetes by 5B'X, but did with new onset heart failure. However. valsartan-sacubitril is not reduce CVD events. contraindicated in patients with a history of angioedema with either ACE inhibitor or ARB therapy Therefore, this patient KIY POIflTS should not be switched to valsadan sacubitril (Option D). . Smoking cessation substantially reduces cardiovascular K EY PO I]tT risk within 2 years, with risk returning to the level of a o Aldosterone antagonist therapy (spironolactone, nonsmoker after approximately 15 years. eplerenone) is indicated in all patients with sympto o Smoking status should be assessed at every visit, and matic heart failure with reduced ejection fraction and cessation counseling and pharmacologic therapy should normal kidney function to improve survival. be offered to active smokers.

eplerenone) is indicated in all patients with sympto o Smoking status should be assessed at every visit, and matic heart failure with reduced ejection fraction and cessation counseling and pharmacologic therapy should normal kidney function to improve survival. be offered to active smokers. 175

Answers and Critiques Bibliography discontinue trastuzumab is made by the oncologist in con Arnett DK. Blumenthal RS, Albert MA. et al. 2019 ACC/AHA guideline on the sultation with a cardiologist. primary prevention of cardiovascular disease: a report of the American College ofCardiologr/American Heart Association Task Force on Clinical XEY POITII Pract-ice Guidelines. Circulation. 2019 ; 140:e596 e646. IPMID: 30879355] doi:l o. I 61 /CIR.000000000O000678 1 . In patients receiving trastuzumab therapy at high risk for cardiac dysfunction, periodic echocardiographic I surveillance is recommended. Item 4O Answer: B Educational Objective: Screen for myocardial dysfunc- Bibliography tion with echocardiography during trastuzumab therapy. Armenian SH. Lacchetti C. Lenihan D. Prevention and monitoring ofcardiac d1'sfunction in survivors of adult cancers: American Society of Clinical This patient should undergo surveillance with echocardiog Oncolos' clinical practice guideline summary. J Oncol Pract. 20u;13: raphy (Option B). Trastuzumab is an anti-HER2 monoclonal 270 s. [PMID, 279227 96] doi:10.1 200/JoP.20i6.018770

surveillance is recommended. Item 4O Answer: B Educational Objective: Screen for myocardial dysfunc- Bibliography tion with echocardiography during trastuzumab therapy. Armenian SH. Lacchetti C. Lenihan D. Prevention and monitoring ofcardiac d1'sfunction in survivors of adult cancers: American Society of Clinical This patient should undergo surveillance with echocardiog Oncolos' clinical practice guideline summary. J Oncol Pract. 20u;13: raphy (Option B). Trastuzumab is an anti-HER2 monoclonal 270 s. [PMID, 279227 96] doi:10.1 200/JoP.20i6.018770 D antibody that decreases the risk for breast cancer recurrence t,I and breast cancer related death. It may result in revers- Item 41 Answer: C E (D ible cardiotoxicity that manifests as left ventricular systolic Educational Objective: Manage persistent symptomatic rtt dysfunction, causing symptoms of heart failure in 3'7, to o, chronic stable angina. 7'7, of patients. Routine surveillance imaging with echocar- diography may be offered during treatment in asymptom Coronary angiography (Option C) is the most appropriate n atic patients at increased risk for cardiac dysfunction. The management for this patient who has persistent angina lt 2017 American Society of Clinical Oncologz (ASCO) practice despite maximally tolerated medical therapy. In this set et guideline recommends echocardiography as the surveil- ting, invasive imaging for revascularization assessment is vt lance imaging modality of choice. ASCO identifles patients appropriate to improve symptom status and quality of life. receiving trastuzumab as having increased risk for cardiac Revascularization targets are identifled on the basis of ana dysfunction if any of the following are present: two or more tomic and functional physiologic characteristics associated traditional cardiovascular risk factors (smoking, hyperten- with myocardial ischemia. Techniques such as fractional sion, diabetes mellitus, dyslipidemia, and obesity), older flow reserve and instantaneous wave-free ratio provide age (>60 years) at cancer treatment, borderline left ventric- information on the functional hemodynamic signiflcance of ular ejection fraction (50'1, to ss'z,), history of myocardial indeterminate lesions identifled on angiographic imaging, infarction, moderate or greater valvular heart disease, and reducing both unnecessary stenting and the need for urgent treatment combined with lower dose anthracycline. This revascularization. In contrast, in unstable or in many acute patient has three risk factors (hypertension, hyperlipidemia, presentations, revascularization is indicated to prevent and borderline ejection fraction) and should undergo echo- future events and improve survival. The risks and beneflts of cardiographic surveillance. ASCO recommends that the fre and alternatives to angiography should be discussed, along quency of cardiac imaging for each patient be determined with potential findings and therapeutic options. Other indi by the patient's physician on the basis of clinical judg- cations for coronary artery imaging include the presence ol ment and patient circumstances. Common practice includes clinical flndings or indications on noninvasive testing that a baseline evaluation and repeat imaging at 3, 6, 9, and are associated with severe ischemic heart disease. Other 12 months after trastuzumab initiation. ASCO suggests that patients who may benefit from coronary artery imaging an echocardiogram be obtained between 6 and 12 months are those with Ieft ventricular systolic dysfunction and the after completion of cancer directed therapy in asymptomatic presence olischemia and other high-risk criteria on nonin- patients considered to be at increased risk. vasive testing. ASCO recommends echocardiography in patients who Aspirin reduces the risk for myocardial infarction and develop heart failure symptoms. Cardiac magnetic reso cardiovascular death in patients with stable angina. Guide nance (CMR) imaging (Option A) or multigated acquisition lines recommend low dose aspirin (75 162 mg/d) for sec (MUGA) scan (Option C) is recommended if echocardi- ondary prevention because it is as effective as high dose ography is not available or has resulted in poor image aspirin (SZS mg/d) in preventing myocardial infarction and qualify, with preference given to CMR imaging. Neither confers a lower bleeding risk. In aspirin-intolerant patients, CMR imaging nor MUGA scan is recommended for routine clopidogrel, a platelet P2Y,, receptor inhibitor, is an accept- surveillance. able alternative. There is no role for dual antiplatelet therapy Performing no surveillance (Option D) is not in the with aspirin and clopidogrel (Option A) in patients with best interest of this patient. The incidence of signiflcant left chronic stable angina in the absence ofrevascularization. ventricular ejection fraction decline in trials has ranged from This patient's current medication regimen has been 7.1"1, to 18.6'1,, with a rate of New York Heart Association optimized. With a resting pulse rate in the range of 55 to functional class III or IV heart failure ranging from 0.4'X, to 60/min and a well-controlled blood pressure, additional 4.1"1,. Early intervention in asymptomatic patients, including vasoactive medical therapy, such as isosorbide mononitrate cessation of trastuzumab and consideration of cardioprotec (Option B), is unlikely to be necessary. In addition, given the tive medications, may help reduce this risk. The decision to presence of orthostatic symptoms with his current regimen,

D antibody that decreases the risk for breast cancer recurrence t,I and breast cancer related death. It may result in revers- Item 41 Answer: C E (D ible cardiotoxicity that manifests as left ventricular systolic Educational Objective: Manage persistent symptomatic rtt dysfunction, causing symptoms of heart failure in 3'7, to o, chronic stable angina. 7'7, of patients. Routine surveillance imaging with echocar- diography may be offered during treatment in asymptom Coronary angiography (Option C) is the most appropriate n atic patients at increased risk for cardiac dysfunction. The management for this patient who has persistent angina lt 2017 American Society of Clinical Oncologz (ASCO) practice despite maximally tolerated medical therapy. In this set et guideline recommends echocardiography as the surveil- ting, invasive imaging for revascularization assessment is vt lance imaging modality of choice. ASCO identifles patients appropriate to improve symptom status and quality of life. receiving trastuzumab as having increased risk for cardiac Revascularization targets are identifled on the basis of ana dysfunction if any of the following are present: two or more tomic and functional physiologic characteristics associated traditional cardiovascular risk factors (smoking, hyperten- with myocardial ischemia. Techniques such as fractional sion, diabetes mellitus, dyslipidemia, and obesity), older flow reserve and instantaneous wave-free ratio provide age (>60 years) at cancer treatment, borderline left ventric- information on the functional hemodynamic signiflcance of ular ejection fraction (50'1, to ss'z,), history of myocardial indeterminate lesions identifled on angiographic imaging, infarction, moderate or greater valvular heart disease, and reducing both unnecessary stenting and the need for urgent treatment combined with lower dose anthracycline. This revascularization. In contrast, in unstable or in many acute patient has three risk factors (hypertension, hyperlipidemia, presentations, revascularization is indicated to prevent and borderline ejection fraction) and should undergo echo- future events and improve survival. The risks and beneflts of cardiographic surveillance. ASCO recommends that the fre and alternatives to angiography should be discussed, along quency of cardiac imaging for each patient be determined with potential findings and therapeutic options. Other indi by the patient's physician on the basis of clinical judg- cations for coronary artery imaging include the presence ol ment and patient circumstances. Common practice includes clinical flndings or indications on noninvasive testing that a baseline evaluation and repeat imaging at 3, 6, 9, and are associated with severe ischemic heart disease. Other 12 months after trastuzumab initiation. ASCO suggests that patients who may benefit from coronary artery imaging an echocardiogram be obtained between 6 and 12 months are those with Ieft ventricular systolic dysfunction and the after completion of cancer directed therapy in asymptomatic presence olischemia and other high-risk criteria on nonin- patients considered to be at increased risk. vasive testing. ASCO recommends echocardiography in patients who Aspirin reduces the risk for myocardial infarction and develop heart failure symptoms. Cardiac magnetic reso cardiovascular death in patients with stable angina. Guide nance (CMR) imaging (Option A) or multigated acquisition lines recommend low dose aspirin (75 162 mg/d) for sec (MUGA) scan (Option C) is recommended if echocardi- ondary prevention because it is as effective as high dose ography is not available or has resulted in poor image aspirin (SZS mg/d) in preventing myocardial infarction and qualify, with preference given to CMR imaging. Neither confers a lower bleeding risk. In aspirin-intolerant patients, CMR imaging nor MUGA scan is recommended for routine clopidogrel, a platelet P2Y,, receptor inhibitor, is an accept- surveillance. able alternative. There is no role for dual antiplatelet therapy Performing no surveillance (Option D) is not in the with aspirin and clopidogrel (Option A) in patients with best interest of this patient. The incidence of signiflcant left chronic stable angina in the absence ofrevascularization. ventricular ejection fraction decline in trials has ranged from This patient's current medication regimen has been 7.1"1, to 18.6'1,, with a rate of New York Heart Association optimized. With a resting pulse rate in the range of 55 to functional class III or IV heart failure ranging from 0.4'X, to 60/min and a well-controlled blood pressure, additional 4.1"1,. Early intervention in asymptomatic patients, including vasoactive medical therapy, such as isosorbide mononitrate cessation of trastuzumab and consideration of cardioprotec (Option B), is unlikely to be necessary. In addition, given the tive medications, may help reduce this risk. The decision to presence of orthostatic symptoms with his current regimen, 176

Answers and Critiques he is unlikely to tolerate further uptitration of vasoactive patient's aneurysm is greater than 5.5 cm. The risk for rup- medications. ture is signiflcantly higher once the maximal diameter is Exercise testing, such as exercise echocardiography greater than 5.5 cm or if the AAA grows quickly (>0.5 cm/ (Option D), may provide additional prognostic informa- year); therefore, proceeding with a plan for aortic repair is tion. However, it cannot identily target lesions that might warranted. be amenable to revascularization to improve this patient's quality of life. KIY POIilTS o The U.S. Preventive Services Task Force recommends I(EY POI l{I one-time screening with duplex ultrasonography in r In the setting of persistent symptoms despite maximally all men aged 65 to 75 years who have smoked at least tolerated medical therapy, invasive imaging for revascu- 100 cigarettes in their lifetime and selective screening Iarization assessment is appropriate to improve slmptom in men in this age group who have never smoked. status and quality of life. . CT angiogfaphy or magnetic resonance angiography is t o, the imaging procedure of choice to identiflz the exact ET Bibliography location of an abdominal aneurysm and plan opera- Katz D, Gavin MC. Stable ischemic heart disease. Ann Intern Med. 2019;177: ITCIT-lTC32. IPMID: 313822881 doi:10.7326lAITC201908060 tive repair. (, =, Bibliography a! t^ Item 42 Answer: C Chaikof EL, Dalman RL, Eskandari MK, et al. The Society for Vascular C, Surgery practice guidelines on the care of patients \a.ith an abdominal Ed u cati o na I O bjective : Perform noninvasive anatomic aortic aneurysm. J Vasc Surg. 201&67:2 77 .e2. IPMID:29268916] doi:10. ut imaging to identiS the location of an abdominal aortic l0l6r'j.jvs.2017.10.044 = E aneurysm.

he is unlikely to tolerate further uptitration of vasoactive patient's aneurysm is greater than 5.5 cm. The risk for rup- medications. ture is signiflcantly higher once the maximal diameter is Exercise testing, such as exercise echocardiography greater than 5.5 cm or if the AAA grows quickly (>0.5 cm/ (Option D), may provide additional prognostic informa- year); therefore, proceeding with a plan for aortic repair is tion. However, it cannot identily target lesions that might warranted. be amenable to revascularization to improve this patient's quality of life. KIY POIilTS o The U.S. Preventive Services Task Force recommends I(EY POI l{I one-time screening with duplex ultrasonography in r In the setting of persistent symptoms despite maximally all men aged 65 to 75 years who have smoked at least tolerated medical therapy, invasive imaging for revascu- 100 cigarettes in their lifetime and selective screening Iarization assessment is appropriate to improve slmptom in men in this age group who have never smoked. status and quality of life. . CT angiogfaphy or magnetic resonance angiography is t o, the imaging procedure of choice to identiflz the exact ET Bibliography location of an abdominal aneurysm and plan opera- Katz D, Gavin MC. Stable ischemic heart disease. Ann Intern Med. 2019;177: ITCIT-lTC32. IPMID: 313822881 doi:10.7326lAITC201908060 tive repair. (, =, Bibliography a! t^ Item 42 Answer: C Chaikof EL, Dalman RL, Eskandari MK, et al. The Society for Vascular C, Surgery practice guidelines on the care of patients \a.ith an abdominal Ed u cati o na I O bjective : Perform noninvasive anatomic aortic aneurysm. J Vasc Surg. 201&67:2 77 .e2. IPMID:29268916] doi:10. ut imaging to identiS the location of an abdominal aortic l0l6r'j.jvs.2017.10.044 = E aneurysm. In this patient with an abdominal aortic aneurysm (AAA) Item 43 Answer: A greater than 5.5 cm in diameter, the most appropriate next Educational Objective: Assess the severit5r of mitral step is CT angiography (CTA) (Option C) to identify the loca- stenosis with exercise echocardiography. tion of the AAA (suprarenal, juxtarenal, or infrarenal) and plan for repair. Because of the high mortality rate associated The most appropriate management is to perform exercise with aneurysm rupture, the U.S. Preventive Services Task echocardiography (Option A). The patient's history (fatigue Force recommends one time screening with duplex ultra- and exertional dyspnea) and examination flndings (open sonography in all men aged 65 to 75 years who have smoked ing snap and diastolic rumble) are consistent with mitral at least 100 cigarettes in their lifetime and selective screening stenosis, which the echocardiogram conflrms. However, in men in this age group who have never smoked. The choice quantitation of the mitral stenosis reveals a gradient and between open surgical repair and endovascular aneurysm valve area consistent with moderate, rather than severe, repair (EVAR) is driven by the location of the AAA and mitral stenosis. Severe mitral stenosis is deflned by a mitral involvement of the renal and mesenteric arteries. Suprarenal valve area of 1.5 cm2 or less, which usually corresponds to and juxtarenal aneurysms often necessitate open surgical a mean mitral gradient of more than 5 to 10 mm Hg at a repair, whereas infrarenal aneurysms often can be treated normal heart rate. This patient's symptoms are predomi with EVAR. Other factors, including patient age, comorbid nantly exertional, and decreased diastolic fllling time with conditions, and ability to tolerate open surgical repair, also exertion typically results in an increased mitral gradient determine which procedure should be performed in patients and left atrial and pulmonary pressures in mitral stenosis. with an infrarenal AAA. In patients with a discrepancy between the clinical and Although abdominal aortography (Option A) has been echocardiographic flndings, exercise echocardiography or used fbr AAA sizing and location, the advent of CTA and exercise testing during cardiac catheterization should be magnetic resonance angiography has relegated invasive aor- pursued to assess the response of the mitral gradient and tography to a second- or third-line option. pulmonary pressures to an increased heart rate. Exercise There is limited evidence that ACE inhibitors (Option B) testing is important because percutaneous balloon mitral and angiotensin receptor blockers can halt the progression commissurotomy is indicated for patients with severe mitral of AAA growth. However, this patient has an AAA greater stenosis and favorable valve morphology. than 5.5 cm in diameter and thus needs aortic repair fol Although cardiac catheterization (Option B), cardiac lowing CTA. magnetic resonance (CMR) imaging (Option C), or trans- A decision to perform open surgical repair (Option D) esophageal echocardiography (Option E) may be used to is premature. The most prudent next step is to determine the measure the transmitral gradient and calculate or measure anatomic location of the AAA with CIA to plan for surgical mitral valve area, each does so with the patient in a resting or endovascular repair. state and thus would not likely demonstrate the heart rate- Repeat duplex ultrasonography (Option E) is not indi- related increases in mitral gradient, pulmonary pressures, cated in this patient because the maximal diameter of this and left atrial pressures often seen in mitral stenosis. None of

In this patient with an abdominal aortic aneurysm (AAA) Item 43 Answer: A greater than 5.5 cm in diameter, the most appropriate next Educational Objective: Assess the severit5r of mitral step is CT angiography (CTA) (Option C) to identify the loca- stenosis with exercise echocardiography. tion of the AAA (suprarenal, juxtarenal, or infrarenal) and plan for repair. Because of the high mortality rate associated The most appropriate management is to perform exercise with aneurysm rupture, the U.S. Preventive Services Task echocardiography (Option A). The patient's history (fatigue Force recommends one time screening with duplex ultra- and exertional dyspnea) and examination flndings (open sonography in all men aged 65 to 75 years who have smoked ing snap and diastolic rumble) are consistent with mitral at least 100 cigarettes in their lifetime and selective screening stenosis, which the echocardiogram conflrms. However, in men in this age group who have never smoked. The choice quantitation of the mitral stenosis reveals a gradient and between open surgical repair and endovascular aneurysm valve area consistent with moderate, rather than severe, repair (EVAR) is driven by the location of the AAA and mitral stenosis. Severe mitral stenosis is deflned by a mitral involvement of the renal and mesenteric arteries. Suprarenal valve area of 1.5 cm2 or less, which usually corresponds to and juxtarenal aneurysms often necessitate open surgical a mean mitral gradient of more than 5 to 10 mm Hg at a repair, whereas infrarenal aneurysms often can be treated normal heart rate. This patient's symptoms are predomi with EVAR. Other factors, including patient age, comorbid nantly exertional, and decreased diastolic fllling time with conditions, and ability to tolerate open surgical repair, also exertion typically results in an increased mitral gradient determine which procedure should be performed in patients and left atrial and pulmonary pressures in mitral stenosis. with an infrarenal AAA. In patients with a discrepancy between the clinical and Although abdominal aortography (Option A) has been echocardiographic flndings, exercise echocardiography or used fbr AAA sizing and location, the advent of CTA and exercise testing during cardiac catheterization should be magnetic resonance angiography has relegated invasive aor- pursued to assess the response of the mitral gradient and tography to a second- or third-line option. pulmonary pressures to an increased heart rate. Exercise There is limited evidence that ACE inhibitors (Option B) testing is important because percutaneous balloon mitral and angiotensin receptor blockers can halt the progression commissurotomy is indicated for patients with severe mitral of AAA growth. However, this patient has an AAA greater stenosis and favorable valve morphology. than 5.5 cm in diameter and thus needs aortic repair fol Although cardiac catheterization (Option B), cardiac lowing CTA. magnetic resonance (CMR) imaging (Option C), or trans- A decision to perform open surgical repair (Option D) esophageal echocardiography (Option E) may be used to is premature. The most prudent next step is to determine the measure the transmitral gradient and calculate or measure anatomic location of the AAA with CIA to plan for surgical mitral valve area, each does so with the patient in a resting or endovascular repair. state and thus would not likely demonstrate the heart rate- Repeat duplex ultrasonography (Option E) is not indi- related increases in mitral gradient, pulmonary pressures, cated in this patient because the maximal diameter of this and left atrial pressures often seen in mitral stenosis. None of 177

Answers and Critiques these tests would provide evidence to explain this patient's In patients u'ith sinus rtode dysfhllction associated u ith symptoms. s_ynrptoms or hemociyllxnlic contpromise rt'ho are at lou' Conclusively demonstrating the severilz of mitral ste likelihood of coronary ischemia, isoproterenol (Option D). nosis with exercise echocardiography would be necessary dopamine. dobutamine, or epinephrir.re may be considered before recommending an intervention as invasive as percu to increase heart rate ancl intprove symptoms. In general. taneous balloon mitral commissurotomy (Option D). guidelines relegate chronotropic irgents as second-line ther apy to atropine in the ilcute resuscitiltion of patients w'ith XEY POIilI hemodl'nanricalll' r-urstable bracll'cirrdia. . In patients with rheumatic mitral stenosis and a dis crepancy between resting echocardiographic findings XEY POIXIS and clinical symptoms, exercise echocardiography or . The treatment of hemodynamically unstable sinus exercise testing during cardiac catheterization is rec bradycardia in patients with a pulse is intravenous ommended to further assess the valve. atropine. ta . The most common extrinsic cause of sinus bradycardia o Bibliography is medication use (p-blockers, donepezil, neostigmine, = t^ Otto CM, Nishimura RA, Bonow RO. et al. 2020 ACC/AHA guideline for the pyridostigmine). o, management of patients with valvular heart disease: a report of the American College of Cardiolog//American Heart Association Joint CL n Committee on Clinical Practice Guidelines. Circulation. 2021 ;143:e72 e227. IPMID: 333321501 doi:10.1161'CIR.0000000000000923 Bibliography Kusul.ltoto FNI. Schoenfeld MH. Barrett c. et al. 2018 ACC AHA HRS guide line on the e\aluation and mirnagement ofpatients t{ith bradlcardia and 4t cardiac conduction delay: a report ofthe American College ofCardiobg' (D vt tr Item 44 Answer: C Ed ucationa I Objective: Manage acute bradycardia. American Heart Association Task Force on Clinical Practice Cuidelines irnd the Heart Rhythm Society. Circulation.2019:1.10:e382 e.182. [PMIL): :1O5a677 2l doi:10.1161 /CIR.0000000000000628

these tests would provide evidence to explain this patient's In patients u'ith sinus rtode dysfhllction associated u ith symptoms. s_ynrptoms or hemociyllxnlic contpromise rt'ho are at lou' Conclusively demonstrating the severilz of mitral ste likelihood of coronary ischemia, isoproterenol (Option D). nosis with exercise echocardiography would be necessary dopamine. dobutamine, or epinephrir.re may be considered before recommending an intervention as invasive as percu to increase heart rate ancl intprove symptoms. In general. taneous balloon mitral commissurotomy (Option D). guidelines relegate chronotropic irgents as second-line ther apy to atropine in the ilcute resuscitiltion of patients w'ith XEY POIilI hemodl'nanricalll' r-urstable bracll'cirrdia. . In patients with rheumatic mitral stenosis and a dis crepancy between resting echocardiographic findings XEY POIXIS and clinical symptoms, exercise echocardiography or . The treatment of hemodynamically unstable sinus exercise testing during cardiac catheterization is rec bradycardia in patients with a pulse is intravenous ommended to further assess the valve. atropine. ta . The most common extrinsic cause of sinus bradycardia o Bibliography is medication use (p-blockers, donepezil, neostigmine, = t^ Otto CM, Nishimura RA, Bonow RO. et al. 2020 ACC/AHA guideline for the pyridostigmine). o, management of patients with valvular heart disease: a report of the American College of Cardiolog//American Heart Association Joint CL n Committee on Clinical Practice Guidelines. Circulation. 2021 ;143:e72 e227. IPMID: 333321501 doi:10.1161'CIR.0000000000000923 Bibliography Kusul.ltoto FNI. Schoenfeld MH. Barrett c. et al. 2018 ACC AHA HRS guide line on the e\aluation and mirnagement ofpatients t{ith bradlcardia and 4t cardiac conduction delay: a report ofthe American College ofCardiobg' (D vt tr Item 44 Answer: C Ed ucationa I Objective: Manage acute bradycardia. American Heart Association Task Force on Clinical Practice Cuidelines irnd the Heart Rhythm Society. Circulation.2019:1.10:e382 e.182. [PMIL): :1O5a677 2l doi:10.1161 /CIR.0000000000000628 'lhis patient should receir.e intrar.cnous atropine (Option C). llc has altered mental status ancl hypotcnsion in the set Item 45 Answer: C ting of profbund bradycardia. According to the advanccd Educational Objective: Manage uptitration of p-blocker carcliovtrscular life support algorithnr for bradl,cardirr in therapy in a patient with heart failure with reduced ejection patients lr,ith a pulse. atropine is the most appropriate first fraction. stcp. It may acutely, ir.nprove hexrt rate and perlusion but r,r'ill likell, require repeat closing if efl'ectir.e. Alternatir,cs The most appropriate management is to increase the dos include intravenous doparline or epir-rephrine or trans age of carvedilol (Option C). This patient has recent-onset cutaneous pacing. rvhich is painful. Ultimatell-. the goal is heart failure with reduced ejection fraction (HFTEF) and is to determine the nnderll,ing cxusc of'his acute condition. undergoing medication titration. B-Blockers should be ini 'Ihc brrrd-v-cardia m:r1, be either the cause or the rcsult tiated in all patients with HFTEF. These agents can improve ol his decompensation. Pathologic sinus bradl,cardia is remodeling, increase left ventricular ejection fraction, and most commonly causecl b1, sinus node dysfunction clue reduce hospitalization and mortality when added to ACE to age re'lated myocarclial fibrosis. Less comnronh: sinus inhibitor and diuretic therapy. In contrast to ACE inhibi nocle dysf unction ma!, result trom right coronary iscl.rernia. tors, the beneflts ofp blocker therapy do not seem to be a Irypothl'roidism. intracranial hr,pertension. postoperative class effect, and one of three agents shown to have a mor scirrring or fibrosis fion.r carcliothrtracic surgery or ir.rfiltra tality beneflt (bisoprolol, carvedilol, metoprolol succinate) tive or inflirmmatory disurders (e.g.. sarcoidosis).lhe nrost should be used. p Blockers are generally well tolerated but common extrinsic cause is mcdication use (B blockers. should not be started when the patient is acutely decom doncpezil, neostigmine, pyriclostigrnine). Permanent pirc pensated. These agents have negative inotropic properties i ng nriry' be indicatecl eventual 11: and may exacerbate heart failure in patients with acute Amiodarone (Option A) is l rnultichannel antiarrhyth volume overload. B Blockers should be initiated at low nric agent used prirnarily to treat vcntricular arrhythmias dosages and uptitrated slowly over weeks (not days) until ancl atrial fibrillation. It lras no role in the management the patient achieves the guideline-directed target dos ol symptomatic bradycardia ancl is n.r<tre likely to worsen age or maximum tolerable dosage. The target dosage for his conclition through its B bl<tcking and negative inotropic carvedilol is 25 mg twice daily (SO mg twice daily if weight properties. >85 kg [187 1b]). 'lhis patient is profbundlv bradvcardic and hlpoten Ivabradine has been shown to reduce hospitalizations sive. but he does har,e a pulse and is arousable. Therefbre. in patients with New York Heart Association functional class chcst conrpressions (Option B) arc not currentlv indi III to IV heart failure on maximally tolerated B blocker ther- cated. If the pulse beconres no longer palpable, he n,ould apy. This patient's heart rate is elevated; however, she is not be in pulseless electrical ilctivit), :rrrest. in which case receiving the maximum dosage of carvedilol, and carvedilol chest compressions to facilitate svstemic perfusion may should be increased before considering adding ivabradine br. lif'e saving. (Option A).

'lhis patient should receir.e intrar.cnous atropine (Option C). llc has altered mental status ancl hypotcnsion in the set Item 45 Answer: C ting of profbund bradycardia. According to the advanccd Educational Objective: Manage uptitration of p-blocker carcliovtrscular life support algorithnr for bradl,cardirr in therapy in a patient with heart failure with reduced ejection patients lr,ith a pulse. atropine is the most appropriate first fraction. stcp. It may acutely, ir.nprove hexrt rate and perlusion but r,r'ill likell, require repeat closing if efl'ectir.e. Alternatir,cs The most appropriate management is to increase the dos include intravenous doparline or epir-rephrine or trans age of carvedilol (Option C). This patient has recent-onset cutaneous pacing. rvhich is painful. Ultimatell-. the goal is heart failure with reduced ejection fraction (HFTEF) and is to determine the nnderll,ing cxusc of'his acute condition. undergoing medication titration. B-Blockers should be ini 'Ihc brrrd-v-cardia m:r1, be either the cause or the rcsult tiated in all patients with HFTEF. These agents can improve ol his decompensation. Pathologic sinus bradl,cardia is remodeling, increase left ventricular ejection fraction, and most commonly causecl b1, sinus node dysfunction clue reduce hospitalization and mortality when added to ACE to age re'lated myocarclial fibrosis. Less comnronh: sinus inhibitor and diuretic therapy. In contrast to ACE inhibi nocle dysf unction ma!, result trom right coronary iscl.rernia. tors, the beneflts ofp blocker therapy do not seem to be a Irypothl'roidism. intracranial hr,pertension. postoperative class effect, and one of three agents shown to have a mor scirrring or fibrosis fion.r carcliothrtracic surgery or ir.rfiltra tality beneflt (bisoprolol, carvedilol, metoprolol succinate) tive or inflirmmatory disurders (e.g.. sarcoidosis).lhe nrost should be used. p Blockers are generally well tolerated but common extrinsic cause is mcdication use (B blockers. should not be started when the patient is acutely decom doncpezil, neostigmine, pyriclostigrnine). Permanent pirc pensated. These agents have negative inotropic properties i ng nriry' be indicatecl eventual 11: and may exacerbate heart failure in patients with acute Amiodarone (Option A) is l rnultichannel antiarrhyth volume overload. B Blockers should be initiated at low nric agent used prirnarily to treat vcntricular arrhythmias dosages and uptitrated slowly over weeks (not days) until ancl atrial fibrillation. It lras no role in the management the patient achieves the guideline-directed target dos ol symptomatic bradycardia ancl is n.r<tre likely to worsen age or maximum tolerable dosage. The target dosage for his conclition through its B bl<tcking and negative inotropic carvedilol is 25 mg twice daily (SO mg twice daily if weight properties. >85 kg [187 1b]). 'lhis patient is profbundlv bradvcardic and hlpoten Ivabradine has been shown to reduce hospitalizations sive. but he does har,e a pulse and is arousable. Therefbre. in patients with New York Heart Association functional class chcst conrpressions (Option B) arc not currentlv indi III to IV heart failure on maximally tolerated B blocker ther- cated. If the pulse beconres no longer palpable, he n,ould apy. This patient's heart rate is elevated; however, she is not be in pulseless electrical ilctivit), :rrrest. in which case receiving the maximum dosage of carvedilol, and carvedilol chest compressions to facilitate svstemic perfusion may should be increased before considering adding ivabradine br. lif'e saving. (Option A). 178

Answers and Critiques In patients with symptomatic heart failure, valsartan dose titration or discontinuation when needed for inr,asive sacubitril has been shown to reduce morbidity and mor- procedures. tality compared with enalapril. It will occasionally cause Intravenous systemic thrombolysis, such as with tenec symptomatic hypotension, a reason to lower the dosage. This teplase (Option C), has not been provecl efl'ective in most patient has no indication to lower the dosage (Option B). patients with acute limb ischemi:i. lJor,r,ever, catheter based This patient has no evidence of volume overload on thrombolvsis is elfective for patients with acute limb physical examination (no jugular venous distention or ischemia and a salvageable limb. edema). Therefore, there is no need to increase the dosage of Venous duplex ultrasonography (Option E) is rTot incli furosemide (Option D). catecl in this patient r,r,,ho has no evidence of massive venous thron-rbosis. Iliof'emoral \enous thrombosis is a rare cause rtv Potr{Ts . oi acute limb ischemia and should be suspected in patients o p-Blockers should be initiated in all patients with heart r,vith sudden severe pain, sr,velling. cyanosis, and edenra. failure with reduced ejection fraction. These findings are not present in this patient. UI (u . In patients with heart failure with reduced ejection XEY POIlIIS CT fraction, B-blockers should be initiated at low dosages and slowly uptitrated over weeks (not days) until the . Classically, patients with acute limb ischemia present with at least one of the six P's: paresthesia, pain, pal- tJ patient achieves the guideline-directed target dosage t, 1or, pulselessness, poikilothermia (coolness), and or maximum tolerable dosage. IE paralysis. UI

In patients with symptomatic heart failure, valsartan dose titration or discontinuation when needed for inr,asive sacubitril has been shown to reduce morbidity and mor- procedures. tality compared with enalapril. It will occasionally cause Intravenous systemic thrombolysis, such as with tenec symptomatic hypotension, a reason to lower the dosage. This teplase (Option C), has not been provecl efl'ective in most patient has no indication to lower the dosage (Option B). patients with acute limb ischemi:i. lJor,r,ever, catheter based This patient has no evidence of volume overload on thrombolvsis is elfective for patients with acute limb physical examination (no jugular venous distention or ischemia and a salvageable limb. edema). Therefore, there is no need to increase the dosage of Venous duplex ultrasonography (Option E) is rTot incli furosemide (Option D). catecl in this patient r,r,,ho has no evidence of massive venous thron-rbosis. Iliof'emoral \enous thrombosis is a rare cause rtv Potr{Ts . oi acute limb ischemia and should be suspected in patients o p-Blockers should be initiated in all patients with heart r,vith sudden severe pain, sr,velling. cyanosis, and edenra. failure with reduced ejection fraction. These findings are not present in this patient. UI (u . In patients with heart failure with reduced ejection XEY POIlIIS CT fraction, B-blockers should be initiated at low dosages and slowly uptitrated over weeks (not days) until the . Classically, patients with acute limb ischemia present with at least one of the six P's: paresthesia, pain, pal- tJ patient achieves the guideline-directed target dosage t, 1or, pulselessness, poikilothermia (coolness), and or maximum tolerable dosage. IE paralysis. UI o Patients with acute limb ischemia should receive o Bibliography tt = Yancy CW, Januzzi JL Jr, Allen LA, et al. 2017 ACC expert consensus decision emergent systemic anticoagulation and diagnostic pathway for optimization ofheart failure treatment: answers to 1O pivotal issues about heart failure with reduced ejection fraction: a report ofthe angiography in preparation for revascularization. American College ofCardiolopy Task Force on Expert Consensus Decision Pathways. J Am Coll Cardiol. 2018;71:201 230. IPMID: 29277252] doi:LO. 1016/j.jacc.2017.11.02s Bibliography Gerhard-Herman MD, Gornik HL, Barrett C, et a]. 2016 AHA/ACC guideline on the management of patients with lower extremity peripheral artery disease: executive summary: a report of the American College of

o Patients with acute limb ischemia should receive o Bibliography tt = Yancy CW, Januzzi JL Jr, Allen LA, et al. 2017 ACC expert consensus decision emergent systemic anticoagulation and diagnostic pathway for optimization ofheart failure treatment: answers to 1O pivotal issues about heart failure with reduced ejection fraction: a report ofthe angiography in preparation for revascularization. American College ofCardiolopy Task Force on Expert Consensus Decision Pathways. J Am Coll Cardiol. 2018;71:201 230. IPMID: 29277252] doi:LO. 1016/j.jacc.2017.11.02s Bibliography Gerhard-Herman MD, Gornik HL, Barrett C, et a]. 2016 AHA/ACC guideline on the management of patients with lower extremity peripheral artery disease: executive summary: a report of the American College of tr Item 45 Answer: D Educational Objective: Treat acute limb ischemia with Cardiologr/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2017;135:e686 e725. [PMID: 27840332] doi:10. 1161 /CIR.0000000000000470 anticoagulation.

tr Item 45 Answer: D Educational Objective: Treat acute limb ischemia with Cardiologr/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2017;135:e686 e725. [PMID: 27840332] doi:10. 1161 /CIR.0000000000000470 anticoagulation. lhe most appropriate next step in management is to admin. Item 47 Answer: C ister intra\enous unfiactionated heparin (Option D). Clas- Ed ucationa I Objective: Diagnose peripartum sponta EI sically, patients nith acllte limb ischemia present with at neous coronary artery dissection. least one of the six P's: paresthesia, pain, pallor, pulseless- ness, poikilothermia (coolness), and paralysis. Acute limb The most likely cliagnosis is spontaneous coronary artery iscl-ren.ria is most commonly caused by acute thrombosis dissection (SCAD) (Option C). SCAD is the most common of a lower extremity artery stent, or bypass graft. Other cause ol pregnancy associated myocardial infirrction iind causes include thromboembolism, vessel dissection (usually commonly occurs during pregnancy or in the first month occurring periprocedurally), or trar-lma. This patient's pre postpartum. SCAD involves development of a nontraumatic sentation is consistent with acute lirr,b ischemia ciue to atrial and non iatrogenic intramural hematoma with or r,rrithout fibrillation related thromboembolism, and the most appro' intimal dissection with luminal conrmunication. the enlarg priate first steps are to (l) initiate intrar,enous anticoagula ing hematoma in the false lumen compresses the true lumen tion with unfractionated heparin, (2) perforrn angiography, of the coronary artery and in potential combination rvith and (3) establish a plan for reperfusion ofrhe leg. obstructing dissection leads to chest pain, ischemia. and/or Invasive angiography of the lower extremity (Option A) infarction. the diagnosis requires coronary C'f or coronary should be expedited, as endovzrscular or surgical rev:rs. angiography to confirm the characteristic imaging features. cularization is warr:rnted to preserve limb Iunction and When associated r,r,ith ST-elerzation myocardial infarction, prevent major amputation. llow'ever. anticoagulation, SCAD rnay be managed inrasivelyr however, percutaneous typically r,l'ith unfraction:ited heparin, should be initiated coronary intervention may be safely detbrred r.then coro- as soon as the diagnosis is suspected, beliire perfbrming nary flow is preserved and symptoms can be controlled and diagnostic testing. closely monitored. This patient, r,r,ho has atrial fibrillation, needs antico 'ITe pathogenesis of ST elevation myocardial infarction agulation fbllorving this e'rent. However, because interuen typically ir.r,,,olves plaque rupture (Option A) within a coro tion is needeci to restore blood flovrl unf'racticlnated heparin nary artery 'lhe rupture causes platelet adhesion, activation, should be initiated no\ r, not an oral irnticoagulant snch as irnd aggrcgation, resultiug in a thrombosed coronary artery apixaban (Option B). Unfractionated heparin has a rapid irnd acute vessel occlnsion. 'lhe sudden loss of coronary onset and offset of action, alkru''ing for more flexibility in blood flort, leacis to transmural ischenria of the nryocardiunt

lhe most appropriate next step in management is to admin. Item 47 Answer: C ister intra\enous unfiactionated heparin (Option D). Clas- Ed ucationa I Objective: Diagnose peripartum sponta EI sically, patients nith acllte limb ischemia present with at neous coronary artery dissection. least one of the six P's: paresthesia, pain, pallor, pulseless- ness, poikilothermia (coolness), and paralysis. Acute limb The most likely cliagnosis is spontaneous coronary artery iscl-ren.ria is most commonly caused by acute thrombosis dissection (SCAD) (Option C). SCAD is the most common of a lower extremity artery stent, or bypass graft. Other cause ol pregnancy associated myocardial infirrction iind causes include thromboembolism, vessel dissection (usually commonly occurs during pregnancy or in the first month occurring periprocedurally), or trar-lma. This patient's pre postpartum. SCAD involves development of a nontraumatic sentation is consistent with acute lirr,b ischemia ciue to atrial and non iatrogenic intramural hematoma with or r,rrithout fibrillation related thromboembolism, and the most appro' intimal dissection with luminal conrmunication. the enlarg priate first steps are to (l) initiate intrar,enous anticoagula ing hematoma in the false lumen compresses the true lumen tion with unfractionated heparin, (2) perforrn angiography, of the coronary artery and in potential combination rvith and (3) establish a plan for reperfusion ofrhe leg. obstructing dissection leads to chest pain, ischemia. and/or Invasive angiography of the lower extremity (Option A) infarction. the diagnosis requires coronary C'f or coronary should be expedited, as endovzrscular or surgical rev:rs. angiography to confirm the characteristic imaging features. cularization is warr:rnted to preserve limb Iunction and When associated r,r,ith ST-elerzation myocardial infarction, prevent major amputation. llow'ever. anticoagulation, SCAD rnay be managed inrasivelyr however, percutaneous typically r,l'ith unfraction:ited heparin, should be initiated coronary intervention may be safely detbrred r.then coro- as soon as the diagnosis is suspected, beliire perfbrming nary flow is preserved and symptoms can be controlled and diagnostic testing. closely monitored. This patient, r,r,ho has atrial fibrillation, needs antico 'ITe pathogenesis of ST elevation myocardial infarction agulation fbllorving this e'rent. However, because interuen typically ir.r,,,olves plaque rupture (Option A) within a coro tion is needeci to restore blood flovrl unf'racticlnated heparin nary artery 'lhe rupture causes platelet adhesion, activation, should be initiated no\ r, not an oral irnticoagulant snch as irnd aggrcgation, resultiug in a thrombosed coronary artery apixaban (Option B). Unfractionated heparin has a rapid irnd acute vessel occlnsion. 'lhe sudden loss of coronary onset and offset of action, alkru''ing for more flexibility in blood flort, leacis to transmural ischenria of the nryocardiunt 179

Answers and Critiques tr c0NI. and the ECG manifestation of ST segment eleration. Acute coronary thrombosis is a less likely cause of m1'ocardial infarction than coronary artery dissection in this postpar of 3.4')i, at 5 )€ars) and risks (periprocedural complication rate of 3.9'),, and increased absolute rate of non periproce dural atrial fibrillation of 0.113'/, per year). Data regarding tum young woman with no atherosclerotic cardiovascular benefit of PFO closure in patients older than 60 years are disease risk factors. lacking. Honever, current guidelines indicate that PFO clo- This patient's clinical picture is inconsistent sure may be considered in patients aged 60 to 65 years u'ith "t,ith peripartum cardiomyopathy (Option B), which is r-rert'ly feu' traditional vascular risk factors lor stroke and no other noted left ventricular systolic dysfunction with onset in the mechanism of stroke detected after a thorough evaluation. rnonths after delivery or toward the end of pregnancy in the including prolonged monitoring fbr atrial fibrillation. absence ofanother identifiable cause. Patients nith peripar \bung patients witl.r a PFO and embolic stroke of unde tum cardiomyopathy usually present '"t,ith features of heart termined source should be treated u'ith PFO closure in tailure. Echocardiography in peripartum cardioml,opathy addition to antipiatelet therapy: Aspirin alone (Option A) usually demonstrates gtobal reduction in systolic function. is generally recommended for patients u'ho are older than UI not tbcal hypokinesis, as seen in this patient. 60 years or patients who decline PFO closure. Stress-induced (takotsubo) cardiomyopathy (Option D) In patients who opt to receive n.redical therapy alone = .D art is characterized by transient regional cardiac dysfunction. without PF-O closure. either an antiplatelet medicatiort. such q, usually involving the apical and mid portions of the left ven as aspirin. or anticoagulation (using a vitamin K antago EL tricle. This is commonly precipitated by a stressful physical nist [Option C], a direct thrombin inl.ribitor. or a factor Xa n or emotional event. PostpartLlm cases ofstress-induced car inhibitor) seems to be equally efl'ective in reducing the risk diomyopathy have been reported. especially after cesarean for stroke by about 30')1,, but confidence inten'als are u'ide. ll delivery. Patients rn,ith stress induced cardiomyopathy pre leading to uncertainty of benefit. In patients $'ith a history of o ta sent with features that mimic an acute coronary syndrome. venous thromboembolism or hypercoagulable state. expert this patient's clinical picture is inconsistent with stress opinion endorses anticoagulation. induced cardiomyopathy given the regional r.tall hypokine Observation alone (Option D) has been associated lvith sis, which is more typical of coronary artery ischemia. I.righer event rates in patients u,ith PFO and stroke. There fbre, it is not appropriate to simply observe u'ithout therapl: I(EY POI TI . Spontaneous coronary artery dissection is the most TEY POIilTS common cause of pregnancy-associated myocardial . In patients younger than 60 years with a patent fora- infarction and occurs most commonly in the first men ovale (PFO) and embolic stroke of undetermined month postparhrm. source, current guidelines recommend PFO closure following a discussion of potential benefits and risks. Bibliography . In patients 60 years or older, patent foramen ovale Tweet MS, Hayes SN, Codsi E, et al. Spontaneous coronary artery dissection associated with pregnancy. J Am Coll Cardiol.2OtTJo:426-435. [PMID: closure may be considered for those who have few 287 28686) doi:10. 1016 /j. jacc. 2O17. 05.055 traditional risk factors for stroke and no other mecha- nism ofstroke detected, although the benefit is more uncertain than in younger patients.

tr c0NI. and the ECG manifestation of ST segment eleration. Acute coronary thrombosis is a less likely cause of m1'ocardial infarction than coronary artery dissection in this postpar of 3.4')i, at 5 )€ars) and risks (periprocedural complication rate of 3.9'),, and increased absolute rate of non periproce dural atrial fibrillation of 0.113'/, per year). Data regarding tum young woman with no atherosclerotic cardiovascular benefit of PFO closure in patients older than 60 years are disease risk factors. lacking. Honever, current guidelines indicate that PFO clo- This patient's clinical picture is inconsistent sure may be considered in patients aged 60 to 65 years u'ith "t,ith peripartum cardiomyopathy (Option B), which is r-rert'ly feu' traditional vascular risk factors lor stroke and no other noted left ventricular systolic dysfunction with onset in the mechanism of stroke detected after a thorough evaluation. rnonths after delivery or toward the end of pregnancy in the including prolonged monitoring fbr atrial fibrillation. absence ofanother identifiable cause. Patients nith peripar \bung patients witl.r a PFO and embolic stroke of unde tum cardiomyopathy usually present '"t,ith features of heart termined source should be treated u'ith PFO closure in tailure. Echocardiography in peripartum cardioml,opathy addition to antipiatelet therapy: Aspirin alone (Option A) usually demonstrates gtobal reduction in systolic function. is generally recommended for patients u'ho are older than UI not tbcal hypokinesis, as seen in this patient. 60 years or patients who decline PFO closure. Stress-induced (takotsubo) cardiomyopathy (Option D) In patients who opt to receive n.redical therapy alone = .D art is characterized by transient regional cardiac dysfunction. without PF-O closure. either an antiplatelet medicatiort. such q, usually involving the apical and mid portions of the left ven as aspirin. or anticoagulation (using a vitamin K antago EL tricle. This is commonly precipitated by a stressful physical nist [Option C], a direct thrombin inl.ribitor. or a factor Xa n or emotional event. PostpartLlm cases ofstress-induced car inhibitor) seems to be equally efl'ective in reducing the risk diomyopathy have been reported. especially after cesarean for stroke by about 30')1,, but confidence inten'als are u'ide. ll delivery. Patients rn,ith stress induced cardiomyopathy pre leading to uncertainty of benefit. In patients $'ith a history of o ta sent with features that mimic an acute coronary syndrome. venous thromboembolism or hypercoagulable state. expert this patient's clinical picture is inconsistent with stress opinion endorses anticoagulation. induced cardiomyopathy given the regional r.tall hypokine Observation alone (Option D) has been associated lvith sis, which is more typical of coronary artery ischemia. I.righer event rates in patients u,ith PFO and stroke. There fbre, it is not appropriate to simply observe u'ithout therapl: I(EY POI TI . Spontaneous coronary artery dissection is the most TEY POIilTS common cause of pregnancy-associated myocardial . In patients younger than 60 years with a patent fora- infarction and occurs most commonly in the first men ovale (PFO) and embolic stroke of undetermined month postparhrm. source, current guidelines recommend PFO closure following a discussion of potential benefits and risks. Bibliography . In patients 60 years or older, patent foramen ovale Tweet MS, Hayes SN, Codsi E, et al. Spontaneous coronary artery dissection associated with pregnancy. J Am Coll Cardiol.2OtTJo:426-435. [PMID: closure may be considered for those who have few 287 28686) doi:10. 1016 /j. jacc. 2O17. 05.055 traditional risk factors for stroke and no other mecha- nism ofstroke detected, although the benefit is more uncertain than in younger patients. tr Item 48 Answer: B Educational Objective: Treat patent foramen ovale in a Bibliography patient with embolic stroke of undetermined source. Messd SR, Gronseth GS, Kent DM, et al. Practice advisory update summary: patent foramen ovale and secondary stroke prevention: report of the The rnost appropriate management is patent foramen ovale Guideline Subcommittee of the American Academy of Neurolog,: Neurologr. 202O:94:876 85. IPMID: 32350058] doi:10.1212 WNL. (PFO) device closure (Option B). The fbramen ovale. a pas 0000000000009443 sage in the superior portion of the fbssa ovalis that allows oxygenated placental blood to transfer to the fetal circulation, remains patent in 25"1,Io 30'/,, of the population. Patients are Item 49 Answer: E usually asymptomatic. PFO has been identified at increased rates in patients with embolic stroke of undetermined Educational Obiective: Evaluate a cardiac murmur with transthoracic echocardiography. source, and several randomized studies have demonstrated that percutaneous PFO closure is more efi'ective for prevent The most appropriate diagnostic test is transthoracic echo ing recurrent ischemic stroke than antiplatelet therapy for cardiography (fff) (Option E) in this patient with physical patients younger than 60 years who have an embolic stroke examination flndings suggestive of structural heart disease, of'undetermined source with PFO. Device closure decreases speciflcally aortic regurgitation. T'TE is the mainstay of non- the risk for recurrent stroke by approximately 60',?, com invasive imaging to detect structural heart abnormalities pared with medical therapy. Current guidelines recommend and to evaluate new or worsening murmurs. This patient's PFC) closure in this population fbllowing a discussion of murmur suggests aortic regurgitation, which should ini- potential heneflts (absolute recurrent stroke risk reduction tially be evaluated with TTE. TTE also allows for evaluation

tr Item 48 Answer: B Educational Objective: Treat patent foramen ovale in a Bibliography patient with embolic stroke of undetermined source. Messd SR, Gronseth GS, Kent DM, et al. Practice advisory update summary: patent foramen ovale and secondary stroke prevention: report of the The rnost appropriate management is patent foramen ovale Guideline Subcommittee of the American Academy of Neurolog,: Neurologr. 202O:94:876 85. IPMID: 32350058] doi:10.1212 WNL. (PFO) device closure (Option B). The fbramen ovale. a pas 0000000000009443 sage in the superior portion of the fbssa ovalis that allows oxygenated placental blood to transfer to the fetal circulation, remains patent in 25"1,Io 30'/,, of the population. Patients are Item 49 Answer: E usually asymptomatic. PFO has been identified at increased rates in patients with embolic stroke of undetermined Educational Obiective: Evaluate a cardiac murmur with transthoracic echocardiography. source, and several randomized studies have demonstrated that percutaneous PFO closure is more efi'ective for prevent The most appropriate diagnostic test is transthoracic echo ing recurrent ischemic stroke than antiplatelet therapy for cardiography (fff) (Option E) in this patient with physical patients younger than 60 years who have an embolic stroke examination flndings suggestive of structural heart disease, of'undetermined source with PFO. Device closure decreases speciflcally aortic regurgitation. T'TE is the mainstay of non- the risk for recurrent stroke by approximately 60',?, com invasive imaging to detect structural heart abnormalities pared with medical therapy. Current guidelines recommend and to evaluate new or worsening murmurs. This patient's PFC) closure in this population fbllowing a discussion of murmur suggests aortic regurgitation, which should ini- potential heneflts (absolute recurrent stroke risk reduction tially be evaluated with TTE. TTE also allows for evaluation 180

Answers and Critiques of hemodynamic and functional consequences of valvular but with New York Heart Association functional class III to heart disease, which will assist in managing this patient. IV heart failure symptoms or recurrent syncope believed to In patients with moderate or severe aortic regurgita- be related to left ventricular outflow tract (LVOT) obstruction tion and suboptimal TTE images or a discrepancy between and an LVOT gradient of 50 mm Hg (resting or provoked) or clinical and TTE flndings, transesophageal echocardiogra greater should be considered for SRT. Adult patients in whom phy (TEE), cardiac catheterization (Option A), or cardiac surgical septal myectomy is contraindicated or the risk is magnetic resonance imaging (Option B) is indicated for the considered unacceptable because of serious comorbidities assessment of left ventricular systolic function, systolic and or advanced age, alcohol septal ablation, performed at expe- diastolic volumes, aortic size, and aortic regurgitation sever rienced centers, is recommended. This patient is young and 1 ity. However, before consideration ofany ofthese tests, initial without significant comorbidities; thus, he should be consid evaluation with TTE should be performed. ered for surgical septal myectomy. In patients with suspected low-flow low gradient severe Both valsartan-sacubitril and carvedilol may reduce aortic stenosis with reduced left ventricular ejection frac afterload. Adding valsartan sacubitril (Option A) or switch vt q, tion, low-dose dobutamine stress testing with echocardio- ing metoprolol to carvedilol (Option C) may worsen this graphic (Option C) or invasive hemodynamic measurements patient's symptoms and degree of LVOT obstruction. .g is reasonable to further deflne severity and assess contractile This patient has no clear indication for implantable L' reserve. However, this patient's auscultation flndings are most cardioverter deflbrillator (lCD) placement (Option B). An =, consistent with aortic regurgitation. Even if this patient had ICD is recommended for patients with HCM and previous t! UI aortic stenosis, the initial diagnostic test remains TTE. documented cardiac arrest or sustained ventricular tachycar- TEE (Option D) is not the most appropriate next step dia. ICD placement is considered reasonable in the presence o ta = for this patient because it is unnecessarily invasive at this of one or more major risk factors for sudden cardiac death, E point in her evaluation. TEE is usually performed if TTE including sudden death in a flrst degree or close relative at image quality is iow; it also can be particularly helpful if age 50 years or younger, lelt ventricular (LV) hypertrophy of an evaluation of left atrial appendage thrombus or a cardi 30 mm or greater, syncope thought to be arrhythmogenic, LV oembolic source is indicated or when there is suspicion of aneurysm, and an LV ejection fraction of 50% or less. endocarditis, prosthetic valve dysfunction, or aortic disease. I(EY POII{I TEE is also useful in patients with moderate or severe aortic o Patients with hypertrophic cardiomyopathy who are regurgitation and suboptimal TTE images or a discrepancy between clinical and TTE lindings. receiving guideline-directed medical therapy but with New York Heart Association functional class III to IV I(IY POI ]II heart failure symptoms or recurrent syncope believed . Transthoracic echocardiography is the mainstay of to be related to left ventricular outflow tract (LVOT) noninvasive imaging to detect structural heart abnor obstruction and an LVOT gradient of 50 mm Hg (rest evaluate new or worsening cardiac ing or provoked) or greater should be considered lor ffi,J*"ff*,o septal reduction therapY.

of hemodynamic and functional consequences of valvular but with New York Heart Association functional class III to heart disease, which will assist in managing this patient. IV heart failure symptoms or recurrent syncope believed to In patients with moderate or severe aortic regurgita- be related to left ventricular outflow tract (LVOT) obstruction tion and suboptimal TTE images or a discrepancy between and an LVOT gradient of 50 mm Hg (resting or provoked) or clinical and TTE flndings, transesophageal echocardiogra greater should be considered for SRT. Adult patients in whom phy (TEE), cardiac catheterization (Option A), or cardiac surgical septal myectomy is contraindicated or the risk is magnetic resonance imaging (Option B) is indicated for the considered unacceptable because of serious comorbidities assessment of left ventricular systolic function, systolic and or advanced age, alcohol septal ablation, performed at expe- diastolic volumes, aortic size, and aortic regurgitation sever rienced centers, is recommended. This patient is young and 1 ity. However, before consideration ofany ofthese tests, initial without significant comorbidities; thus, he should be consid evaluation with TTE should be performed. ered for surgical septal myectomy. In patients with suspected low-flow low gradient severe Both valsartan-sacubitril and carvedilol may reduce aortic stenosis with reduced left ventricular ejection frac afterload. Adding valsartan sacubitril (Option A) or switch vt q, tion, low-dose dobutamine stress testing with echocardio- ing metoprolol to carvedilol (Option C) may worsen this graphic (Option C) or invasive hemodynamic measurements patient's symptoms and degree of LVOT obstruction. .g is reasonable to further deflne severity and assess contractile This patient has no clear indication for implantable L' reserve. However, this patient's auscultation flndings are most cardioverter deflbrillator (lCD) placement (Option B). An =, consistent with aortic regurgitation. Even if this patient had ICD is recommended for patients with HCM and previous t! UI aortic stenosis, the initial diagnostic test remains TTE. documented cardiac arrest or sustained ventricular tachycar- TEE (Option D) is not the most appropriate next step dia. ICD placement is considered reasonable in the presence o ta = for this patient because it is unnecessarily invasive at this of one or more major risk factors for sudden cardiac death, E point in her evaluation. TEE is usually performed if TTE including sudden death in a flrst degree or close relative at image quality is iow; it also can be particularly helpful if age 50 years or younger, lelt ventricular (LV) hypertrophy of an evaluation of left atrial appendage thrombus or a cardi 30 mm or greater, syncope thought to be arrhythmogenic, LV oembolic source is indicated or when there is suspicion of aneurysm, and an LV ejection fraction of 50% or less. endocarditis, prosthetic valve dysfunction, or aortic disease. I(EY POII{I TEE is also useful in patients with moderate or severe aortic o Patients with hypertrophic cardiomyopathy who are regurgitation and suboptimal TTE images or a discrepancy between clinical and TTE lindings. receiving guideline-directed medical therapy but with New York Heart Association functional class III to IV I(IY POI ]II heart failure symptoms or recurrent syncope believed . Transthoracic echocardiography is the mainstay of to be related to left ventricular outflow tract (LVOT) noninvasive imaging to detect structural heart abnor obstruction and an LVOT gradient of 50 mm Hg (rest evaluate new or worsening cardiac ing or provoked) or greater should be considered lor ffi,J*"ff*,o septal reduction therapY. Bibliography Bibliography otto cM, Nishimura RA, Bonon, RO. et al. 2020 ACC/AHA guideline for the Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC guideline for the diag- management of patients with valvular heart disease: a report of the nosis and treatment of patients with hypertrophic cardiomyopathy: exec American College of Cardiolory/American Ileart Association Joint utive summary: a report of the American College of Cardiologl/American Committee on Clinical Practice Guidelines. Circulation. 2021;143: Heart Association Joint Committee on Clinical Practice Guidelines. e72 e227. IPMID: 33332150] doi:10.1161 /CIR.0000000000000923 Circulation. 2020:142:e533 e557. IPMID: 33215938] doi:10.1161/CIR. 0000000000000938

Bibliography Bibliography otto cM, Nishimura RA, Bonon, RO. et al. 2020 ACC/AHA guideline for the Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC guideline for the diag- management of patients with valvular heart disease: a report of the nosis and treatment of patients with hypertrophic cardiomyopathy: exec American College of Cardiolory/American Ileart Association Joint utive summary: a report of the American College of Cardiologl/American Committee on Clinical Practice Guidelines. Circulation. 2021;143: Heart Association Joint Committee on Clinical Practice Guidelines. e72 e227. IPMID: 33332150] doi:10.1161 /CIR.0000000000000923 Circulation. 2020:142:e533 e557. IPMID: 33215938] doi:10.1161/CIR. 0000000000000938 ttem 50 Answer: D Ed u cati o n a I O bj ective : Treat hypertrophic cardiomy- opathy with obstructive symptoms with septal reduction Item 51 Answer: C Educational Objective: Treat hemodynamic complica- tr therapy. tions of inferior myocardial infarction with right ventricu lar involvement. Septal reduction therapy (SRT) (Option D) is the most appro priate treatment. Pharmacotherapy and lifestyle modification Intravenous (t.9')1, saline (Option C) is indicated firr this are appropriate initial choices for treatment of hypertrophic patierlt lvith iut inferior rnyocarclial infarctiot.t (MI) compli cardiomyopathy (HCM) with obstructive symptoms. Non cated tr1' right r,entricular (RV) inf'arction. RV infarction is vasodilating p blockers and/or nondihydropyridine calcium rarely nn isolirted cvent: it rlccurs in as nlan!'JS olle third channel blockers (verapamil, diltiazem) are flrst-line choices. ol paticnts with an inf'erior Ir4l and is nrost comnlonly asso For patients with persistent symptoms, adding disopyramide, ciltecl r,r,ith proxitrtll rigl'tt coronary artery cvents. Acutc a class IA antiarrhythmic drug with potent negative ino resuscil:rtiotr of patients with RV ischenlic dysiunction is tropic activity, to one of the other drugs is a recommended irinrecl itt reversing tlre resultant clecrease in lelt ventricular option. Patients receiving guideline-directed medical therapy (tV) preloacl itnd sr-rbseqr'rent recluctiorl in cardiac output.

ttem 50 Answer: D Ed u cati o n a I O bj ective : Treat hypertrophic cardiomy- opathy with obstructive symptoms with septal reduction Item 51 Answer: C Educational Objective: Treat hemodynamic complica- tr therapy. tions of inferior myocardial infarction with right ventricu lar involvement. Septal reduction therapy (SRT) (Option D) is the most appro priate treatment. Pharmacotherapy and lifestyle modification Intravenous (t.9')1, saline (Option C) is indicated firr this are appropriate initial choices for treatment of hypertrophic patierlt lvith iut inferior rnyocarclial infarctiot.t (MI) compli cardiomyopathy (HCM) with obstructive symptoms. Non cated tr1' right r,entricular (RV) inf'arction. RV infarction is vasodilating p blockers and/or nondihydropyridine calcium rarely nn isolirted cvent: it rlccurs in as nlan!'JS olle third channel blockers (verapamil, diltiazem) are flrst-line choices. ol paticnts with an inf'erior Ir4l and is nrost comnlonly asso For patients with persistent symptoms, adding disopyramide, ciltecl r,r,ith proxitrtll rigl'tt coronary artery cvents. Acutc a class IA antiarrhythmic drug with potent negative ino resuscil:rtiotr of patients with RV ischenlic dysiunction is tropic activity, to one of the other drugs is a recommended irinrecl itt reversing tlre resultant clecrease in lelt ventricular option. Patients receiving guideline-directed medical therapy (tV) preloacl itnd sr-rbseqr'rent recluctiorl in cardiac output. 181

Answers and Critiques : ffi Prompt reperfusion follor.ted by intravenous volume expan- with heafi failure r,r'ithin 30 days oi the index hospitaliza El s16n with up to sereral liters of intrarenous iluirls increases tion. Tr,r,o key elements are associated r,rrith a successful tran coNT right ventricular preload and contractility. tl-rus increasing sition fiorn hospital to home: a follor,r, r-rp phone call u,ithin ftow through the pulmonary circuit into the lell atrium 2 to l3 days of discharge and an oflice visit $'ithin 7 to 1,1 days 1 and ultimately enhancing LV preload and carcliac output. ol'hospital discharge. The pttrpose of the fbllor,l'-up phone Although long-term prognosis is good r,r,hen appropriale call is to address signs ofcongestion. provide education and ,t treatment is initiated promptly, RV infarction is associated review adherence to the meclication regimen, and confirm ! with high inpatient morbidity and morlality. Early recog fbllor,", up appointments and adequate transportation. The . nition is therefore essential and may be facilitated by iden expert consensus decision pathr,r,ay recommends a stan a tiflcation of 1 mm or more of ST segment elevation in lead clardized approach to the fbllou, up telephone call, including V, or V.,R (right sided V). Findings of normal or modestly use ofa checklist to help organize the call. l

nition is therefore essential and may be facilitated by iden expert consensus decision pathr,r,ay recommends a stan a tiflcation of 1 mm or more of ST segment elevation in lead clardized approach to the fbllou, up telephone call, including V, or V.,R (right sided V). Findings of normal or modestly use ofa checklist to help organize the call. l elevated central venous pressure r.r,ith clear lungs despite For patients with an initial dingnosis ol heart firilure. it is tachycardia and/or hypotension are suggestive of an RV allpropriate to repeat echocardiography in 3 rnonths (Option A) i aa infarction complicating infbrior ST-elevation MI: honever, 1r; zrssess the eflect ot medical therapy on ejectior-r lraction : € .D these findings also may be seen in cardiac tamponade, ancl and need for an implantable cardioverter defibrillator (lCl)). r UI conflrmation of RV infarction physiolog, and absence of lichocardiographl,was perlbrmed in this patient in the hos q, pericardial effusion by echocardiography is indicated. pital, and fbr a patient lvith kno.,vn lou' ejection 1'raction a Support with intra'aortic balloon pump placement and an lCD, there is l1o reason for echocardiography so soon rl (Option A) or other mechanical IV supportive measllres shoulcl unless there is a clinical change. be reserved fbr stabilization in the setting ofpersistent shock, 1he first postdischarge appointment lbcuses on changes lt (D especially with evidence of concomitant LV systolic failure. in clinical status, patient education. medication rer,ierv and : UI When volume resuscitation does not improve signs of acljustn.rent of dosages, and iclentification and correctioll 1

elevated central venous pressure r.r,ith clear lungs despite For patients with an initial dingnosis ol heart firilure. it is tachycardia and/or hypotension are suggestive of an RV allpropriate to repeat echocardiography in 3 rnonths (Option A) i aa infarction complicating infbrior ST-elevation MI: honever, 1r; zrssess the eflect ot medical therapy on ejectior-r lraction : € .D these findings also may be seen in cardiac tamponade, ancl and need for an implantable cardioverter defibrillator (lCl)). r UI conflrmation of RV infarction physiolog, and absence of lichocardiographl,was perlbrmed in this patient in the hos q, pericardial effusion by echocardiography is indicated. pital, and fbr a patient lvith kno.,vn lou' ejection 1'raction a Support with intra'aortic balloon pump placement and an lCD, there is l1o reason for echocardiography so soon rl (Option A) or other mechanical IV supportive measllres shoulcl unless there is a clinical change. be reserved fbr stabilization in the setting ofpersistent shock, 1he first postdischarge appointment lbcuses on changes lt (D especially with evidence of concomitant LV systolic failure. in clinical status, patient education. medication rer,ierv and : UI When volume resuscitation does not improve signs of acljustn.rent of dosages, and iclentification and correctioll 1 cardiogenic shock associated r.tith RV infarction or when of issues that might leaci to rvorsening of heirrt lailure and intravenous fluids result in development ol pulmonary readmission. 'Ihe recommended tinring ol the first follort up edema, inotropic therapy may be necessary. ln this patient visit is u,ithin 7 to 10 days of hospital discharge: 30 days 1 r.tith tachycardia on presentation. clear lungs. and stable (Option B) is too 1:rte. hypotension. dobutamine infusion (Option B) may be asso lnadequate diuretic dosage is a common cause of heart ciated with worsening tachycardia and further l.remody- failure readmissions. This patieltt required an increased furo- namic deterioration. Inotropic therapy should be resenred semide dosage to achier,e adequate diuresis. 'lhis suglests i

cardiogenic shock associated r.tith RV infarction or when of issues that might leaci to rvorsening of heirrt lailure and intravenous fluids result in development ol pulmonary readmission. 'Ihe recommended tinring ol the first follort up edema, inotropic therapy may be necessary. ln this patient visit is u,ithin 7 to 10 days of hospital discharge: 30 days 1 r.tith tachycardia on presentation. clear lungs. and stable (Option B) is too 1:rte. hypotension. dobutamine infusion (Option B) may be asso lnadequate diuretic dosage is a common cause of heart ciated with worsening tachycardia and further l.remody- failure readmissions. This patieltt required an increased furo- namic deterioration. Inotropic therapy should be resenred semide dosage to achier,e adequate diuresis. 'lhis suglests i fbr iailure of volume erpansion. that the prerrious home diur-etic dosage uus inadequate, and 'i i Nitrates, diuretics, opioid analgesic agents. calcium an increase of at least double that dosage should be consid \ channel blockers, and B blockers (metoprolol) (Option D) ered. Restarling the previous home dosage (Option D) might can aclversely contribute to reduced cardiac preload and be considered fbr a patient w'ho did not adhere to the medi cardiac output and should be avoided in patients rvith acute c:rtion regimen befbre hospitalization. RV infarction physiologr. XEY POIIII ' trl.Y. rPOlt.f]:ir r. ri, r Two key elements are associated with a successful : . A patient with an inferior myocardial infarction with transition to home following hospitalization for heart .

fbr iailure of volume erpansion. that the prerrious home diur-etic dosage uus inadequate, and 'i i Nitrates, diuretics, opioid analgesic agents. calcium an increase of at least double that dosage should be consid \ channel blockers, and B blockers (metoprolol) (Option D) ered. Restarling the previous home dosage (Option D) might can aclversely contribute to reduced cardiac preload and be considered fbr a patient w'ho did not adhere to the medi cardiac output and should be avoided in patients rvith acute c:rtion regimen befbre hospitalization. RV infarction physiologr. XEY POIIII ' trl.Y. rPOlt.f]:ir r. ri, r Two key elements are associated with a successful : . A patient with an inferior myocardial infarction with transition to home following hospitalization for heart . right ventricular involvement and hypotension should failure: a follow-up phone call within 2 to 3 days of l receive intravenous fl uids. discharge and an office visit within 7 to 14 days of 1 : hospital discharge. Bibliography Ibanez B, James S, Agewall S, et al; ESC Scientific Document Group. 2017 Bibliography ESC guidelines for the management of acute myocardial infarction in Hollenberg SM, Warner Stevenson L, Ahmad T, et al. 2019 ACC expert consen- l patients presenting with ST segment elevation: the Task Force for the Management ofAcute Myocardial Infarction in patients presenting With sus decisionpathway on risk assessment, management, and clinical trajec ST Segment Elevation of the European Society of Cardiologz (ESC). Eur tory ol patients hospitalized with heart failure: a report of the American Heart J. 2018;39:1 19 77 . lPMlDt 288866211 doi:10.1 093/eurheartj/ehx393 College of Cardiolos/ Solution Set Oversight Committee. J Am Coll Cardiol. 2019;74:7966 20ll- IPMID: 31526538] doi:10.1016/j.jacc.2019.08.001

right ventricular involvement and hypotension should failure: a follow-up phone call within 2 to 3 days of l receive intravenous fl uids. discharge and an office visit within 7 to 14 days of 1 : hospital discharge. Bibliography Ibanez B, James S, Agewall S, et al; ESC Scientific Document Group. 2017 Bibliography ESC guidelines for the management of acute myocardial infarction in Hollenberg SM, Warner Stevenson L, Ahmad T, et al. 2019 ACC expert consen- l patients presenting with ST segment elevation: the Task Force for the Management ofAcute Myocardial Infarction in patients presenting With sus decisionpathway on risk assessment, management, and clinical trajec ST Segment Elevation of the European Society of Cardiologz (ESC). Eur tory ol patients hospitalized with heart failure: a report of the American Heart J. 2018;39:1 19 77 . lPMlDt 288866211 doi:10.1 093/eurheartj/ehx393 College of Cardiolos/ Solution Set Oversight Committee. J Am Coll Cardiol. 2019;74:7966 20ll- IPMID: 31526538] doi:10.1016/j.jacc.2019.08.001 tr Item 52 Ed ucatio n a I O bj ective Answer: C : Prevent healt failure readmission Item 53 Answer: A Educational Objective: Diagnose severe aortic stenosis with early follow-up. in a patient with discrepant clinical and echocardiographic A telephone call within 2 to 3 days (Option C) is recom flndings. mended to prevent this patient's early readmission to the The most appropriate next step in management is to perform hospital. The 2019 American College of Cardiolog; expert cardiac catheterization (Option A). This patient's symptoms of consensus decision pathway fbr patients hospitalizecl lvith dyspnea and syncope are consistent with qrmptomatic, poten heart failure notes that up to 25')l, of patients are readrnitted tially severe aortic stenosis. When caused by aortic stenosis,

tr Item 52 Ed ucatio n a I O bj ective Answer: C : Prevent healt failure readmission Item 53 Answer: A Educational Objective: Diagnose severe aortic stenosis with early follow-up. in a patient with discrepant clinical and echocardiographic A telephone call within 2 to 3 days (Option C) is recom flndings. mended to prevent this patient's early readmission to the The most appropriate next step in management is to perform hospital. The 2019 American College of Cardiolog; expert cardiac catheterization (Option A). This patient's symptoms of consensus decision pathway fbr patients hospitalizecl lvith dyspnea and syncope are consistent with qrmptomatic, poten heart failure notes that up to 25')l, of patients are readrnitted tially severe aortic stenosis. When caused by aortic stenosis, 142

Answers and Critiques syncope is usually a late finding and raises concern for sud moderate intensity statin therapy. Guidelines from the U.S. den cardiac death if aortic stenosis is not adequately treated. Department of Veterans AIIairs/U.S. Department of Delbnse Severe aortic stenosis is typically defined by a small valve area recommend at least moderate intensity statin therapy for (<t.0 cm2), high peak velocity (>a m/s), and/or high mean gra the secondary prevention of ASCVD. As many as 45'X, ol dient (>40 mm Hg). However, althclugh the two-dimensional patients with PAD are not prescribed or do not flll a prescrip morphologic description of this patient's aortic valve is consis tion for statin medications. Patients with PAD may confuse tent with severe aortic stenosis (severely thickened, minimally symptoms of intermittent claudication with adverse efI'ects mobile tricuspid aortic valve), the mean valve gradient and of statins (namely myalgia), which may contribute to the low aortic valve area are consistent with moderate aortic stenosis. adherence rate. The most appropriate treatment is patient Because technicai considerations may result in either over or education and reintroduction of atorvastatin. underestimation of aortic valve gradient and aortic valve area Colestipol (Option B) is a bile acid sequestrant. The by echocardiography, further hemodynamic testing with car AHATACC cholesterol guideline suggests consideration of diac catheterization should be pursued in cases ofdiscrepant a bile acid sequestrant in patients aged 20 to 75 years with ah {, clinicai and echocardiographic fi ndings. a baseline LDL cholesterol level o1'190 mg/dl or greater E CT of the aortic valve (Option B) is a useful diagnostic (>4.9 mmol/L) who achieve less than a 50'2, reduction in LDL modality fbr severe aortic stenosis in low flow iow gradient cholesterol and have a fasting triglyceride level of 300 mg/dL (J disease with normal or reduced cardiac output. However, the or less (<3.4 mmol/L) while receiving maximally tolerated -, issue at present is discrepant clinical and echocardiographic statin and ezetimibe therapy. Monotherapy with a bile acid t! t flndings. A study that can provide hemodynamic data, such sequestrant is not recommended as a substitute for statin as cardiac catheterization, is pref'erred. therapy in the secondary prevention of ASCVD. o Exercise stress testing (Option C) is not appropriate Ezetimibe (Option C) is a cholesterol absorption inhibi tt = E fbr this patient. Exercise stress testing is contraindicated tor. the AHAi'ACC cholesterol guideline suggests considering in most patients with symptomatic severe aortic stenosis, the addition of ezetimibe to high intensity statin therapy in given the increased risk lbr sudden cardiac death during the patients with clinical ASCVD whose LDL cholesterol level test. A symptom limited treadmill test may be perfbrmed in remains 70 mgldL (1.8 mmol/L) or greater on maximally asymptomatic patients with severe aortic stenosis to conflrm tolerated statin therapy. Monritherapy with ezetimibe is not asymptomatic status. a substitute fbr statin therapy. Neither surgical aortic valve replacement (Option D) Icosapent ethyl (Option D), a highly purilied eicosa nor transcatheter aortic valve implantation (Option E) is pentaenoic acid ethyl ester, lowers triglyceride levels. In appropriate until hemodynamic confirmation of severe patients with ASCVD or other cardiac risk I'actors on a statin aortic stenosis is made. with controlled LDL cholesterol but elevated triglyceride levels (135 499 mg/dl [t.sz s.os mmol/L]), the addition of KTY POIl{I icosapent ethyl may be considered to reduce cardiovascular o Guidelines recommend cardiac catheterization to risk. Therapy with icosapent ethyl monotherapy is not rec \ evaluate patients with suspected significant aortic ste ommended for the secondary prevention of ASCVD and is nosis when there is a discrepancy between the clinical not a substitute Ibr statin therapy. evaluation and the echocardiogram. t(Ev P0ltTs

syncope is usually a late finding and raises concern for sud moderate intensity statin therapy. Guidelines from the U.S. den cardiac death if aortic stenosis is not adequately treated. Department of Veterans AIIairs/U.S. Department of Delbnse Severe aortic stenosis is typically defined by a small valve area recommend at least moderate intensity statin therapy for (<t.0 cm2), high peak velocity (>a m/s), and/or high mean gra the secondary prevention of ASCVD. As many as 45'X, ol dient (>40 mm Hg). However, althclugh the two-dimensional patients with PAD are not prescribed or do not flll a prescrip morphologic description of this patient's aortic valve is consis tion for statin medications. Patients with PAD may confuse tent with severe aortic stenosis (severely thickened, minimally symptoms of intermittent claudication with adverse efI'ects mobile tricuspid aortic valve), the mean valve gradient and of statins (namely myalgia), which may contribute to the low aortic valve area are consistent with moderate aortic stenosis. adherence rate. The most appropriate treatment is patient Because technicai considerations may result in either over or education and reintroduction of atorvastatin. underestimation of aortic valve gradient and aortic valve area Colestipol (Option B) is a bile acid sequestrant. The by echocardiography, further hemodynamic testing with car AHATACC cholesterol guideline suggests consideration of diac catheterization should be pursued in cases ofdiscrepant a bile acid sequestrant in patients aged 20 to 75 years with ah {, clinicai and echocardiographic fi ndings. a baseline LDL cholesterol level o1'190 mg/dl or greater E CT of the aortic valve (Option B) is a useful diagnostic (>4.9 mmol/L) who achieve less than a 50'2, reduction in LDL modality fbr severe aortic stenosis in low flow iow gradient cholesterol and have a fasting triglyceride level of 300 mg/dL (J disease with normal or reduced cardiac output. However, the or less (<3.4 mmol/L) while receiving maximally tolerated -, issue at present is discrepant clinical and echocardiographic statin and ezetimibe therapy. Monotherapy with a bile acid t! t flndings. A study that can provide hemodynamic data, such sequestrant is not recommended as a substitute for statin as cardiac catheterization, is pref'erred. therapy in the secondary prevention of ASCVD. o Exercise stress testing (Option C) is not appropriate Ezetimibe (Option C) is a cholesterol absorption inhibi tt = E fbr this patient. Exercise stress testing is contraindicated tor. the AHAi'ACC cholesterol guideline suggests considering in most patients with symptomatic severe aortic stenosis, the addition of ezetimibe to high intensity statin therapy in given the increased risk lbr sudden cardiac death during the patients with clinical ASCVD whose LDL cholesterol level test. A symptom limited treadmill test may be perfbrmed in remains 70 mgldL (1.8 mmol/L) or greater on maximally asymptomatic patients with severe aortic stenosis to conflrm tolerated statin therapy. Monritherapy with ezetimibe is not asymptomatic status. a substitute fbr statin therapy. Neither surgical aortic valve replacement (Option D) Icosapent ethyl (Option D), a highly purilied eicosa nor transcatheter aortic valve implantation (Option E) is pentaenoic acid ethyl ester, lowers triglyceride levels. In appropriate until hemodynamic confirmation of severe patients with ASCVD or other cardiac risk I'actors on a statin aortic stenosis is made. with controlled LDL cholesterol but elevated triglyceride levels (135 499 mg/dl [t.sz s.os mmol/L]), the addition of KTY POIl{I icosapent ethyl may be considered to reduce cardiovascular o Guidelines recommend cardiac catheterization to risk. Therapy with icosapent ethyl monotherapy is not rec \ evaluate patients with suspected significant aortic ste ommended for the secondary prevention of ASCVD and is nosis when there is a discrepancy between the clinical not a substitute Ibr statin therapy. evaluation and the echocardiogram. t(Ev P0ltTs Bibliography . Peripheral artery disease is considered a clinical athero Otto CM. Nishimura RA. Bonou' RO. et al. 2020 ACC AHA guideline fbr the sclerotic cardiovascular disease. nranagement of patients u'ith lalvuhr herrt disease: a report of the o Statin therapy is recommended for secondary preven r\r'nerican College of CarclioloS''American Ileart Association Joint Comnrittee on Clinical Practice (lui(lelines. Circulation. 2o2l:143:e7') tion of atherosclerotic cardiovascular disease in patients e227. IPl\'llDr 33332150] doi: 10. I l6l Cl R.0000000000000923 with peripheral artery disease.

Bibliography . Peripheral artery disease is considered a clinical athero Otto CM. Nishimura RA. Bonou' RO. et al. 2020 ACC AHA guideline fbr the sclerotic cardiovascular disease. nranagement of patients u'ith lalvuhr herrt disease: a report of the o Statin therapy is recommended for secondary preven r\r'nerican College of CarclioloS''American Ileart Association Joint Comnrittee on Clinical Practice (lui(lelines. Circulation. 2o2l:143:e7') tion of atherosclerotic cardiovascular disease in patients e227. IPl\'llDr 33332150] doi: 10. I l6l Cl R.0000000000000923 with peripheral artery disease. Item 54 Answer: A Bibliography (;rundy Sl\4, Stone NJ, Bailey At.. et rl. 20l8 AIIA/ACC/AACVPRIAAPA/AB(l/ Educational Objective: Treat a patient with peripheral ACPM/ADAIAGSlAPhA/ASPC/NLA/l'CNA guideline on the management artery disease with statin therapy. of blood cholesterol: a report ol the American College ol Cardioloryr American Heart Association'lirsk Iirrce on Clinical Practice Cuidelines' Circulation. 2019;139:e1082 ell'1i:1. IPMID: :105867741 doi:10'1161 /ClR' Tl.re most appropriate treatment is to reintroduce atorvasta 0000000000000625 tin (Option A). Peripheral artery disease (PAD) is considered ir clinical atherosclerotic cardiovascular disease (ASCVD), ancl high intensity statin therapy (atorvastatin or rosuva Item 55 Answer: C statin) is recommended in patients with clinical ASCVD Educational Objective: Treat symptomatic premature tbr secondary prevention, accordir.rg to guidelines from the ventricular contractions with a p-blocker. American Heart Association/American College of Cardiolory (AF{A/ACC). Patients with PAD who are older than 75 years 'lhe most appropriate treatment is propranolol (Option or intolerant of high intensity statins should be treated with C). This patient has symptomatic premature ventricular

Item 54 Answer: A Bibliography (;rundy Sl\4, Stone NJ, Bailey At.. et rl. 20l8 AIIA/ACC/AACVPRIAAPA/AB(l/ Educational Objective: Treat a patient with peripheral ACPM/ADAIAGSlAPhA/ASPC/NLA/l'CNA guideline on the management artery disease with statin therapy. of blood cholesterol: a report ol the American College ol Cardioloryr American Heart Association'lirsk Iirrce on Clinical Practice Cuidelines' Circulation. 2019;139:e1082 ell'1i:1. IPMID: :105867741 doi:10'1161 /ClR' Tl.re most appropriate treatment is to reintroduce atorvasta 0000000000000625 tin (Option A). Peripheral artery disease (PAD) is considered ir clinical atherosclerotic cardiovascular disease (ASCVD), ancl high intensity statin therapy (atorvastatin or rosuva Item 55 Answer: C statin) is recommended in patients with clinical ASCVD Educational Objective: Treat symptomatic premature tbr secondary prevention, accordir.rg to guidelines from the ventricular contractions with a p-blocker. American Heart Association/American College of Cardiolory (AF{A/ACC). Patients with PAD who are older than 75 years 'lhe most appropriate treatment is propranolol (Option or intolerant of high intensity statins should be treated with C). This patient has symptomatic premature ventricular 183

Answers and Critiques contractions (PVCs) with a normal heart on echocardio Item 56 Answer: A gram. Laboratory studies have excluded common second- Educational Objective: Treat atrial septal defect. ary causes of PVCs (anemia, hyperthyroidism, pregnancy). The PVCs are likely contributing to her anxiety, which may Atrial septal defect (ASD) closure (Option A) is indicated in this in turn increase their number. p Blockers, particularly patient with a 1.5 cm ASD associated with right heart enlarge- those with some anxiolytic effect (such as propranolol), are ment, symptoms, and no pulmonary hypertension. An ASD is first-line therapy for PVCs. B-Blockers are also preferred in a defect in the atrial septum resulting in a left-to-right shunt patients with ventricular dysfunction. Among patients with with eventual right sided cardiac chamber dilatation in most depression or very poor tolerance of B-blockers, a nondihy patients. Ostium secundum defects, the most common ty'pe of dropyridine calcium channel blocker, such as verapamil, ASD (757, of cases), are typically located in the mid portion of may be used. the atrial septum and are usually isolated anomalies. In asymp- This patient's PVC burden may be quite high if she tomatic patients with a small ASD and no right heart enlarge- has several PVCs on a standard l2-lead ECG. Ambula- ment, periodic clinical monitoring and echocardiographic UI tory ECG monitoring can help clarify whether her PVCs imagrng are recornnended. The main indications for ASD clo- E are episodic and of low overall burden or if they persist sure include right sided cardiac chamber enlargement, dys- .D ul throughout the day. Patients with PVCs that account for pnea, or paradoxical embolization. Most patients with ostium o, more than l0% to 15% of beats may be at risk for develop- secundum ASD are candidates for device closure ofthe ASD. a TL ing PVC induced cardiomyopathy and subsequent heart procedure performed in the cardiac catheterization laboratory. ..t failure, which is an additional reason to treat this patient's Cardiopulmonary exercise testing (Option B) may be symptomatic PVCs. If she develops cardiomyopathy, it may helpful in evaluating dyspnea if the initial evaluation is unre- 4t E be reversible with more aggressive treatment of PVCs (e.g., vealing, deconditioning is a possibility. or several problems .D (a catheter ablation). may be contributing to dyspnea. This patient's dyspnea and Amiodarone (Option A) is an antiarrhythmic agent that right heart enlargement are caused by the ASD. and cardio- may be very effective at suppressing this patient's PVCs. pulmonary testing is not necessary. However, it may be toxic over the long term, potentially Coronary angiography (Option C) is considered before causing devastating injury to the lungs, liver, and/or thyroid. cardiac surgery or intervention for noncoronary cardiac Furthermore, it may be unnecessary in this young patient. issues in patients with symptoms of angina, evidence of cor Amiodarone is therefore not an appropriate flrst-line choice onary ischemia, decreased left ventricular systolic function, in this clinical setting. When amiodarone is used, it should a history ol coronary artery disease, or risk factors for coro be taken for the shortest possible time at the lowest effective nary artery disease. This patient's symptoms and evaluation dose, with close monitoring. are consistent with ASD, not cardiac ischemia, and coronary This patient has no exertional symptoms, no speciflc angiography is not required. risk factors for coronary ischemia, and normal echocar Echocardiographic surveillance (Option D) is considered diogram results. Exercise ECG (Option B) is unlikely to be for patients with an ASD if there is no associated right heart high yield in this setting. However, PVCs often cease during enlargement, if severe pulmonary hypertension is present, or exercise in a structurally normal heart, which would be if there are no severe comorbid conditions that may adversely reassuring. affect outcome. Transesophageal echocardiography may be This patient's symptoms are likely attributable to pVCs needed to conflrm the presence of an ASD if transthoracic and are described as intolerable; therefore, she warrants echocardiography is nondiagnostic or for the purposes of treatment, and reassurance alone (Option D) is not appro procedure planning. ASD closure, not serial surveillance with priate. echocardiography, is recommended for this patient with a symptomatic ASD and right heart enlargement. rEY POIilTS o First-line treatment for q.rrnptomatic premature ven- TEY POIXTT tricular contraction suppression is p-blocker or calcium o Atrial septal defect closure is indicated in patients channel blocker therapy; p-blockers are preferred in with symptoms or evidence of right-sided cardiac patients with ventricular dysfunction. chamber enlargement and without severe pulmonary o Ambulatory ECG monitoring can help clariflz the bur- hypertension. den of premature ventricular contractions (pVCs); o Most patients with ostium secundum atrial septal defect patients with PVCs that account for more than 10% are candidates for device closure performed in the cardiac to 15% of beats may be at risk for pVC induced catheterization laboratory. cardiomyopathy. Bibliography Bibliography Stout KK. Daniels CJ. Aboulhosn JA. er al. 2018 AHA,ACC guideline for the management of adults w.ith congenital heart disease; a report of the Marcus GM. Evaluation and management of premature ventricular com American College of Cardiologr/American Heart Association Task Force plexes. Circulation. 2020;141 :1404 18. [PMID: 32339046] doi:10.1161 / on Clinical Practice Guidelines. J Am Coll Cardiol. 2O79:23:e81-e192. CIRCULATIONAH A.179.042434 IPMID: 30121239] doi:10.1016/j.jacc.2018.08.1029

contractions (PVCs) with a normal heart on echocardio Item 56 Answer: A gram. Laboratory studies have excluded common second- Educational Objective: Treat atrial septal defect. ary causes of PVCs (anemia, hyperthyroidism, pregnancy). The PVCs are likely contributing to her anxiety, which may Atrial septal defect (ASD) closure (Option A) is indicated in this in turn increase their number. p Blockers, particularly patient with a 1.5 cm ASD associated with right heart enlarge- those with some anxiolytic effect (such as propranolol), are ment, symptoms, and no pulmonary hypertension. An ASD is first-line therapy for PVCs. B-Blockers are also preferred in a defect in the atrial septum resulting in a left-to-right shunt patients with ventricular dysfunction. Among patients with with eventual right sided cardiac chamber dilatation in most depression or very poor tolerance of B-blockers, a nondihy patients. Ostium secundum defects, the most common ty'pe of dropyridine calcium channel blocker, such as verapamil, ASD (757, of cases), are typically located in the mid portion of may be used. the atrial septum and are usually isolated anomalies. In asymp- This patient's PVC burden may be quite high if she tomatic patients with a small ASD and no right heart enlarge- has several PVCs on a standard l2-lead ECG. Ambula- ment, periodic clinical monitoring and echocardiographic UI tory ECG monitoring can help clarify whether her PVCs imagrng are recornnended. The main indications for ASD clo- E are episodic and of low overall burden or if they persist sure include right sided cardiac chamber enlargement, dys- .D ul throughout the day. Patients with PVCs that account for pnea, or paradoxical embolization. Most patients with ostium o, more than l0% to 15% of beats may be at risk for develop- secundum ASD are candidates for device closure ofthe ASD. a TL ing PVC induced cardiomyopathy and subsequent heart procedure performed in the cardiac catheterization laboratory. ..t failure, which is an additional reason to treat this patient's Cardiopulmonary exercise testing (Option B) may be symptomatic PVCs. If she develops cardiomyopathy, it may helpful in evaluating dyspnea if the initial evaluation is unre- 4t E be reversible with more aggressive treatment of PVCs (e.g., vealing, deconditioning is a possibility. or several problems .D (a catheter ablation). may be contributing to dyspnea. This patient's dyspnea and Amiodarone (Option A) is an antiarrhythmic agent that right heart enlargement are caused by the ASD. and cardio- may be very effective at suppressing this patient's PVCs. pulmonary testing is not necessary. However, it may be toxic over the long term, potentially Coronary angiography (Option C) is considered before causing devastating injury to the lungs, liver, and/or thyroid. cardiac surgery or intervention for noncoronary cardiac Furthermore, it may be unnecessary in this young patient. issues in patients with symptoms of angina, evidence of cor Amiodarone is therefore not an appropriate flrst-line choice onary ischemia, decreased left ventricular systolic function, in this clinical setting. When amiodarone is used, it should a history ol coronary artery disease, or risk factors for coro be taken for the shortest possible time at the lowest effective nary artery disease. This patient's symptoms and evaluation dose, with close monitoring. are consistent with ASD, not cardiac ischemia, and coronary This patient has no exertional symptoms, no speciflc angiography is not required. risk factors for coronary ischemia, and normal echocar Echocardiographic surveillance (Option D) is considered diogram results. Exercise ECG (Option B) is unlikely to be for patients with an ASD if there is no associated right heart high yield in this setting. However, PVCs often cease during enlargement, if severe pulmonary hypertension is present, or exercise in a structurally normal heart, which would be if there are no severe comorbid conditions that may adversely reassuring. affect outcome. Transesophageal echocardiography may be This patient's symptoms are likely attributable to pVCs needed to conflrm the presence of an ASD if transthoracic and are described as intolerable; therefore, she warrants echocardiography is nondiagnostic or for the purposes of treatment, and reassurance alone (Option D) is not appro procedure planning. ASD closure, not serial surveillance with priate. echocardiography, is recommended for this patient with a symptomatic ASD and right heart enlargement. rEY POIilTS o First-line treatment for q.rrnptomatic premature ven- TEY POIXTT tricular contraction suppression is p-blocker or calcium o Atrial septal defect closure is indicated in patients channel blocker therapy; p-blockers are preferred in with symptoms or evidence of right-sided cardiac patients with ventricular dysfunction. chamber enlargement and without severe pulmonary o Ambulatory ECG monitoring can help clariflz the bur- hypertension. den of premature ventricular contractions (pVCs); o Most patients with ostium secundum atrial septal defect patients with PVCs that account for more than 10% are candidates for device closure performed in the cardiac to 15% of beats may be at risk for pVC induced catheterization laboratory. cardiomyopathy. Bibliography Bibliography Stout KK. Daniels CJ. Aboulhosn JA. er al. 2018 AHA,ACC guideline for the management of adults w.ith congenital heart disease; a report of the Marcus GM. Evaluation and management of premature ventricular com American College of Cardiologr/American Heart Association Task Force plexes. Circulation. 2020;141 :1404 18. [PMID: 32339046] doi:10.1161 / on Clinical Practice Guidelines. J Am Coll Cardiol. 2O79:23:e81-e192. CIRCULATIONAH A.179.042434 IPMID: 30121239] doi:10.1016/j.jacc.2018.08.1029 184

Answers and Critiques tr Item 57 Answer: D Educational Objective: Evaluate chest pain using Item 58 Answer: C Educational Objective: Diagnose constrictive tr vasodilator single-photon emission CT. pericarditis. Vasodilator single photon emission CT (Option D) using per The diagnostic findings are consistent with constrictive fusion witl.r adcnosine, regadenoson, or dipyridamole is the pericarditis (Option C), which typically presents with most appropriate and pref'erred stress testing option for this ir.rdolent, progressive signs and symptoms of righl l.reart patient with lcfl bundle branch block (LBBB). In patients with failure, including latigue and excrtional dyspnea. On LBBB undergoing my'ocardial perfusion imaging, vasodilator physical examination, the central venous pressure is ele stress minimizes septal abnormalities frequently seen with vated in nearly all patients, with prominent x and y exercise and dobutamine, which are associated with higher descents. The height of'the wavefbrm does not fall or may heart rates. Although this paticnt can exercise, the presence increase during inspiration (Kussmaul sign), reflecting of LBBB lirnits interpretation fbr heart rate dependent stress the fixed diastolic volume of the right heart. Early dia- vt (l, modalities. stolic filling is unimpaired or even accentuated and is fbl Dobutamine echocardiography (Option A) is not recom- lowed by sudden cessation when total acceptable volume ET

tr Item 57 Answer: D Educational Objective: Evaluate chest pain using Item 58 Answer: C Educational Objective: Diagnose constrictive tr vasodilator single-photon emission CT. pericarditis. Vasodilator single photon emission CT (Option D) using per The diagnostic findings are consistent with constrictive fusion witl.r adcnosine, regadenoson, or dipyridamole is the pericarditis (Option C), which typically presents with most appropriate and pref'erred stress testing option for this ir.rdolent, progressive signs and symptoms of righl l.reart patient with lcfl bundle branch block (LBBB). In patients with failure, including latigue and excrtional dyspnea. On LBBB undergoing my'ocardial perfusion imaging, vasodilator physical examination, the central venous pressure is ele stress minimizes septal abnormalities frequently seen with vated in nearly all patients, with prominent x and y exercise and dobutamine, which are associated with higher descents. The height of'the wavefbrm does not fall or may heart rates. Although this paticnt can exercise, the presence increase during inspiration (Kussmaul sign), reflecting of LBBB lirnits interpretation fbr heart rate dependent stress the fixed diastolic volume of the right heart. Early dia- vt (l, modalities. stolic filling is unimpaired or even accentuated and is fbl Dobutamine echocardiography (Option A) is not recom- lowed by sudden cessation when total acceptable volume ET mended fbr this patient because ol the presence of LBtsB, which is met, resulting ir.r a high frequency early diastolic sound rr, may limit echocardiographic image interpretation. Other sce (pericardiai knock, heard in <50'X, ol patients). Pulsus par narios in which dobutamine echocardiography is not an opti- adoxus is less frequent (<2O"/,, of patients) in constrictive tr =l ag mal stress option include resting wall motion abnormalities pericarditis than in cardiac tamponade. Peripheral eclema, Ul q, and contrainclications to using dobutamine. Contraindications irscites, hepatomegaly, and pleural eftusions are com to dobutamine stress ech<lcardiography include ircute coronary mon. Diagnosis of constrictive pericarditis is made rvith UI = syndromes; severe aortic stenosisr hypertrophic obstrrrctive imaging studies and hemodynamic evaluation. Trans cardiomyopathy; and uncontrollecl hyperterrsion, urrhyhmias, thoracic echocardiography reveals nrlrmal right and lcll or heart failure. Dobutamine echocardiography is recom- ventricular size and systolic function despite prominenl mended in patients who cannot exercise or when infbnnation symptoms ancl finclings suggestive of heart failure. Dilat:r- on an area of myocardium at risk is needed. tion olthe inf'erior vena cava reflects elevated right sided Exercisc ECG (Option B) is usually the preferred stress filling (right atrial) pressure. Doppler echocardiography test lbr patients unless there are compellirrg reasons to add and tissue Doppler velocity are rcquired to differentialc imaging to the stress test or if'the patient cannot exercise. constrictive pericarditis fiom restrictive cardiomyopathy. The compelling indication to avoid exercise ECG in this Al t hough an underlying cause o{' constrictive pericardi tis patient is thc presence of LtsBB. LBBB renders the exercise is not always identified, previous pericarditis, cardiac ECG nearly impossibie to appropriately interpret unless the surgery, chest irradiati<in, connectivc tissue disorders, and patient devclops the equivalent of'an ST segment elevation uremia are comnron precipitants. myocardial intarction during the test. Cardiac tamponade (Option A) can easily be conlused Exercise single photon ernission CT (Option C) is not with constrictive pericarditis. However, cardiac tamponade the most appropriate stress modality fbr this patient because is typically associated with pulsus paradoxus and not asso ol the prcsence of LBBB. Inraging modalities that require ciated with Kussmaul sign. heart rate increases, such as exercise, are not rccommended A not uncomrnon misdiagnosis in patients with con for patients with LBBB because the abnormal septal wall strictive pericarditis is cirrhosis. Likc patients with con motion may limit interpretation. With the exception of strictive pericarditis, those with cirrhosis may have a LBBB, exercise single photon ernission CT is recommended palpable livet ascites, pleural eftusions, and periphcral when baselinc ECC flndings are abnormal or whcn infbrma edema. Patients with chronic liver dise:rse (Option B) do not tion on a particular area ot myocardium at risk is needed. have jugular venous distention, Kussmaul sign, or a pericur With LBBB, c<-rnduction delay in the septunl may cause dial knock. as detected in this patient. false positive abnormalities: vasodilator stress can improve In most cases. clinically diflerentiating restrictivc cilr the accurlcy oI perlusion itnlgittg. diomyopathy (Option D) from constrictive pericarditis is impossible. Restrictive cardiomyopathy is more likely in a IEY POITI patient with a predisposing systemic clisease, such as clia o In the evaluation of patients with chest pain, vasodila- betes mellitus or arnyloidosis. In this case, constrictive peri tor myocardial perfusion imaging with adenosine, carditis is suggested by the previous coronary artery bypass regadenoson, or dipyridamole minimizes septal surgery. Restrictive cardioml'opathy is not associated with a abnormalities frequently seen with exercise or dobu- pcricardial knocl<. lrut this flnding is sometimes difficult ttt tamine myocardial perfusion imaging. distinguish fiom irn S.,.

mended fbr this patient because ol the presence of LBtsB, which is met, resulting ir.r a high frequency early diastolic sound rr, may limit echocardiographic image interpretation. Other sce (pericardiai knock, heard in <50'X, ol patients). Pulsus par narios in which dobutamine echocardiography is not an opti- adoxus is less frequent (<2O"/,, of patients) in constrictive tr =l ag mal stress option include resting wall motion abnormalities pericarditis than in cardiac tamponade. Peripheral eclema, Ul q, and contrainclications to using dobutamine. Contraindications irscites, hepatomegaly, and pleural eftusions are com to dobutamine stress ech<lcardiography include ircute coronary mon. Diagnosis of constrictive pericarditis is made rvith UI = syndromes; severe aortic stenosisr hypertrophic obstrrrctive imaging studies and hemodynamic evaluation. Trans cardiomyopathy; and uncontrollecl hyperterrsion, urrhyhmias, thoracic echocardiography reveals nrlrmal right and lcll or heart failure. Dobutamine echocardiography is recom- ventricular size and systolic function despite prominenl mended in patients who cannot exercise or when infbnnation symptoms ancl finclings suggestive of heart failure. Dilat:r- on an area of myocardium at risk is needed. tion olthe inf'erior vena cava reflects elevated right sided Exercisc ECG (Option B) is usually the preferred stress filling (right atrial) pressure. Doppler echocardiography test lbr patients unless there are compellirrg reasons to add and tissue Doppler velocity are rcquired to differentialc imaging to the stress test or if'the patient cannot exercise. constrictive pericarditis fiom restrictive cardiomyopathy. The compelling indication to avoid exercise ECG in this Al t hough an underlying cause o{' constrictive pericardi tis patient is thc presence of LtsBB. LBBB renders the exercise is not always identified, previous pericarditis, cardiac ECG nearly impossibie to appropriately interpret unless the surgery, chest irradiati<in, connectivc tissue disorders, and patient devclops the equivalent of'an ST segment elevation uremia are comnron precipitants. myocardial intarction during the test. Cardiac tamponade (Option A) can easily be conlused Exercise single photon ernission CT (Option C) is not with constrictive pericarditis. However, cardiac tamponade the most appropriate stress modality fbr this patient because is typically associated with pulsus paradoxus and not asso ol the prcsence of LBBB. Inraging modalities that require ciated with Kussmaul sign. heart rate increases, such as exercise, are not rccommended A not uncomrnon misdiagnosis in patients with con for patients with LBBB because the abnormal septal wall strictive pericarditis is cirrhosis. Likc patients with con motion may limit interpretation. With the exception of strictive pericarditis, those with cirrhosis may have a LBBB, exercise single photon ernission CT is recommended palpable livet ascites, pleural eftusions, and periphcral when baselinc ECC flndings are abnormal or whcn infbrma edema. Patients with chronic liver dise:rse (Option B) do not tion on a particular area ot myocardium at risk is needed. have jugular venous distention, Kussmaul sign, or a pericur With LBBB, c<-rnduction delay in the septunl may cause dial knock. as detected in this patient. false positive abnormalities: vasodilator stress can improve In most cases. clinically diflerentiating restrictivc cilr the accurlcy oI perlusion itnlgittg. diomyopathy (Option D) from constrictive pericarditis is impossible. Restrictive cardiomyopathy is more likely in a IEY POITI patient with a predisposing systemic clisease, such as clia o In the evaluation of patients with chest pain, vasodila- betes mellitus or arnyloidosis. In this case, constrictive peri tor myocardial perfusion imaging with adenosine, carditis is suggested by the previous coronary artery bypass regadenoson, or dipyridamole minimizes septal surgery. Restrictive cardioml'opathy is not associated with a abnormalities frequently seen with exercise or dobu- pcricardial knocl<. lrut this flnding is sometimes difficult ttt tamine myocardial perfusion imaging. distinguish fiom irn S.,. f,EY POIt{T Bibliography Balfour PC Jr, Conzalez JA, Kramer CM. Non-invasive assessment of low- . Kussmaul sign and pericardial knock, if present, are and intermediate risk patients with chest pain. Trends Cardiovasc Med. helpfirl clues to the presence ofconstrictive pericarditis. 2017 :27 :182 189. IPMID: 27717538] doi:10.1016/i.tcm.2016.08.006

f,EY POIt{T Bibliography Balfour PC Jr, Conzalez JA, Kramer CM. Non-invasive assessment of low- . Kussmaul sign and pericardial knock, if present, are and intermediate risk patients with chest pain. Trends Cardiovasc Med. helpfirl clues to the presence ofconstrictive pericarditis. 2017 :27 :182 189. IPMID: 27717538] doi:10.1016/i.tcm.2016.08.006 185

{ry1vers ana !{!i11e1 Bibliography Bibliography Geske JB, Ana"ekar NS, Nishimura RA. et al. Differentiation of constriction Anderson JL, Morrow DA. Acute myocardial infarction. \ Engl J \'led. 2017: and restriction: complex cardiovascular hemodl'namics. J Am Coll Cardiol. 376:2053 64. IP\'llD: 28538121] doi:10.1056 NEJ\{ra1606915 2Ol6:68:2329 -17. IPMID: 278842.52] doi:10.1016 j.iacc.2016.08.050

Bibliography Bibliography Geske JB, Ana"ekar NS, Nishimura RA. et al. Differentiation of constriction Anderson JL, Morrow DA. Acute myocardial infarction. \ Engl J \'led. 2017: and restriction: complex cardiovascular hemodl'namics. J Am Coll Cardiol. 376:2053 64. IP\'llD: 28538121] doi:10.1056 NEJ\{ra1606915 2Ol6:68:2329 -17. IPMID: 278842.52] doi:10.1016 j.iacc.2016.08.050 Item 59 Item 60 Answer: D tr Answer: D Ed ucati ona I Objective : Manage non- ST-elevation acute Educational Objective: Evaluate a patient with palpita- tions using a 30-day event monitor. eoronary syndrome with coronary angiography. A 30-day event monitor (Option D) is the most appropriate Urgent or irnrnediate angiographl' (Option D) uitl.r intent diagnostic testing option for this patient $,ith palpitations. to perftrnn revascularization is indicatecl in pitients $'ith Event monitors are patient-triggered devices that are ideally non S1'clevation acute coronirry syndronre (NS'I'E-ACS) suited to capture symptomatic arrhythmias. The choice of who have retiactory angina or hemodynamic or electri cal instabilityr 'll.ris patient's presentatioll is l.riglrlv sugges ambulatory cardiac rhl.thm monitor depends on the fre- t, quency and duration of the symptoms as uell as any other € tive ol Nsl'lj ACS given his l.ristorl: ph1'sical exirmination .D associated symptoms, signs, or findings. For patients such UI findings, ischernic ECG clunges. and troponin level. This q, patient has an intermecliate'l'lNI I risk score ol,1 given his age as this one, with symptoms that occur frequently over the (>65 years): evidence of myocardial ischenria. including course of a month but not daily, a 30 day event monitor EL f.t ischemic ECG ST segment changes and elevatecl t()ponin is most appropriate. The patient can activate the monitor level; and recurrent chest pain episodes. Cornpared vlith when symptoms occur, provided that the symptoms last lt an ischernia guided approach. an invasive strrrteg,' ofl'ers long enough to be captured by the device's active and ret .D improved olltcomes ancl is inclicated in most prtients $'ith rospective capture. Symptoms that last longer than 1 to a,l 2 minutes are ideally suited for event monitors. higher risk ACS. r,r,ith underll,ing patient risk determining An exercise ECG (Option A) allows diagnosis of exercise- the urgency and timir.rg. Whereas an invasivc assessment with coronary angiography ancl consideratiou of revascu related arrhythmias and also allows lor assessment of the larizatior.r are appropriate lvitl.rir.r 25 Io72 l.ururs ol presen- efl'ect of exercise on blood pressure and symptoms. Most tation in patients u'ith a'flN'll score of 3 or.1. this patient has arrhythmias are not exercise induced, and this patient ongoing chcst cliscomfbn refiactor\, to stanclarcl rneasures: clearly indicated that there were no triggering events for her palpations; therefore, exercise ECG is not indicated. thereibre, urgent angiography (r,r,ithin 2 honrs ol presenta tion) is indicated. An implantable loop recorder (Option B) is most appropri ate for infrequent or highly syrnptomatic arrhlthmias in which ln low risk patients with NSI'E-ACS or in those r'vho elect an initial ischemia guided therapeutic pathuay. 9616 the symptoms, such as syncope, might preclude a patient from cardiographl, (Option A) or stress testing can iclentifl' those activating the device. These monitors are implanted under the rvho nright benefit fiorn lurtl.rer ir.rvasive assessnrent rvith skin and can be used for months to years. This patient's symp subsequent revascularization. ln patients rvith increased toms occw weekly and are not associated with slmcope; thus, risk and active mlocardial ischemia or hemodynirnric or an implantable loop recorder is not necessary.

Item 59 Item 60 Answer: D tr Answer: D Ed ucati ona I Objective : Manage non- ST-elevation acute Educational Objective: Evaluate a patient with palpita- tions using a 30-day event monitor. eoronary syndrome with coronary angiography. A 30-day event monitor (Option D) is the most appropriate Urgent or irnrnediate angiographl' (Option D) uitl.r intent diagnostic testing option for this patient $,ith palpitations. to perftrnn revascularization is indicatecl in pitients $'ith Event monitors are patient-triggered devices that are ideally non S1'clevation acute coronirry syndronre (NS'I'E-ACS) suited to capture symptomatic arrhythmias. The choice of who have retiactory angina or hemodynamic or electri cal instabilityr 'll.ris patient's presentatioll is l.riglrlv sugges ambulatory cardiac rhl.thm monitor depends on the fre- t, quency and duration of the symptoms as uell as any other € tive ol Nsl'lj ACS given his l.ristorl: ph1'sical exirmination .D associated symptoms, signs, or findings. For patients such UI findings, ischernic ECG clunges. and troponin level. This q, patient has an intermecliate'l'lNI I risk score ol,1 given his age as this one, with symptoms that occur frequently over the (>65 years): evidence of myocardial ischenria. including course of a month but not daily, a 30 day event monitor EL f.t ischemic ECG ST segment changes and elevatecl t()ponin is most appropriate. The patient can activate the monitor level; and recurrent chest pain episodes. Cornpared vlith when symptoms occur, provided that the symptoms last lt an ischernia guided approach. an invasive strrrteg,' ofl'ers long enough to be captured by the device's active and ret .D improved olltcomes ancl is inclicated in most prtients $'ith rospective capture. Symptoms that last longer than 1 to a,l 2 minutes are ideally suited for event monitors. higher risk ACS. r,r,ith underll,ing patient risk determining An exercise ECG (Option A) allows diagnosis of exercise- the urgency and timir.rg. Whereas an invasivc assessment with coronary angiography ancl consideratiou of revascu related arrhythmias and also allows lor assessment of the larizatior.r are appropriate lvitl.rir.r 25 Io72 l.ururs ol presen- efl'ect of exercise on blood pressure and symptoms. Most tation in patients u'ith a'flN'll score of 3 or.1. this patient has arrhythmias are not exercise induced, and this patient ongoing chcst cliscomfbn refiactor\, to stanclarcl rneasures: clearly indicated that there were no triggering events for her palpations; therefore, exercise ECG is not indicated. thereibre, urgent angiography (r,r,ithin 2 honrs ol presenta tion) is indicated. An implantable loop recorder (Option B) is most appropri ate for infrequent or highly syrnptomatic arrhlthmias in which ln low risk patients with NSI'E-ACS or in those r'vho elect an initial ischemia guided therapeutic pathuay. 9616 the symptoms, such as syncope, might preclude a patient from cardiographl, (Option A) or stress testing can iclentifl' those activating the device. These monitors are implanted under the rvho nright benefit fiorn lurtl.rer ir.rvasive assessnrent rvith skin and can be used for months to years. This patient's symp subsequent revascularization. ln patients rvith increased toms occw weekly and are not associated with slmcope; thus, risk and active mlocardial ischemia or hemodynirnric or an implantable loop recorder is not necessary. electrical instrbility. echocardiography oflers lirnited early Mobile cardiac telemetry (MCT) (Option C) provides con benefit in the absence of signs or s).rlptolls ot rnechanical tinuous ambulatory ECG recording for precise quantification cardiopuh.nonar y conrplicatirlns. or capture of rare arrhlthmias. MCT is not indicated for this Eplerenone (Option B). an irldosterone ilntagonist, hits patient whose symptoms have not yet been correlated to any provecl beneficial in pttients u'ith myocarclial intarction specific arrhyhmia; thus, quantification of arrhlthmia bur- who are rc'ceiving therapeutic closes ot ACE inhibitrtrs ancl den is unnecessary at this time. MCT is often used to capture arrhythmias that may not be associated with symptoms (e.9.. B blockers and have a lelt ventricular ejection fiactior, of' 40'X, or less ancl either diabetes nrellitus or heart Iailure. lhis occult atrial flbrillation). but this patient's symptom complex patient cloes not meet the criteria fbr eplerenone tl.rerapl:. seems fairly reproducible. Furthermore, her symptoms occur Routine oxygen therap), (Option C) l.ras lteen shou'n to frequently enough that an event monitor would be the most provide no benefit in ACS anci ma1, increase rclverse events resource-appropriate test to order at this time. in the absence olhypoxenria. Cuidelines recontntend against TEY POIilIS orygen aclnrinistration in patients rvith ACS irnd rixygen sat . A 30-day event monitor is most appropriate for evalu uratior] greater than 90')1, to 92'X,. ating patients with palpitations who have symptoms t(tY PottT that occur less than daily but frequently over the course . Urgent or immediate diagnostic angiography with of a month. intent to perform revascularization is indicated in o An implantable looping event recorder is most appro- patients with non-ST-elevation acute coronary syn priate for infrequent or highly symptomatic arrhyth- drome who have refractory angina or hemodynamic mias in which the symptoms might preclude a patient or electrical instability. from activating the device, such as syncope.

electrical instrbility. echocardiography oflers lirnited early Mobile cardiac telemetry (MCT) (Option C) provides con benefit in the absence of signs or s).rlptolls ot rnechanical tinuous ambulatory ECG recording for precise quantification cardiopuh.nonar y conrplicatirlns. or capture of rare arrhlthmias. MCT is not indicated for this Eplerenone (Option B). an irldosterone ilntagonist, hits patient whose symptoms have not yet been correlated to any provecl beneficial in pttients u'ith myocarclial intarction specific arrhyhmia; thus, quantification of arrhlthmia bur- who are rc'ceiving therapeutic closes ot ACE inhibitrtrs ancl den is unnecessary at this time. MCT is often used to capture arrhythmias that may not be associated with symptoms (e.9.. B blockers and have a lelt ventricular ejection fiactior, of' 40'X, or less ancl either diabetes nrellitus or heart Iailure. lhis occult atrial flbrillation). but this patient's symptom complex patient cloes not meet the criteria fbr eplerenone tl.rerapl:. seems fairly reproducible. Furthermore, her symptoms occur Routine oxygen therap), (Option C) l.ras lteen shou'n to frequently enough that an event monitor would be the most provide no benefit in ACS anci ma1, increase rclverse events resource-appropriate test to order at this time. in the absence olhypoxenria. Cuidelines recontntend against TEY POIilIS orygen aclnrinistration in patients rvith ACS irnd rixygen sat . A 30-day event monitor is most appropriate for evalu uratior] greater than 90')1, to 92'X,. ating patients with palpitations who have symptoms t(tY PottT that occur less than daily but frequently over the course . Urgent or immediate diagnostic angiography with of a month. intent to perform revascularization is indicated in o An implantable looping event recorder is most appro- patients with non-ST-elevation acute coronary syn priate for infrequent or highly symptomatic arrhyth- drome who have refractory angina or hemodynamic mias in which the symptoms might preclude a patient or electrical instability. from activating the device, such as syncope. : 186

Answers and Critiques Bibliography Steinberg JS, Varma N, Cygankiewicz I, et al. 2017 ISHNE HRS expert consen sus statement on ambulatory ECG and external cardiac monitoring/ . Treatment of takotsubo cardiomyopathy is similar to telemetry. Heart Rhythm. 2017;14:e55-e96. [pMID: 28495301] doi:10.1016/ that for heart failure of other causes; most patients i.hrthm.2017.03.038 recover cardiac function over several months.

Bibliography Steinberg JS, Varma N, Cygankiewicz I, et al. 2017 ISHNE HRS expert consen sus statement on ambulatory ECG and external cardiac monitoring/ . Treatment of takotsubo cardiomyopathy is similar to telemetry. Heart Rhythm. 2017;14:e55-e96. [pMID: 28495301] doi:10.1016/ that for heart failure of other causes; most patients i.hrthm.2017.03.038 recover cardiac function over several months. tr Item 61 Answer: D Educational Objective: Diagnose takotsubo (stress- Bibliography Pal S, Broker M, Wagner H, et al. Stress (takotsubo) cardiomyopathy: a review of its pathophysiolo$/, manifestations, and factors that affect induced) cardiomyopathy. prognosis. Cardiol Rev 2021 Jul Aug OL;292O5-2O9. [PMID: 32282392] doi :10.1097/CRD.0000000000000309 The most likely diagnosis is takotsubo (stress.induced) cardiomyopathy (Option D). Takotsubo cardiomyopathy is a syndrome characterized by transient regional systolic ventricular dyslunction mimicking myocardial infarcticln Item 52 Answer: C Educational Objective: Treat acute ascending aortic tr UI (l, (reduced ejection fraction, eievated cardiac enzymes, and dissection with open aortic repair. E signs of ischemia on ECC) in the absence of angiographic evi- The most appropriate treatment fbr this patient with acute IJ dence olobstrrrctive coronary afiery disease. In most cases of type A aortic dissection is immediate open aortic repair takotsubo cardiomyopathy, the regional wall motion abnor- (Option C). The in-hospital mortality rate for patients =t .E mality extends beyond the territory perf'used by a single t with acute type A aortic dissection is greater than 50'i1, (I, epicardial coronary afiery. The syndrome is of'ten precipitated with conservative measures and typically 1O"/,, to 20"/,, by extreme emotional stress, such as death of a loved one. tt fbllowing surgery. In this patient with hypotension, asym = The pathogenesis of' takotsubo cardiomyopathy is unknown, metric arm blood pressures and pulses, and murmur of but the condition is postulated to result from reversible myo- aortic regurgitation, emergency repair of the aorta and cardial toxicily induced by very l-righ catecholamine levels. aortic valve repair or replacement are indicated. Delaying Women are affected more fiequently than are men. Treat- surgical repair has been associated with higher morbid- ment is generally srlppoftive and is similar to that for heart ity and mortality rates, and expert consensus guidelines lailure ofother causes; most patients recover cardiac function recommend emergency repair in patients without clear over several months. Additional imaging studies may inciude contraindications. cardiac magnetic resonance imaging to exclude myocarditis. A retrospective study evaluated the role of coronary Acute ascending aortic dissection (Option A) c'lassically angiography (Option A) in patients r,r,ith grpe A aortic presents as severe, sudden onset chest or back pain that has a dissection who underwent emergency aodic surgery. In- tearing or ripping quality Other presenting fbatures may inc{ude hospital mortality rates \,\,ere no difl'erent in those who hypertension, syncope, a murrnur of aortic regurgitation, and underwent coronary angiography cclmpared with those whr-r heafi failure. Acute ascending aortic dissection may cause acute did not. I.-urthermore, coronary angiography had no impact coronary occlusion; however, wall motion abnormalities would on coronary aftery bypass grafting, as most of these proce most likely involve a single coronary artery distribution, and dures were performed fbr coronary artery dissection, not obstructior.r would be detected by angiography In addition, acute atherosclerotic coronary ar1ery disease. These flndings sup ascending aortic dissection can be visuaiized on echocardiogram. port the need to perlbrm aortic surgery as soon as possible Coronary aftery dissection (Option B) is usualiy identified and not delay surgery fbr coronary angiography. by coronary angiography, although the lindings may be subtle. Although most guidelines recommend that patients A single coronary artery dissection causes regionalwall motion with acute aortic dissection be treated aggressively with abnormalities in a single coronary artery distribution pattem blood pressure reduction (systolic blood pressure goal of rather than global mid- and apical ventricular dysfunction. <120 mm Hg in the first hour), this patient should undergo Coronary artery embolism (Option C) is a potential emergent aortic repair due to evidence of' cardiogenic cause of acute myocardial infarction, resulting in abnormal shock. Interventions to reduce his blood pressure are not ventricular function in a patient with no obstructive coro- needed. When indicated, intravenous p-blocker therapy is nary artery disease; however, a coronary artery embolism used initially to lower blood pressure; decrease the veloc- generally causes regional wa1l motion abnormalities in a ity of left ventricular contraction; and reduce heart rate, single coronary artery distribution rather than global mid contractility, and aortic shear stress. Vasodilator therapy, and apical ventricular dysf unction. using agents such as nitroprusside (Option B), foilows B-blockade. o Takotsubo cardiomyopathy is a syndrome character- There are reports of endovascular repair (Option D) ized by transient regional systolic ventricular dysfunc- of ascending aortic dissection; however, open surgical repair remains the standard of care and is recommended tion mimicking myocardial infarction in the absence by current guidelines. Furthermore, this patient requires of angiographic evidence of obstructive coronary aortic valve repair or replacement due to evidence of aor- arterydisease. (Continued) tic regurgitation, and endovascular repair has not been

tr Item 61 Answer: D Educational Objective: Diagnose takotsubo (stress- Bibliography Pal S, Broker M, Wagner H, et al. Stress (takotsubo) cardiomyopathy: a review of its pathophysiolo$/, manifestations, and factors that affect induced) cardiomyopathy. prognosis. Cardiol Rev 2021 Jul Aug OL;292O5-2O9. [PMID: 32282392] doi :10.1097/CRD.0000000000000309 The most likely diagnosis is takotsubo (stress.induced) cardiomyopathy (Option D). Takotsubo cardiomyopathy is a syndrome characterized by transient regional systolic ventricular dyslunction mimicking myocardial infarcticln Item 52 Answer: C Educational Objective: Treat acute ascending aortic tr UI (l, (reduced ejection fraction, eievated cardiac enzymes, and dissection with open aortic repair. E signs of ischemia on ECC) in the absence of angiographic evi- The most appropriate treatment fbr this patient with acute IJ dence olobstrrrctive coronary afiery disease. In most cases of type A aortic dissection is immediate open aortic repair takotsubo cardiomyopathy, the regional wall motion abnor- (Option C). The in-hospital mortality rate for patients =t .E mality extends beyond the territory perf'used by a single t with acute type A aortic dissection is greater than 50'i1, (I, epicardial coronary afiery. The syndrome is of'ten precipitated with conservative measures and typically 1O"/,, to 20"/,, by extreme emotional stress, such as death of a loved one. tt fbllowing surgery. In this patient with hypotension, asym = The pathogenesis of' takotsubo cardiomyopathy is unknown, metric arm blood pressures and pulses, and murmur of but the condition is postulated to result from reversible myo- aortic regurgitation, emergency repair of the aorta and cardial toxicily induced by very l-righ catecholamine levels. aortic valve repair or replacement are indicated. Delaying Women are affected more fiequently than are men. Treat- surgical repair has been associated with higher morbid- ment is generally srlppoftive and is similar to that for heart ity and mortality rates, and expert consensus guidelines lailure ofother causes; most patients recover cardiac function recommend emergency repair in patients without clear over several months. Additional imaging studies may inciude contraindications. cardiac magnetic resonance imaging to exclude myocarditis. A retrospective study evaluated the role of coronary Acute ascending aortic dissection (Option A) c'lassically angiography (Option A) in patients r,r,ith grpe A aortic presents as severe, sudden onset chest or back pain that has a dissection who underwent emergency aodic surgery. In- tearing or ripping quality Other presenting fbatures may inc{ude hospital mortality rates \,\,ere no difl'erent in those who hypertension, syncope, a murrnur of aortic regurgitation, and underwent coronary angiography cclmpared with those whr-r heafi failure. Acute ascending aortic dissection may cause acute did not. I.-urthermore, coronary angiography had no impact coronary occlusion; however, wall motion abnormalities would on coronary aftery bypass grafting, as most of these proce most likely involve a single coronary artery distribution, and dures were performed fbr coronary artery dissection, not obstructior.r would be detected by angiography In addition, acute atherosclerotic coronary ar1ery disease. These flndings sup ascending aortic dissection can be visuaiized on echocardiogram. port the need to perlbrm aortic surgery as soon as possible Coronary aftery dissection (Option B) is usualiy identified and not delay surgery fbr coronary angiography. by coronary angiography, although the lindings may be subtle. Although most guidelines recommend that patients A single coronary artery dissection causes regionalwall motion with acute aortic dissection be treated aggressively with abnormalities in a single coronary artery distribution pattem blood pressure reduction (systolic blood pressure goal of rather than global mid- and apical ventricular dysfunction. <120 mm Hg in the first hour), this patient should undergo Coronary artery embolism (Option C) is a potential emergent aortic repair due to evidence of' cardiogenic cause of acute myocardial infarction, resulting in abnormal shock. Interventions to reduce his blood pressure are not ventricular function in a patient with no obstructive coro- needed. When indicated, intravenous p-blocker therapy is nary artery disease; however, a coronary artery embolism used initially to lower blood pressure; decrease the veloc- generally causes regional wa1l motion abnormalities in a ity of left ventricular contraction; and reduce heart rate, single coronary artery distribution rather than global mid contractility, and aortic shear stress. Vasodilator therapy, and apical ventricular dysf unction. using agents such as nitroprusside (Option B), foilows B-blockade. o Takotsubo cardiomyopathy is a syndrome character- There are reports of endovascular repair (Option D) ized by transient regional systolic ventricular dysfunc- of ascending aortic dissection; however, open surgical repair remains the standard of care and is recommended tion mimicking myocardial infarction in the absence by current guidelines. Furthermore, this patient requires of angiographic evidence of obstructive coronary aortic valve repair or replacement due to evidence of aor- arterydisease. (Continued) tic regurgitation, and endovascular repair has not been 187

Answers and Critiques tr CONT shown to be efl'ective in patients with evidence of valvuiar dysfunction. r(EY P0il{TS . Surgery for chronic primary severe mitral regurgitation xEY potltT is indicated in the presence of symptoms, left ventric- . In patients with ascending aortic dissection, immediate ular dilation, or reduced ejection fraction. open aortic repair is imperative to improve survival and . Surgical mitral valve repair is first line therapy for reduce morbidity. patients with primary severe mitral regurgitation meeting indications for intervention. Bibliography Lawton JS, Liu l, Kulshrestha K, et al. The impact ofsurgical strate$/ on Bibliography survival after repair of type A aortic dissection. J Thorac Cardiovasc Bonow RO, O'Gara PT, Adams DH, et al. 2020 Focused update ofthe 20U Surg. 2015;150:294 301.e1. IPMID: 260050601 doi:10.1016/j.jtcvs.2015. ACC expert consensus decision pathway on the management of mitral 03.023 regurgitationr a report ofthe American College ofCardiologr Solution Set Oversight Committee. I Am Coll Cardiol. 2020;75:2236 2270. IPMID: 320680841 doi:10.1016/j.jacc.2020.02.005 u! E Item 63 Answer: B .D Educational Objective: Treat primary (degenerative) vr o, a severe mitral regurgitation with surgical mitral valve repair. Item 64 Answer: B Educational Objective: Manage cardiac implantable tr n The most appropriate next step in management is surgical device infection.

tr CONT shown to be efl'ective in patients with evidence of valvuiar dysfunction. r(EY P0il{TS . Surgery for chronic primary severe mitral regurgitation xEY potltT is indicated in the presence of symptoms, left ventric- . In patients with ascending aortic dissection, immediate ular dilation, or reduced ejection fraction. open aortic repair is imperative to improve survival and . Surgical mitral valve repair is first line therapy for reduce morbidity. patients with primary severe mitral regurgitation meeting indications for intervention. Bibliography Lawton JS, Liu l, Kulshrestha K, et al. The impact ofsurgical strate$/ on Bibliography survival after repair of type A aortic dissection. J Thorac Cardiovasc Bonow RO, O'Gara PT, Adams DH, et al. 2020 Focused update ofthe 20U Surg. 2015;150:294 301.e1. IPMID: 260050601 doi:10.1016/j.jtcvs.2015. ACC expert consensus decision pathway on the management of mitral 03.023 regurgitationr a report ofthe American College ofCardiologr Solution Set Oversight Committee. I Am Coll Cardiol. 2020;75:2236 2270. IPMID: 320680841 doi:10.1016/j.jacc.2020.02.005 u! E Item 63 Answer: B .D Educational Objective: Treat primary (degenerative) vr o, a severe mitral regurgitation with surgical mitral valve repair. Item 64 Answer: B Educational Objective: Manage cardiac implantable tr n The most appropriate next step in management is surgical device infection. tt mitral valve repair (Option B). This patient's echocar- Urgent pacemaker extraction (Option B) is the most CD diogram is consistent with severe mitral regurgitation, appropriate additional management. this patient pre- ,t, deflned as an effective regurgitant oriflce area of 0.4 cm2 sents r,^"'ith clinical signs of a pacemaker pclcket infection, or greater, a regurgitant volume of 60 mL or greater, or possibly due to skin contamination from a superficial a vena contracta of 0.7 cm or greater. The mitral regur- wound. Altl-rough infections most commonly are seen gitation is primary (degenerative), as indicated by the shortly after pocket instrunlentation (e.g., following ini patient's midsystolic click and late mitral regurgitation tial implantation or generator change). they may occur (both seen in mitral valve prolapse) and the demonstra- spontaneously and may present lvith only localized pain tion of anterior prolapse by echocardiography. Although or erythema over the pocket u,ithout systemic signs or the presence of symptoms resulting from severe mitral synlptoms ol inf'ection. This patient l.ras relatively clear regurgitation (such as shortness of breath and volume erythema. scabbing, and dimpling, likely rvith impending overload) is an indication for intervention, class 1 indica- erosion: however, pocket infection may be more insidious tions for intervention in asymptomatic patients include a ancl subtle. ln the absence of'major contraindications to left ventricular (LV) ejection fraction of 60% or less and/or extraction andror extreme risk factors, curative therapy an LV end systolic dimension of 40 mm or greater. Surgi- requires extraction ol all implanted cardiac hardr,r,are, cal mitral valve repair is flrst-line therapy for patients with debriden-rent ot the pocket, sustained antibiotic therapy primary severe mitral regurgitation meeting indications and reimplantation at a new location at'ter int'ection has for intervention. been eradicated. This patient does not har,e any obvious In most cases, transthoracic echocardiography (TTE) contraindications to device extraction or extreme risk tac provides the data needed for adequate cardiac evaluation tors (primarily age and comorbid conditions) that would of the patient with mitral regurgitation. However, in cases be prohibitive. in which TTE image quality is poor, cardiac magnetic reso- Aspiration of a cardiac implantable device pocket nance (CMR) imaging (Option A) may be of value in mitral (Option A) should never be perfbnr.red fbr diagr.rostic pur regurgitation evaluation. This patient does not have an indi poses. Device pocket infection is a clinical diagnosis. and cation for CMR imaging. aspiration will only sene to inoculate a possibly sterile. In severely symptomatic patients (New York Heart Asso uninlected pocket. Furthermore. the diagnostic 1,'ield is ciation class III or IV) with primary severe mitral regurgi likely to be very lor,r,. tation and high or prohibitive surgical risk, transcatheter Topical mupirocin (Option C) is indicated for very mitral valve repair (transcatheter edge to edge repair [TEER]) superficial skin infections. such as impetigo or fblliculitis. (Option C) is reasonable if mitral valve anatomy is favorable 'lbpical antibiotics are ineft'ective fbr deeper skin or soft tis- for the repair procedure and the patient's life expectancy is at sue infections, such as cellulitis. and are totally inadequate Ieast 1year. This patient meets no indication for TEER. for this patient r,l'ith a possible pacemaker pocket inf'ection. Transesophageal echocardiography (Option D) may In addition, topical antibiotics often \\'orsen the clinical sit be pursued when TTE is insufficient to determine either uation, as they may improve the appearance of the skin and the exact severity or the mechanism of mitral regurgita delay definitive care. tion (primary versus secondary); this patient's TTE was Clinical observation and reassessment (Option D) sufflcient to identify the nature and severity of the mitral are not appropriate in the setting ofdevice pocket infec regurgitation. tion. The inf'ection tikely will progress and might cause

tt mitral valve repair (Option B). This patient's echocar- Urgent pacemaker extraction (Option B) is the most CD diogram is consistent with severe mitral regurgitation, appropriate additional management. this patient pre- ,t, deflned as an effective regurgitant oriflce area of 0.4 cm2 sents r,^"'ith clinical signs of a pacemaker pclcket infection, or greater, a regurgitant volume of 60 mL or greater, or possibly due to skin contamination from a superficial a vena contracta of 0.7 cm or greater. The mitral regur- wound. Altl-rough infections most commonly are seen gitation is primary (degenerative), as indicated by the shortly after pocket instrunlentation (e.g., following ini patient's midsystolic click and late mitral regurgitation tial implantation or generator change). they may occur (both seen in mitral valve prolapse) and the demonstra- spontaneously and may present lvith only localized pain tion of anterior prolapse by echocardiography. Although or erythema over the pocket u,ithout systemic signs or the presence of symptoms resulting from severe mitral synlptoms ol inf'ection. This patient l.ras relatively clear regurgitation (such as shortness of breath and volume erythema. scabbing, and dimpling, likely rvith impending overload) is an indication for intervention, class 1 indica- erosion: however, pocket infection may be more insidious tions for intervention in asymptomatic patients include a ancl subtle. ln the absence of'major contraindications to left ventricular (LV) ejection fraction of 60% or less and/or extraction andror extreme risk factors, curative therapy an LV end systolic dimension of 40 mm or greater. Surgi- requires extraction ol all implanted cardiac hardr,r,are, cal mitral valve repair is flrst-line therapy for patients with debriden-rent ot the pocket, sustained antibiotic therapy primary severe mitral regurgitation meeting indications and reimplantation at a new location at'ter int'ection has for intervention. been eradicated. This patient does not har,e any obvious In most cases, transthoracic echocardiography (TTE) contraindications to device extraction or extreme risk tac provides the data needed for adequate cardiac evaluation tors (primarily age and comorbid conditions) that would of the patient with mitral regurgitation. However, in cases be prohibitive. in which TTE image quality is poor, cardiac magnetic reso- Aspiration of a cardiac implantable device pocket nance (CMR) imaging (Option A) may be of value in mitral (Option A) should never be perfbnr.red fbr diagr.rostic pur regurgitation evaluation. This patient does not have an indi poses. Device pocket infection is a clinical diagnosis. and cation for CMR imaging. aspiration will only sene to inoculate a possibly sterile. In severely symptomatic patients (New York Heart Asso uninlected pocket. Furthermore. the diagnostic 1,'ield is ciation class III or IV) with primary severe mitral regurgi likely to be very lor,r,. tation and high or prohibitive surgical risk, transcatheter Topical mupirocin (Option C) is indicated for very mitral valve repair (transcatheter edge to edge repair [TEER]) superficial skin infections. such as impetigo or fblliculitis. (Option C) is reasonable if mitral valve anatomy is favorable 'lbpical antibiotics are ineft'ective fbr deeper skin or soft tis- for the repair procedure and the patient's life expectancy is at sue infections, such as cellulitis. and are totally inadequate Ieast 1year. This patient meets no indication for TEER. for this patient r,l'ith a possible pacemaker pocket inf'ection. Transesophageal echocardiography (Option D) may In addition, topical antibiotics often \\'orsen the clinical sit be pursued when TTE is insufficient to determine either uation, as they may improve the appearance of the skin and the exact severity or the mechanism of mitral regurgita delay definitive care. tion (primary versus secondary); this patient's TTE was Clinical observation and reassessment (Option D) sufflcient to identify the nature and severity of the mitral are not appropriate in the setting ofdevice pocket infec regurgitation. tion. The inf'ection tikely will progress and might cause 188

Answers and Critiques tr CONT Iurtl-rcr pocket erosion and,.or blrcteremia urith endo ca r.i it is. recent studies have evaluated the potential benefit of P2Y, inhibitor monotherapy (ticagrelor) after DES-based pCI, xlY P0ttTs currently no guideline consensus exists for this practice; thus, discontinuing aspirin (Option B) is not appropriate. o Although infections of the cardiac device pocket most Proton pump inhibitors (PPIs), such as omeprazole, are commonly are seen shortly after pocket instrumenta- indicated in patients treated with DAPT who have a history tion (e.g., following initial implantation or generator ofupper gastrointestinal (UGI) bleeding and are reasonable change), they may occur spontaneously and may pre- in patients at high risk for UGI bleeding. Whereas pharma- sent with only pain or ery.thema over the pocket codynamic studies suggested that omeprazole may attenuate without systemic signs or symptoms of infection. the effect of clopidogrel, subsequent clinical studies have r Effective treatment of cardiac device infection usually not shown a meaningful increase in adverse cardiovascular includes complete extraction of all hardware, debride- outcomes among patients taking these medications together. ment of the pocket, sustained antibiotic therapy, and Discontinuing omeprazole (Option D) may be appropriate vt (l, reimplantation at a new location after infection has for this patient if she remains without symptoms of gas- 3 ET troesophageal reflux disease. PPI use is not recommended been eradicated. routinely in patients receiving DAPT. (J Bibliography f,rY POtl{TS =t .E Baddour LM, Epstein AE, Erickson CC, et al; American Heart Association Rheumatic Fever, Endocarditis. and Kawasaki Disease Committee. . In a patient treated with dual antiplatelet therapy for vt Update on cardiovascular implantable electronic device infections and coronary artery disease at low bleeding risk, guide- (l, their management: a scientific statement fiom the American lJeart Iines suggest treatment duration of at Ieast 6 months U! Association. Circulation. 20101121:458 77. IPMID: 20048212] doi:10.1161/ = CIRCU LATIONAHA.1O9.192665 after elective drug-eluting stent placement. o Dual antiplatelet therapy for at least 3 months may be Item 65 Answer: C reasonable following elective placement of a drug- Educational Obiective: Discontinue clopidogrel after eluting stent in some patients at high risk for bleeding. drug-eluting stent placement in a patient with high bleeding risk. Bibliography Levine CN, Bates ER, Bittl JA, et al. 2016 ACC/AI IA guideline fbcused update The most appropriate management is to discontinue clopido on duration ofdual antiplatelet therapy in patients with coronary artery disease: a report ofthe American College ot Cardiolos//American Heart grel (Option C). Current guidelines suggest treating patients Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. with stable angina with dual antiplatelet therapy (DAPT) for 2016;68:1082-115. IPMID: 27036918] doi:10.1016/j.jacc.2Ol6.03.513 at least 6 months after elective drug eluting stent (DES) place- ment, although the optimal duration for any patient should be selected on the basis of the patient's relative risk for throm- botic and/or ischemic complications. Factors associated with Item 66 Answer: B Educational Objective: Treat end stage primary restric- tr tive cardiomyopathy with cardiac transplantation. increased bleeding risk include advanced age; female sex; anemia; low body weight; chronic kidney disease (CKD); dia- Cardiac transplarrtation (Option B) is the most eppropri betes mellitus; and concomitant therapy with glucocorticoids, ate treatment lbr this patient. 'lhe patient has syr.nptonrs of' NSAIDS, or oral anticoagulant therapy. Risks for ischemic or refractorl' heart failure despitc eflofls at diuresis and rhl thnr thrombotic complications include a complex or suboptimal control. 'lhe f'eatures of preserved sy'stolic tlrnction. signif outcome of percutaneous coronary intervention (PCI), an icant biltrial dilatation, ancl pulmonary hypcrtensit.rr.r on acute coronary syndrome, left ventricular dysfunction, exten- cchocanliogram supl)ofi thc diiigr.rosis of reslrictire carclio sive coronary disease/ischemic history advanced age, diabetes m1opathl, (RCIVI). Sun'ival is poor in patients with RCM. r,r'ith mellitus, and CKD. Current guidelines suggest that at least :r 5 year rnortality rete of 36'/;, and a lO-year rnortality rltc 3 months of DAPT in patients at high risk for bleeding may be o{ 63')1,. Cardiovascular nrurtaliff is predominlntly rclatecl reasonable. This patient has several conditions with increased to progressire l.rerrt failure and arrhl'thnrias. Nlortality rates risk for bleeding; after 4 months of DAPT, discontinuation of increasc with malc sex, scvcrity ol left atrial dilatation. clopidogrel is a reasonable consideration. age oldcr than 70 _years, iind Nerv \irrk lIeart Association Platelet function analysis (Option A) has been proposed (NYHA) functional class. -lhe patient should be retbrrecl to as a method to optimize antiplatelet therapy in those at high ln ad.uuncecl heart failure ancl transplantation specialist ltrr risk for bleeding or thrombosis. Routine use of platelet reac evirluation lbr possible cardiac transplanlatior.r. Heafi trlns tivity assessment to guide medical therapy, however, has not pl antati on r.na1' be I i rn iteci b1' pulmonrr ry, h1'pertension. been associated with improved clinical outcomes and is not Cardiac resyrrchronization therirl'ry (CR'l') (Option A) indicated. is indicated for patients rtho have ref'ractory hearl lirilure In the absence of contraindications, lifeiong aspirin svnlptonls despite guidelinc clirectecl tneclicrrl thcrapl' 'nr itl't (ls toz mg/d) is recommended for secondary prevention in lett ventricular ejcction filctiott less than l)S')i, and QItS patients with established coronary artery disease. Although duratiorr grcater than 150 ms, optimally lelt bundle "vith 189

Answers and Critiques branch block configuratittn ancl sinus rhythnl. Ihis l"rittient guide imrnecliate treatlxent decisions, st"tch as the' neecl tbr does not have an indicltior.r for CItl. revl scula rizatictt-t. CONT. Placement of an implantable cardiovertcr defibrillator Lxercise echocirrdiogrlphy (Option C) adcls echocardio (Option C) is recommended in patients r,t'ith heart lailure grrrphic irnaging to an EC(l stress lest. F]xercise stress testing \ who have an ejection liactior.r of 35',{, or less and \\'H,\ n itl.r imirgirrg is irtdicated in pirticnts u'ho lrirve baseline F-CG lunctional class Il or III symptoms while receiving guicleline rrbnormalities that limit interpretatioll of'the cxcrcise F.CG. \ directed medical therap1,.'[here is no accepted indication lbr or u,ho have indeterntinate firrclir.rgs on the erercise UCG. primary prevention IOI) placernent in patiellts \\'ith RCM lor this patient, adding echocarcliogrlphy is not necessary rvho have preserved systolic function. ancl nould not be a cost ef fective methoci to diagtrose CAI). Pulmonary vein isolation ttrr rhythrn control (Option D) Ambulatory l.CG (Option D) woulcl be appropriate it the nray be appropriate in c<tnjunction with thcrapy tci patient's s!'mptolxs or ll(l(l lirlclings sttggestcd arrhythmia reduce stroke risk in patients with s)'mptornatic atrial as the cause ol his slinlpttlms. Irirst clegree atrioventricular fibrillation unresponsive to irntiarrhytl.rmic ttedicatiot-ts. block is il comnton finclirtg ort tiCG and does not neces UI However. in this patient with severe left atrial dilation. strrih' increase tl.tc suspicit)n that the patient is havirlg an persistcnt atrial fibrillation fbr more than 1 year. ancl arrhllhmil. Tl-tis patient's sylllptoms ilrc nlosl consistent = rD vr evidence of underlyir.rg RCM. it is unlikely to prttvide a rvith angina. q, durable solution to the patierlt's problcnl and carries t(EY P0l llTs CL procedural risk. n o The evaluation of undiagnosed chest pain begins with I(EY POII{I assessing the patient's pretest probability of coronary lt o Heart transplantation is an effective therapy for select artery disease. (D Ut patients with end-stage restrictive cardiomyopathy. o Stress testing is most effectively used in patients with an intermediate pretest probability of coronary artery Bibliography disease. and exercise ECG is recommended as the ini- Pereira NL, Grogan M, Dec CW. Spectrum of restrictive and infiltrative car diomyopathies: part 2 ofa 2.part series. J Am Coll Cardiol. 2018171:1149 tial test of choice in patients who are able to exercise 66. [PMID: 29519356] doi:10.1016'j.Fcc.2018.01.017 and have normal findings on baseline ECG.

branch block configuratittn ancl sinus rhythnl. Ihis l"rittient guide imrnecliate treatlxent decisions, st"tch as the' neecl tbr does not have an indicltior.r for CItl. revl scula rizatictt-t. CONT. Placement of an implantable cardiovertcr defibrillator Lxercise echocirrdiogrlphy (Option C) adcls echocardio (Option C) is recommended in patients r,t'ith heart lailure grrrphic irnaging to an EC(l stress lest. F]xercise stress testing \ who have an ejection liactior.r of 35',{, or less and \\'H,\ n itl.r imirgirrg is irtdicated in pirticnts u'ho lrirve baseline F-CG lunctional class Il or III symptoms while receiving guicleline rrbnormalities that limit interpretatioll of'the cxcrcise F.CG. \ directed medical therap1,.'[here is no accepted indication lbr or u,ho have indeterntinate firrclir.rgs on the erercise UCG. primary prevention IOI) placernent in patiellts \\'ith RCM lor this patient, adding echocarcliogrlphy is not necessary rvho have preserved systolic function. ancl nould not be a cost ef fective methoci to diagtrose CAI). Pulmonary vein isolation ttrr rhythrn control (Option D) Ambulatory l.CG (Option D) woulcl be appropriate it the nray be appropriate in c<tnjunction with thcrapy tci patient's s!'mptolxs or ll(l(l lirlclings sttggestcd arrhythmia reduce stroke risk in patients with s)'mptornatic atrial as the cause ol his slinlpttlms. Irirst clegree atrioventricular fibrillation unresponsive to irntiarrhytl.rmic ttedicatiot-ts. block is il comnton finclirtg ort tiCG and does not neces UI However. in this patient with severe left atrial dilation. strrih' increase tl.tc suspicit)n that the patient is havirlg an persistcnt atrial fibrillation fbr more than 1 year. ancl arrhllhmil. Tl-tis patient's sylllptoms ilrc nlosl consistent = rD vr evidence of underlyir.rg RCM. it is unlikely to prttvide a rvith angina. q, durable solution to the patierlt's problcnl and carries t(EY P0l llTs CL procedural risk. n o The evaluation of undiagnosed chest pain begins with I(EY POII{I assessing the patient's pretest probability of coronary lt o Heart transplantation is an effective therapy for select artery disease. (D Ut patients with end-stage restrictive cardiomyopathy. o Stress testing is most effectively used in patients with an intermediate pretest probability of coronary artery Bibliography disease. and exercise ECG is recommended as the ini- Pereira NL, Grogan M, Dec CW. Spectrum of restrictive and infiltrative car diomyopathies: part 2 ofa 2.part series. J Am Coll Cardiol. 2018171:1149 tial test of choice in patients who are able to exercise 66. [PMID: 29519356] doi:10.1016'j.Fcc.2018.01.017 and have normal findings on baseline ECG. Bibliography Item 67 tr Answer: B Educational Objective: Diagnose coronary artery disease Ferraro R. Latina JM. Alfaddagh A, et al. Evaluation and management of patients with stable angina: beyond the ischemia paradigm: JACC state of the art review. J Am Coll Cardiol. 2020176,2252 2266. IPMIDI with exercise ECG. 331535861 doi:10.10161j.jacc.2020.08.078

Bibliography Item 67 tr Answer: B Educational Objective: Diagnose coronary artery disease Ferraro R. Latina JM. Alfaddagh A, et al. Evaluation and management of patients with stable angina: beyond the ischemia paradigm: JACC state of the art review. J Am Coll Cardiol. 2020176,2252 2266. IPMIDI with exercise ECG. 331535861 doi:10.10161j.jacc.2020.08.078 'lhe most appropriate managemcnt is exercise IICG (Option B) lbr this patient with typical angina sy'rnptor.t.ts. 'lhe eval Item 68 Answer: D uation of' undiagnosed chesl pain begins with assessittg Educational Objective: Continue warfarin during preg- the patient's pretest probabilitl' ol coronarl' artery diseasc nancy in a patient with a prosthetic mechanical valve. (CAD). This patient's age. sex. and nreclical hiskrry place lrim in the ir.rtcrmediate risk category. and exercisc llCG fttr CAI) Continuing the INR adjusted warfarin regimen (Option D) is best applied to patients in this group. Unless there are is most appropriate for this patient. Mechanical mitral valve contraindications to exercise. exercise testing is pref'erred prostheses increase risks to the patient and fetus during to pharmacologic stress testing. Absolute contraindicatiot.ts pregnancy. Warfarin anticoagulation seems to be the safest tci exercise include unstable angina or acute myocirrdial agent to prevent maternal prosthetic valve thrombosis; how infarction. uncontrollecl arrhythmias. decompensated heart ever, warfarin poses increased fetal risks, including terato Iailure, acute pulmonrry embolism or deep venous throm genicity, miscarriage, and fetal loss because of intracranial bosis. acute pericarditis or myocarditis, acute aortic dissec hemorrhage. Risk to the fetus is dose related; warfarin is tion. and severc symptonlatic aortic stenosis. Exercise ECC the preferred anticoagulant during the first trimester if the is recommended as the initial test of choice in patients lt ith dosage is 5 mg/d or less. During the second and early third normal findings on baseline ECG. 'llris patient's baselinc trimesters, warfarin is the preferred anticoagulant. irCC has no findings that u,ould in.rpair interprctation of the Bivalirudin (Option A) has not been demonstrated to results. such as S'f segment depression greater than 1 mm. provide adequate anticoagulation coverage for a pregnant lctt bunclle branch block. left ventricular hypertrophl: paccd patient with a prosthetic mechanical valve and should not rhythm. or preexcitation. be used. Calcification of the coronirry arteries is indicutive ol For patients with a mechanical valve prosthesis, the atherosclerosis and may be quantifled with C'l. Although direct thrombin inhibitor dabigatran (Option B) should coronary artery calcium scoring (Option A) provides inlbr not be used because of increased risk for harm. A ran mtrtion regarding the burder.r ot disease, i1 canl-rot confirnr domized clinical trial of dabigatran in nonpregnant patients that thc patient's symptoms are due to obstructive CAD or with a mechanical heart valve showed an increased rate of

'lhe most appropriate managemcnt is exercise IICG (Option B) lbr this patient with typical angina sy'rnptor.t.ts. 'lhe eval Item 68 Answer: D uation of' undiagnosed chesl pain begins with assessittg Educational Objective: Continue warfarin during preg- the patient's pretest probabilitl' ol coronarl' artery diseasc nancy in a patient with a prosthetic mechanical valve. (CAD). This patient's age. sex. and nreclical hiskrry place lrim in the ir.rtcrmediate risk category. and exercisc llCG fttr CAI) Continuing the INR adjusted warfarin regimen (Option D) is best applied to patients in this group. Unless there are is most appropriate for this patient. Mechanical mitral valve contraindications to exercise. exercise testing is pref'erred prostheses increase risks to the patient and fetus during to pharmacologic stress testing. Absolute contraindicatiot.ts pregnancy. Warfarin anticoagulation seems to be the safest tci exercise include unstable angina or acute myocirrdial agent to prevent maternal prosthetic valve thrombosis; how infarction. uncontrollecl arrhythmias. decompensated heart ever, warfarin poses increased fetal risks, including terato Iailure, acute pulmonrry embolism or deep venous throm genicity, miscarriage, and fetal loss because of intracranial bosis. acute pericarditis or myocarditis, acute aortic dissec hemorrhage. Risk to the fetus is dose related; warfarin is tion. and severc symptonlatic aortic stenosis. Exercise ECC the preferred anticoagulant during the first trimester if the is recommended as the initial test of choice in patients lt ith dosage is 5 mg/d or less. During the second and early third normal findings on baseline ECG. 'llris patient's baselinc trimesters, warfarin is the preferred anticoagulant. irCC has no findings that u,ould in.rpair interprctation of the Bivalirudin (Option A) has not been demonstrated to results. such as S'f segment depression greater than 1 mm. provide adequate anticoagulation coverage for a pregnant lctt bunclle branch block. left ventricular hypertrophl: paccd patient with a prosthetic mechanical valve and should not rhythm. or preexcitation. be used. Calcification of the coronirry arteries is indicutive ol For patients with a mechanical valve prosthesis, the atherosclerosis and may be quantifled with C'l. Although direct thrombin inhibitor dabigatran (Option B) should coronary artery calcium scoring (Option A) provides inlbr not be used because of increased risk for harm. A ran mtrtion regarding the burder.r ot disease, i1 canl-rot confirnr domized clinical trial of dabigatran in nonpregnant patients that thc patient's symptoms are due to obstructive CAD or with a mechanical heart valve showed an increased rate of 190

Answers and C thromboembolic and bleeding complications with dabiga resting ABIs are normal or borderline. ABI testing is also tran compared with rrarfarin. The effectiveness of apixaban, useful to differentiate claudication from pseudoclaudication rivaroxaban, and edoxaban (anti-Xa direct oral anticoagu (spinal stenosis) in persons with exertional leg symptoms. lants) has not been established in patients with a mechanical This asymptomatic patient has established PAD based on an heart valve, and the safety ofthese agents in pregnancy is not abnormal resting ABI, and additional testing with exercise known; therefore, they are not recommended. ABI is not needed. In patients who prefer not to take warfarin during the CT angiography (Option B) and magnetic resonance flrst trimester of pregnancy or if the warfarin dosage is more angiography are often reserved for planning endovascular than 5 mg/d, intravenous dose adjusted unfractionated hep or surgical revascularization in patients with PAD. Because arin may be used. However, subcutaneous unfractionated this patient is asymptomatic, there is no indication for CT heparin (Option C) does not provide adequate anticoagu angiography. lation coverage for a patient with a mechanical prosthetic In patients with conflrmed PAD, toe-brachial index valve. Intravenous unfractionated heparin is the preferred testing (Option C) has no added utility. The toe brachial t (l, anticoagulant option for patients with a mechanical valve index is useful when the resting ABI is greater than 1.40, CT around the time of delivery. indicating the presence of noncompressible, calcifled arter- ies in the lower extremities. In these patients, an appropriate (J l(EY P0r1{rs .E, next step is great toe pressure measurement or toe-brachial o For pregnant patients with a mechanical valve pros index calculation (systolic great toe pressure divided by sys .u thesis, warfarin is the preferred anticoagulant during tolic brachial pressure). r

thromboembolic and bleeding complications with dabiga resting ABIs are normal or borderline. ABI testing is also tran compared with rrarfarin. The effectiveness of apixaban, useful to differentiate claudication from pseudoclaudication rivaroxaban, and edoxaban (anti-Xa direct oral anticoagu (spinal stenosis) in persons with exertional leg symptoms. lants) has not been established in patients with a mechanical This asymptomatic patient has established PAD based on an heart valve, and the safety ofthese agents in pregnancy is not abnormal resting ABI, and additional testing with exercise known; therefore, they are not recommended. ABI is not needed. In patients who prefer not to take warfarin during the CT angiography (Option B) and magnetic resonance flrst trimester of pregnancy or if the warfarin dosage is more angiography are often reserved for planning endovascular than 5 mg/d, intravenous dose adjusted unfractionated hep or surgical revascularization in patients with PAD. Because arin may be used. However, subcutaneous unfractionated this patient is asymptomatic, there is no indication for CT heparin (Option C) does not provide adequate anticoagu angiography. lation coverage for a patient with a mechanical prosthetic In patients with conflrmed PAD, toe-brachial index valve. Intravenous unfractionated heparin is the preferred testing (Option C) has no added utility. The toe brachial t (l, anticoagulant option for patients with a mechanical valve index is useful when the resting ABI is greater than 1.40, CT around the time of delivery. indicating the presence of noncompressible, calcifled arter- ies in the lower extremities. In these patients, an appropriate (J l(EY P0r1{rs .E, next step is great toe pressure measurement or toe-brachial o For pregnant patients with a mechanical valve pros index calculation (systolic great toe pressure divided by sys .u thesis, warfarin is the preferred anticoagulant during tolic brachial pressure). r the first trimester if the dosage is 5 mg/d or less; war- (l, t(EY POtltrS vl farin is the preferred anticoagulant during the second = and early third trimesters. r The American College of Cardiologz recommends o Direct oral anticoagulants are not recommended in resting ankle brachial index testing in patients with patients with a mechanical valve prosthesis. history or physical examination findings suggestive of peripheral artery disease. Bibliography o Patients with both coronary artery disease and otto CM, Nishinrura RA, Bonow RO. er al. 2020 ACO AIIA guideline tbr rhe peripheral artery disease are at higher risk for major nranagement of patients with valvular heart disease: a report of the adverse cardiovascular events. American College of Cardiologr/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulatirn.2O2l:143:e7 ) e))7. IPMID: 333321501 doi:l0.ll6l/CIR.0000000000000923 Bibliography Gerhard Ilerman MD, Gornik HL, Barrett C, et al. 2016 AHA/ACC guideline on the management of patients with lower extremity peripheral artery disease: executive summary: a report of the American College of Item 69 Answer: D Cardiology/American []eart Association Task Force on Clinical Educational Objective: Avoid unnecessary testing in a Practice (luidelines. Circulation. 201 7;135:e686-e725. IPMID: 27840332) doi:10.1161 iCIR.00000O0000000470 patient with asymptomatic peripheral artery disease.

the first trimester if the dosage is 5 mg/d or less; war- (l, t(EY POtltrS vl farin is the preferred anticoagulant during the second = and early third trimesters. r The American College of Cardiologz recommends o Direct oral anticoagulants are not recommended in resting ankle brachial index testing in patients with patients with a mechanical valve prosthesis. history or physical examination findings suggestive of peripheral artery disease. Bibliography o Patients with both coronary artery disease and otto CM, Nishinrura RA, Bonow RO. er al. 2020 ACO AIIA guideline tbr rhe peripheral artery disease are at higher risk for major nranagement of patients with valvular heart disease: a report of the adverse cardiovascular events. American College of Cardiologr/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulatirn.2O2l:143:e7 ) e))7. IPMID: 333321501 doi:l0.ll6l/CIR.0000000000000923 Bibliography Gerhard Ilerman MD, Gornik HL, Barrett C, et al. 2016 AHA/ACC guideline on the management of patients with lower extremity peripheral artery disease: executive summary: a report of the American College of Item 69 Answer: D Cardiology/American []eart Association Task Force on Clinical Educational Objective: Avoid unnecessary testing in a Practice (luidelines. Circulation. 201 7;135:e686-e725. IPMID: 27840332) doi:10.1161 iCIR.00000O0000000470 patient with asymptomatic peripheral artery disease. No additional testing (Option D) is necessary. This patient Item 70 has both coronary afiery disease and peripheral artery dis ease (PAD), a combination associated with a higher risk fbr major adverse cardiovascular events. In patients with a Answer: C Educational Objective: Treat new onset symptomatic tr heart failure with an ACE inhibitor. history or physical examination flndings suggestive of PAD, the American College of Cardiologr recommends resting 'lhc most uppropriirte trcatment is rrn ACI: inhibitor. such as ankle brachial index (ABI) testing to establish the diagnosis. cnalapril (Option C), ttrr this patient l'nith new onsct 1>eri This patient's diagnosis of PAD was confirmed by a low ABI l)artum crrrcliomyr4rrrtIr1' anci hcart lailure. Follou,ing dcliv in both lower extremities (0.80 on the right and 0.86 on er\. patients u,ith peripirrtunr clrcliomyoplthy are treated the left), and he does not require additional testing. He is the samc rrs rrll other l)atients r,r,ith heart tailure. ACI inhib being treated appropriately with guideline directed medi itors reclucc morbidity and nrurtalitlr in pltients rtith hcart cal therapy, including tvvo antiplatelet agents, a p-blocker, Iirilure."n'ith reclucccl cjection fiaction (HFrl.-l) and should be an ACE inhibitor, and a statin. There is also a 45-mm Hg r-rscd in botl.r s1-r.nplonratic and ilsymptonlatic patients. r\CE difference in arm blood pressures in this patient. Although irrlribitors cirn be startecl immccliately in l)atients r,r,ith acute a difference in arm systolic pressures of greater than 15 to hcart failurc in thc absence of hyperkalenria; the estinrated 20 mm Hg suggests subclavian or innominate artery ste gkrmerular liltration rxte shollld lre monitoleri during upti nosis, in the absence of symptoms (arm claudication or trirtion. lrnrrlapril. captopril, cluinapril, ancl benazcpril are symptoms olvertebral artery steal), no further imaging or I)rcsenl in vcry low lcvels in breasl milk ancl are consiclered intervention is warranted. s:rfe during breastll'ccling. \hlslrtan-sacubitril shoulcl r.tot Exercise ABI testing (Option A) is useful in establish be used cluring brclstf-eeding beciruse ol thc potcntial fbr ing the diagnosis of PAD in the symptomatic patient when serious aclverse reactions in infants.

No additional testing (Option D) is necessary. This patient Item 70 has both coronary afiery disease and peripheral artery dis ease (PAD), a combination associated with a higher risk fbr major adverse cardiovascular events. In patients with a Answer: C Educational Objective: Treat new onset symptomatic tr heart failure with an ACE inhibitor. history or physical examination flndings suggestive of PAD, the American College of Cardiologr recommends resting 'lhc most uppropriirte trcatment is rrn ACI: inhibitor. such as ankle brachial index (ABI) testing to establish the diagnosis. cnalapril (Option C), ttrr this patient l'nith new onsct 1>eri This patient's diagnosis of PAD was confirmed by a low ABI l)artum crrrcliomyr4rrrtIr1' anci hcart lailure. Follou,ing dcliv in both lower extremities (0.80 on the right and 0.86 on er\. patients u,ith peripirrtunr clrcliomyoplthy are treated the left), and he does not require additional testing. He is the samc rrs rrll other l)atients r,r,ith heart tailure. ACI inhib being treated appropriately with guideline directed medi itors reclucc morbidity and nrurtalitlr in pltients rtith hcart cal therapy, including tvvo antiplatelet agents, a p-blocker, Iirilure."n'ith reclucccl cjection fiaction (HFrl.-l) and should be an ACE inhibitor, and a statin. There is also a 45-mm Hg r-rscd in botl.r s1-r.nplonratic and ilsymptonlatic patients. r\CE difference in arm blood pressures in this patient. Although irrlribitors cirn be startecl immccliately in l)atients r,r,ith acute a difference in arm systolic pressures of greater than 15 to hcart failurc in thc absence of hyperkalenria; the estinrated 20 mm Hg suggests subclavian or innominate artery ste gkrmerular liltration rxte shollld lre monitoleri during upti nosis, in the absence of symptoms (arm claudication or trirtion. lrnrrlapril. captopril, cluinapril, ancl benazcpril are symptoms olvertebral artery steal), no further imaging or I)rcsenl in vcry low lcvels in breasl milk ancl are consiclered intervention is warranted. s:rfe during breastll'ccling. \hlslrtan-sacubitril shoulcl r.tot Exercise ABI testing (Option A) is useful in establish be used cluring brclstf-eeding beciruse ol thc potcntial fbr ing the diagnosis of PAD in the symptomatic patient when serious aclverse reactions in infants. 191

Answers and Critiques t m lhe p blockers rnetoprolol. can'edilol. and bisoprolol linear downsloping ST segment) in leads V, through V" with llJ 19p1;6n A) aiso reduce mortalig in patients rvith HFTEF. or without right bundle branch block. Brugada syndrome is coNT but trextment should be clelayed in patierlts lr,ith volunre the association of Brugada pattern with ventricular fibril- ove'rload (jugular venous distentior.r. crackles. ederna) and lation, arrhythmogenic syncope, or cardiac arrest. Brugada reduced cardiac output (S.) bccause treatment in these syndrome has an increased prevalence in men and persons patients may \\'orselt symptonts. Guidelines recommend of Asian descent. Arrhythmic events, including sudden car reclucing intrar,'ascular volume with a loop diuretic and ini diac death, in patients with Brugada syndrome are more tiating an ACE inhibitor; B blockers ntay be cautiously intro common at night, during sleep. Abnormalities on ECG may ducecl rvhen the patient is closer to being euvolemic. be intermittent and may be elicited by fever or pharma In small trials, the nondihldropyridine calcium chan cologic challenge with sodium channel blockade, such as nel blockers diltiazern (Option B) and',eraparnil have been procainamide infusion. The presence of Brugada pattern on associated w-ith :rn increase in rnortali[,- in patients with ECG, an unexplained syncopal event, and relevant family heart failure. Ifthis patient's hypertension persists after she history (father who died in his sleep at age 45 years) are 3 art receives maximal doses of an ACF. inhibitor ancl B blocker. highly suggestive of Brugada syndrome. E one might consider adding a dihydropvridine calcium chan This patient has no exertional symptoms or ischemic .D U! nel blocker (e.g.. anrlodipine. felodipine); these agents have changes on ECG, and his symptoms are paroxysmal. Inter- o, been shown to be saf'e in patients with heart failure. mittent syncope would be a very unusual presentation of CL lvabradine (Option D) inhibits the sinus node and coronary artery disease (Option B), particular$ in this age n reduces heafi rate in patients with heart lailure. lt has been group. =. sholr,n to reduce heirrl failure hospitalizations r,r'hen added Long QT syndrome (Option C) is among the most com- tt c .D to nr:rximally tolerated B blocker therapyl This patient is uot mon inherited arrhythmias, affecting between 1 in 1000 ut tal<ing a B blocker, making this an inappropriate addition at and 1 in 5000 persons. The presence of a prolonged QTc this time. (>440 ms in men and >460 ms in women) alone is insuf- flcient to diagnose long QT syndrome. This patient's QTc rEY POITTS interval is normal, and long QT syndrome is not associated . ACE inhibitors reduce morbidity and mortality in with the findings seen on this patient's ECG. patients with heart failure with reduced ejection frac- This patient has no prodrome offlushing, light-headedness, tion and should be used in both symptomatic and or dizziness, which is typical of vasovagal slmcope (Option D). asymptomatic patients. Finally his s,.ncope and associated ECG findings are of great o Metoprolol, carvedilol, and bisoprolol reduce mortal- concern and are consistent with Brugada qmdrome. ity in patients with heart failure with reduced ejection f,IY POI lII! fraction, but treatment should be delayed in patients . Cardiovascular syncopal events often occur suddenly with volume overload until the patient is closer to and usually without a significant prodrome, although being euvolemic. chest pain and palpitations may be present.

m lhe p blockers rnetoprolol. can'edilol. and bisoprolol linear downsloping ST segment) in leads V, through V" with llJ 19p1;6n A) aiso reduce mortalig in patients rvith HFTEF. or without right bundle branch block. Brugada syndrome is coNT but trextment should be clelayed in patierlts lr,ith volunre the association of Brugada pattern with ventricular fibril- ove'rload (jugular venous distentior.r. crackles. ederna) and lation, arrhythmogenic syncope, or cardiac arrest. Brugada reduced cardiac output (S.) bccause treatment in these syndrome has an increased prevalence in men and persons patients may \\'orselt symptonts. Guidelines recommend of Asian descent. Arrhythmic events, including sudden car reclucing intrar,'ascular volume with a loop diuretic and ini diac death, in patients with Brugada syndrome are more tiating an ACE inhibitor; B blockers ntay be cautiously intro common at night, during sleep. Abnormalities on ECG may ducecl rvhen the patient is closer to being euvolemic. be intermittent and may be elicited by fever or pharma In small trials, the nondihldropyridine calcium chan cologic challenge with sodium channel blockade, such as nel blockers diltiazern (Option B) and',eraparnil have been procainamide infusion. The presence of Brugada pattern on associated w-ith :rn increase in rnortali[,- in patients with ECG, an unexplained syncopal event, and relevant family heart failure. Ifthis patient's hypertension persists after she history (father who died in his sleep at age 45 years) are 3 art receives maximal doses of an ACF. inhibitor ancl B blocker. highly suggestive of Brugada syndrome. E one might consider adding a dihydropvridine calcium chan This patient has no exertional symptoms or ischemic .D U! nel blocker (e.g.. anrlodipine. felodipine); these agents have changes on ECG, and his symptoms are paroxysmal. Inter- o, been shown to be saf'e in patients with heart failure. mittent syncope would be a very unusual presentation of CL lvabradine (Option D) inhibits the sinus node and coronary artery disease (Option B), particular$ in this age n reduces heafi rate in patients with heart lailure. lt has been group. =. sholr,n to reduce heirrl failure hospitalizations r,r'hen added Long QT syndrome (Option C) is among the most com- tt c .D to nr:rximally tolerated B blocker therapyl This patient is uot mon inherited arrhythmias, affecting between 1 in 1000 ut tal<ing a B blocker, making this an inappropriate addition at and 1 in 5000 persons. The presence of a prolonged QTc this time. (>440 ms in men and >460 ms in women) alone is insuf- flcient to diagnose long QT syndrome. This patient's QTc rEY POITTS interval is normal, and long QT syndrome is not associated . ACE inhibitors reduce morbidity and mortality in with the findings seen on this patient's ECG. patients with heart failure with reduced ejection frac- This patient has no prodrome offlushing, light-headedness, tion and should be used in both symptomatic and or dizziness, which is typical of vasovagal slmcope (Option D). asymptomatic patients. Finally his s,.ncope and associated ECG findings are of great o Metoprolol, carvedilol, and bisoprolol reduce mortal- concern and are consistent with Brugada qmdrome. ity in patients with heart failure with reduced ejection f,IY POI lII! fraction, but treatment should be delayed in patients . Cardiovascular syncopal events often occur suddenly with volume overload until the patient is closer to and usually without a significant prodrome, although being euvolemic. chest pain and palpitations may be present. Bibliography o Causes of cardiovascular syncope include cardiac Yancy CW, Jessup M, Bozkurt B, et al; American College of Cardiologr arrhythmia; coronary artery disease; and structural Foundation. 2013 ACCF/AHA guideline for the management of heart and obstructive disease, including aortic and pulmo- failure: a report of the American College of Cardiolory Foundationr American Heart Association Task Force on Practice Guidelines. J Am Coll nary valve stenosis, obstructive hypertrophic cardio Cardiol.2013;62:e147 n9.lPMlDt23747642ldoi:LO.1O16/j.iacc.2013.05.019 myopathy, aortic dissection, and cardiac tamponade.

Bibliography o Causes of cardiovascular syncope include cardiac Yancy CW, Jessup M, Bozkurt B, et al; American College of Cardiologr arrhythmia; coronary artery disease; and structural Foundation. 2013 ACCF/AHA guideline for the management of heart and obstructive disease, including aortic and pulmo- failure: a report of the American College of Cardiolory Foundationr American Heart Association Task Force on Practice Guidelines. J Am Coll nary valve stenosis, obstructive hypertrophic cardio Cardiol.2013;62:e147 n9.lPMlDt23747642ldoi:LO.1O16/j.iacc.2013.05.019 myopathy, aortic dissection, and cardiac tamponade. Bibliography Item 71 Answer: A Al-Khatib SM. Stevenson WG. Ackerman Ml. et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and Educational Objective: Diagnose Brugada syndrome. the prevention ofsudden cardiac death: a report ofthe American College ofCardiologr/American Heart Association Task Force on Clinical Practice The most likely diagnosis in this patient with recurrent Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2018;72: syncope is Brugada syndrome (Option A). Cardiovascular e91-e220. IPMID: 290972961 doi:10.1016/j.jacc.2017.10.054

Bibliography Item 71 Answer: A Al-Khatib SM. Stevenson WG. Ackerman Ml. et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and Educational Objective: Diagnose Brugada syndrome. the prevention ofsudden cardiac death: a report ofthe American College ofCardiologr/American Heart Association Task Force on Clinical Practice The most likely diagnosis in this patient with recurrent Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2018;72: syncope is Brugada syndrome (Option A). Cardiovascular e91-e220. IPMID: 290972961 doi:10.1016/j.jacc.2017.10.054 syncopal events often occur suddenly and usually with Item72 out a signiflcant prodrome, although chest pain and palpi tations may be present. Causes of cardiovascular syncope include cardiac arrhythmia; coronary artery disease; and Answer: B Educational Objective: Treat infective endocarditis with tr early valve replacement surgery. structural and obstructive disease, including aortic and pulmonary valve stenosis, obstructive hypertrophic car- The most appropriate nlrnagement is earlv surgical aortic diomyopathy, aortic dissection, and cardiac tamponade. valve replacement (Option B). This llatient's history and Brugada pattern is distinguished by a structurally normal physical examination findings are consistent with infec- heart (normal echocardiogram) and right precordial ECG tive endocarditis (lE), severe aortic regurgitation (murmur, abnormalities, including ST segment coving (concave or bounding pulses. widened pulse pressure), and heart failure.

syncopal events often occur suddenly and usually with Item72 out a signiflcant prodrome, although chest pain and palpi tations may be present. Causes of cardiovascular syncope include cardiac arrhythmia; coronary artery disease; and Answer: B Educational Objective: Treat infective endocarditis with tr early valve replacement surgery. structural and obstructive disease, including aortic and pulmonary valve stenosis, obstructive hypertrophic car- The most appropriate nlrnagement is earlv surgical aortic diomyopathy, aortic dissection, and cardiac tamponade. valve replacement (Option B). This llatient's history and Brugada pattern is distinguished by a structurally normal physical examination findings are consistent with infec- heart (normal echocardiogram) and right precordial ECG tive endocarditis (lE), severe aortic regurgitation (murmur, abnormalities, including ST segment coving (concave or bounding pulses. widened pulse pressure), and heart failure. 192

: Answers and Critiques tr CONT. In addition. the liCG denronstrating prolonged first dcgree atrior,entricular block is concerning fbr involvernent of the a rapid increase in erythrocyte mass. When the hemoglobin level and hematocrit begin to increase in 7 to 10 days, iron atrio'"entricular nocle. rn,hich sits close to the aortic vllve therapy should be discontinued. Correction of iron defl and may be involved in aortic valve endocarditis, especially ciency is associated with increased exercise capacity and ilan aortic abscess is present. In patients r,r,ith IE r,vho pre improved quality of Iife. sent with valve dysfunction resulting in sympk)ms ol heart Menorrhagia is the presumed cause of relative anemia in failurc, or [E complicated by hearl block, annular or arlrtic this patient, and management of menorrhagia is indicated. I abscess, or destructive penetrating lesions, early surgery Treatment may involve endometrial ablation, intrauterine during the initial hospitalization ancl before completiorr of a device placement, and, rarely, hysterectomy (Option A). Sur full therapeutic course of antibiotics is indicatecl. gical interventions are generally avoided in patients with Occasionally. cardiac crtheterization (Option A) to Eisenmenger syndrome unless they are necessary owing to define coronary ilnatomy rnay be pursued before surgical increased perioperative risk. The initial treatment is to cor aortic valve replaccment to determine whether adjunctive rect iron deflciency anemia. aa (l, coronary artery bypass grafting is needed. l]owever. the In patients with cyanotic congenital heart disease, ET catheterization finclings would not change the need fbr aor phlebotomy (Option C) is recommended for symptomatic tic valve replacement and should not clelay surgical manage hyperviscosity (headaches, reduced concentration) with a fr, ment in tl.ris patient. hemoglobin level greater than 20 g/dl (200 g/L) and hema- 'El Sinrilarly', ltlacement of a tentporary pacemaker tocrit greater than 65% in the absence ofdehydration. Phle |! (Option C) does not address the undcrlying worsening rtrr botomy is not indicated in this patient with a hemoglobin t (, tic valve infection ar.rd conductioll systeln contpromise by an level that is low for a patient with Eisenmenger syndrome. UI abscess: therefbre, it shoulcl llot delay surgical management. In patients with cyanotic heart disease, guidelines rec- = Patients with IE and heart failure treated with surgery ommend supplemental oxygen (Option D) as needed for have a 2l'X, in hospital mortality rate c<tmpared with a ratc of symptom relief of dyspnea but not to a target oxygen satura- 45'li in those tlcated medicallli In aclclition. extensive pxra- tion level and not to be continued if there is no symptomatic valvular inf'ections (including annular or ilortic abscesses beneflt. A more physiologic strateg/ to address this patient's and destructive penetrating lesions or fistulae) irre associated exertional dyspnea is to treat her iron deflciency anemia. n'ith a mortality rate of .,l0')1, or higher ar.rd heart block. Earll' Her symptoms will improve quickly with appropriate iron surgery is associated vvith ln actuarill survival rate ol 75')1, at replacement. .5 years. Continuing current therapy withollt early surgery (Option D) is not inclicatecl. TEY POIl{IS o Correction of iron deficiency is associated with I(EY POI ]IT increased exercise capacity and improved quality of . Early surgical valve replacement is indicated in life in patients with cyanotic congenital heart disease. patients with infective endocarditis and heart failure, . Adaptive erythrocytosis is well tolerated in patients annular or aortic abscess, or destructive penetrating with cyanotic congenital heart disease, and therapeutic lesions. phlebotomy is not indicated until hemoglobin con centration is greater than 20 gldL (2OO glL). Bibliography Otto CM. Nishimura RA. Bonow RO, et aI.2020 ACC/AIIA guideline for the management of patients with valvular heart disease: a report of the Bibliography American College of Cardiology/American Heart Association Joint Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC guideline for the Committee on Clinical Practice Guidelines. Circulation. 2O2l:143:e72 management of adults with congenital heart disease: a report of the e227. I PMID: 33332lsol doi:10. I 161 /CIR.000000000000o923 American College of Cardiolog//American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2019:73:e81-e192. IPMID: 30121239] doi:10.1016/j.jacc.2018.08.1029

tr CONT. In addition. the liCG denronstrating prolonged first dcgree atrior,entricular block is concerning fbr involvernent of the a rapid increase in erythrocyte mass. When the hemoglobin level and hematocrit begin to increase in 7 to 10 days, iron atrio'"entricular nocle. rn,hich sits close to the aortic vllve therapy should be discontinued. Correction of iron defl and may be involved in aortic valve endocarditis, especially ciency is associated with increased exercise capacity and ilan aortic abscess is present. In patients r,r,ith IE r,vho pre improved quality of Iife. sent with valve dysfunction resulting in sympk)ms ol heart Menorrhagia is the presumed cause of relative anemia in failurc, or [E complicated by hearl block, annular or arlrtic this patient, and management of menorrhagia is indicated. I abscess, or destructive penetrating lesions, early surgery Treatment may involve endometrial ablation, intrauterine during the initial hospitalization ancl before completiorr of a device placement, and, rarely, hysterectomy (Option A). Sur full therapeutic course of antibiotics is indicatecl. gical interventions are generally avoided in patients with Occasionally. cardiac crtheterization (Option A) to Eisenmenger syndrome unless they are necessary owing to define coronary ilnatomy rnay be pursued before surgical increased perioperative risk. The initial treatment is to cor aortic valve replaccment to determine whether adjunctive rect iron deflciency anemia. aa (l, coronary artery bypass grafting is needed. l]owever. the In patients with cyanotic congenital heart disease, ET catheterization finclings would not change the need fbr aor phlebotomy (Option C) is recommended for symptomatic tic valve replacement and should not clelay surgical manage hyperviscosity (headaches, reduced concentration) with a fr, ment in tl.ris patient. hemoglobin level greater than 20 g/dl (200 g/L) and hema- 'El Sinrilarly', ltlacement of a tentporary pacemaker tocrit greater than 65% in the absence ofdehydration. Phle |! (Option C) does not address the undcrlying worsening rtrr botomy is not indicated in this patient with a hemoglobin t (, tic valve infection ar.rd conductioll systeln contpromise by an level that is low for a patient with Eisenmenger syndrome. UI abscess: therefbre, it shoulcl llot delay surgical management. In patients with cyanotic heart disease, guidelines rec- = Patients with IE and heart failure treated with surgery ommend supplemental oxygen (Option D) as needed for have a 2l'X, in hospital mortality rate c<tmpared with a ratc of symptom relief of dyspnea but not to a target oxygen satura- 45'li in those tlcated medicallli In aclclition. extensive pxra- tion level and not to be continued if there is no symptomatic valvular inf'ections (including annular or ilortic abscesses beneflt. A more physiologic strateg/ to address this patient's and destructive penetrating lesions or fistulae) irre associated exertional dyspnea is to treat her iron deflciency anemia. n'ith a mortality rate of .,l0')1, or higher ar.rd heart block. Earll' Her symptoms will improve quickly with appropriate iron surgery is associated vvith ln actuarill survival rate ol 75')1, at replacement. .5 years. Continuing current therapy withollt early surgery (Option D) is not inclicatecl. TEY POIl{IS o Correction of iron deficiency is associated with I(EY POI ]IT increased exercise capacity and improved quality of . Early surgical valve replacement is indicated in life in patients with cyanotic congenital heart disease. patients with infective endocarditis and heart failure, . Adaptive erythrocytosis is well tolerated in patients annular or aortic abscess, or destructive penetrating with cyanotic congenital heart disease, and therapeutic lesions. phlebotomy is not indicated until hemoglobin con centration is greater than 20 gldL (2OO glL). Bibliography Otto CM. Nishimura RA. Bonow RO, et aI.2020 ACC/AIIA guideline for the management of patients with valvular heart disease: a report of the Bibliography American College of Cardiology/American Heart Association Joint Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC guideline for the Committee on Clinical Practice Guidelines. Circulation. 2O2l:143:e72 management of adults with congenital heart disease: a report of the e227. I PMID: 33332lsol doi:10. I 161 /CIR.000000000000o923 American College of Cardiolog//American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2019:73:e81-e192. IPMID: 30121239] doi:10.1016/j.jacc.2018.08.1029 Item 73 Answer: B Educational Obiective: Treat iron deficiency in cyanotic congenital heart disease.

tr CONT. In addition. the liCG denronstrating prolonged first dcgree atrior,entricular block is concerning fbr involvernent of the a rapid increase in erythrocyte mass. When the hemoglobin level and hematocrit begin to increase in 7 to 10 days, iron atrio'"entricular nocle. rn,hich sits close to the aortic vllve therapy should be discontinued. Correction of iron defl and may be involved in aortic valve endocarditis, especially ciency is associated with increased exercise capacity and ilan aortic abscess is present. In patients r,r,ith IE r,vho pre improved quality of Iife. sent with valve dysfunction resulting in sympk)ms ol heart Menorrhagia is the presumed cause of relative anemia in failurc, or [E complicated by hearl block, annular or arlrtic this patient, and management of menorrhagia is indicated. I abscess, or destructive penetrating lesions, early surgery Treatment may involve endometrial ablation, intrauterine during the initial hospitalization ancl before completiorr of a device placement, and, rarely, hysterectomy (Option A). Sur full therapeutic course of antibiotics is indicatecl. gical interventions are generally avoided in patients with Occasionally. cardiac crtheterization (Option A) to Eisenmenger syndrome unless they are necessary owing to define coronary ilnatomy rnay be pursued before surgical increased perioperative risk. The initial treatment is to cor aortic valve replaccment to determine whether adjunctive rect iron deflciency anemia. aa (l, coronary artery bypass grafting is needed. l]owever. the In patients with cyanotic congenital heart disease, ET catheterization finclings would not change the need fbr aor phlebotomy (Option C) is recommended for symptomatic tic valve replacement and should not clelay surgical manage hyperviscosity (headaches, reduced concentration) with a fr, ment in tl.ris patient. hemoglobin level greater than 20 g/dl (200 g/L) and hema- 'El Sinrilarly', ltlacement of a tentporary pacemaker tocrit greater than 65% in the absence ofdehydration. Phle |! (Option C) does not address the undcrlying worsening rtrr botomy is not indicated in this patient with a hemoglobin t (, tic valve infection ar.rd conductioll systeln contpromise by an level that is low for a patient with Eisenmenger syndrome. UI abscess: therefbre, it shoulcl llot delay surgical management. In patients with cyanotic heart disease, guidelines rec- = Patients with IE and heart failure treated with surgery ommend supplemental oxygen (Option D) as needed for have a 2l'X, in hospital mortality rate c<tmpared with a ratc of symptom relief of dyspnea but not to a target oxygen satura- 45'li in those tlcated medicallli In aclclition. extensive pxra- tion level and not to be continued if there is no symptomatic valvular inf'ections (including annular or ilortic abscesses beneflt. A more physiologic strateg/ to address this patient's and destructive penetrating lesions or fistulae) irre associated exertional dyspnea is to treat her iron deflciency anemia. n'ith a mortality rate of .,l0')1, or higher ar.rd heart block. Earll' Her symptoms will improve quickly with appropriate iron surgery is associated vvith ln actuarill survival rate ol 75')1, at replacement. .5 years. Continuing current therapy withollt early surgery (Option D) is not inclicatecl. TEY POIl{IS o Correction of iron deficiency is associated with I(EY POI ]IT increased exercise capacity and improved quality of . Early surgical valve replacement is indicated in life in patients with cyanotic congenital heart disease. patients with infective endocarditis and heart failure, . Adaptive erythrocytosis is well tolerated in patients annular or aortic abscess, or destructive penetrating with cyanotic congenital heart disease, and therapeutic lesions. phlebotomy is not indicated until hemoglobin con centration is greater than 20 gldL (2OO glL). Bibliography Otto CM. Nishimura RA. Bonow RO, et aI.2020 ACC/AIIA guideline for the management of patients with valvular heart disease: a report of the Bibliography American College of Cardiology/American Heart Association Joint Stout KK, Daniels CJ, Aboulhosn JA, et al. 2018 AHA/ACC guideline for the Committee on Clinical Practice Guidelines. Circulation. 2O2l:143:e72 management of adults with congenital heart disease: a report of the e227. I PMID: 33332lsol doi:10. I 161 /CIR.000000000000o923 American College of Cardiolog//American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2019:73:e81-e192. IPMID: 30121239] doi:10.1016/j.jacc.2018.08.1029 Item 73 Answer: B Educational Obiective: Treat iron deficiency in cyanotic congenital heart disease. The most appropriate management is a short course of Item 74 Answer: C Educational Objective: Treat ST elevation myocardial tr infarction with thrombolysis. iron therapy (Option B). This patient has patent ductus arteriosus related Eisenmenger syndrome and symptom- This patient u'ith an inf'erolateral S'l' elevation myocardial atic relative anemia. Most patients with cyanosis have com- inlarction (STEMI) is best mirnaged by thrombolysis folloned pensated erythrocytosis with stable hemoglobin levels. Iron by transfer to a pcrcutaneous coronilry intervenlion (l']Cl) deflciency and resultant microcytosis in these patients are center within 24 hours (Option C). 'lhrombolytic thcrapy often caused by inappropriate phlebotomy or blood loss, is recomnrended lirr patients with STEMI if symptom <lnset such as menorrhagia, as in this case. This patient's baseline is $,ithin 12 hours and primary PCI is r.rot available rt,ithin hemoglobin level was nearly 18 g/dl (180 g/L), and initial 120 minutes of first medical contact. If symptonrs began l2 to therapy should include oral iron therapy, which often causes 24 hours befbre presentatior.r and/or tl.rere is hemodynamic

The most appropriate management is a short course of Item 74 Answer: C Educational Objective: Treat ST elevation myocardial tr infarction with thrombolysis. iron therapy (Option B). This patient has patent ductus arteriosus related Eisenmenger syndrome and symptom- This patient u'ith an inf'erolateral S'l' elevation myocardial atic relative anemia. Most patients with cyanosis have com- inlarction (STEMI) is best mirnaged by thrombolysis folloned pensated erythrocytosis with stable hemoglobin levels. Iron by transfer to a pcrcutaneous coronilry intervenlion (l']Cl) deflciency and resultant microcytosis in these patients are center within 24 hours (Option C). 'lhrombolytic thcrapy often caused by inappropriate phlebotomy or blood loss, is recomnrended lirr patients with STEMI if symptom <lnset such as menorrhagia, as in this case. This patient's baseline is $,ithin 12 hours and primary PCI is r.rot available rt,ithin hemoglobin level was nearly 18 g/dl (180 g/L), and initial 120 minutes of first medical contact. If symptonrs began l2 to therapy should include oral iron therapy, which often causes 24 hours befbre presentatior.r and/or tl.rere is hemodynamic 193

t Answers and Critiques tr CONI, instability, significant myocardium at risk (such as rvith anterior MI). or ercessive bleeding risk. transler fbr printlry PCI (thc preferrecl strategn,) can bc consiclered. although aflects the patient's ability to continue to participate in ath- letics as well as the consideration of further testing and treat- ment. Structural adaptations of the left ventricle in response thrombolytic therirpy shoulcl be consiclered if timeil.transf'er to rigorous training include dilatation and increased wall (<120 minutes) is not arailiible. Thronrbolytic therapl,is n.rost thickness; these flndings do not necessarily indicate pathol effectirre u,ithin the flrst lJ to 6 hours irom syrnptom onset. ogr. In a study of elite athletes, left ventricular (LV) end ln additior-r to thrornboll,tic therapy. all patier.rts rtithout a diastolic diameters ranged from 38 to 66 mm in women (mean, specific contrainclication should recei\e a loacling dose of 48 mm) and from 43 to 70 mm in men (mean, 55 mm). aspirin as rtell as intravenous unfractionatecl heparin. error Markedly dilated LV chambers (>60 mm) were most common aparin. or fbndaparinux. Olopidogrcl loading (SOO mg oralty) in athletes with higher body mass and those participating has been demonstrated to increase rittes of vcssel patencl' in endurance sporls. Increased wall thickness is common, and is also recommended ir1 this setting. but wall thickness greater than 13 mm is uncommon in elite D This p:rtient has clear evidence of :rcute Sl'Fllvll. ancl ther athletes and should raise suspicion for possible underlying gt apeutic clelal,-fbr completion olC'f angiographl' (Option A) or pathologr. LV diastolic fllling in athletes is most often normal E other inraging nrodalities is not rvarranted. but may show enhanced passive LV fllling. Abnormal diastolic .D t thron.rbolytic therapy' is r,r,idely availablc and is a rc':r fllling patterns are more common in patients with pathologic A' sonable therapeutic choicc u-hen primary I'Cl is delal,ed conditions. LV ejection fraction is usually normal in athletes. EL b1, more than 120 minutes. '[hromboll,tic therapv has been Fabry disease (Option B) is associated with increased n showr.r to be most beneficial rvhen incorporatccl into a phar LV wall thickness. However, it is also associated with fatigue, macoinvlrsive trelrtment protocol at non-PCI centers. This burning dysesthesia in the extremities, and angiokeratoma, 4r E involves delivery'of thron.rboly'tic therapy earll' alter st'rnp- none of which is present in this patient. .D (^ tom onsct fbllowcd by transler to a l)CI capable hospit:rl fbr This patient has no history of hypertension, making elective angiography ancl re'vascularization. Early routine hypertensive heart disease (Option C) an unlikely cause of transfbr has shor,r,n benef it in allou'ing earl1, "rescue" PCI fbr load dependent hypertrophy. patierlts r,vho do not denlonslrate evidence o{ reperfusion or Although the patient has no family history of hyper sufl'er rcocclusion irnd reinfarction af ter delivery of throm- trophic cardiomyopathy (HCM), spontaneous genetic muta- bol)'tic therapl.l Thromboh,sis and adrnission to a telenretry tions may occur. This patient's flndings are consistent with bed (Option B) is not the most appropriate option. athlete heart, but il wall thickness were greater or if clinical Whcreas primary PCI delilered rvithin 12 htiurs of synrp concern remained high, a period of several months of decon tom ulset is associirted r'r'ith louer rates of deatl.t. reinf'arction. ditioning lollowed by re evaluation, or cardiac magnetic and blcecling tlran thrombollrtic therapy, delays in reperfusior-t resonance imaging with gadolinium, would be useful to limit this potential benefit firr patients unable to receive PCI differentiate betvveen athlete heart and nonobstructive HCM rvithir.r 'l20 minutes of first medical contact (Option D). Pri (Option D) or another condition. rnary I'}Cl rentains tl.re prelbrred stratcp5' urhen rcadill, ar,ailirble I(EY POIl{I (first nrcdical contirct to balloon time ol <90 minutes). Prinrlry PCI is also reconrmended fbr high risk patients rvith a late . Increased left ventricular (LV) wall thickness and LV cav- presentation or hernodl,narnic,'electrical instabilitli at the clis ity dilatation may be normal findings in highly trained cretion o1'providers assessing the perceived risk benefit rltio. athletes; s).irnmetric wall thickness of 13 mm or less and normal diastolic filling favor the diagnosis of athlete heart XEY POIIIT over the diagrosis of hypertrophic cardiomyopathy. . For patients with ST-elevation myocardial infarction, thrombolytic therapy is recommended if symptom Bibliography onset is within 12 hours and primary percutaneous Baggish AL. Wood MJ. Athlete's heart and cardiorascular care ofthe athlete: coronary intervention is not available within 120 min- scientitic and clinical update. Circulation. 2oll;123:2723 35. IPMID: 2767 0241 I doi:10.1 l 6l /cIRCULA IIONAHA. 110.981s71 utes of first medical contact.

tr CONI, instability, significant myocardium at risk (such as rvith anterior MI). or ercessive bleeding risk. transler fbr printlry PCI (thc preferrecl strategn,) can bc consiclered. although aflects the patient's ability to continue to participate in ath- letics as well as the consideration of further testing and treat- ment. Structural adaptations of the left ventricle in response thrombolytic therirpy shoulcl be consiclered if timeil.transf'er to rigorous training include dilatation and increased wall (<120 minutes) is not arailiible. Thronrbolytic therapl,is n.rost thickness; these flndings do not necessarily indicate pathol effectirre u,ithin the flrst lJ to 6 hours irom syrnptom onset. ogr. In a study of elite athletes, left ventricular (LV) end ln additior-r to thrornboll,tic therapy. all patier.rts rtithout a diastolic diameters ranged from 38 to 66 mm in women (mean, specific contrainclication should recei\e a loacling dose of 48 mm) and from 43 to 70 mm in men (mean, 55 mm). aspirin as rtell as intravenous unfractionatecl heparin. error Markedly dilated LV chambers (>60 mm) were most common aparin. or fbndaparinux. Olopidogrcl loading (SOO mg oralty) in athletes with higher body mass and those participating has been demonstrated to increase rittes of vcssel patencl' in endurance sporls. Increased wall thickness is common, and is also recommended ir1 this setting. but wall thickness greater than 13 mm is uncommon in elite D This p:rtient has clear evidence of :rcute Sl'Fllvll. ancl ther athletes and should raise suspicion for possible underlying gt apeutic clelal,-fbr completion olC'f angiographl' (Option A) or pathologr. LV diastolic fllling in athletes is most often normal E other inraging nrodalities is not rvarranted. but may show enhanced passive LV fllling. Abnormal diastolic .D t thron.rbolytic therapy' is r,r,idely availablc and is a rc':r fllling patterns are more common in patients with pathologic A' sonable therapeutic choicc u-hen primary I'Cl is delal,ed conditions. LV ejection fraction is usually normal in athletes. EL b1, more than 120 minutes. '[hromboll,tic therapv has been Fabry disease (Option B) is associated with increased n showr.r to be most beneficial rvhen incorporatccl into a phar LV wall thickness. However, it is also associated with fatigue, macoinvlrsive trelrtment protocol at non-PCI centers. This burning dysesthesia in the extremities, and angiokeratoma, 4r E involves delivery'of thron.rboly'tic therapy earll' alter st'rnp- none of which is present in this patient. .D (^ tom onsct fbllowcd by transler to a l)CI capable hospit:rl fbr This patient has no history of hypertension, making elective angiography ancl re'vascularization. Early routine hypertensive heart disease (Option C) an unlikely cause of transfbr has shor,r,n benef it in allou'ing earl1, "rescue" PCI fbr load dependent hypertrophy. patierlts r,vho do not denlonslrate evidence o{ reperfusion or Although the patient has no family history of hyper sufl'er rcocclusion irnd reinfarction af ter delivery of throm- trophic cardiomyopathy (HCM), spontaneous genetic muta- bol)'tic therapl.l Thromboh,sis and adrnission to a telenretry tions may occur. This patient's flndings are consistent with bed (Option B) is not the most appropriate option. athlete heart, but il wall thickness were greater or if clinical Whcreas primary PCI delilered rvithin 12 htiurs of synrp concern remained high, a period of several months of decon tom ulset is associirted r'r'ith louer rates of deatl.t. reinf'arction. ditioning lollowed by re evaluation, or cardiac magnetic and blcecling tlran thrombollrtic therapy, delays in reperfusior-t resonance imaging with gadolinium, would be useful to limit this potential benefit firr patients unable to receive PCI differentiate betvveen athlete heart and nonobstructive HCM rvithir.r 'l20 minutes of first medical contact (Option D). Pri (Option D) or another condition. rnary I'}Cl rentains tl.re prelbrred stratcp5' urhen rcadill, ar,ailirble I(EY POIl{I (first nrcdical contirct to balloon time ol <90 minutes). Prinrlry PCI is also reconrmended fbr high risk patients rvith a late . Increased left ventricular (LV) wall thickness and LV cav- presentation or hernodl,narnic,'electrical instabilitli at the clis ity dilatation may be normal findings in highly trained cretion o1'providers assessing the perceived risk benefit rltio. athletes; s).irnmetric wall thickness of 13 mm or less and normal diastolic filling favor the diagnosis of athlete heart XEY POIIIT over the diagrosis of hypertrophic cardiomyopathy. . For patients with ST-elevation myocardial infarction, thrombolytic therapy is recommended if symptom Bibliography onset is within 12 hours and primary percutaneous Baggish AL. Wood MJ. Athlete's heart and cardiorascular care ofthe athlete: coronary intervention is not available within 120 min- scientitic and clinical update. Circulation. 2oll;123:2723 35. IPMID: 2767 0241 I doi:10.1 l 6l /cIRCULA IIONAHA. 110.981s71 utes of first medical contact. Bibliography Item 76 Answer: C Anderson JL, Morrow DA. Acute myocardial infarction. N Engl J Med. 2017; 376:2053 64. [PMID: 28538121] doi:10.1056 NEJMral606915 Educational Objective: Diagnose radiation-associated coronary artery disease.

Bibliography Item 76 Answer: C Anderson JL, Morrow DA. Acute myocardial infarction. N Engl J Med. 2017; 376:2053 64. [PMID: 28538121] doi:10.1056 NEJMral606915 Educational Objective: Diagnose radiation-associated coronary artery disease. Item 75 Answer: A The most likely diagnosis is coronary artery disease (Option C). Although the patient has no typical risk factors for athero Educational Objective: Diagnose athlete heart. sclerosis, she underwent significant radiotherapy at an early The most likely diagnosis is athlete hearl (Option A). It is age that included the heart within the fleld. Cancer survivors important, and sometimes difficult, to distinguish normal who received such radiotherapy are at risk for the late devel- training-related adaptive changes of the heart from poten opment of cardiovascular complications, including pericar tially life-threatening pathologic processes. This distinction dial constriction, valvular heart disease, and coronary artery 194

Answers and Critiques disease. Stenosis is often ostial within the coronary arteries symptomatic heart failure who is receiving guideline- and may be more fibrous or fibrocalciflc than typical ather directed medical therapy. CRT is indicated in patients with oma. Anginal symptoms, especially in women, may not be an ejection fraction of, 35% or less, New York Heart Asso typical. Given the exertional nature of this patient's symp ciation (NYHA) functional class ll to lV symptoms despite toms and the lack of other features supporting a pericar guideline directed medical therapy, sinus rhythm, and dial or valvular underlying cause, a high index of suspicion Ieft bundle branch block (LBBB) with a QRS duration of should be maintained for ischemic disease. 150 ms or longer (class 1 recommendation). For patients Patients with signiflcant aortic or mitral valvular disease with LBBB and QRS duration of 120 to 149 ms, CRT can be may present with exertional dyspnea, but this patient's normal useful and should be considered (class 2a recommenda flndings on auscultation make the diagrosis of valr.ular heart tion). A recent echocardiogram shows that this patient's disease less likely. Severe aortic stenosis (Option A) is associated ejection fraction is still less than 35')(,, and his ECG shows with a late-peaking systolic murmur, a diminished or absent LBBB; therefore, it would be appropriate to place a biven aortic component of the Sr, and a delay in the carotid upstroke tricular pacemaker (which will improve ejection fraction) t (pulsus tardus). Mitral stenosis (Option D) produces a low o with a cardioverter deflbrillator. This therapy would give E frequency diastolic murmur heard best at the cardiac apex. him a survival benefit over continued medical therapy and Pericardial disease is a potential cardiac sequela ofradio improve his functional capacity. (J a therapy, but late constrictive pericarditis (Option B) generally Implantable cardioverler defibrillators (lCDs) (Option B) !, presents in an indolent fashion with symptoms of fatigue and have also been shown to provide a sun,ival benefit in patients E .E dyspnea limiting exertion. Jugular venous distention is usually with symptomatic heart failure and an ejection fraction less U! present, and the Kussmaul venous sign may be seen (no change than 35',1,. In contrast to CRT. ICDs have no eflect on either o or rise in jugular pressure with inspiration). An early diastolic ejection lraction or functional capacity. = U!

disease. Stenosis is often ostial within the coronary arteries symptomatic heart failure who is receiving guideline- and may be more fibrous or fibrocalciflc than typical ather directed medical therapy. CRT is indicated in patients with oma. Anginal symptoms, especially in women, may not be an ejection fraction of, 35% or less, New York Heart Asso typical. Given the exertional nature of this patient's symp ciation (NYHA) functional class ll to lV symptoms despite toms and the lack of other features supporting a pericar guideline directed medical therapy, sinus rhythm, and dial or valvular underlying cause, a high index of suspicion Ieft bundle branch block (LBBB) with a QRS duration of should be maintained for ischemic disease. 150 ms or longer (class 1 recommendation). For patients Patients with signiflcant aortic or mitral valvular disease with LBBB and QRS duration of 120 to 149 ms, CRT can be may present with exertional dyspnea, but this patient's normal useful and should be considered (class 2a recommenda flndings on auscultation make the diagrosis of valr.ular heart tion). A recent echocardiogram shows that this patient's disease less likely. Severe aortic stenosis (Option A) is associated ejection fraction is still less than 35')(,, and his ECG shows with a late-peaking systolic murmur, a diminished or absent LBBB; therefore, it would be appropriate to place a biven aortic component of the Sr, and a delay in the carotid upstroke tricular pacemaker (which will improve ejection fraction) t (pulsus tardus). Mitral stenosis (Option D) produces a low o with a cardioverter deflbrillator. This therapy would give E frequency diastolic murmur heard best at the cardiac apex. him a survival benefit over continued medical therapy and Pericardial disease is a potential cardiac sequela ofradio improve his functional capacity. (J a therapy, but late constrictive pericarditis (Option B) generally Implantable cardioverler defibrillators (lCDs) (Option B) !, presents in an indolent fashion with symptoms of fatigue and have also been shown to provide a sun,ival benefit in patients E .E dyspnea limiting exertion. Jugular venous distention is usually with symptomatic heart failure and an ejection fraction less U! present, and the Kussmaul venous sign may be seen (no change than 35',1,. In contrast to CRT. ICDs have no eflect on either o or rise in jugular pressure with inspiration). An early diastolic ejection lraction or functional capacity. = U! sound (pericardial knock) may be heard. Increased abdominal Implantabie pulmonary ar1ery presswe sensors (Option C) girth (ascites) may be present, and peripheral edema is com are placed in the distal pulmonary artery and are used mon. This patient's presentation is not compatible with the to remotely monitor pulmonary hemodynamics. In the diagnosis of constrictive pericarditis. CHAMPION trial. the use of these sensors was shown to Radiation also damages the microvasculature, caus reduce hearl failure hospitalizations in patients with NYHA ing endothelial dysfunction and ischemia that result in class III s),mptoms compared with patients in the control myocardial flbrosis, diastolic dysfunction. and restrictive arm. These monitors are often placed in patients who have physiology. Radiation induced cardiomyopathy presents frequer.rt hospitalizations to more closely monitor their heart similarly to primary restrictive cardiomyopathy (Option E), failure hemodynamics, but they have no efl'ect on ejection with symptoms ol dyspnea, peripheral edema, and exercise fractior.r. Despite significant ongoing symptoms, this patient intolerance. There is usually evidence of significant pulmct has not had frequent hospitalizations and would not be a nary hypertension (loud S, and eventually widely split 52), candidate fbr this device. and tricuspid and mitral valve regurgitation are commonly A randomized controiled trial showed that a wearable present. In this patient with a normal cardiac examination. cardioverter defibrillator (Option D) after acute myocar coronary artery disease is the most likely cause of exertional dial inlarction did not reduce the incidence of sudden dyspnea and burning throat pain. cardiac death but did reduce the secondary outcome of all cause mortality. There are no guideline recommenda I( EY PO I lII tions on the use of a wearable cardioverter.defibrillator o Cancer survivors who received chest radiotherapy are in patients with heart failure, but this device might be at risk for the late development of cardiovascular an option for patients at high risk for arrhythmias as a complications, including pericardial constriction, val bridge to ICD therapy. Unlike resynchronization therapy, vular heart disease, restrictive cardiomyopathy, and a wearable cardioverter defibrillator will not improve coronary artery disease. this patient's ejection fraction.

sound (pericardial knock) may be heard. Increased abdominal Implantabie pulmonary ar1ery presswe sensors (Option C) girth (ascites) may be present, and peripheral edema is com are placed in the distal pulmonary artery and are used mon. This patient's presentation is not compatible with the to remotely monitor pulmonary hemodynamics. In the diagnosis of constrictive pericarditis. CHAMPION trial. the use of these sensors was shown to Radiation also damages the microvasculature, caus reduce hearl failure hospitalizations in patients with NYHA ing endothelial dysfunction and ischemia that result in class III s),mptoms compared with patients in the control myocardial flbrosis, diastolic dysfunction. and restrictive arm. These monitors are often placed in patients who have physiology. Radiation induced cardiomyopathy presents frequer.rt hospitalizations to more closely monitor their heart similarly to primary restrictive cardiomyopathy (Option E), failure hemodynamics, but they have no efl'ect on ejection with symptoms ol dyspnea, peripheral edema, and exercise fractior.r. Despite significant ongoing symptoms, this patient intolerance. There is usually evidence of significant pulmct has not had frequent hospitalizations and would not be a nary hypertension (loud S, and eventually widely split 52), candidate fbr this device. and tricuspid and mitral valve regurgitation are commonly A randomized controiled trial showed that a wearable present. In this patient with a normal cardiac examination. cardioverter defibrillator (Option D) after acute myocar coronary artery disease is the most likely cause of exertional dial inlarction did not reduce the incidence of sudden dyspnea and burning throat pain. cardiac death but did reduce the secondary outcome of all cause mortality. There are no guideline recommenda I( EY PO I lII tions on the use of a wearable cardioverter.defibrillator o Cancer survivors who received chest radiotherapy are in patients with heart failure, but this device might be at risk for the late development of cardiovascular an option for patients at high risk for arrhythmias as a complications, including pericardial constriction, val bridge to ICD therapy. Unlike resynchronization therapy, vular heart disease, restrictive cardiomyopathy, and a wearable cardioverter defibrillator will not improve coronary artery disease. this patient's ejection fraction. Bibliography I(EY POIl{T Groarke JD, Nguyen PL, Nohria A, et ,1. Cardiovascular complications ol o Cardiac resynchronization therapy is indicated in ridiation therapy fi)r thoracic malignancies: the role tor non invlsive imilging for detection ofcardiovascular disease. Eur I Ieart J. 2014i35:612 patients with New York Heart Association functional 23. IPMID: 23666251] doi:10.109i1 eurhearti,'eht11.l class II to IV symptoms despite guideline-directed medical therapy who have an ejection fraction of 35'1, or less, sinus rhythm, and left bundle branch block llem77 Answer: A with a QRS duration of 150 ms or longer. Educational Objective: Treat heart failure with a cardiac resynchronization therapy defibrillator. Bibliography Henin M. Ragr I [, Mannion J, et al. Indications ofcardiac resynchronization A cardiac resynchronization therapy (CRI') deflbrillator in non left bundle branch block: clinical review of available evidence. (Option A) is indicated in this patient with relatively new onset Cardiol Res. 2020;ll:l 8. [PMlDr 32095190] doi:10.1,1740/cr989

Bibliography I(EY POIl{T Groarke JD, Nguyen PL, Nohria A, et ,1. Cardiovascular complications ol o Cardiac resynchronization therapy is indicated in ridiation therapy fi)r thoracic malignancies: the role tor non invlsive imilging for detection ofcardiovascular disease. Eur I Ieart J. 2014i35:612 patients with New York Heart Association functional 23. IPMID: 23666251] doi:10.109i1 eurhearti,'eht11.l class II to IV symptoms despite guideline-directed medical therapy who have an ejection fraction of 35'1, or less, sinus rhythm, and left bundle branch block llem77 Answer: A with a QRS duration of 150 ms or longer. Educational Objective: Treat heart failure with a cardiac resynchronization therapy defibrillator. Bibliography Henin M. Ragr I [, Mannion J, et al. Indications ofcardiac resynchronization A cardiac resynchronization therapy (CRI') deflbrillator in non left bundle branch block: clinical review of available evidence. (Option A) is indicated in this patient with relatively new onset Cardiol Res. 2020;ll:l 8. [PMlDr 32095190] doi:10.1,1740/cr989 195

Answers and Critiques Item 78 Item 79 Answer: B tr Answer: B Educational Objective: Treat aortic dissection with Educational Objective: Treat a patient with diabetes emergent surgery. mellitus and atherosclerotic cardiovascular disease with a glucagon-like peptide I receptor agonist. The most appropriate next stcp in managenlent is emer gent surgery (Option B), inclucling surgical aortic dissec The most appropriate additional treatment is liraglutide tion repair and aortic valve replacement. Causes of acute (Option B). The 2021 Standards of Medical Care in Diabe- aortic regurgitation it.tclude er.rdocarditis. blunt trauma tes from the American Diabetes Association, endorsed by to the chest. iatrogenic causes (such as cornplicatiot.ts the American College of Cardiologr, recommends either a of balloon aortic valvuloplastl'). and aortic dissection. sodium-glucose cotransporter 2 (SGLT2) inhibitor or a Patients with acute aortic dissection rt,ithout evidence glucagon-like peptide 1 (GLP-1) receptor agonist in patients of cardiogcnic sl-rock or acutc aortic regurgitation sl-rould with type 2 diabetes mellitus who have established atheroscle be treated rt,ith medicaI tl.rcrapy'to control heart rate and rotic cardiovascular disease, as part ofcomprehensive cardio- vt reduce blood pressure. Current guidelines recommend vascular risk reduction and/or the glucose lowering regimen. E (D reducing systolic blood pressure to 120 mnt IIg or less In this population, both drugs are associated with reduced IA in the lirst hour in patier.rts r,r,ith aortic clisscctior.r. Pain rates ofadverse cardiovascular events, including stroke, myo o, control is oflen necessary and is best accornplished cardial infarction, and cardiovascular death. In this patient "t'ith with obesity, the GLP 1 receptor agonist liraglutide may be EL intravenous opioids. Acute aortic regurgilation due to -r aortic dissection is a surgical emergency and is espe preferred to an SGUI2 inhibitor because it is associated with cially urgent in the prescnce of hvpotension. pulmonarl' weight loss. Furthermore, the hypoglycemic effect of SGLI2 E edema. or cardiogenic shock: it generalll' requires aortic inhibitors is diminished if the estimated glomerular flltration .D UT valve repair or replacement, even for moclcrate aortic rate is less than 45 ml/min/1.73 m2, as it is in this patient. regurgitdtion. Long-term treatment with dual antiplatelet therapy, Cardiac magnetic resonance imagir.rg (Option A) may such as aspirin and clopidogrel (Option A), should be con be used k) quantitate tl.re degree of aortic regllrgitation sidered for patients with prior coronary intervention, high and to diagnose aortic dissection: hou'evcr, in tl.ris case, ischemic risk, and low bleeding risk to prevent major adverse further quantitation of aurtic regurgitation ancl diagnosis cardiovascular events. However, this patient is already taking ofaortic dissection are unnecessarl,becanse the CT angio- rivaroxaban and aspirin. Combination therapy with aspirin grarn and echocardiogram have already established type plus low-dose rivaroxaban should be considered in patients A dissection rt"ith involvement of the aortic valve (aortic with stable coronary and/or peripheral artery disease and regurgitation). low bleeding risk to prevent major adverse limb and cardio Intra aortic balloon counterpulsation (Option C) is vascular events. The addition of clopidogrel to this regimen contraindic:lted in patients \\,ith acute severe iiortic regur- (triple antithrombotic therapy) is generally avoided because gitation because inflation of the balloor-r in cliastole r.r'ould of the increased risk for bleeding. worsen thc rcgurgitation severil). Statin plus niacin (Option C) combination therapy has 'l'ransesophageal echocardiography ('ltiD) (Option D) not been shown to provide additional cardiovascular beneflt also may be used to qualitatively and quantitatively evaluate above statin therapy alone, may increase side effects, and is aortic regurgitation. but in cases of native valvc iiortic regur generally not recommended. gitation. it typically does not provide additional inforntation Pramlintide (Option D), an injectable agent used to beyoncl that provided by transthoracic echocardiographl: treat diabetes, is an amylin mimetic that slows gastric emp TEE r,toulcl be usef'ul if CT lr.rgiography lr,erc unavailable. In tying, suppresses glucagon secretion, and increases satiety. that case, 'l'Flti could providc inlormation on both the aortic It is associated with weight loss but has no known effects on valve and the ascending aorta. 'lEE is also useful in intraop the incidence of cardiovascular events, including myocardial eratirre assessment of aortic valr,e function befbrc and after infarction, stroke, or cardiovascular death, and would not be the surgical intenention. the best choice for this high risk patient.

Item 78 Item 79 Answer: B tr Answer: B Educational Objective: Treat aortic dissection with Educational Objective: Treat a patient with diabetes emergent surgery. mellitus and atherosclerotic cardiovascular disease with a glucagon-like peptide I receptor agonist. The most appropriate next stcp in managenlent is emer gent surgery (Option B), inclucling surgical aortic dissec The most appropriate additional treatment is liraglutide tion repair and aortic valve replacement. Causes of acute (Option B). The 2021 Standards of Medical Care in Diabe- aortic regurgitation it.tclude er.rdocarditis. blunt trauma tes from the American Diabetes Association, endorsed by to the chest. iatrogenic causes (such as cornplicatiot.ts the American College of Cardiologr, recommends either a of balloon aortic valvuloplastl'). and aortic dissection. sodium-glucose cotransporter 2 (SGLT2) inhibitor or a Patients with acute aortic dissection rt,ithout evidence glucagon-like peptide 1 (GLP-1) receptor agonist in patients of cardiogcnic sl-rock or acutc aortic regurgitation sl-rould with type 2 diabetes mellitus who have established atheroscle be treated rt,ith medicaI tl.rcrapy'to control heart rate and rotic cardiovascular disease, as part ofcomprehensive cardio- vt reduce blood pressure. Current guidelines recommend vascular risk reduction and/or the glucose lowering regimen. E (D reducing systolic blood pressure to 120 mnt IIg or less In this population, both drugs are associated with reduced IA in the lirst hour in patier.rts r,r,ith aortic clisscctior.r. Pain rates ofadverse cardiovascular events, including stroke, myo o, control is oflen necessary and is best accornplished cardial infarction, and cardiovascular death. In this patient "t'ith with obesity, the GLP 1 receptor agonist liraglutide may be EL intravenous opioids. Acute aortic regurgilation due to -r aortic dissection is a surgical emergency and is espe preferred to an SGUI2 inhibitor because it is associated with cially urgent in the prescnce of hvpotension. pulmonarl' weight loss. Furthermore, the hypoglycemic effect of SGLI2 E edema. or cardiogenic shock: it generalll' requires aortic inhibitors is diminished if the estimated glomerular flltration .D UT valve repair or replacement, even for moclcrate aortic rate is less than 45 ml/min/1.73 m2, as it is in this patient. regurgitdtion. Long-term treatment with dual antiplatelet therapy, Cardiac magnetic resonance imagir.rg (Option A) may such as aspirin and clopidogrel (Option A), should be con be used k) quantitate tl.re degree of aortic regllrgitation sidered for patients with prior coronary intervention, high and to diagnose aortic dissection: hou'evcr, in tl.ris case, ischemic risk, and low bleeding risk to prevent major adverse further quantitation of aurtic regurgitation ancl diagnosis cardiovascular events. However, this patient is already taking ofaortic dissection are unnecessarl,becanse the CT angio- rivaroxaban and aspirin. Combination therapy with aspirin grarn and echocardiogram have already established type plus low-dose rivaroxaban should be considered in patients A dissection rt"ith involvement of the aortic valve (aortic with stable coronary and/or peripheral artery disease and regurgitation). low bleeding risk to prevent major adverse limb and cardio Intra aortic balloon counterpulsation (Option C) is vascular events. The addition of clopidogrel to this regimen contraindic:lted in patients \\,ith acute severe iiortic regur- (triple antithrombotic therapy) is generally avoided because gitation because inflation of the balloor-r in cliastole r.r'ould of the increased risk for bleeding. worsen thc rcgurgitation severil). Statin plus niacin (Option C) combination therapy has 'l'ransesophageal echocardiography ('ltiD) (Option D) not been shown to provide additional cardiovascular beneflt also may be used to qualitatively and quantitatively evaluate above statin therapy alone, may increase side effects, and is aortic regurgitation. but in cases of native valvc iiortic regur generally not recommended. gitation. it typically does not provide additional inforntation Pramlintide (Option D), an injectable agent used to beyoncl that provided by transthoracic echocardiographl: treat diabetes, is an amylin mimetic that slows gastric emp TEE r,toulcl be usef'ul if CT lr.rgiography lr,erc unavailable. In tying, suppresses glucagon secretion, and increases satiety. that case, 'l'Flti could providc inlormation on both the aortic It is associated with weight loss but has no known effects on valve and the ascending aorta. 'lEE is also useful in intraop the incidence of cardiovascular events, including myocardial eratirre assessment of aortic valr,e function befbrc and after infarction, stroke, or cardiovascular death, and would not be the surgical intenention. the best choice for this high risk patient. rEY POIXT rtY P0ttT o In patients with type 2 diabetes mellitus, sodium- . In patients with acute aortic regurgitation due to aortic glucose cotransporter 2 inhibitors and glucagon-like dissection, emergent surgery including aortic valve peptide 1 receptor agonists are associated with reduced replacement or repair and aortic dissection repair, is rates of adverse cardiovascular events, including stroke, indicated. myocardial infarction, and cardiovascular death, com- pared with placebo. Bibliography Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with vahular heart disease: a report of the Bibliography American College of Cardiolos//American Heart Association Joint American Diabetes Association. 10. Cardiovascular disease and risk man Committee on Clinical Practice Guidelines. Circulation. 2O2t;743:e72- agement: standards of medical care in diabetes-2o2l. Diabetes Care. e227. IPMID: 33332150] doi:1O.1161/CIR.O0OO00OOOOOO0923 2O21;44:5125 S150. IPMID: 33298421) doi:10.2337ldc21-S01O

rEY POIXT rtY P0ttT o In patients with type 2 diabetes mellitus, sodium- . In patients with acute aortic regurgitation due to aortic glucose cotransporter 2 inhibitors and glucagon-like dissection, emergent surgery including aortic valve peptide 1 receptor agonists are associated with reduced replacement or repair and aortic dissection repair, is rates of adverse cardiovascular events, including stroke, indicated. myocardial infarction, and cardiovascular death, com- pared with placebo. Bibliography Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with vahular heart disease: a report of the Bibliography American College of Cardiolos//American Heart Association Joint American Diabetes Association. 10. Cardiovascular disease and risk man Committee on Clinical Practice Guidelines. Circulation. 2O2t;743:e72- agement: standards of medical care in diabetes-2o2l. Diabetes Care. e227. IPMID: 33332150] doi:1O.1161/CIR.O0OO00OOOOOO0923 2O21;44:5125 S150. IPMID: 33298421) doi:10.2337ldc21-S01O ) 196

Answers and Critiques tr Item 80 Answer: D Educational Objective: 'l'reat left atrial myxoma. Item 81 Answer: C Educational Objective: Treat a symptomatic patient tr 'ilre most appropriilte managcnlent with transient heart block following an inferior myocardial is rlrgent sr_rrgical exci sion (Option D). 'lhis paticnt's ecl.rocirrcliograrn demor.r infarction. strates a large left atrial ntass consistcnt r,r,ith ntyxonra, 'l he most appropriate trcatment tbr this patient is temporary with attachment by a stalk to the intcratrial scptum. t,elt pacing (Option C). Gtnduction al)normalitics are cornntonly rtrial myxon-ras tnost cornntonly occur in rniddle agcd idcntified in the settillg ol acute rnyocardial infarction (Ml) and persolls and are more frc'clucnt in uonlen. 'll-rcy ntay prc irrc marutgccl on the basis of'the type oi block and the location scnt rvitl.r valvular occlusivc symptolls, such as dyspnct ot nryocardial injury Symptomatic patients with inferior MI and t irnd syncope, or with ernbolic phenomena, including transic'nt heirft block rnty be trcated lr,ith tcr.nporury, pacing stroke or transient ischentic events. Atrial myxomas ntily beciluse concluction block in this setting, including Mobitz t),pe produce cytclkines that result in constitutional symptortrs. 1 irncl complcte hearl block, is causcd by high vagal tone affect vt I such as fever. anorexia, ancl weight loss, which are pre iug the atrioventricular (AV) node. is genemlly transient, and is a, I sent in up to one third of patients. Central ner\ous systcltl accompanic'cl b1'an adcquate escapc rhlthrn. Whereas tentpo ET \ embolic cvents shoulcl herald urgent cirrdiac sirrgical eval r-irry pacing support may occasionally be neccssary pcrmirnent Llation xnd excision in paticnts with acceptaltle surgical pacing (Option D) is rarely indicatect. Vagally mediatcd hearl U L t risk. Because of' the possibility of' recurrence. l<tr.rgitudinal block occur-ring at the AV node ntust be distinguishecl fiom the (E screening \^,ith echocardiogrrrphy is appropriate. less In-rigr and potentially lethal Mobiz type 2 seconci degree rr! Anticoagulation with a direct rtral anticoagulant AV block, which occurs more fieclnently in the settir.rg of'ex1en. o, (Option A) or vitan.rin K ar.rtagonist would be appropriatc sire anterior M I and danrage to the c<tnduction system bclow the t! = g fbr prevcntion or treatment of thrombus of thc lcft atriultl AV nocle. Ahhough Mobitz tlpe 1 bl<rck occurs at the AV node ar-rd or lell atrial appendage. I lowever, the rounded nature is iclcntified by cyclical. repetitive prolongatirin of the PR ir.rterval of this nrass and attachment [o the interatrial septulx is Ieacting to a "dropped beat" ancl a regularly irregular rlrythm. ry'pical firr mvxor.na. Lelt atrial or left atrill appendage Mubitz tlpe 2 btock is typified by block conduction r,vithout thrombus would be more likely ir.r pltients with under associated PR prolongation and nray preclispose to extendecl lying atrial fibrillation, mitral stenosis, or :r mitral valvc periods of asysklle, requiring permanent pacemaker support. prosthesis with abnormal lur.rction. none of rvhich is pre Atropine (Option A) may ir.npr<)ve AV noclalconduction ancl scnt in this patient. incrcase the sinus rate througl-r vagolytic activity. Hove\er, it pro 'lhcrc is no indicati<ln fbr thrornbolytic therapy vicles only lcrxporary benefit and is neither necessary nor sufti- (Option B) in this patient r,r,hose neurologic svmptoms cient as treatnrent for asymptomatic heart bkrck in this setting. clemonstrated complete and rapid resolution, and thc Although unfiactior.rated heparin (Option B) and other administration of'thrombolytic therapy ir-r such a patielrt intravenous antithronlbin therapy would bc indicated in the n.ray be harmful. presence of' thrombotic con-rplications or atrial librillation, Bloocl cultures and erxpiric antibiotic therapy (Option C) it is not irrdicated roLltinely after successtul primary percu \'voulcl bc considcrcd fbr suspectecl infective endocardi tancous coronary inlervention rir lor treatment of irregular tis. Fkrwever, lhis prtient's mass docs not appear to be rhytl.rms associated with heart block. However. dual anti clirectll, iissociatecl with thc valve in its attachrnent. and it platelet thcrapy is indicated. nould be unusually large fbr a vegetition. In adclitiot-t. this KEY POITT tl:rtient has no ur.rclcrtying risk factors lilr enciocarditis rtrd hirs not undergone a recent procedure likely to etrgender . Symptomatic patients with transient heart block, I including Mobitz type t heart block and complete bacterenr ia. heart block, after inferior myocardial infarction may i XEY POTIITS be treated with temporary pacing. :

tr Item 80 Answer: D Educational Objective: 'l'reat left atrial myxoma. Item 81 Answer: C Educational Objective: Treat a symptomatic patient tr 'ilre most appropriilte managcnlent with transient heart block following an inferior myocardial is rlrgent sr_rrgical exci sion (Option D). 'lhis paticnt's ecl.rocirrcliograrn demor.r infarction. strates a large left atrial ntass consistcnt r,r,ith ntyxonra, 'l he most appropriate trcatment tbr this patient is temporary with attachment by a stalk to the intcratrial scptum. t,elt pacing (Option C). Gtnduction al)normalitics are cornntonly rtrial myxon-ras tnost cornntonly occur in rniddle agcd idcntified in the settillg ol acute rnyocardial infarction (Ml) and persolls and are more frc'clucnt in uonlen. 'll-rcy ntay prc irrc marutgccl on the basis of'the type oi block and the location scnt rvitl.r valvular occlusivc symptolls, such as dyspnct ot nryocardial injury Symptomatic patients with inferior MI and t irnd syncope, or with ernbolic phenomena, including transic'nt heirft block rnty be trcated lr,ith tcr.nporury, pacing stroke or transient ischentic events. Atrial myxomas ntily beciluse concluction block in this setting, including Mobitz t),pe produce cytclkines that result in constitutional symptortrs. 1 irncl complcte hearl block, is causcd by high vagal tone affect vt I such as fever. anorexia, ancl weight loss, which are pre iug the atrioventricular (AV) node. is genemlly transient, and is a, I sent in up to one third of patients. Central ner\ous systcltl accompanic'cl b1'an adcquate escapc rhlthrn. Whereas tentpo ET \ embolic cvents shoulcl herald urgent cirrdiac sirrgical eval r-irry pacing support may occasionally be neccssary pcrmirnent Llation xnd excision in paticnts with acceptaltle surgical pacing (Option D) is rarely indicatect. Vagally mediatcd hearl U L t risk. Because of' the possibility of' recurrence. l<tr.rgitudinal block occur-ring at the AV node ntust be distinguishecl fiom the (E screening \^,ith echocardiogrrrphy is appropriate. less In-rigr and potentially lethal Mobiz type 2 seconci degree rr! Anticoagulation with a direct rtral anticoagulant AV block, which occurs more fieclnently in the settir.rg of'ex1en. o, (Option A) or vitan.rin K ar.rtagonist would be appropriatc sire anterior M I and danrage to the c<tnduction system bclow the t! = g fbr prevcntion or treatment of thrombus of thc lcft atriultl AV nocle. Ahhough Mobitz tlpe 1 bl<rck occurs at the AV node ar-rd or lell atrial appendage. I lowever, the rounded nature is iclcntified by cyclical. repetitive prolongatirin of the PR ir.rterval of this nrass and attachment [o the interatrial septulx is Ieacting to a "dropped beat" ancl a regularly irregular rlrythm. ry'pical firr mvxor.na. Lelt atrial or left atrill appendage Mubitz tlpe 2 btock is typified by block conduction r,vithout thrombus would be more likely ir.r pltients with under associated PR prolongation and nray preclispose to extendecl lying atrial fibrillation, mitral stenosis, or :r mitral valvc periods of asysklle, requiring permanent pacemaker support. prosthesis with abnormal lur.rction. none of rvhich is pre Atropine (Option A) may ir.npr<)ve AV noclalconduction ancl scnt in this patient. incrcase the sinus rate througl-r vagolytic activity. Hove\er, it pro 'lhcrc is no indicati<ln fbr thrornbolytic therapy vicles only lcrxporary benefit and is neither necessary nor sufti- (Option B) in this patient r,r,hose neurologic svmptoms cient as treatnrent for asymptomatic heart bkrck in this setting. clemonstrated complete and rapid resolution, and thc Although unfiactior.rated heparin (Option B) and other administration of'thrombolytic therapy ir-r such a patielrt intravenous antithronlbin therapy would bc indicated in the n.ray be harmful. presence of' thrombotic con-rplications or atrial librillation, Bloocl cultures and erxpiric antibiotic therapy (Option C) it is not irrdicated roLltinely after successtul primary percu \'voulcl bc considcrcd fbr suspectecl infective endocardi tancous coronary inlervention rir lor treatment of irregular tis. Fkrwever, lhis prtient's mass docs not appear to be rhytl.rms associated with heart block. However. dual anti clirectll, iissociatecl with thc valve in its attachrnent. and it platelet thcrapy is indicated. nould be unusually large fbr a vegetition. In adclitiot-t. this KEY POITT tl:rtient has no ur.rclcrtying risk factors lilr enciocarditis rtrd hirs not undergone a recent procedure likely to etrgender . Symptomatic patients with transient heart block, I including Mobitz type t heart block and complete bacterenr ia. heart block, after inferior myocardial infarction may i XEY POTIITS be treated with temporary pacing. : i . Patients with a myxoma may present with valvular I occlusive symptoms, such as dyspnea and syncope; Bibliography embolic phenomena, including stroke or transient O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST elevation myocardial infarction: a report of the I ischemic events; and/or constitutional symptoms, American College of Cardiolory Foundation/American Heart Association I such as fever, anorexia, and weight loss. Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;61:e78 e14o. \ . In patients with atrial myxoma and a central nervous IPMID: 232569141 doi:10.1016/j.jacc.2012.11.019 I

i . Patients with a myxoma may present with valvular I occlusive symptoms, such as dyspnea and syncope; Bibliography embolic phenomena, including stroke or transient O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST elevation myocardial infarction: a report of the I ischemic events; and/or constitutional symptoms, American College of Cardiolory Foundation/American Heart Association I such as fever, anorexia, and weight loss. Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;61:e78 e14o. \ . In patients with atrial myxoma and a central nervous IPMID: 232569141 doi:10.1016/j.jacc.2012.11.019 I I 5 system embolic event, urgent cardiac surgical evalua- l tion and excision are indicated. Itenn 82 Answer: A I Educational Objective: Diagnose heart failure with t preserved ejection fraction. Bibliography Wang Z, Chen S, Zhu M, et al. Risk prediction fbr emboli and recurrence of I t primary cardiac m,r(omas after resection. J Cardiothorac Surg. 2016ill: The most likely diagnosis is heart failure with preserved ejec- i 22. [PMID: 268328O6] doi:10.1186/s13019 016 O42O-4 tion fraction (HFpEF) (Option A). The diagnosis of HFpEF I 197 \ I

Answers and Critiques should be suspected in patients who meet the following Item 83 Answer: D three criteria: symptoms of heart failure, left ventricular Educational Objective: Prevent stroke in a patient with (LV) ejection fraction of50'/, or greatet and no other appar incidentally diagnosed atrial fibrillation. ent cause of heart failure symptoms. I{FpEF accounts tbr : approximately half of heart failure cases. Classic symptoms The most appropriate management is to initiate oral antico- include exertional dyspnea, paroxysmal nocturnal dyspnea, agulation (Option D). This patient likely has persistent, and I and orthopnea. Physical flndings in heart failure. such as:rn possibly symptomatic, atrial fibrillation (AF). AF is usually S.,, elevated central venous pressure, crackles. and peripheral the result of long standing risk factors, such as diabetes mel edema. are highly speciflc but insensitive, and their absence litus, obesity. hypertension, coronary artery disease, heart .} does not exclude heart failure. Natriuretic peptide levels failure, and obstructive sleep apnea. In stable patients with may be normal in patients with heart failure. particularly AF, the primary goals of therapy are to (1) prevent stroke. in those with obesity or only exertional symptoms. Echo (2) control heart rate, (3) minimize or eliminate symptoms,

approximately half of heart failure cases. Classic symptoms The most appropriate management is to initiate oral antico- include exertional dyspnea, paroxysmal nocturnal dyspnea, agulation (Option D). This patient likely has persistent, and I and orthopnea. Physical flndings in heart failure. such as:rn possibly symptomatic, atrial fibrillation (AF). AF is usually S.,, elevated central venous pressure, crackles. and peripheral the result of long standing risk factors, such as diabetes mel edema. are highly speciflc but insensitive, and their absence litus, obesity. hypertension, coronary artery disease, heart .} does not exclude heart failure. Natriuretic peptide levels failure, and obstructive sleep apnea. In stable patients with may be normal in patients with heart failure. particularly AF, the primary goals of therapy are to (1) prevent stroke. in those with obesity or only exertional symptoms. Echo (2) control heart rate, (3) minimize or eliminate symptoms, D cardiographic features of HFpEF include normal LV cavity and (4) modify underlying risk factors. The 2019 American u) size, increased LV wall thickness, left atrial enlargement. College of Cardiologr/American Heart Association/Heart abnormal diastolic function. and elevated pulmonary artery Rhythm Society focused update on AF recommends antico { = .D UI systolic pressure (>35 mm Hg). agulation to prevent stroke in patients with nonvalvular AF q, who have a CHATDST-VASc score of 2 or greater in men or 3 High output heart failure (Option B) is characterized by CL symptoms of heart failure in the setting of a cardiac index or greater in women. In this patient with a CHATDS, VASc n .

D cardiographic features of HFpEF include normal LV cavity and (4) modify underlying risk factors. The 2019 American u) size, increased LV wall thickness, left atrial enlargement. College of Cardiologr/American Heart Association/Heart abnormal diastolic function. and elevated pulmonary artery Rhythm Society focused update on AF recommends antico { = .D UI systolic pressure (>35 mm Hg). agulation to prevent stroke in patients with nonvalvular AF q, who have a CHATDST-VASc score of 2 or greater in men or 3 High output heart failure (Option B) is characterized by CL symptoms of heart failure in the setting of a cardiac index or greater in women. In this patient with a CHATDS, VASc n . greater than 4 L/min/m2. Causes include obesity, anemia, score of 4 (age >75 years [2 pointsl, female [1 pointl, hyper- 1 i hyperthyroidism, Paget disease of bone, thiamine deficiency, tension [f pointl), consideration oforal anticoagulation for ll i and arteriovenous fistula. The patient's normal cardiac index stroke prevention is warranted. Aspirin alone (Option A) is i .D U! rules out this diagnosis. insufflcient for stroke prevention in this patient at high risk t Hypertrophic obstructive cardiomyopathy (Option C) for stroke. may cause dyspnea; however, a systolic murmur would In addition, given this patient's exertional limitation, 'a

greater than 4 L/min/m2. Causes include obesity, anemia, score of 4 (age >75 years [2 pointsl, female [1 pointl, hyper- 1 i hyperthyroidism, Paget disease of bone, thiamine deficiency, tension [f pointl), consideration oforal anticoagulation for ll i and arteriovenous fistula. The patient's normal cardiac index stroke prevention is warranted. Aspirin alone (Option A) is i .D U! rules out this diagnosis. insufflcient for stroke prevention in this patient at high risk t Hypertrophic obstructive cardiomyopathy (Option C) for stroke. may cause dyspnea; however, a systolic murmur would In addition, given this patient's exertional limitation, 'a be present on examination, and the echocardiogran.r her AF may be symptomatic, and rhythm control, with l would demonstrate resting or provoked outllow tract appropriate stroke prevention, should be considered as a obstruction. means of improving her fatigue. Lastly, her loud snoring may -l

be present on examination, and the echocardiogran.r her AF may be symptomatic, and rhythm control, with l would demonstrate resting or provoked outllow tract appropriate stroke prevention, should be considered as a obstruction. means of improving her fatigue. Lastly, her loud snoring may -l The patient's t.V hypertrophy and elevated right suggest underlying obstructive sleep apnea, which may be ventricular systolic pressure make noncardiac dyspnea driving the AF, and she should be asked about symptoms of (Option D) less likely. Predictive scores can exclude non excessive daytime sleepiness. cardiac causes of' dyspnea with a high degree of reli This patient does not require emergent cardioversion ability. The Heart Failure Preserved Ejection Fraction (Option B), as she is not hemodynamically unstable, has a (HrFpEF) risk score, which relies on simple clinical and well controlled heart rate, and has no signs of heart failure. echocardiographic characteristics, is a means to assess Increasing the metoprolol dosage (Option C) is not indi the likelihood of HFpEF and is used to discriminate cated in this patient with a well-controlled heart rate and cardiac versus noncardiac causes of dyspnea. Predictive normal blood pressure. Increasing the metoprolol dosage variables include obesity (2 points), atrial fibrillation also may worsen her flatigue. (3 points), age older than 60 years (l point), treatment Reassurance (Option E) is not appropriate management with at least two antihypertensive drugs (1 point), echo because this patient's stroke risk, possible symptoms of AF, cardiographic E/e' ratio greater than 9 (1 point), and and possible sleep apnea should be addressed. echocardiographic pulmonary artery systolic pressure rEY POIilIS greater than 35 mm Hg (1 point). This patient's HTFpEF o In stable patients with atrial fibrillation, the primary risk score is B, suggesting that her dyspnea has a cardiac cause and that further diagnostic evaluation of dyspnea goals oftherapy are to (1) prevent stroke, (2) control is unnecessary. heart rate, (3) minimize or eliminate symptoms, and (4) modify underlying risk factors. f,tY POIilT . Anticoagulation is indicated for stroke prevention in o Heart failure with preserved ejection fraction should patients with nonvalvular atrial fibrillation who have be suspected in patients who meet the following three a CHATDST-VASc score of 2 or greater in men or 3 or criteria: symptoms of heart failure, left ventricular greater in women. ejection fraction of 50'7, or greater, and no other apparent cause of heart failure symptoms. Bibliography January CT. \Urnn LS. Calkins H. et al. 2019 AHr\ A(-(l I IRS focused r-rpdate Bibliography ol the 201.1 AIIi\ ACC IIRS guideline ti)r the nttnagement ol patients Rcddy YN\,i Crrter RI.l. Obokata M, et al. A sinrple. o,idcnce basecl with atrial fibrillation: a report ol tlte American College of Oanliologl approach to help guide diagnosis of heart fai lurc with presrnr'ed eject iotl American Heart Association Task Rrrce on Clinical Practice Guidelines fraction. Circulation. 2018;138:u6t 70. IPMll): 297g22gql doi:lO.l t(>1,' rnd the Ilcart Rhytlrm Society. J Ant Coll (lardiol.2019;71:104 132. ClRCUI.r\TIONAHA. I t8.03,16.16 I PMID: 30703 13ll doi:10. l0l6 j.jacc.2019.01.011

The patient's t.V hypertrophy and elevated right suggest underlying obstructive sleep apnea, which may be ventricular systolic pressure make noncardiac dyspnea driving the AF, and she should be asked about symptoms of (Option D) less likely. Predictive scores can exclude non excessive daytime sleepiness. cardiac causes of' dyspnea with a high degree of reli This patient does not require emergent cardioversion ability. The Heart Failure Preserved Ejection Fraction (Option B), as she is not hemodynamically unstable, has a (HrFpEF) risk score, which relies on simple clinical and well controlled heart rate, and has no signs of heart failure. echocardiographic characteristics, is a means to assess Increasing the metoprolol dosage (Option C) is not indi the likelihood of HFpEF and is used to discriminate cated in this patient with a well-controlled heart rate and cardiac versus noncardiac causes of dyspnea. Predictive normal blood pressure. Increasing the metoprolol dosage variables include obesity (2 points), atrial fibrillation also may worsen her flatigue. (3 points), age older than 60 years (l point), treatment Reassurance (Option E) is not appropriate management with at least two antihypertensive drugs (1 point), echo because this patient's stroke risk, possible symptoms of AF, cardiographic E/e' ratio greater than 9 (1 point), and and possible sleep apnea should be addressed. echocardiographic pulmonary artery systolic pressure rEY POIilIS greater than 35 mm Hg (1 point). This patient's HTFpEF o In stable patients with atrial fibrillation, the primary risk score is B, suggesting that her dyspnea has a cardiac cause and that further diagnostic evaluation of dyspnea goals oftherapy are to (1) prevent stroke, (2) control is unnecessary. heart rate, (3) minimize or eliminate symptoms, and (4) modify underlying risk factors. f,tY POIilT . Anticoagulation is indicated for stroke prevention in o Heart failure with preserved ejection fraction should patients with nonvalvular atrial fibrillation who have be suspected in patients who meet the following three a CHATDST-VASc score of 2 or greater in men or 3 or criteria: symptoms of heart failure, left ventricular greater in women. ejection fraction of 50'7, or greater, and no other apparent cause of heart failure symptoms. Bibliography January CT. \Urnn LS. Calkins H. et al. 2019 AHr\ A(-(l I IRS focused r-rpdate Bibliography ol the 201.1 AIIi\ ACC IIRS guideline ti)r the nttnagement ol patients Rcddy YN\,i Crrter RI.l. Obokata M, et al. A sinrple. o,idcnce basecl with atrial fibrillation: a report ol tlte American College of Oanliologl approach to help guide diagnosis of heart fai lurc with presrnr'ed eject iotl American Heart Association Task Rrrce on Clinical Practice Guidelines fraction. Circulation. 2018;138:u6t 70. IPMll): 297g22gql doi:lO.l t(>1,' rnd the Ilcart Rhytlrm Society. J Ant Coll (lardiol.2019;71:104 132. ClRCUI.r\TIONAHA. I t8.03,16.16 I PMID: 30703 13ll doi:10. l0l6 j.jacc.2019.01.011 198

Answers and Critiques Item 84 Answer: A Item 85 Answer: A Educational Objective: Assess the severity of mitral Educational Objective: Evaluate for coronary artery regurgitation with cardiac magnetic resonance imaging. disease in a patient with new-onset heart failure.

Item 84 Answer: A Item 85 Answer: A Educational Objective: Assess the severity of mitral Educational Objective: Evaluate for coronary artery regurgitation with cardiac magnetic resonance imaging. disease in a patient with new-onset heart failure. The most appropriate next step in management is cardiac Cardiac catheterization (Option A) is the most appropriate magnetic resonance (CMR) imaging (OptionA). The patient's test to perform in this patient with new onset heart failure history and examination findings are consistent with heart ofunclear cause. Echocardiography should be performed ini failure and volume overload (dyspnea, orthopnea, S., tially in all patients with new heart failure; this patient's echo elevated central venous pressure, puimonary crackles, pul- cardiogram is notable for a low ejection fraction, anterior wall monary edema on the chest radiograph) despite guideline- hypokinesis, and absence of left ventricular (LV) hlpertrophy. directed medical therapy. The systolic click and radiation of The anterior wall motion abnormality increases suspicion fbr the murmur to the back suggest posteriorly directed mitral coronary artery disease (CAD), the most common underlying regurgitation (MR) with prolapse (primary MR). Despite cause of heart failure. The patient also has exertional chest vt these flndings, the quantitative echocardiographic data are heaviness; thus, clinical suspicion tbr CAD should be high. o consistent with moderate MR. However. two dimensional Cardiac catheterization offers the most direct information ET quantitative echocardiographic data may underestimate the about coronary anatomy and therefore is the best method fbr CJ severity of MR. In that case, additional imaging is required. assessing ischemia in such patients. If the patient has CAD, E In patients with primary MR, iltransthoracic echocardiogra- revascularization has been associated with improved survival E t! phy provides insufficient or discordant information, current rates and often with improved ejection fiaction. t,l guidelines recommend either transesophageal echocardiog Cardiac magnetic resonance (CMR) imaging (Option B) o raphy or CMR imaging to assess the severity of MR (class 1 wtiuld be reasonable to perfbrm afterechocardiography and after t,l = E recommendations). This assessment is important in deter CAD has been excluded. CMR imaging can help identi! infiltra- mining whether mitral valve intervention is indicated. Surgi tive processes, such as sarcoidosis, hemochromatosis, amyloido- cal and transcatheter interventions are performed primarily sis, I.-abry disease, or endomyocardial fibrosis, and has distinct in patients with severe valvular heart disease, but diagnosis, imaging pattems that can suggest the diagnosis of myocarditis. patient education, periodic monitoring, and medical therapy CMR imaging is also becoming more widely used to evaluate fbr are essential elements in the management of patients with ischemia and hibernating myocardium, but guidelines recom mild to moderate val'ue dyslunction. mend either stress testing or cardiac catheterization as the first ln symptomatic patients with confirmed mild to mod study in the evaluation of possible ischemic cardiomyopathy. erate MR, starting guideline directed medical therapy with Cardiac PET (Option C) can aid in assessing LV function periodic imaging surveillance is appropriate. Repeat echo- and evaluating for ischemia. It may help distinguish between cardiographic imaging is recommended every 1 to 2 years inflammation and fibrosis and therefbre can guide decisions (Option B) in patients with moderate primary MR. How- about therapy. However, given this patient's high likelihood ever, the severity of this patient's symptoms is at odds with of CAD, cardiac catheterization is the most direct and apprcr the echocardiographic flndings, and additional imaging is priate modality to assess for CAD. required to establish the degree of valve dysfunction and Cardiac amyloidosis is suggested by heart failure with select the appropriate treatment. restrictive physiologi, increased wall thickness, and low Neither surgical (Option C) nor transcatheter (Option D) ECG voltage. Technetium-99m pyrophosphate scintigraphy mitral valve repair is appropriate before confirming the (Option D) is used to diagnose the transthyretin variant of severity of MR. Documentation of severe MR would be an cardiac amyloidcisis. This patient's lack ol LV hypertrriphy indication fbr surgical mitral valve repair. ln patients with on echocardiogram and anterior hypokinesis argue against high or prohibitive surgical risk, transcatheter mitral valve the diagnosis of amyloidosis, an infiltrative cardiomyopathy. repair (transcatheter edge to edge repair) is reasonable. KEY POITI KEY POII{T . Patients with new-onset heart failure and a high like- o For patients in whom there is a discrepancy between lihood ofcoronary artery disease should be evaluated physical examination flndings and transthoracic echo with cardiac catheterization. cardiographic assessment of mitral regurgitation severity, Bibliography cardiac magnetic resonance imaging or transesophageal Wu A. I leart failure. Ann Intcrn Med. 20l8r168:l lC8l I lC96. [PMID: 2986tt8161 echocardiography should be used to quantitatively rloi:10.7326 1AITC20l 806050 assess mitral regurgitation and resolve the discrepancy. Item 86 Answer: E Bibliography Educational Objective: Treat a patient with intermittent tsonow RO, o'(;Nra Pl'. Adams DH. et al. 2020 Focused Llpdrte of the 2017 claudication with supervised exercise training. ACC exper( consensus decision pathway on the manrgcment of mitral regurgitNtion: J report ofthe American College ol Carditllol5, Solution Set The most appropriate treatment for this patient with symp Oversight Committee. J Am Qrll Crrdiol. 2020;75:22116 2270. [PMID: 3206808.1 | doi: I 0.r 016 ',j.jacc.2020.o2.005 tomatic peripheral artery disease (PAD) is to start a supervised

The most appropriate next step in management is cardiac Cardiac catheterization (Option A) is the most appropriate magnetic resonance (CMR) imaging (OptionA). The patient's test to perform in this patient with new onset heart failure history and examination findings are consistent with heart ofunclear cause. Echocardiography should be performed ini failure and volume overload (dyspnea, orthopnea, S., tially in all patients with new heart failure; this patient's echo elevated central venous pressure, puimonary crackles, pul- cardiogram is notable for a low ejection fraction, anterior wall monary edema on the chest radiograph) despite guideline- hypokinesis, and absence of left ventricular (LV) hlpertrophy. directed medical therapy. The systolic click and radiation of The anterior wall motion abnormality increases suspicion fbr the murmur to the back suggest posteriorly directed mitral coronary artery disease (CAD), the most common underlying regurgitation (MR) with prolapse (primary MR). Despite cause of heart failure. The patient also has exertional chest vt these flndings, the quantitative echocardiographic data are heaviness; thus, clinical suspicion tbr CAD should be high. o consistent with moderate MR. However. two dimensional Cardiac catheterization offers the most direct information ET quantitative echocardiographic data may underestimate the about coronary anatomy and therefore is the best method fbr CJ severity of MR. In that case, additional imaging is required. assessing ischemia in such patients. If the patient has CAD, E In patients with primary MR, iltransthoracic echocardiogra- revascularization has been associated with improved survival E t! phy provides insufficient or discordant information, current rates and often with improved ejection fiaction. t,l guidelines recommend either transesophageal echocardiog Cardiac magnetic resonance (CMR) imaging (Option B) o raphy or CMR imaging to assess the severity of MR (class 1 wtiuld be reasonable to perfbrm afterechocardiography and after t,l = E recommendations). This assessment is important in deter CAD has been excluded. CMR imaging can help identi! infiltra- mining whether mitral valve intervention is indicated. Surgi tive processes, such as sarcoidosis, hemochromatosis, amyloido- cal and transcatheter interventions are performed primarily sis, I.-abry disease, or endomyocardial fibrosis, and has distinct in patients with severe valvular heart disease, but diagnosis, imaging pattems that can suggest the diagnosis of myocarditis. patient education, periodic monitoring, and medical therapy CMR imaging is also becoming more widely used to evaluate fbr are essential elements in the management of patients with ischemia and hibernating myocardium, but guidelines recom mild to moderate val'ue dyslunction. mend either stress testing or cardiac catheterization as the first ln symptomatic patients with confirmed mild to mod study in the evaluation of possible ischemic cardiomyopathy. erate MR, starting guideline directed medical therapy with Cardiac PET (Option C) can aid in assessing LV function periodic imaging surveillance is appropriate. Repeat echo- and evaluating for ischemia. It may help distinguish between cardiographic imaging is recommended every 1 to 2 years inflammation and fibrosis and therefbre can guide decisions (Option B) in patients with moderate primary MR. How- about therapy. However, given this patient's high likelihood ever, the severity of this patient's symptoms is at odds with of CAD, cardiac catheterization is the most direct and apprcr the echocardiographic flndings, and additional imaging is priate modality to assess for CAD. required to establish the degree of valve dysfunction and Cardiac amyloidosis is suggested by heart failure with select the appropriate treatment. restrictive physiologi, increased wall thickness, and low Neither surgical (Option C) nor transcatheter (Option D) ECG voltage. Technetium-99m pyrophosphate scintigraphy mitral valve repair is appropriate before confirming the (Option D) is used to diagnose the transthyretin variant of severity of MR. Documentation of severe MR would be an cardiac amyloidcisis. This patient's lack ol LV hypertrriphy indication fbr surgical mitral valve repair. ln patients with on echocardiogram and anterior hypokinesis argue against high or prohibitive surgical risk, transcatheter mitral valve the diagnosis of amyloidosis, an infiltrative cardiomyopathy. repair (transcatheter edge to edge repair) is reasonable. KEY POITI KEY POII{T . Patients with new-onset heart failure and a high like- o For patients in whom there is a discrepancy between lihood ofcoronary artery disease should be evaluated physical examination flndings and transthoracic echo with cardiac catheterization. cardiographic assessment of mitral regurgitation severity, Bibliography cardiac magnetic resonance imaging or transesophageal Wu A. I leart failure. Ann Intcrn Med. 20l8r168:l lC8l I lC96. [PMID: 2986tt8161 echocardiography should be used to quantitatively rloi:10.7326 1AITC20l 806050 assess mitral regurgitation and resolve the discrepancy. Item 86 Answer: E Bibliography Educational Objective: Treat a patient with intermittent tsonow RO, o'(;Nra Pl'. Adams DH. et al. 2020 Focused Llpdrte of the 2017 claudication with supervised exercise training. ACC exper( consensus decision pathway on the manrgcment of mitral regurgitNtion: J report ofthe American College ol Carditllol5, Solution Set The most appropriate treatment for this patient with symp Oversight Committee. J Am Qrll Crrdiol. 2020;75:22116 2270. [PMID: 3206808.1 | doi: I 0.r 016 ',j.jacc.2020.o2.005 tomatic peripheral artery disease (PAD) is to start a supervised 199

Answers and Critiques exercise program (Option E), regardless ofthe ankle brachial Item 87 Answer: C index value. In patients with intermittent claudication, super- Educational Objective: Manage a patient with Marfan vised exercise training is recommended to improve functional syndrome and aortic root dilation who is considering status (maximal walking distance and pain-free walking pregnancy. distance) and qualiff of life and to reduce leg symptoms. Studies with intermediate and long term follow-up also have Aortic repair before pregnancy (Option C) is the most demonstrated a persistent beneflt of supervised exercise in appropriate management option for this patient. All these patients. The risk benefit ratio for supervised exercise is women with Marfan syndrome have an increased risk for favorable for patients with PAD (including those with comor pregnancy-related aortic dissection and rupture. To reduce bid conditions), and training is recommended for a minimum this risk, aortic repair surgery is recommended before con- of 30 to 45 minutes, at least three times weekly for a minimum ception for women with Marfan syndrome who have an of 12 weeks. The Centers for Medicare & Medicaid Services ascending aortic diameter greater than 4.0 cm and risk provides reimbursement for supervised exercise programs in factors for aortic dissection, such as a family or personal U) patients with symptomatic PAD. Cilostazol, a phosphodies- history of aortic dissection or aortic dilatation of more € .D terase inhibitor, is also recommended to improve symptoms than 5 mm per year. Pregnancy is considered Iow risk if aa and increase walking distance in patients with claudication. the aortic diameter is smaller than 4.0 cm. This patient has o, Noninvasive imagrng, such as CT angiography (Option A), both a family history of aortic dissection and evidence of EL magnetic resonance angiography, or duplex ultrasonogra an expanding aneurysm; aortic repair before attempting o phy, should be reserved for patients being considered for pregnancy should be advised. revascularization. In this patient, guideline directed medical There is limited information and no randomized con- a therapy and a supervised exercise program should be started trolled trials on the clinical outcomes of statin therapy, such .D t^ before consideration of CT angiography. as atorvastatin (Option A), in slowing the expansion of the Chelation therapy with ethylenediaminetetraacetic acid aortic root in patients with aortic or thoracic aneurysm. (Option B) is not beneflcial for treatment of claudication In addition, statin therapy is contraindicated in patients (American Heart Association/American College of Cardiol who wish to become pregnant or are pregnant. Population ogr class 3 recommendation). A Cochrane systematic review studies suggest that there may be an increase in congen and meta-analysis concluded that there was no signiflcant ital central nervous system and limb abnormalities with difference in maximal and pain-free walking distance with exposure to lipophilic statins during the flrst trimester. chelation therapy versus placebo. Starting atorvastatin and continuing with pregnancy is not Pentoxifylline (Option C) has no beneflt for the treat- recommended. ment of symptomatic PAD (class 3 recommendation) and Angiotensin receptor blockers, such as losartan (Option B), should not be prescribed to this patient. are contraindicated during pregnancy because of fetal toxic- Although this patient has progressive symptoms, revas ity. Exposure to these agents during the flrst trimester may cularization (Option D) is not appropriate at this time. cause central nervous system and cardiovascular malfor Patients with intermittent claudication should be started mations; exposure during the second trimester may lead to on a supervised exercise program and medical therapy (e.g., urogenital and renal developmental malformations. These cilostazol, vascular disease risk reduction) before referral for agents are often used in nonpregnant patients with Marfan revascularization. If symptoms persist despite these inter- syndrome as alternatives to B-blocker therapy for slowing ventions, counseling about the risks and beneflts ofrevascu, aortic root expansion. larization (endovascular or surgical) is appropriate. The size of this patient's aortic root in the context of the patient's family history of aortic dissection and the rate I(EY POIilT5 of aortic root expansion are all factors that support aortic . In patients with peripheral artery disease and inter- repair prior to pregnancy. Proceeding directly to pregnancy mittent claudication, supervised exercise training is (Option D) is not advisable. the most effective treatment to improve maximal I(EY POIlIT walking distance and pain free walking distance. o Cilostazol, a phosphodiesterase inhibitor, is recom- o Women with Marfan syndrome have an increased risk for pregnancy-related aortic dissection and rupture; mended in addition to a supervised exercise program aortic repair surgery is recommended before concep to improve symptoms and increase walking distance in patients with claudication. tion to reduce this risk in those with an ascending aortic diameter greater than 4.0 cm and who have risk factors for aortic dissection. Bibliography Gerhard-Heman MD, Gomik HL, Barrett C, et al. 2016 AHA/ACC guideline on the management of patients with lower extremity peripheral artery disease: Bibliography executive summary: a report of the American College of Cardiologr/ Regitz Zagrosek V Roos Hesselink IW, Bauersachs J, et al; ESC Scientific American Heart Association Task Force on Clinical praclice Guidelines. Document Croup. 2018 ESC guidelines fbr the management ofcardiovas Circulation. 2017;135:e686 e725. IPMID: 27540382) doi:10.1161/CIR. cular diseases during pregnancy. Eur Heart J. ZO1S;S9,gtOS-aZ+1. [pMlD: 0000000000000470 301655441 doi:10.1093/eurheartj/ehy340

exercise program (Option E), regardless ofthe ankle brachial Item 87 Answer: C index value. In patients with intermittent claudication, super- Educational Objective: Manage a patient with Marfan vised exercise training is recommended to improve functional syndrome and aortic root dilation who is considering status (maximal walking distance and pain-free walking pregnancy. distance) and qualiff of life and to reduce leg symptoms. Studies with intermediate and long term follow-up also have Aortic repair before pregnancy (Option C) is the most demonstrated a persistent beneflt of supervised exercise in appropriate management option for this patient. All these patients. The risk benefit ratio for supervised exercise is women with Marfan syndrome have an increased risk for favorable for patients with PAD (including those with comor pregnancy-related aortic dissection and rupture. To reduce bid conditions), and training is recommended for a minimum this risk, aortic repair surgery is recommended before con- of 30 to 45 minutes, at least three times weekly for a minimum ception for women with Marfan syndrome who have an of 12 weeks. The Centers for Medicare & Medicaid Services ascending aortic diameter greater than 4.0 cm and risk provides reimbursement for supervised exercise programs in factors for aortic dissection, such as a family or personal U) patients with symptomatic PAD. Cilostazol, a phosphodies- history of aortic dissection or aortic dilatation of more € .D terase inhibitor, is also recommended to improve symptoms than 5 mm per year. Pregnancy is considered Iow risk if aa and increase walking distance in patients with claudication. the aortic diameter is smaller than 4.0 cm. This patient has o, Noninvasive imagrng, such as CT angiography (Option A), both a family history of aortic dissection and evidence of EL magnetic resonance angiography, or duplex ultrasonogra an expanding aneurysm; aortic repair before attempting o phy, should be reserved for patients being considered for pregnancy should be advised. revascularization. In this patient, guideline directed medical There is limited information and no randomized con- a therapy and a supervised exercise program should be started trolled trials on the clinical outcomes of statin therapy, such .D t^ before consideration of CT angiography. as atorvastatin (Option A), in slowing the expansion of the Chelation therapy with ethylenediaminetetraacetic acid aortic root in patients with aortic or thoracic aneurysm. (Option B) is not beneflcial for treatment of claudication In addition, statin therapy is contraindicated in patients (American Heart Association/American College of Cardiol who wish to become pregnant or are pregnant. Population ogr class 3 recommendation). A Cochrane systematic review studies suggest that there may be an increase in congen and meta-analysis concluded that there was no signiflcant ital central nervous system and limb abnormalities with difference in maximal and pain-free walking distance with exposure to lipophilic statins during the flrst trimester. chelation therapy versus placebo. Starting atorvastatin and continuing with pregnancy is not Pentoxifylline (Option C) has no beneflt for the treat- recommended. ment of symptomatic PAD (class 3 recommendation) and Angiotensin receptor blockers, such as losartan (Option B), should not be prescribed to this patient. are contraindicated during pregnancy because of fetal toxic- Although this patient has progressive symptoms, revas ity. Exposure to these agents during the flrst trimester may cularization (Option D) is not appropriate at this time. cause central nervous system and cardiovascular malfor Patients with intermittent claudication should be started mations; exposure during the second trimester may lead to on a supervised exercise program and medical therapy (e.g., urogenital and renal developmental malformations. These cilostazol, vascular disease risk reduction) before referral for agents are often used in nonpregnant patients with Marfan revascularization. If symptoms persist despite these inter- syndrome as alternatives to B-blocker therapy for slowing ventions, counseling about the risks and beneflts ofrevascu, aortic root expansion. larization (endovascular or surgical) is appropriate. The size of this patient's aortic root in the context of the patient's family history of aortic dissection and the rate I(EY POIilT5 of aortic root expansion are all factors that support aortic . In patients with peripheral artery disease and inter- repair prior to pregnancy. Proceeding directly to pregnancy mittent claudication, supervised exercise training is (Option D) is not advisable. the most effective treatment to improve maximal I(EY POIlIT walking distance and pain free walking distance. o Cilostazol, a phosphodiesterase inhibitor, is recom- o Women with Marfan syndrome have an increased risk for pregnancy-related aortic dissection and rupture; mended in addition to a supervised exercise program aortic repair surgery is recommended before concep to improve symptoms and increase walking distance in patients with claudication. tion to reduce this risk in those with an ascending aortic diameter greater than 4.0 cm and who have risk factors for aortic dissection. Bibliography Gerhard-Heman MD, Gomik HL, Barrett C, et al. 2016 AHA/ACC guideline on the management of patients with lower extremity peripheral artery disease: Bibliography executive summary: a report of the American College of Cardiologr/ Regitz Zagrosek V Roos Hesselink IW, Bauersachs J, et al; ESC Scientific American Heart Association Task Force on Clinical praclice Guidelines. Document Croup. 2018 ESC guidelines fbr the management ofcardiovas Circulation. 2017;135:e686 e725. IPMID: 27540382) doi:10.1161/CIR. cular diseases during pregnancy. Eur Heart J. ZO1S;S9,gtOS-aZ+1. [pMlD: 0000000000000470 301655441 doi:10.1093/eurheartj/ehy340 200

Answers and Critiques Item 88 Answer: C of structural heart disease is an impofiant distinction in the Educational Objective: Evaluate atypical angina with nlarlagenlent of'ventricular tachycardia (VT). CMR imag pharmacologic myocardial perfusion imaglng. ing generally allows for tissue characterization, rnaking it an important method fbr evaluating myocardial diseases Pharmacologic myocardial perfusion imaging (Option C) that may manifest as Vl'. including arrhythmogenic right is the most appropriate next test. The evaluation of angina ventricular cardiomyopathy, cardiac sarcoidosis, and other should include a physical examination to detect conditions infiltrative cardiornyrpathies (e.g., amyloidosis). that may mimic symptomatic coronary artery disease (CAD), Fllectrophysiologic testing (Option B) is not indicated as well as a focused history to assist in determining the as part of the initial management ol this patient. It may be pretest probabiliff of CAD. A resting ECG is required to uselul to establisl.r the diagnosis of sustained monomor evaluate for ongoing ischemic insult and to guide the choice phic tachycardia if the diagnosis is in doubt. It is similarly of subsequent diagnostic testing. This 66-year-old woman useful to establish the mechanism of VT and to identify the with clinical features of atlpical angina has an intermedi- krcation of the arrhythmogenic lbcus if ablation is being ta o, ate pretest likelihood of CAD, an indication for stress test considered. However, the initial management should fbcus ET diagnostic evaluation. Stress testing with imaging is indi- on (1) assessment fbr structural heart disease and (2) iden cated in patients with an inability to exercise, baseline ECG tification of correctable causes of V'1. including myocarclial TJ abnormalities (such as left bundle branch block [LBBB]) that ischemia, heart failure, drug effects, anemia, and electrolyte E limit interpretation of the exercise ECG, or indeterminate abnormalities. a! flndings on the exercise ECG. In patients able to exercise but UI It is premature to consider an implantable cardioverter (l, with underlying LBBB, such as this patient, pharmacologic defibrillakir (lCD) (Option C) fbr this patient. lf CMR imag stress testing with imaging (myocardial perfusion, cardiac .A ing demonstrates significant structural heart disease, lCIf = magnetic resonance, or echocardiographic) is appropriate to placement or additional testing may be warranted before reduce the rate of false positive test results associated with discharge. An ICD is indicated for secondary preventittn of exercise ECG (Option B) in this population. sudden cardiac death as well as for primary prevention ol Coronary angiography (Option A) is not indicated for sudden cardiac death in patients with an ejection fraction stable, low-risk clinical features. It should be reserved for of 35'/, or less and New York Heart Asstlciation functional patients with a high pretest likelihood of CAD and unstable class II or III hearl failure symptoms while receiving guide symptoms, or for those in whom optimal medical therapy line directed medical therapy. ICD placernent is generally has been ineffective. unnecessary in idiopathic V'f, owing to the benign prognrtsis Resting transthoracic echocardiography (Option D) can and high eflicacy ol'other therapies. provide helpful prognostic information related to ventricular lf the patient has idiopathic V'l', which is Vf in the function and is usefui in assessing for noncoronary cardiac absence of structural heart disease, an implantable loop causes of chest pain. It is not as helpful as exercise stress recorder (ll-R) (Option D) may be appropriate. Idiopathic testing as an initial test for symptomatic CAD. VT typically n-ianifests as palpitations in the third to fifth Reassurance without additional testing (Option E) may decades ol lif'e, otten triggered by stress, emotion, or be appropriate when an alternative cause of chest discomfort sleeplessness. It would be premature to consicier ll,R has been identifled in a patient with a low pretest probability placement befbre assessment for structural heart disease. of CAD, but this patient's ongoing exertional chest pain and An ILR rn:ry be valuable to assess rare recurrences o[' intermediate likelihood of CAD require further investigation. arrhytl-rmia and/or to assess symptoms, but further eval uation is needed first. I(EY POITI o Stress testing with imaging is indicated in patients f,EY POIilTS with an inability to exercise, baseline ECG abnormali- o The initial evaluation ofventricular tachycardia focuses ties that limit interpretation of the exercise ECG, or on the identification of reversible causes and includes indeterminate findings on the exercise ECG. echocardiography, cardiac magnetic resonance imaging, and exercise ECG. Bibliography r Idiopathic ventricular tachycardia occurs in the absence Katz D, Gavin MC. Stable ischemic heart disease. Ann Intern Med. 2019; of structural heart disease, $pically manifesting as 171:lTC17lTC32. [PMID: 31382288] doi:10.7326/AITC201908060 palpitations in the third to fifth decades of life, often triggered by stress, emotion, or sleeplessness. Answer: A tr Item 89 Educational Objective: Evaluate a patient with ventric- Bibliography ular tachycardia. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhlthmias and The most appropriate initial management is an evaluation ihe prevention ofsudden cardiac death: a report ofthe American College of CardioloryiAmerican Heart Association Task Force on Clinical Practice lbr structural heart disease r.tith cardiac magnetic reso Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2018;72re91 nance (CMR) imaging (Option A). The presence or absence e220. [PMID: 29097296] doi:10.1016/j.jacc.20i7.10.054

Item 88 Answer: C of structural heart disease is an impofiant distinction in the Educational Objective: Evaluate atypical angina with nlarlagenlent of'ventricular tachycardia (VT). CMR imag pharmacologic myocardial perfusion imaglng. ing generally allows for tissue characterization, rnaking it an important method fbr evaluating myocardial diseases Pharmacologic myocardial perfusion imaging (Option C) that may manifest as Vl'. including arrhythmogenic right is the most appropriate next test. The evaluation of angina ventricular cardiomyopathy, cardiac sarcoidosis, and other should include a physical examination to detect conditions infiltrative cardiornyrpathies (e.g., amyloidosis). that may mimic symptomatic coronary artery disease (CAD), Fllectrophysiologic testing (Option B) is not indicated as well as a focused history to assist in determining the as part of the initial management ol this patient. It may be pretest probabiliff of CAD. A resting ECG is required to uselul to establisl.r the diagnosis of sustained monomor evaluate for ongoing ischemic insult and to guide the choice phic tachycardia if the diagnosis is in doubt. It is similarly of subsequent diagnostic testing. This 66-year-old woman useful to establish the mechanism of VT and to identify the with clinical features of atlpical angina has an intermedi- krcation of the arrhythmogenic lbcus if ablation is being ta o, ate pretest likelihood of CAD, an indication for stress test considered. However, the initial management should fbcus ET diagnostic evaluation. Stress testing with imaging is indi- on (1) assessment fbr structural heart disease and (2) iden cated in patients with an inability to exercise, baseline ECG tification of correctable causes of V'1. including myocarclial TJ abnormalities (such as left bundle branch block [LBBB]) that ischemia, heart failure, drug effects, anemia, and electrolyte E limit interpretation of the exercise ECG, or indeterminate abnormalities. a! flndings on the exercise ECG. In patients able to exercise but UI It is premature to consider an implantable cardioverter (l, with underlying LBBB, such as this patient, pharmacologic defibrillakir (lCD) (Option C) fbr this patient. lf CMR imag stress testing with imaging (myocardial perfusion, cardiac .A ing demonstrates significant structural heart disease, lCIf = magnetic resonance, or echocardiographic) is appropriate to placement or additional testing may be warranted before reduce the rate of false positive test results associated with discharge. An ICD is indicated for secondary preventittn of exercise ECG (Option B) in this population. sudden cardiac death as well as for primary prevention ol Coronary angiography (Option A) is not indicated for sudden cardiac death in patients with an ejection fraction stable, low-risk clinical features. It should be reserved for of 35'/, or less and New York Heart Asstlciation functional patients with a high pretest likelihood of CAD and unstable class II or III hearl failure symptoms while receiving guide symptoms, or for those in whom optimal medical therapy line directed medical therapy. ICD placernent is generally has been ineffective. unnecessary in idiopathic V'f, owing to the benign prognrtsis Resting transthoracic echocardiography (Option D) can and high eflicacy ol'other therapies. provide helpful prognostic information related to ventricular lf the patient has idiopathic V'l', which is Vf in the function and is usefui in assessing for noncoronary cardiac absence of structural heart disease, an implantable loop causes of chest pain. It is not as helpful as exercise stress recorder (ll-R) (Option D) may be appropriate. Idiopathic testing as an initial test for symptomatic CAD. VT typically n-ianifests as palpitations in the third to fifth Reassurance without additional testing (Option E) may decades ol lif'e, otten triggered by stress, emotion, or be appropriate when an alternative cause of chest discomfort sleeplessness. It would be premature to consicier ll,R has been identifled in a patient with a low pretest probability placement befbre assessment for structural heart disease. of CAD, but this patient's ongoing exertional chest pain and An ILR rn:ry be valuable to assess rare recurrences o[' intermediate likelihood of CAD require further investigation. arrhytl-rmia and/or to assess symptoms, but further eval uation is needed first. I(EY POITI o Stress testing with imaging is indicated in patients f,EY POIilTS with an inability to exercise, baseline ECG abnormali- o The initial evaluation ofventricular tachycardia focuses ties that limit interpretation of the exercise ECG, or on the identification of reversible causes and includes indeterminate findings on the exercise ECG. echocardiography, cardiac magnetic resonance imaging, and exercise ECG. Bibliography r Idiopathic ventricular tachycardia occurs in the absence Katz D, Gavin MC. Stable ischemic heart disease. Ann Intern Med. 2019; of structural heart disease, $pically manifesting as 171:lTC17lTC32. [PMID: 31382288] doi:10.7326/AITC201908060 palpitations in the third to fifth decades of life, often triggered by stress, emotion, or sleeplessness. Answer: A tr Item 89 Educational Objective: Evaluate a patient with ventric- Bibliography ular tachycardia. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhlthmias and The most appropriate initial management is an evaluation ihe prevention ofsudden cardiac death: a report ofthe American College of CardioloryiAmerican Heart Association Task Force on Clinical Practice lbr structural heart disease r.tith cardiac magnetic reso Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2018;72re91 nance (CMR) imaging (Option A). The presence or absence e220. [PMID: 29097296] doi:10.1016/j.jacc.20i7.10.054 201

Answers and Critiques Item 90 Answer: B relrlacement and aortic repair (Option B). When patients have an indication ttrr cardiac surgell' (such as coronary Ed u cationa I O bj ective : Diagnose low-fl ow low- gradient artery bl.pass grafting [CABG]) and have concomitant aortic severe symptomatic aortic stenosis. stenosis and thoracic aofiic aneurysnr. the risks and bene The most appropriate next step in management is dobu fits of aortic rah,'e replacement ancl lortic repair should be -lhis patient's tamine stress echocardiography (Option B). considered. Aortic rcpair should be perfbrmed at the tirne examination findings (late-peaking crescendo decrescendo of cardiac surgery if' the ascenclinll aofta or aortic rorll is murmur at the right upper sternal border, crackles, and llrgcr than .1.5 cnr. ln this patient r,r'ith a maxinral aortic elevated central venous pressure) and elevated B type natri dimension of 5.6 cn.r. the annual risk tbr rllpture of the thcr uretic peptide level are consistent with signiflcant aortic ste rxcic aofia is significant enough to refer l.rer lor aorlic repair. nosis and associated volume overload. On echocardiography, 'll.rc additional risk associated with aortic val-ne replacement low-flow low gradient severe aortic stenosis is suggested cluring CABC is srnall, and replacenlellt nor,r'r.tould prevcnt D by a severely reduced valve area (<1.0 cm2) and a modestly subsequent aortic valve clperations tbr symptomatic severe UI increased peak aortic velocity (<+ m/s) in the setting of a aortic stenosis. reduced ejection fraction (<sO'2,). The most appropriate next Performing CABG and aortic r,alve replacentcnt = .D step in management is to confirm the diagnosis of severe (Option A) concurrently is appropriate in patients \\'ith Ut o, aortic stenosis with low-dose dobutamine stress echocar three-r,essel coronary artery diselsc ((lAD) and moderate tc) a diography. If dobutamine infusion results in an increase in severe aortic stenosis. However. in the presence of thoracic n stroke volume by at least 20')(,, severe aortic stenosis is diag aortic aneurysnr with maxirnal aortic climension grcatcr nosed by an increase in peak velocity to 4.0 m/s or greater than 4.5 c111. aortic repair also shoulci lre performecl. It with the valve area remaining 1.0 cm2 or less. ln patients Although transcatheter aortic virlve irnplantation (Tl\\'l) .D 6 with suspected low flow low gradient severe aortic stenosis (Option C) has beconle a conrnlon treiltlnent for patients with normal or reduced left ventricular ejection fraction, u'ith severe aortic stenosis. the proccdure is contraindicatecl measurement of aortic valve calcium score by CT is also rea- in tl.ris patient because of her conconritant CAD and thorrrcic sonable to further deflne aortic stenosis severity. xortic aneurysnr. TAVI is often perfbrn.red in patients rvitlr In this patient who likely has low cardiac output, direct severe aortic stenosis and conconritar-rt CAD: hou'ever. the measurement of the aortic valve gradient by cardiac cath- coronary anatom)' typically should fhvor percutaneous cor eterization (Option A) would result in iow gradients that onarf intervention (rthich it does rlot in this case). ancl the underestimate the severity of the aortic stenosis, similar to pr-ocedures shoulcl be performed in sequence. gradient and velocity values on resting echocardiography. Perforrning no rrclditional interyention (Option D) in Dobutamine catheterization may be performed in lieu of this patient with two surgically correct:rble life linritir-rg dobutamine echocardiography in this case. lcsions rtho is lrlrcady nndergoing open heart surger-t' is Proceeding to surgical (Option C) or transcatheter inappropriate. 'lhe benefits of aortic r':rlve replacement rrr-rcl aortic valve implantation (Option D) is inappropriate at aurtic repair u'ill n.rost likelv outucigl.r the harnts in this this timel the resting echocardiogram does not adequately pirtient. differentiate between pseudosevere aortic stenosis due to insufflcient stroke volume and low flow Iow gradient severe I(EY POIilT aortic stenosis. . In patients with an ascending aorta or aortic root larger than 4.5 cm in diameter who require surgery l(tY P0tltT for coronary artery disease or valve pathologr, aortic . Dobutamine stress echocardiography can be used to repair should be performed at the time of cardiac differentiate between pseudosevere aortic stenosis surgery. and low-flow low-gradient severe aortic stenosis. Bibliography Bibliography Su,erdlon NJ, Wu WW Schermerhom ML. Open and endovascular manage Ofto CM. Nishimura RA, Bonow RO. et al. 2020 ACC,,AI1A guideline for the ment of aortic aneurysms. Circ Res. 2019112,1:617 661. [PMID: 30761]2061 management of patients with valvular heart disease: a report of the doi:10.1161 ClRCRESAHA.ll8.313186 American College of Cardiologr' American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2O21:143:e72- e227. IPMI I): 333321501 doi:10.1161 /ClR.O00OOOOOOOOoO923

Item 90 Answer: B relrlacement and aortic repair (Option B). When patients have an indication ttrr cardiac surgell' (such as coronary Ed u cationa I O bj ective : Diagnose low-fl ow low- gradient artery bl.pass grafting [CABG]) and have concomitant aortic severe symptomatic aortic stenosis. stenosis and thoracic aofiic aneurysnr. the risks and bene The most appropriate next step in management is dobu fits of aortic rah,'e replacement ancl lortic repair should be -lhis patient's tamine stress echocardiography (Option B). considered. Aortic rcpair should be perfbrmed at the tirne examination findings (late-peaking crescendo decrescendo of cardiac surgery if' the ascenclinll aofta or aortic rorll is murmur at the right upper sternal border, crackles, and llrgcr than .1.5 cnr. ln this patient r,r'ith a maxinral aortic elevated central venous pressure) and elevated B type natri dimension of 5.6 cn.r. the annual risk tbr rllpture of the thcr uretic peptide level are consistent with signiflcant aortic ste rxcic aofia is significant enough to refer l.rer lor aorlic repair. nosis and associated volume overload. On echocardiography, 'll.rc additional risk associated with aortic val-ne replacement low-flow low gradient severe aortic stenosis is suggested cluring CABC is srnall, and replacenlellt nor,r'r.tould prevcnt D by a severely reduced valve area (<1.0 cm2) and a modestly subsequent aortic valve clperations tbr symptomatic severe UI increased peak aortic velocity (<+ m/s) in the setting of a aortic stenosis. reduced ejection fraction (<sO'2,). The most appropriate next Performing CABG and aortic r,alve replacentcnt = .D step in management is to confirm the diagnosis of severe (Option A) concurrently is appropriate in patients \\'ith Ut o, aortic stenosis with low-dose dobutamine stress echocar three-r,essel coronary artery diselsc ((lAD) and moderate tc) a diography. If dobutamine infusion results in an increase in severe aortic stenosis. However. in the presence of thoracic n stroke volume by at least 20')(,, severe aortic stenosis is diag aortic aneurysnr with maxirnal aortic climension grcatcr nosed by an increase in peak velocity to 4.0 m/s or greater than 4.5 c111. aortic repair also shoulci lre performecl. It with the valve area remaining 1.0 cm2 or less. ln patients Although transcatheter aortic virlve irnplantation (Tl\\'l) .D 6 with suspected low flow low gradient severe aortic stenosis (Option C) has beconle a conrnlon treiltlnent for patients with normal or reduced left ventricular ejection fraction, u'ith severe aortic stenosis. the proccdure is contraindicatecl measurement of aortic valve calcium score by CT is also rea- in tl.ris patient because of her conconritant CAD and thorrrcic sonable to further deflne aortic stenosis severity. xortic aneurysnr. TAVI is often perfbrn.red in patients rvitlr In this patient who likely has low cardiac output, direct severe aortic stenosis and conconritar-rt CAD: hou'ever. the measurement of the aortic valve gradient by cardiac cath- coronary anatom)' typically should fhvor percutaneous cor eterization (Option A) would result in iow gradients that onarf intervention (rthich it does rlot in this case). ancl the underestimate the severity of the aortic stenosis, similar to pr-ocedures shoulcl be performed in sequence. gradient and velocity values on resting echocardiography. Perforrning no rrclditional interyention (Option D) in Dobutamine catheterization may be performed in lieu of this patient with two surgically correct:rble life linritir-rg dobutamine echocardiography in this case. lcsions rtho is lrlrcady nndergoing open heart surger-t' is Proceeding to surgical (Option C) or transcatheter inappropriate. 'lhe benefits of aortic r':rlve replacement rrr-rcl aortic valve implantation (Option D) is inappropriate at aurtic repair u'ill n.rost likelv outucigl.r the harnts in this this timel the resting echocardiogram does not adequately pirtient. differentiate between pseudosevere aortic stenosis due to insufflcient stroke volume and low flow Iow gradient severe I(EY POIilT aortic stenosis. . In patients with an ascending aorta or aortic root larger than 4.5 cm in diameter who require surgery l(tY P0tltT for coronary artery disease or valve pathologr, aortic . Dobutamine stress echocardiography can be used to repair should be performed at the time of cardiac differentiate between pseudosevere aortic stenosis surgery. and low-flow low-gradient severe aortic stenosis. Bibliography Bibliography Su,erdlon NJ, Wu WW Schermerhom ML. Open and endovascular manage Ofto CM. Nishimura RA, Bonow RO. et al. 2020 ACC,,AI1A guideline for the ment of aortic aneurysms. Circ Res. 2019112,1:617 661. [PMID: 30761]2061 management of patients with valvular heart disease: a report of the doi:10.1161 ClRCRESAHA.ll8.313186 American College of Cardiologr' American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2O21:143:e72- e227. IPMI I): 333321501 doi:10.1161 /ClR.O00OOOOOOOOoO923 Item 91 Item 92 Answer: D Educational Objective: Diagnose pulmonary regurgita- tr tr Answer: B Educational Objective: Treat thoracic aortic aneurysm tion in a patient with repaired tetralory of Fallot. 'I he most likel1'cliirgnosis iu this prlticnt \\,ith repaired tetral with aortic repair in a patient who requires open heart ogy of Fallot ('l OIi) is pulmonary regLrrgitation (Option D). surgery. 'l'Ol is characterized lry a large subaortic ventricular septal The most appropriate additional inten'ention to intprove defL'ct (VSD), intirr.rdibr-rlar and/or v:tlvular pulmonary ste clinical orltcomes in this complex patient is aortic l,alrre nosis. aortic ovcrriclc. ancl right ventricnlar \pertroph1,.

Item 91 Item 92 Answer: D Educational Objective: Diagnose pulmonary regurgita- tr tr Answer: B Educational Objective: Treat thoracic aortic aneurysm tion in a patient with repaired tetralory of Fallot. 'I he most likel1'cliirgnosis iu this prlticnt \\,ith repaired tetral with aortic repair in a patient who requires open heart ogy of Fallot ('l OIi) is pulmonary regLrrgitation (Option D). surgery. 'l'Ol is characterized lry a large subaortic ventricular septal The most appropriate additional inten'ention to intprove defL'ct (VSD), intirr.rdibr-rlar and/or v:tlvular pulmonary ste clinical orltcomes in this complex patient is aortic l,alrre nosis. aortic ovcrriclc. ancl right ventricnlar \pertroph1,. 202

Answers and Critiques tr CONT, TOF replir involves VSD putch closure and relief'of pul lnor1ary stenosis, right r,entricular ontflon tract <tbstruction by transannular patch plirccr-nent. 'fhe trans:rnnulirr patch with empagliflozin (Option A). Optimal medical therapy, including qqgressive risk factor reduction and glucose control, is fbundational for patients with diabetes mellitus to reduce disrupts integrit),of the pulmor.rary ralve. resulting in severe the risk for clinical ASCVD events. The American Diabetes pulmonary regurgitation, which in turn caLlses right heart Association (ADA) and the American College of Cardiologz eniargement, tricuspid rcgllrgitation, excrcise Iimitation, recommend introducing a sodium-glucose cotransporter 2 and both atriirl and ventricular arrhythn.rias. l)uhnonary (SGLI2) inhibitor or glucagon-like peptide 1 (GLP 1) receptor regurgitation is the mctst contnton reason fbr reoperatior-r agonist with demonstrated cardiovascular benefit as part of after TOF repair. Severe pulntonary regurgitiition causes a glycemic control regimen in patients with tlpe 2 diabetes a diastolic [lurmur heard at the left sternal burder that and clinical ASCVD. If the patient is already taking metformin increases in intensity with inspiration. Adclitional clinical combined with another therapeutic agent or agents and is not fbatures include a parasternal lift ancl a soft sysblic pulmo taking an SGLI2 inhibitor or GLP-I receptor agonist, the ADA nary outllor,r, lnurmur. A singlc S, is heard because pulmo- recommends considering switching to one of these agents, tt nary rralve iutcgrity is disruptcd bt,the transannular p:rtch. which reduce the risk for ASCVD events regardless of the o Aortic corrctation (Option A) is associated \{ith a s}-s- hemoglobin A,. level. 'lhis patient has high risk cardiovas C' tolic or continuous murntLtr hcard in the left infiaclarricular cular features given his diabetes and history ofnondisabling rJ region or over the back. A lrurrrlur fion.r collatcral intercos stroke. Use of SGLI2 inhibitors in this population is associ !, tal vcsscls nray also be audible and palpablc over the chest ated with a 14'1, reduction in cardiovascular death. Patients tu r'r,a1l. Filty percent of patients rvith aortic corrrctation hare with previous amputation, severe peripheral vascular disease, UI

tr CONT, TOF replir involves VSD putch closure and relief'of pul lnor1ary stenosis, right r,entricular ontflon tract <tbstruction by transannular patch plirccr-nent. 'fhe trans:rnnulirr patch with empagliflozin (Option A). Optimal medical therapy, including qqgressive risk factor reduction and glucose control, is fbundational for patients with diabetes mellitus to reduce disrupts integrit),of the pulmor.rary ralve. resulting in severe the risk for clinical ASCVD events. The American Diabetes pulmonary regurgitation, which in turn caLlses right heart Association (ADA) and the American College of Cardiologz eniargement, tricuspid rcgllrgitation, excrcise Iimitation, recommend introducing a sodium-glucose cotransporter 2 and both atriirl and ventricular arrhythn.rias. l)uhnonary (SGLI2) inhibitor or glucagon-like peptide 1 (GLP 1) receptor regurgitation is the mctst contnton reason fbr reoperatior-r agonist with demonstrated cardiovascular benefit as part of after TOF repair. Severe pulntonary regurgitiition causes a glycemic control regimen in patients with tlpe 2 diabetes a diastolic [lurmur heard at the left sternal burder that and clinical ASCVD. If the patient is already taking metformin increases in intensity with inspiration. Adclitional clinical combined with another therapeutic agent or agents and is not fbatures include a parasternal lift ancl a soft sysblic pulmo taking an SGLI2 inhibitor or GLP-I receptor agonist, the ADA nary outllor,r, lnurmur. A singlc S, is heard because pulmo- recommends considering switching to one of these agents, tt nary rralve iutcgrity is disruptcd bt,the transannular p:rtch. which reduce the risk for ASCVD events regardless of the o Aortic corrctation (Option A) is associated \{ith a s}-s- hemoglobin A,. level. 'lhis patient has high risk cardiovas C' tolic or continuous murntLtr hcard in the left infiaclarricular cular features given his diabetes and history ofnondisabling rJ region or over the back. A lrurrrlur fion.r collatcral intercos stroke. Use of SGLI2 inhibitors in this population is associ !, tal vcsscls nray also be audible and palpablc over the chest ated with a 14'1, reduction in cardiovascular death. Patients tu r'r,a1l. Filty percent of patients rvith aortic corrrctation hare with previous amputation, severe peripheral vascular disease, UI a bicuspicl aortic valve. Auscultation of the hcirrt mir1, rereal neuropathy, or diabetic foot ulcers should exercise caution o I t an ejection click. a sl.stolic nrurnrur at the cardiac base. or. with canagliflozin and ertugliflozin. It is unclear whether this = tr sometinles, arr Sr. Tl-ris paticnt's murmur is not compat- caution should be applied to all drugs in the class. ible with coirrctation. and coarttation is not a long term This patient's LDL cholesterol level is well controlled, and expectecl outcome forTOF repair. the potential benefit of lowering LDL cholesterol levels below In aortic regurgitation (Option B), :r cliastolic murmur this Ievel using ezetimibe (Option B) has not been shown. is generalll,heard at the lclt stcrnal borcler ancl cloes not Screening for asymptomatic coronary artery disease increase in inter-rsit1' $'itli inspiration. Right ventricular in patients with diabetes is controversial. Without proven prominence on physical exarrirldtioll would not be erpectecl outcome beneflt, routine stress testing with exercise ECG i in a paticnt rvith aortic regurgitation. (Option C) in asymptomatic individuals, such as this patient, The rumbling diastolic murmur of mitral stenosis is not recommended. I (Option C) is best hearci at thc apex and does not vary with No additional management (Option D) is inappropriate inspiration. 'lhe murmur is typicalll,preceded b1'an opening for this patient at increased risk for additional ASCVD events. snap. N,{itral stenosis is not a recognized late con.rplication of Tight glycemic control reduces microvascular complications; TOF repair. however, it does not reduce the risk fbr myocardial infarction ; (MI). The use of SGLI2 inhibitors and GLP-I receptor agonists IEY POIl{IT in patients with type 2 diabetes has been shown to reduce o Severe pulmonary regurgitation causes a diastolic rates oflacute MI, stroke, and cardiovascular death. These ben- murmur heard at the left sternal border that increases efits seem to be unrelated to their glucose lowering eflects. : in intensity with inspiration, a parasternal lift, and a f,EY POIf,Is soft systolic pulmonary outflow murmur. o Pulmonary regurgitation is the most common postop . A sodium-glucose cotransporter 2 inhibitor or glucagon- I like peptide 1 receptor agonist with demonstrated car- erative sequela of tetralory of Fallot repair. diovascular disease benefit should be included as part of a g$cemic control regimen in patients with type 2 Bibliography L diabetes mellitus and clinical atherosclerotic cardio- Stout KK. Daniels CJ. Aboulhosn JA. et al. 2018 AHA ACC guideline fbr the management of adults with congenital heart disease: s report of the vascular disease. American College of Cardiologr,rAmerican Heart Association Task Force I on Clinical Practice Guidelines. J Am Coll Cardiol. 2019r73:e81-e192. . The benefits of sodium-glucose cotransporter 2 inhib- I IPMID: 301212391 doi:10.1016/j.jacc.2018.08.1029 itors or glucagon-like peptide 1 receptor agonists in reducing atherosclerotic cardiovascular disease events t seem to be unrelated to their glucose-lowering effects.

a bicuspicl aortic valve. Auscultation of the hcirrt mir1, rereal neuropathy, or diabetic foot ulcers should exercise caution o I t an ejection click. a sl.stolic nrurnrur at the cardiac base. or. with canagliflozin and ertugliflozin. It is unclear whether this = tr sometinles, arr Sr. Tl-ris paticnt's murmur is not compat- caution should be applied to all drugs in the class. ible with coirrctation. and coarttation is not a long term This patient's LDL cholesterol level is well controlled, and expectecl outcome forTOF repair. the potential benefit of lowering LDL cholesterol levels below In aortic regurgitation (Option B), :r cliastolic murmur this Ievel using ezetimibe (Option B) has not been shown. is generalll,heard at the lclt stcrnal borcler ancl cloes not Screening for asymptomatic coronary artery disease increase in inter-rsit1' $'itli inspiration. Right ventricular in patients with diabetes is controversial. Without proven prominence on physical exarrirldtioll would not be erpectecl outcome beneflt, routine stress testing with exercise ECG i in a paticnt rvith aortic regurgitation. (Option C) in asymptomatic individuals, such as this patient, The rumbling diastolic murmur of mitral stenosis is not recommended. I (Option C) is best hearci at thc apex and does not vary with No additional management (Option D) is inappropriate inspiration. 'lhe murmur is typicalll,preceded b1'an opening for this patient at increased risk for additional ASCVD events. snap. N,{itral stenosis is not a recognized late con.rplication of Tight glycemic control reduces microvascular complications; TOF repair. however, it does not reduce the risk fbr myocardial infarction ; (MI). The use of SGLI2 inhibitors and GLP-I receptor agonists IEY POIl{IT in patients with type 2 diabetes has been shown to reduce o Severe pulmonary regurgitation causes a diastolic rates oflacute MI, stroke, and cardiovascular death. These ben- murmur heard at the left sternal border that increases efits seem to be unrelated to their glucose lowering eflects. : in intensity with inspiration, a parasternal lift, and a f,EY POIf,Is soft systolic pulmonary outflow murmur. o Pulmonary regurgitation is the most common postop . A sodium-glucose cotransporter 2 inhibitor or glucagon- I like peptide 1 receptor agonist with demonstrated car- erative sequela of tetralory of Fallot repair. diovascular disease benefit should be included as part of a g$cemic control regimen in patients with type 2 Bibliography L diabetes mellitus and clinical atherosclerotic cardio- Stout KK. Daniels CJ. Aboulhosn JA. et al. 2018 AHA ACC guideline fbr the management of adults with congenital heart disease: s report of the vascular disease. American College of Cardiologr,rAmerican Heart Association Task Force I on Clinical Practice Guidelines. J Am Coll Cardiol. 2019r73:e81-e192. . The benefits of sodium-glucose cotransporter 2 inhib- I IPMID: 301212391 doi:10.1016/j.jacc.2018.08.1029 itors or glucagon-like peptide 1 receptor agonists in reducing atherosclerotic cardiovascular disease events t seem to be unrelated to their glucose-lowering effects. i Item 93 Answer: A : Educational Objective: Treat a patient with type 2 dia- Bibliography betes mellitus and atherosclerotic cardiovascular disease I)rs SR, Everett BM, Birtcher KK, et al. 2018 ACC expert consensus decision pathway on novel therapies for cardiovascular risk reduction in patients i with a sodium-glucose cotransporter 2 inhibitor. with type 2 diabetes xnd atherosclerotic cardiovascular disease: a report of the American College of Cardiologl Task Ft)rce on Expeft Consensus The most appropriate management of this patient's athero- Decision Pathways. J Am Coll Cardiol. 2018;72:3200 3223. [PMID: sclerotic cardiovascular disease (ASCVD) is to begin treatment 304978811 doi:10.1016rj.jacc.2018.09.020

i Item 93 Answer: A : Educational Objective: Treat a patient with type 2 dia- Bibliography betes mellitus and atherosclerotic cardiovascular disease I)rs SR, Everett BM, Birtcher KK, et al. 2018 ACC expert consensus decision pathway on novel therapies for cardiovascular risk reduction in patients i with a sodium-glucose cotransporter 2 inhibitor. with type 2 diabetes xnd atherosclerotic cardiovascular disease: a report of the American College of Cardiologl Task Ft)rce on Expeft Consensus The most appropriate management of this patient's athero- Decision Pathways. J Am Coll Cardiol. 2018;72:3200 3223. [PMID: sclerotic cardiovascular disease (ASCVD) is to begin treatment 304978811 doi:10.1016rj.jacc.2018.09.020 203

Answers and Critiques Item 94 Answer: C Ed ucatio n a I O bj ective : Treat high-risk acute pericarditis. Item 95 Answer: B Educational Objective: Diagnose coronary vasospasm. tr The nlost appropriate management is to hospitalize the This patient's findings of transient dif fuse ST-segment elevation patient and begin tl,erapy with ibuprofen and colchicine with associated hemodynamic instability are most consistent (Option C). This patient meets the diagnostic criteria defin- rvith serere multivessel coronary vasospasm (Option B). Coro ing acute pericarditis, with pericarditic chest pain, a friction nary vasospasm occurs either spontaneousll' from \asomo rub on examination, ECG ch:rnges consistent rt'ith acute tor dy'sfunction or after exposure to dmgs (such as cocaine pericarditis, and a pericardial eflusion. Most patients u'ith or chemotherapeutic irgents) and is olten a diagnosis of acute pericarditis can be managed as outpatientsr hor,r,ever, exclusion. Invasive testing n,ith coronary angiographl' ma1' those rn,ith accompanying high risk features may require not reveal spontaneous vasoconstriction. and additional hospitalization for treatment and monitoring. Patients with pro\,ocative testing u,ith acetylcholine or ergonovine infu pericarditis and high-risk features, including temperature sion may be necessary to confirtn irn abnormal vasoconstric ut higher than 38.0'C (100.4'F), subacute onset. a large peri tive response. With the use ol provocative testing. coronary E cardial effusion or tamponade at presentation, oral anti vasospasm has been identified in as many as 46'X, of patients (D a^ coagulation therapy, or lack of response to treatment, may with myocardial infarction in the absence of obstructive o, require hospitalization. This patient has a pericardial eflu coronary artery disease. ECG patterns ma1'be nonspecific CL sion smaller than the size connoting high risk (diastolic or suggest ST elevation myocardial infarction. Serere cases n echo free space, 2 cm), and she does not ha\€ clinical or o1'multivessel spasrr may be ass<lciated *'ith n'idespread echocardiographic f'eatures ol tamponade. However. she ST segment elevation and possibll' r'entricular d1'srh1'th Itg does have t\ivo high risk features: subacute onset over the mia and cardiac arrest. Treatment with calcium channel .D Ut course ofa week and fever greater than 38.0 "C (100.4'F). blockade and,or nitrates can rapidly reverse coronary'\aso Because olthese features, hospitalization to initiate therapy constriction. with improventent in my'ocardial perfusion. and evaluate early response is indicated. First-line therapy symptoms, ECG abnormalities, and hernodynamics. fbr acute idiopathic pericarditis is aspirin or NSAIDs. Colchi Myocardial ischemia and injury may be the result of cine is recommended as adjunctive therapy to shorten symp coronary embolism liom atrial fibrillation or left "entric tom duration and reduce treatment failure and recurrence. ular or valvular thrombotic or infbctious processes. Unlike Patients who respond to therapy initially but develop recur coronary spasm, embolism (Option A) is identified as fixed rent pericarditis after treatment completion may benefit ('orolrdry arten obstruction. fiom a longer course ofstandard therapy lvith slow tapering. Although pulmonary embolism (Option C) has been or ttom interleukin-1 signaling blockade with rilonacept. associated rvith syncope and cardiac arrest. marked revers Outpatient treatment with ibuprof'en and colchicine ible ST segment elevation is generally not encountered. (Option A) is appropriate fbr patients with acute pericarditis Stress (takotsubo) cardiomyopath), (Option D) m:r1 who do not have high risk f'eatures. result in ST segment elevation and or deep symmetric Glucocorticoid therapy is reserved fbr patients with peri T wave inl'ersion on ECC associated with chest pain, hemo carditis that is recurrent, incessant (>4 6 weeks' duration), dynamic compromise, and elevated cardiac enzymes. These or chronic (>3 months' duration) despite standard therapy; findings, however are generally in u,clmen and are persistent uremic pericarditis not resporlsive to intensive dialysisr con rather than transient. with slort'resolution over the course traindications to NSAID therapy; or autoimmune mediated ofdays to \\eeks. pericarditis. This patient has no indication for glucocorticoid tl.rerapy, either as an inpatient or oufpatient (Options B, D). rIT POIf,Is . ECG pattems in patients with coronary artery spasm t(tY PotxIs may suggest ST-elevation myocardial infarction; severe o First-line therapy for acute idiopathic pericarditis is cases of multivessel spasm may be associated with aspirin or NSAIDs and colchicine. widespread ST-segment elevation. o Patients with acute pericarditis and high-risk features, . Treatment of coronary artery vasospasm with calcium including temperature higher than 38.0 'C (100.4'F), channel blockade and/or nitrates can rapidly reverse subacute onset, a large pericardial effrrsion or tampon- coronary vasoconstriction, with improvement in ade at presentation, oral anticoagulation therapy, or lack myocardial perfusion, symptoms, ECG abnormalities, of response to treatrnent, may require hospitalization. and hemodlmamics.

Item 94 Answer: C Ed ucatio n a I O bj ective : Treat high-risk acute pericarditis. Item 95 Answer: B Educational Objective: Diagnose coronary vasospasm. tr The nlost appropriate management is to hospitalize the This patient's findings of transient dif fuse ST-segment elevation patient and begin tl,erapy with ibuprofen and colchicine with associated hemodynamic instability are most consistent (Option C). This patient meets the diagnostic criteria defin- rvith serere multivessel coronary vasospasm (Option B). Coro ing acute pericarditis, with pericarditic chest pain, a friction nary vasospasm occurs either spontaneousll' from \asomo rub on examination, ECG ch:rnges consistent rt'ith acute tor dy'sfunction or after exposure to dmgs (such as cocaine pericarditis, and a pericardial eflusion. Most patients u'ith or chemotherapeutic irgents) and is olten a diagnosis of acute pericarditis can be managed as outpatientsr hor,r,ever, exclusion. Invasive testing n,ith coronary angiographl' ma1' those rn,ith accompanying high risk features may require not reveal spontaneous vasoconstriction. and additional hospitalization for treatment and monitoring. Patients with pro\,ocative testing u,ith acetylcholine or ergonovine infu pericarditis and high-risk features, including temperature sion may be necessary to confirtn irn abnormal vasoconstric ut higher than 38.0'C (100.4'F), subacute onset. a large peri tive response. With the use ol provocative testing. coronary E cardial effusion or tamponade at presentation, oral anti vasospasm has been identified in as many as 46'X, of patients (D a^ coagulation therapy, or lack of response to treatment, may with myocardial infarction in the absence of obstructive o, require hospitalization. This patient has a pericardial eflu coronary artery disease. ECG patterns ma1'be nonspecific CL sion smaller than the size connoting high risk (diastolic or suggest ST elevation myocardial infarction. Serere cases n echo free space, 2 cm), and she does not ha\€ clinical or o1'multivessel spasrr may be ass<lciated *'ith n'idespread echocardiographic f'eatures ol tamponade. However. she ST segment elevation and possibll' r'entricular d1'srh1'th Itg does have t\ivo high risk features: subacute onset over the mia and cardiac arrest. Treatment with calcium channel .D Ut course ofa week and fever greater than 38.0 "C (100.4'F). blockade and,or nitrates can rapidly reverse coronary'\aso Because olthese features, hospitalization to initiate therapy constriction. with improventent in my'ocardial perfusion. and evaluate early response is indicated. First-line therapy symptoms, ECG abnormalities, and hernodynamics. fbr acute idiopathic pericarditis is aspirin or NSAIDs. Colchi Myocardial ischemia and injury may be the result of cine is recommended as adjunctive therapy to shorten symp coronary embolism liom atrial fibrillation or left "entric tom duration and reduce treatment failure and recurrence. ular or valvular thrombotic or infbctious processes. Unlike Patients who respond to therapy initially but develop recur coronary spasm, embolism (Option A) is identified as fixed rent pericarditis after treatment completion may benefit ('orolrdry arten obstruction. fiom a longer course ofstandard therapy lvith slow tapering. Although pulmonary embolism (Option C) has been or ttom interleukin-1 signaling blockade with rilonacept. associated rvith syncope and cardiac arrest. marked revers Outpatient treatment with ibuprof'en and colchicine ible ST segment elevation is generally not encountered. (Option A) is appropriate fbr patients with acute pericarditis Stress (takotsubo) cardiomyopath), (Option D) m:r1 who do not have high risk f'eatures. result in ST segment elevation and or deep symmetric Glucocorticoid therapy is reserved fbr patients with peri T wave inl'ersion on ECC associated with chest pain, hemo carditis that is recurrent, incessant (>4 6 weeks' duration), dynamic compromise, and elevated cardiac enzymes. These or chronic (>3 months' duration) despite standard therapy; findings, however are generally in u,clmen and are persistent uremic pericarditis not resporlsive to intensive dialysisr con rather than transient. with slort'resolution over the course traindications to NSAID therapy; or autoimmune mediated ofdays to \\eeks. pericarditis. This patient has no indication for glucocorticoid tl.rerapy, either as an inpatient or oufpatient (Options B, D). rIT POIf,Is . ECG pattems in patients with coronary artery spasm t(tY PotxIs may suggest ST-elevation myocardial infarction; severe o First-line therapy for acute idiopathic pericarditis is cases of multivessel spasm may be associated with aspirin or NSAIDs and colchicine. widespread ST-segment elevation. o Patients with acute pericarditis and high-risk features, . Treatment of coronary artery vasospasm with calcium including temperature higher than 38.0 'C (100.4'F), channel blockade and/or nitrates can rapidly reverse subacute onset, a large pericardial effrrsion or tampon- coronary vasoconstriction, with improvement in ade at presentation, oral anticoagulation therapy, or lack myocardial perfusion, symptoms, ECG abnormalities, of response to treatrnent, may require hospitalization. and hemodlmamics. Bibliography Bibliography Adler Y, Charron B Imazio M, et al; ESC Scientific Document Group. 2O1S Tamis-Holland JE, Jneid H, Reynolds HR, et al; American Heart Association ESC guidelines for the diagnosis and management ofpericardial diseases: Interventional Cardiovascular Care Committee ofthe Council on Clinical the Task Force for the Diagnosis and Management ofPericardial Diseases Cardiologr; Council on Cardiovascular and Stroke Nursing; Council on ofthe European Society of Cardiolory (ESC) Endorsed by: The European Epidemiologi and Prevention; and Council on Quality of Care and Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2015;36: 2921-2964. IPMID' 26320112] doi:10.1093/eurheartj/ehv318 Outcomes Research. Contemporary diagnosis and management of patients with myocardial infarction in the absence ofobstructive coronary \ 204

Answers and Critiques anery disease: a scientific statement from the American Heart Association. Circulation. 2019;139:e891 e908. IPMID: 30913893] doi:10.1161/CIR. rEY POIXI 0000000000000670 . Long-acting nitrates provide a constant level ofvasodi- lation and q.,rnptom relief throughout the day, but a daily nitrate-free interval is required to avoid tolerance. Item 95 Answer: C Educational Objective: Manage nitrate tolerance by Bibliography reducing the dose frequency. Katz D, Gavin MC. Stable ischemic heart disease. Ann Intern Med. 2019: l71tlTc17 ITC32. IPMID: 31382288] doi:10.7326lAlTC2Ol9O8060 Once-daily isosorbide mononitrate dosing (Option C) is the most appropriate management. Nitrates improve myo- cardial oxygen delivery through coronary vasodilation and decrease oxygen consumption by reducing preload. They are an important component of anginal symptom control. Item 97 Answer: B Ed ucationa I Objective: Diagnose ibrutinib-related atrial tr ut fibrillation. (l, Long acting nitrates, such as isosorbide mononitrate and 'lhe most likely contributor k) the patient's atrial fibrilla ET patch formulations, provide a constant level of vasodilation and symptom relief throughout the day. However, a nitrate tion is ibrutinib (Option B). Ibrutinib, a tyrosine kinase rJ fiee interval of B to 12 hours daily is required to avoid nitrate inhibitor, is an efi'ective trcatlncnt lbr chronic lympho E tolerance, the clinically apparent effect ofprolonged nitrate cytic leukemia and various B cell lymphomas. It has becr.t .E rcportecl to cause atrial fibrill:rtion in up to 16')i, of patie uts. tl exposure reducing nitrate efficacy. This patient has experi- (l, enced an increase in anginal symptoms with an increase of anri this can be a tl-rerapy linriting rtclverse efl'ect. In one nreta anall,sis. the incidence ol ibmtinib associatecl atri:ll I,l = isosorbide mononitrate to twice daily dosing, and the most reasonable next step is to decrease the frequency of admin- librillatior.r r,vas 5.77 per 100 persolr years. much highcr istration to once daily to restore a nitrate-free interval and than in tl.re general population. Ne\,\, onset atrial fibrillrt nitrate's beneflcial eflects on blood pressure and symptoms. tion in patients r.t,ith cancer is associated increased risk fbr heart failure anci thronrboenrbolistn."vithp Blockers Calcium channel blockade may be useful in patients with angina who are symptomatic despite B blocker ther lre usually used saf'ely fbr rate control. Although diltiazenr apy or have intolerance to p blockers. This patient is already and verapamil are effective in blocl<ing the atrioventricular taking the nondihydropyridine calcium channel blocker node, they are moderate cytochrornc P450 3A4 inhibi diltiazem for blood pressure and rate control, and given tors. and they may signilicirntly iltcrease plasma lcvcls his persistent hypertension (goal systolic blood pressure of ibrutinib through this nrechanism. Ibrutinib irtcrertscs <130 mm Hg), it would be reasonable to increase diltiazem cligoxin plasma levels. r'r,hich mav increase the potential before adding a dihydropyridine calcium channel blocker, firr digoxin toricity: such as amlodipine (Option A), as long as the resting heart Myocardial inlarction (Option A) is unlikelli 'lhis rate remains above 55/min. However, the patient's blood patient's symptoms have been present fbr 1 to 2 days. Given pressure may reach target by reducing isosorbide mono the nonnal troponin level. irbsence ol chest pain, nortnltl nitrate to restore the eflectiveness of the drug on his blood lcft ventricular systolic lirnctitlt.t without a regittnal wall pressure and anginal symptoms. lurotion abnormality, and altsetrce rif specific liCG changes, it Treatment for hypertension should include drug classes is r-rnlikely that ml,ocardial infar-ction is causing the paticllt's

anery disease: a scientific statement from the American Heart Association. Circulation. 2019;139:e891 e908. IPMID: 30913893] doi:10.1161/CIR. rEY POIXI 0000000000000670 . Long-acting nitrates provide a constant level ofvasodi- lation and q.,rnptom relief throughout the day, but a daily nitrate-free interval is required to avoid tolerance. Item 95 Answer: C Educational Objective: Manage nitrate tolerance by Bibliography reducing the dose frequency. Katz D, Gavin MC. Stable ischemic heart disease. Ann Intern Med. 2019: l71tlTc17 ITC32. IPMID: 31382288] doi:10.7326lAlTC2Ol9O8060 Once-daily isosorbide mononitrate dosing (Option C) is the most appropriate management. Nitrates improve myo- cardial oxygen delivery through coronary vasodilation and decrease oxygen consumption by reducing preload. They are an important component of anginal symptom control. Item 97 Answer: B Ed ucationa I Objective: Diagnose ibrutinib-related atrial tr ut fibrillation. (l, Long acting nitrates, such as isosorbide mononitrate and 'lhe most likely contributor k) the patient's atrial fibrilla ET patch formulations, provide a constant level of vasodilation and symptom relief throughout the day. However, a nitrate tion is ibrutinib (Option B). Ibrutinib, a tyrosine kinase rJ fiee interval of B to 12 hours daily is required to avoid nitrate inhibitor, is an efi'ective trcatlncnt lbr chronic lympho E tolerance, the clinically apparent effect ofprolonged nitrate cytic leukemia and various B cell lymphomas. It has becr.t .E rcportecl to cause atrial fibrill:rtion in up to 16')i, of patie uts. tl exposure reducing nitrate efficacy. This patient has experi- (l, enced an increase in anginal symptoms with an increase of anri this can be a tl-rerapy linriting rtclverse efl'ect. In one nreta anall,sis. the incidence ol ibmtinib associatecl atri:ll I,l = isosorbide mononitrate to twice daily dosing, and the most reasonable next step is to decrease the frequency of admin- librillatior.r r,vas 5.77 per 100 persolr years. much highcr istration to once daily to restore a nitrate-free interval and than in tl.re general population. Ne\,\, onset atrial fibrillrt nitrate's beneflcial eflects on blood pressure and symptoms. tion in patients r.t,ith cancer is associated increased risk fbr heart failure anci thronrboenrbolistn."vithp Blockers Calcium channel blockade may be useful in patients with angina who are symptomatic despite B blocker ther lre usually used saf'ely fbr rate control. Although diltiazenr apy or have intolerance to p blockers. This patient is already and verapamil are effective in blocl<ing the atrioventricular taking the nondihydropyridine calcium channel blocker node, they are moderate cytochrornc P450 3A4 inhibi diltiazem for blood pressure and rate control, and given tors. and they may signilicirntly iltcrease plasma lcvcls his persistent hypertension (goal systolic blood pressure of ibrutinib through this nrechanism. Ibrutinib irtcrertscs <130 mm Hg), it would be reasonable to increase diltiazem cligoxin plasma levels. r'r,hich mav increase the potential before adding a dihydropyridine calcium channel blocker, firr digoxin toricity: such as amlodipine (Option A), as long as the resting heart Myocardial inlarction (Option A) is unlikelli 'lhis rate remains above 55/min. However, the patient's blood patient's symptoms have been present fbr 1 to 2 days. Given pressure may reach target by reducing isosorbide mono the nonnal troponin level. irbsence ol chest pain, nortnltl nitrate to restore the eflectiveness of the drug on his blood lcft ventricular systolic lirnctitlt.t without a regittnal wall pressure and anginal symptoms. lurotion abnormality, and altsetrce rif specific liCG changes, it Treatment for hypertension should include drug classes is r-rnlikely that ml,ocardial infar-ction is causing the paticllt's demonstrated to reduce cardiovascular events in patients :rtrial fibrillation. '[his patient's \Vells score is 2.5 points based on with diabetes mellitus. ACE inhibitors or angiotensin recep tor blockers are recommended as flrst-line therapy for the presence of malignancy ar.rd heart rate gre.ltcr thilll hypertension in patients with diabetes and coronary artery 100,'rnin. placing him into a motlerate risk group (pulnlrr disease. A reduction in the lisinopril dosage (Option B) is nary embolisn.r ur.rlikell. b-y ntodifiecl \Vells criteriir). 'lhc not indicated; an increase in dosage may be indicated to nomal D climer le."'el ancl ttort.t-tal right heart function ot-t attain the desired systolic blood pressure goal of less than cchocirrcliography rech-rce t hc cl i n ical probabi lity of' th rrltn 130 mm Hg if the patient does not respond to isosorbide bocmbolisnr (Option C). 'lhe patient has normirl thyroicl stimulating hormot.tc mononitrate dosage reduction. ar.rcl fiee tl-ryroxine levels. making thyrotoxicosis (Option I)) Coronary angiography is an invasive procedure that carries risk for contrast nephropathy or reactions, vascu- uulike[1r lar complications (1% to 2"1,), myocardial infarction (0.1'1,), XEY POII{T stroke (<0.1%), or death (0.1'1,). It should be reserved for . Ibrutinib, a BT osine kinase inhibitor, is associated with patients with unstable or medically refractory symptoms increased rates of atrial fibrillation. and uncertain anatomy. Given this patient's recently docu- mented nonrevascularizable coronary artery disease with Bibliography out clinical flndings or features suggesting acute coronary Canatra S, Sharma A, Shah S, et al. Ibrutinib associated atrial fibrillation. syndrome, repeat coronary angiography (Option D) is not JACC Clin Electrophysiol. 2018;4:1491 500. IPMID: 30573111] doi:10.1016/ indicated. i.iacep.2018.06.004

demonstrated to reduce cardiovascular events in patients :rtrial fibrillation. '[his patient's \Vells score is 2.5 points based on with diabetes mellitus. ACE inhibitors or angiotensin recep tor blockers are recommended as flrst-line therapy for the presence of malignancy ar.rd heart rate gre.ltcr thilll hypertension in patients with diabetes and coronary artery 100,'rnin. placing him into a motlerate risk group (pulnlrr disease. A reduction in the lisinopril dosage (Option B) is nary embolisn.r ur.rlikell. b-y ntodifiecl \Vells criteriir). 'lhc not indicated; an increase in dosage may be indicated to nomal D climer le."'el ancl ttort.t-tal right heart function ot-t attain the desired systolic blood pressure goal of less than cchocirrcliography rech-rce t hc cl i n ical probabi lity of' th rrltn 130 mm Hg if the patient does not respond to isosorbide bocmbolisnr (Option C). 'lhe patient has normirl thyroicl stimulating hormot.tc mononitrate dosage reduction. ar.rcl fiee tl-ryroxine levels. making thyrotoxicosis (Option I)) Coronary angiography is an invasive procedure that carries risk for contrast nephropathy or reactions, vascu- uulike[1r lar complications (1% to 2"1,), myocardial infarction (0.1'1,), XEY POII{T stroke (<0.1%), or death (0.1'1,). It should be reserved for . Ibrutinib, a BT osine kinase inhibitor, is associated with patients with unstable or medically refractory symptoms increased rates of atrial fibrillation. and uncertain anatomy. Given this patient's recently docu- mented nonrevascularizable coronary artery disease with Bibliography out clinical flndings or features suggesting acute coronary Canatra S, Sharma A, Shah S, et al. Ibrutinib associated atrial fibrillation. syndrome, repeat coronary angiography (Option D) is not JACC Clin Electrophysiol. 2018;4:1491 500. IPMID: 30573111] doi:10.1016/ indicated. i.iacep.2018.06.004 205

I l I I 1 : Answers and Critiques I 1 iI with an ischemic stroke or transient ischemic attack of tr Item 98 Answer: B t undetermined source. occult intermittent atrial flbrillation 1

iI with an ischemic stroke or transient ischemic attack of tr Item 98 Answer: B t undetermined source. occult intermittent atrial flbrillation 1 Educational Objective: Treat cardiogenic shock in the J (AF) is thought to be present in up to 25"/,, of cases, and 1 setting of non- ST-elevation myocardial infarction. I prolonged ambulatory ECG monitoring may be indicated This patient is in cardiogenic shock and requires placement ol for detection. According to the 2019 American College of ! I an intra aortic balloon pump (Option B). Cardirtgenic shock is Cardiologi/American Heart Association/Heart Rhythm t characterizecl by signs ancl syr-nptoms of low cardiac output r,r'itl.r Socieg AF focused update, in a patient with an ischemic 1

Educational Objective: Treat cardiogenic shock in the J (AF) is thought to be present in up to 25"/,, of cases, and 1 setting of non- ST-elevation myocardial infarction. I prolonged ambulatory ECG monitoring may be indicated This patient is in cardiogenic shock and requires placement ol for detection. According to the 2019 American College of ! I an intra aortic balloon pump (Option B). Cardirtgenic shock is Cardiologi/American Heart Association/Heart Rhythm t characterizecl by signs ancl syr-nptoms of low cardiac output r,r'itl.r Socieg AF focused update, in a patient with an ischemic 1 systolic blood pressure less than 90 mm Hg (or suppon to main stroke of unknown cause in whom external ambulatory l I tain blood pressure) and evidence ot end organ hypopefiusion. ECG monitoring is inconclusive, implantation of a cardiac i ! This paticnt has already been revascularized: tl.rus. the fbcus ot monitor (loop recorder) is reasonable to optimize detection i therapy should be on supporting the cardiac outpul. Appropri of silent AF (class 2a recommendation). The 2019 guide- I ate therapics include in<"rtropes, vasopressors, and mechani line on the management of acute stroke from the Amer- I

systolic blood pressure less than 90 mm Hg (or suppon to main stroke of unknown cause in whom external ambulatory l I tain blood pressure) and evidence ot end organ hypopefiusion. ECG monitoring is inconclusive, implantation of a cardiac i ! This paticnt has already been revascularized: tl.rus. the fbcus ot monitor (loop recorder) is reasonable to optimize detection i therapy should be on supporting the cardiac outpul. Appropri of silent AF (class 2a recommendation). The 2019 guide- I ate therapics include in<"rtropes, vasopressors, and mechani line on the management of acute stroke from the Amer- I cal support (such as balloon pumps, percutaneous ventricular ican Heart Association/American Academy of Neurologr ! assist devices, and extracoqrure:rl membrane og,genation). notes that the effectiveness of prolonged cardiac monitoring I vt E I)igoxin (Option A) is a r,r,eak inotrope that has bee'n shou,n during hospitalization after acute ischemic stroke to guide 1

cal support (such as balloon pumps, percutaneous ventricular ican Heart Association/American Academy of Neurologr ! assist devices, and extracoqrure:rl membrane og,genation). notes that the effectiveness of prolonged cardiac monitoring I vt E I)igoxin (Option A) is a r,r,eak inotrope that has bee'n shou,n during hospitalization after acute ischemic stroke to guide 1 ID i to reduce hospitalizations fbr patients $dth chronic hearl fai]ure. treatment selection for prevention of recurrent stroke is UI o, It would not be helpfui fbr this patient in the acutc sctting. uncertain. However, there is some practice variation regard- l i EL In thc outpatient sctting. B blockers have been shown ing the duration of "proionged" monitoring and the burden n to improve survival in patients with heart failure who have of detected, asymptomatic AF that warrants anticoagula I n no signs of volume overload. ln the acute setting. cspecialll' tion. Also, the sequence of evaluation varies for example, st fbr palients receiving norepinephrine. r,r{rich is a potent I

EL In thc outpatient sctting. B blockers have been shown ing the duration of "proionged" monitoring and the burden n to improve survival in patients with heart failure who have of detected, asymptomatic AF that warrants anticoagula I n no signs of volume overload. ln the acute setting. cspecialll' tion. Also, the sequence of evaluation varies for example, st fbr palients receiving norepinephrine. r,r{rich is a potent I .D extended rhythm monitoring flrst versus testing for intracar i vt vasopressor and has inotropic properties mediated through diac shunt with transesophageal echocardiography. I the cardiirc B receptor. addirrg a p blocker, sucl.r irs metopro It would be premature to switch this patient's antiplate I lol (Option C), would not be ilppropriate. let therapy to anticoagulation (Option A) in the absence of I

.D extended rhythm monitoring flrst versus testing for intracar i vt vasopressor and has inotropic properties mediated through diac shunt with transesophageal echocardiography. I the cardiirc B receptor. addirrg a p blocker, sucl.r irs metopro It would be premature to switch this patient's antiplate I lol (Option C), would not be ilppropriate. let therapy to anticoagulation (Option A) in the absence of I 'l ln the short term, thc fbcr-rs should be or.r ltenrodl,'nanric conflrmed AF. l support irr the hopes of imltrovir-rg clrrdiac lirnctior-r ur,er the Similarly, consideration of left atrial appendage occlusion next ,18 hours r,r'ith revlrsculurization rirther thin urgent (Option B) would be premature. This procedure is reserved l .,i transler to a transplant ceuter (Option D). primarily for patients with known AF who are at significant I Vasopressin (Option [) may be addcd to norepinepl-r i risk for stroke and have complicating medical comorbid con- rine to lurther raise bloocl prcssure or rccluce the close ot ditions that make oral anticoagulation high risk or ineflective. I norepinephrine in patients with r,,asodilatory shock (cold .l: This patient does not have conflrmed AF, nor has oral antico and dry). ln general. r'asoprcssir.r shcluld n<tt ltc used in car l agulation failed to prevent stroke associated with AE diogenic (r,r'urm and net) or hypovolemic shock. Thrombophilia evaluation (Option D) is not routinely I

'l ln the short term, thc fbcr-rs should be or.r ltenrodl,'nanric conflrmed AF. l support irr the hopes of imltrovir-rg clrrdiac lirnctior-r ur,er the Similarly, consideration of left atrial appendage occlusion next ,18 hours r,r'ith revlrsculurization rirther thin urgent (Option B) would be premature. This procedure is reserved l .,i transler to a transplant ceuter (Option D). primarily for patients with known AF who are at significant I Vasopressin (Option [) may be addcd to norepinepl-r i risk for stroke and have complicating medical comorbid con- rine to lurther raise bloocl prcssure or rccluce the close ot ditions that make oral anticoagulation high risk or ineflective. I norepinephrine in patients with r,,asodilatory shock (cold .l: This patient does not have conflrmed AF, nor has oral antico and dry). ln general. r'asoprcssir.r shcluld n<tt ltc used in car l agulation failed to prevent stroke associated with AE diogenic (r,r'urm and net) or hypovolemic shock. Thrombophilia evaluation (Option D) is not routinely I rEY PO I lIIS indicated among older patients with embolic stroke of unde- termined source. I . Treatment of cardiogenic shock initially focuses on reversing the cause of shock, such as reperfusion in l(tv PotltI 1

rEY PO I lIIS indicated among older patients with embolic stroke of unde- termined source. I . Treatment of cardiogenic shock initially focuses on reversing the cause of shock, such as reperfusion in l(tv PotltI 1 : the setting of acute coronary syndrome. . In patients with an ischemic stroke of unknown cause 1 . In cardiogenic shock, appropriate therapies to support in whom external ambulatory monitoring is incon- l cardiac output include inotropes, vasopressors, and clusive, implantation of a cardiac monitor (loop : mechanical support (such as balloon pumps, percuta- recorder) is reasonable to optimize detection of silent neous ventricular assist devices, and extracorporeal atrial fibrillation. ;

. In cardiogenic shock, appropriate therapies to support in whom external ambulatory monitoring is incon- l cardiac output include inotropes, vasopressors, and clusive, implantation of a cardiac monitor (loop : mechanical support (such as balloon pumps, percuta- recorder) is reasonable to optimize detection of silent neous ventricular assist devices, and extracorporeal atrial fibrillation. ; I membrane oxygenation). Bibliography Bibliography January Cl. \{hnn LS. Calkins H, et al. 2019 AHATACC,,HRS focused update van Diepen S, Katz JN, Albert NM. et al; American Heart Association Council ol the 201.1 AHATACC,IIRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiologr/ on Clinical Cardiolory; Council on Cardiovascular and Stroke Nursing; American Heart Association Task Force on Clinical practice Guidelines Council on Quality ofCare and Outcomes Research; and Mission: LifelinE. and the Heart Rhythm Society in Collaboration With the Society of Contemporary management ofcardkrgenic shock: a scientific statement 'l'horacic Surgeons. Circulation. 2019;140:e125-51. from the American Heart Association. Circulation. 2017;136:e222 e26g. [pMID: SOOAObat] doi: 10.1161 /CIR.0000000OO000066S ! IPMID: 289239881 doi:10.1161 /CI R.000000000000052s

I membrane oxygenation). Bibliography Bibliography January Cl. \{hnn LS. Calkins H, et al. 2019 AHATACC,,HRS focused update van Diepen S, Katz JN, Albert NM. et al; American Heart Association Council ol the 201.1 AHATACC,IIRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiologr/ on Clinical Cardiolory; Council on Cardiovascular and Stroke Nursing; American Heart Association Task Force on Clinical practice Guidelines Council on Quality ofCare and Outcomes Research; and Mission: LifelinE. and the Heart Rhythm Society in Collaboration With the Society of Contemporary management ofcardkrgenic shock: a scientific statement 'l'horacic Surgeons. Circulation. 2019;140:e125-51. from the American Heart Association. Circulation. 2017;136:e222 e26g. [pMID: SOOAObat] doi: 10.1161 /CIR.0000000OO000066S ! IPMID: 289239881 doi:10.1161 /CI R.000000000000052s Item 99 Answer: C Item 100 Answer: A Educational Objective: Identiff the cause of embolic Educational Objective: Treat a patient with a mechanical stroke of undetermined source. mitral valve with warfarin. The most reasonable management is loop recorder implan_ The most appropriate antithrombotic therapy is to continue tation (Option C). Among patients aged 55 years or older the current dosage of warfarin (Option A). This patient,s

Item 99 Answer: C Item 100 Answer: A Educational Objective: Identiff the cause of embolic Educational Objective: Treat a patient with a mechanical stroke of undetermined source. mitral valve with warfarin. The most reasonable management is loop recorder implan_ The most appropriate antithrombotic therapy is to continue tation (Option C). Among patients aged 55 years or older the current dosage of warfarin (Option A). This patient,s 206

Answers and Critiques history and examination flndings are consistent with a nor Item 101 Answer: B mally functioning mechanical mitral valve. patients with a Educational Objective: Evaluate a patient with a bicuspid mechanical cardiac valve require antithrombotic therapy for aortic valve for aortopathy. thromboembolic prophylaxis. Given the increased throm bogenicity associated with mechanical versus bioprosthetic '[he most appropriate management is to perform CT angiog- cardiac valves, antithrombotic management requires anti- raphy (CTA) (Option B) or magnetic resonance angiography coagulant therapy rather than antiplatelet monotherapy. (MRA) of the thoracic aorta. The patient's symptoms and ECG With the advent of direct oral anticoagulants (dabigatran, are consistent with aortic stenosis, and an echocardiogram apixaban, rivaroxaban, edoxaban), there has been interest in reveals a bicuspid aortic valve associated with severe aortic using these agents in patients with mechanical and biopros- stenosis. Bicuspid aortic valve is frequently associated with thetic cardiac valves. However, given the data from the ran aortopathy resulting in aneurysm, dissection, and coarctation. domized RE ALIGN trial, which showed that dabigatran was Because these flndings may be associated with the need for associated with excess bleeding and thromboembolic events surgical intervention on the aorta itself, appropriate prepro vt €, compared with warfarin, dabigatran (Option D) should cedural planning for aortic valve replacement requires careful evaluation of the thoracic aorta. The initial recommended ET be avoided. The safety of other direct oral anticoagulants, including rivaroxaban (Option E), has not been assessed, imaging test is transthoracic echocardiography However, MRA lr, and these agents should not be used. lnstead, warfarin and/ or CIA is indicated when morphologr of the aortic sinuses, ?, or aspirin should be used, depending on valve type (bio- sinotubular junction, or ascending aorta cannot be assessed E au prosthetic or mechanical) and position (aortic, mitral, pul accurately with echocardiography, as is the case for this patient. Ut q, monary or tricuspid). With mechanical valves in the mitral In patients undergoing valve intervention with low pre position, guidelines recommend anticoagulation with war test probability for coronary artery disease, CT angiography vt = farin, with a goal INR of 3.0. A range ot 2.5 to 3.5 is accept- of the coronary arteries is recommended and can be per able to balance the risks ofunder and over anticoagulation lbrmed at the same time as CT angiography of the aorta. in a patient with a mechanical mitral valve. ln those u,ith intermediate or high pretest probability of Although this patient has ecchymoses, he has a normal coronary disease, invasive coronary angiography is recom hemoglobin level, no clinical evidence of overt bleeding, mended to assess coronary anatomy and guide the need for and a therapeutic INR. As a result, no change should be and type of revascularization. However, assessment of the made to his warfarin dosing or his goal INR (Option B). In aorta should occur first to rule out aortic pathologr, which practice, it is diflicult to control the INR exactly, and in the may complicate cardiac catheterization (Option A). absence of clinically significant overt bleeding, the risk fbr Exercise stress testing (Option C) is not the appropri under-anticoagulation precludes a change in INR range for ate next step in management. Exercise stress testing is con ecchymoses. traindicated in symptomatic severe aortic stenosis, given the Aspirin monotherapy (Option C) should not be used for increased risk fbr severe adverse events (sudden cardiac death). thromboembolic prophylaxis in patients with a mechanical In patients with bicuspid aortic valve and symptomatic valve. Adding aspirin (75 100 mg/d) to warfarin may be con- severe aortic stenosis, transcatheter aortic valve implanta- sidered in patients who have an indicaticin for antiplatelet tion (TAVI) (Option D) may be considered as an alternative therapy (cardiovascular or cerebrovascular disease) if their to surgical aortic valve replacement if the procedure is per bleeding risk is low Aspirin (75-100 mg/d) monotherapy is fbrmed at a Comprehensive Valve Center. However, TAVI also reasonable in patients with a bioprosthetic valve and no may not be a viable therapy in patients who require surgery additional indication for anticoagulation. because of concomitant aortopathy.

history and examination flndings are consistent with a nor Item 101 Answer: B mally functioning mechanical mitral valve. patients with a Educational Objective: Evaluate a patient with a bicuspid mechanical cardiac valve require antithrombotic therapy for aortic valve for aortopathy. thromboembolic prophylaxis. Given the increased throm bogenicity associated with mechanical versus bioprosthetic '[he most appropriate management is to perform CT angiog- cardiac valves, antithrombotic management requires anti- raphy (CTA) (Option B) or magnetic resonance angiography coagulant therapy rather than antiplatelet monotherapy. (MRA) of the thoracic aorta. The patient's symptoms and ECG With the advent of direct oral anticoagulants (dabigatran, are consistent with aortic stenosis, and an echocardiogram apixaban, rivaroxaban, edoxaban), there has been interest in reveals a bicuspid aortic valve associated with severe aortic using these agents in patients with mechanical and biopros- stenosis. Bicuspid aortic valve is frequently associated with thetic cardiac valves. However, given the data from the ran aortopathy resulting in aneurysm, dissection, and coarctation. domized RE ALIGN trial, which showed that dabigatran was Because these flndings may be associated with the need for associated with excess bleeding and thromboembolic events surgical intervention on the aorta itself, appropriate prepro vt €, compared with warfarin, dabigatran (Option D) should cedural planning for aortic valve replacement requires careful evaluation of the thoracic aorta. The initial recommended ET be avoided. The safety of other direct oral anticoagulants, including rivaroxaban (Option E), has not been assessed, imaging test is transthoracic echocardiography However, MRA lr, and these agents should not be used. lnstead, warfarin and/ or CIA is indicated when morphologr of the aortic sinuses, ?, or aspirin should be used, depending on valve type (bio- sinotubular junction, or ascending aorta cannot be assessed E au prosthetic or mechanical) and position (aortic, mitral, pul accurately with echocardiography, as is the case for this patient. Ut q, monary or tricuspid). With mechanical valves in the mitral In patients undergoing valve intervention with low pre position, guidelines recommend anticoagulation with war test probability for coronary artery disease, CT angiography vt = farin, with a goal INR of 3.0. A range ot 2.5 to 3.5 is accept- of the coronary arteries is recommended and can be per able to balance the risks ofunder and over anticoagulation lbrmed at the same time as CT angiography of the aorta. in a patient with a mechanical mitral valve. ln those u,ith intermediate or high pretest probability of Although this patient has ecchymoses, he has a normal coronary disease, invasive coronary angiography is recom hemoglobin level, no clinical evidence of overt bleeding, mended to assess coronary anatomy and guide the need for and a therapeutic INR. As a result, no change should be and type of revascularization. However, assessment of the made to his warfarin dosing or his goal INR (Option B). In aorta should occur first to rule out aortic pathologr, which practice, it is diflicult to control the INR exactly, and in the may complicate cardiac catheterization (Option A). absence of clinically significant overt bleeding, the risk fbr Exercise stress testing (Option C) is not the appropri under-anticoagulation precludes a change in INR range for ate next step in management. Exercise stress testing is con ecchymoses. traindicated in symptomatic severe aortic stenosis, given the Aspirin monotherapy (Option C) should not be used for increased risk fbr severe adverse events (sudden cardiac death). thromboembolic prophylaxis in patients with a mechanical In patients with bicuspid aortic valve and symptomatic valve. Adding aspirin (75 100 mg/d) to warfarin may be con- severe aortic stenosis, transcatheter aortic valve implanta- sidered in patients who have an indicaticin for antiplatelet tion (TAVI) (Option D) may be considered as an alternative therapy (cardiovascular or cerebrovascular disease) if their to surgical aortic valve replacement if the procedure is per bleeding risk is low Aspirin (75-100 mg/d) monotherapy is fbrmed at a Comprehensive Valve Center. However, TAVI also reasonable in patients with a bioprosthetic valve and no may not be a viable therapy in patients who require surgery additional indication for anticoagulation. because of concomitant aortopathy. I(EY POIT{TS rEY POIl{I5 o Patients with a mechanical cardiac valve require war- . Bicuspid aortic valve is frequently associated with farin anticoagulation for thromboembolic prophy aortopathy resulting in aneurysm, dissection, and laxis; dabigatran is associated with excess bleeding coarctation and requires initial assessment with and thrombosis, and the safety of other direct oral transthoracic echocardiography. anticoagulants has not been assessed. o In patients with a bicuspid aortic valve, CT angiography . In patients with a prosthetic cardiac valve, the appro- or magnetic resonance angiogfaphy ofthe thoracic aorta priate INR goal varies by type ofvalve and valve posi is indicated when morphologz olthe aortic sinuses, sino- tion, with a goal INR of 3.0 (range 2.5 3.5) for a tubularjunction, or ascending aorta cannot be assessed mechanical valve in the mitral position. accurately with transthoracic echocardiography.

I(EY POIT{TS rEY POIl{I5 o Patients with a mechanical cardiac valve require war- . Bicuspid aortic valve is frequently associated with farin anticoagulation for thromboembolic prophy aortopathy resulting in aneurysm, dissection, and laxis; dabigatran is associated with excess bleeding coarctation and requires initial assessment with and thrombosis, and the safety of other direct oral transthoracic echocardiography. anticoagulants has not been assessed. o In patients with a bicuspid aortic valve, CT angiography . In patients with a prosthetic cardiac valve, the appro- or magnetic resonance angiogfaphy ofthe thoracic aorta priate INR goal varies by type ofvalve and valve posi is indicated when morphologz olthe aortic sinuses, sino- tion, with a goal INR of 3.0 (range 2.5 3.5) for a tubularjunction, or ascending aorta cannot be assessed mechanical valve in the mitral position. accurately with transthoracic echocardiography. Bibliography Bibliography Otto CM, Nishimurx RA. Bonow RO. et al. 2020 ACC/AUA guideline lbr the Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for thc mrnagement ot patients $,ith valvular heart disease: a report of the management of patients with valvular heart disease: a report of the Anrerican College of Carcliolog American Ilcart Associiltion Joint American College of Clrtiiolory American Heart Association Joint Committee on Clinical Prirctice Guidelines. Circulation. 2021 :113:e7 ) Committee on Clinical l)ractice Guidelines. Circulation. 2o2l:143:e7) e227. IPMID: 333321 50] doi:10. I I 61,'CtR.0000oo0000000923 e227. LPMII): 333321501 doir10.1161 iCIR.0000000000000923 207

!-:*-"I: a1! c1!is1e1 Item 1O2 Answer: C Bibliography I.arber A. Chronic limb threatening ischemia. N Engl J Med. 2018:379:l7l Ed ucati o na I O bjective : Treat chronic limb-threatening 180. IP\'1lD: 2999608s] doi:10.1056/NEJMcp1709326 ischemia (critical limb ischemia).

Item 1O2 Answer: C Bibliography I.arber A. Chronic limb threatening ischemia. N Engl J Med. 2018:379:l7l Ed ucati o na I O bjective : Treat chronic limb-threatening 180. IP\'1lD: 2999608s] doi:10.1056/NEJMcp1709326 ischemia (critical limb ischemia). The most appropriate next step in the management of this patient with chronic limb-threatening ischemia (CLTI), also Item 1O3 Answer: B called critical limb ischemia, is to perform invasive angiog- Educational Objective: Prevent sudden cardiac death in raphy of the affected limb (Option C) with subsequent revas a patient with hypertrophic cardiomyopathy. cularization. CLII is characterized by more than 2 weeks of Implantable cardioverter-deflbrillator (lCD) therapy (Option B) ischemic rest pain, nonhealing wound/ulcers, or gangrene is the most appropriate treatment. Any unexplained episode in one or both legs that is attributable to objectively proven of syncope in a patient with hypertrophic cardiomyopathy peripheral artery disease (PAD). PAD can be conflrmed (HCM) represents a potential arrhythmic event and requires with ankle-brachial index testing (often <0.4 in CLTI), toe- further risk stratiflcation, including echocardiography and (,l brachial index testing, and other measures. Unlike patients ambulatory ECG monitoring for arrhythmia. The 2020 E (D with other symptoms of PAD (e.g., intermittent claudica- American College of Cardiologz/American Heart Association (a tion), patients with CLTI often cannot exercise because of q, Guideline for the Diagnosis and Treatment of Patients With skin ulceration and/or ischemic rest pain. The primary goal Hypertrophic Cardiomyopathy recommends ICD placement CL for patients with CLTI is to revascularize the limb to reduce rr for patients with HCM and previous documented cardiac -t the incidence of major amputation, and invasive angiog- arrest or sustained ventricular tachycardia (class 1 recom raphy expedites the diagnosis and allows for concurrent a endovascular revascularization. In patients who undergo mendation). For adult patients with HCM and one or more (D major risk factors for sudden cardiac death (SCD), offering Vt successful limb revascularization, the 1 year risk for major an ICD is reasonable (class 2a recommendation). Risk factors amputation is signiflcantly lower than in patients who do include SCD judged definitively or likely attributable to HCI\4 not undergo revascularization. in one or more first-degree or close relatives aged 50 years Owing to the high morbidity and mortality associated or younger, left ventricular (LV) hypertrophy of 30 mm or with CLTI, immediate referral for invasive angiography with greater in any LV segment, one or more recent episodes of endovascular revascularization is often the most eflective syncope suspected by clinical history to be arrhy,thmic in strateS/ to preserve tissue viability. Noninvasive imaging stud- nature, LV apical aneurysm, and LV ejection fraction less than ies, such as CT angiography (Option A), would result in treat 50'7,. Based on the patient's recent episode of unexplained ment time delays in this patient with CLTI and a viable limb. syncope and LV wall thickness of 30 mm, it is reasonable to Clinical trials of hyperbaric oxygen therapy (Option B) refer her for consideration ofan ICD to prevent SCD. for the treatment ofarterial ulcers have focused on patients For patients with HCM and symptoms attributable to without severe PAD and have not demonstrated a long term LV outflow tract obstruction, nonvasodilating p blockers beneflt on wound healing or an improvement in amputation- are recommended. Such symptoms typically include effort- free survival compared with sham treatment. Hyperbaric related dyspnea or chest pain. If p-blockers are ineffective or oxygen therapy is not a viable treatment option for this not tolerated, a nondihydropyridine calcium channel blocker patient who needs urgent revascularization. (verapamil or diltiazem) may be substituted. If symptoms Primary amputation (Option D) refers to amputation persist despite p blocker or nondihydropyridine calcium without attempting to salvage the limb. In patients with channel blocker therapy, adding disopyramide in combi- CLTI and limb viability, invasive angiography and revascu nation with one of the other drugs or treatment w'ith sep- larization as an initial strates/ is always preferred to primary tal reduction therapy (SRT) is recommended. This patient's major amputation of the lower extremity. Patients older than obstructive symptoms generally have been well managed on 65 years who undergo major amputation have a 1-year mor metoprolol, and her outflow tract gradient on echocardiog tality rate of nearly 50'7, and a 3-year mortality rate higher raphy does not indicate severe LV outflow tract obstruction; thanTO"/,,. thus, changing this patient's medications (Options A, D) is unnecessary. XEY POIilTS A peak LV outflow tract gradient (resting or provoked) r Chronic limb-threatening ischemia is characterized by of 50 mm Hg or greater is generally considered the threshold more than 2 weeks of ischemic rest pain, nonhealing for SRT (Option C) in patients with drug refractory symp- wound/ulcers, or gangrene in one or both legs that is toms. Referring this patient for SRT is not indicated. attributable to objectively proven peripheral artery I( EY PO I XTS disease. . In patients with chronic limb-threatening ischemia, o An implantable cardioverter-defibrillator is recom immediate invasive angiography with endovascular mended for patients with hypertrophic cardiomyopathy revascularization is often the most effective strateg/ to and previous documented cardiac arrest or sustained preserve tissue viability. ventricular tachycardia. (Continued)

The most appropriate next step in the management of this patient with chronic limb-threatening ischemia (CLTI), also Item 1O3 Answer: B called critical limb ischemia, is to perform invasive angiog- Educational Objective: Prevent sudden cardiac death in raphy of the affected limb (Option C) with subsequent revas a patient with hypertrophic cardiomyopathy. cularization. CLII is characterized by more than 2 weeks of Implantable cardioverter-deflbrillator (lCD) therapy (Option B) ischemic rest pain, nonhealing wound/ulcers, or gangrene is the most appropriate treatment. Any unexplained episode in one or both legs that is attributable to objectively proven of syncope in a patient with hypertrophic cardiomyopathy peripheral artery disease (PAD). PAD can be conflrmed (HCM) represents a potential arrhythmic event and requires with ankle-brachial index testing (often <0.4 in CLTI), toe- further risk stratiflcation, including echocardiography and (,l brachial index testing, and other measures. Unlike patients ambulatory ECG monitoring for arrhythmia. The 2020 E (D with other symptoms of PAD (e.g., intermittent claudica- American College of Cardiologz/American Heart Association (a tion), patients with CLTI often cannot exercise because of q, Guideline for the Diagnosis and Treatment of Patients With skin ulceration and/or ischemic rest pain. The primary goal Hypertrophic Cardiomyopathy recommends ICD placement CL for patients with CLTI is to revascularize the limb to reduce rr for patients with HCM and previous documented cardiac -t the incidence of major amputation, and invasive angiog- arrest or sustained ventricular tachycardia (class 1 recom raphy expedites the diagnosis and allows for concurrent a endovascular revascularization. In patients who undergo mendation). For adult patients with HCM and one or more (D major risk factors for sudden cardiac death (SCD), offering Vt successful limb revascularization, the 1 year risk for major an ICD is reasonable (class 2a recommendation). Risk factors amputation is signiflcantly lower than in patients who do include SCD judged definitively or likely attributable to HCI\4 not undergo revascularization. in one or more first-degree or close relatives aged 50 years Owing to the high morbidity and mortality associated or younger, left ventricular (LV) hypertrophy of 30 mm or with CLTI, immediate referral for invasive angiography with greater in any LV segment, one or more recent episodes of endovascular revascularization is often the most eflective syncope suspected by clinical history to be arrhy,thmic in strateS/ to preserve tissue viability. Noninvasive imaging stud- nature, LV apical aneurysm, and LV ejection fraction less than ies, such as CT angiography (Option A), would result in treat 50'7,. Based on the patient's recent episode of unexplained ment time delays in this patient with CLTI and a viable limb. syncope and LV wall thickness of 30 mm, it is reasonable to Clinical trials of hyperbaric oxygen therapy (Option B) refer her for consideration ofan ICD to prevent SCD. for the treatment ofarterial ulcers have focused on patients For patients with HCM and symptoms attributable to without severe PAD and have not demonstrated a long term LV outflow tract obstruction, nonvasodilating p blockers beneflt on wound healing or an improvement in amputation- are recommended. Such symptoms typically include effort- free survival compared with sham treatment. Hyperbaric related dyspnea or chest pain. If p-blockers are ineffective or oxygen therapy is not a viable treatment option for this not tolerated, a nondihydropyridine calcium channel blocker patient who needs urgent revascularization. (verapamil or diltiazem) may be substituted. If symptoms Primary amputation (Option D) refers to amputation persist despite p blocker or nondihydropyridine calcium without attempting to salvage the limb. In patients with channel blocker therapy, adding disopyramide in combi- CLTI and limb viability, invasive angiography and revascu nation with one of the other drugs or treatment w'ith sep- larization as an initial strates/ is always preferred to primary tal reduction therapy (SRT) is recommended. This patient's major amputation of the lower extremity. Patients older than obstructive symptoms generally have been well managed on 65 years who undergo major amputation have a 1-year mor metoprolol, and her outflow tract gradient on echocardiog tality rate of nearly 50'7, and a 3-year mortality rate higher raphy does not indicate severe LV outflow tract obstruction; thanTO"/,,. thus, changing this patient's medications (Options A, D) is unnecessary. XEY POIilTS A peak LV outflow tract gradient (resting or provoked) r Chronic limb-threatening ischemia is characterized by of 50 mm Hg or greater is generally considered the threshold more than 2 weeks of ischemic rest pain, nonhealing for SRT (Option C) in patients with drug refractory symp- wound/ulcers, or gangrene in one or both legs that is toms. Referring this patient for SRT is not indicated. attributable to objectively proven peripheral artery I( EY PO I XTS disease. . In patients with chronic limb-threatening ischemia, o An implantable cardioverter-defibrillator is recom immediate invasive angiography with endovascular mended for patients with hypertrophic cardiomyopathy revascularization is often the most effective strateg/ to and previous documented cardiac arrest or sustained preserve tissue viability. ventricular tachycardia. (Continued) 208

\ i Answers and Critiques I t Glycoprotein llb/llla inhibitors, such as tirofiban \ t l(EY P0lLTt (cqtlnued) (Option D) and eptifibatide, are potent iutravenous anti t . In patients with hypertrophic cardiomyopathy (HCM) platelet agents that are generally reserved for use at the and risk factors for sudden cardiac death (SCD), such time of coronary angiography and coronary intervention for \ I as SCD attributable to HCM in a first-degree or close treatment of significant intracoronary thrombus burden. t relative aged 50 years or younger, left ventricular (LV) Tirofibar.r rvould have no benefit ir-r tl.ris clinically stable hypertrophy of 30 mm or greater in any LV segment, patient and has the potential to increase bleeding. I \ syncope suspected to be arrhythmic in nature, LV api i cal aneurysm, and LV ejection fraction less than 50%, TEY POTTI \ it is reasonable to offer an implantable cardioverter- . All patients with non-ST-elevation acute coronary t defibrillator. syndrome should be treated with aspirin and a P2Y12 \ inhibitor regardless of reperfusion strates/. Bibliography vt q, i i Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC guideline for the diag Bibliography a nosis and treatment of patients with hypertrophic cardiomyopathy: exec ET Anderson Jt., Morrow DA. Acute myocardial infarction. N Engl J Med. I utive summary: a report of the American College of Cardiolos//American 2077 ;376:2053 64. IPMID: 28538121] doi:10.1056/NEJMral606915 : Heart Association loint Committee on Clinical Practice Cuidelines. Circulation. 2020;142:e533 e557. IPMID: 33215938] doi:10.1161/CIR. tr, a 0000000000000938 !t Item 105 Answer: C EducationaI Objective: Evaluate refractory ischemic chest tr G tt q, \ tr Item 104 Answer: A Educational Objective: Treat a patient with non-ST- pain with invasive coronary angiography.

\ i Answers and Critiques I t Glycoprotein llb/llla inhibitors, such as tirofiban \ t l(EY P0lLTt (cqtlnued) (Option D) and eptifibatide, are potent iutravenous anti t . In patients with hypertrophic cardiomyopathy (HCM) platelet agents that are generally reserved for use at the and risk factors for sudden cardiac death (SCD), such time of coronary angiography and coronary intervention for \ I as SCD attributable to HCM in a first-degree or close treatment of significant intracoronary thrombus burden. t relative aged 50 years or younger, left ventricular (LV) Tirofibar.r rvould have no benefit ir-r tl.ris clinically stable hypertrophy of 30 mm or greater in any LV segment, patient and has the potential to increase bleeding. I \ syncope suspected to be arrhythmic in nature, LV api i cal aneurysm, and LV ejection fraction less than 50%, TEY POTTI \ it is reasonable to offer an implantable cardioverter- . All patients with non-ST-elevation acute coronary t defibrillator. syndrome should be treated with aspirin and a P2Y12 \ inhibitor regardless of reperfusion strates/. Bibliography vt q, i i Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC guideline for the diag Bibliography a nosis and treatment of patients with hypertrophic cardiomyopathy: exec ET Anderson Jt., Morrow DA. Acute myocardial infarction. N Engl J Med. I utive summary: a report of the American College of Cardiolos//American 2077 ;376:2053 64. IPMID: 28538121] doi:10.1056/NEJMral606915 : Heart Association loint Committee on Clinical Practice Cuidelines. Circulation. 2020;142:e533 e557. IPMID: 33215938] doi:10.1161/CIR. tr, a 0000000000000938 !t Item 105 Answer: C EducationaI Objective: Evaluate refractory ischemic chest tr G tt q, \ tr Item 104 Answer: A Educational Objective: Treat a patient with non-ST- pain with invasive coronary angiography. lnvasive coronary angiography (Option C) is the rnost B UI

lnvasive coronary angiography (Option C) is the rnost B UI elevation acute coronary syndrome with dual antiplatelet appropriate imaging test to evaluate this patient's chest therapy. : pain. This procedure is indicated for patients with acute ( All patients u,ith non ST-elevation acute coK)nary synclrome chest pain who arc highly synptomatic with abnormal (NSTE-ACS) sl-rould be treated with aspirin and a P2Y,, inlrib- findings on stress testing or lbr selected patients with an itor. such as clopidogrel (Option A). regarclless of reperfusion acute coronary synclrome. Coronary angiographl, should strateS/. Cun-ent Anrerican Hearl Association,'American Col also be considered fbr patients with ischemic symptoms lege of Cardiologz guidelines recommend aclnrinistration of that are relractory to medication, such as tl-ris patient with mpirin (162 :125 mg at presentation. fbllowecl by 81 162 rng/d) unstable angina refractory to rnedical therapy. If culprit lnci P2\',, inl.ribitior.r cornbined n'ith earl1, inrasive irngiog lesions arnenable to intervention are identilied cluring L raphy rtithin 2,1 hours of presentation in hemodynamically diagnostic coronary angiography, percutaneous revascu stable paticnts who have evidence of NSI'U ACS and elevated larization can be perfbrmed. I risk as determined by prognostic irssessmer.rt with risk scores. Calcification of the coronary arteries indicates athero- such as'flMI and GRACE risk moclels. Clopidogrel or ticagre sclerosis and may be quantified with CT. Although coronary ; lor is indicated at presentation in patients with acute coronary ar1ery calcium (CAC) scoring (Option A) provides inlirrnration syndroure managed with an early inrrasivc strates/ (class 1 regarding the burden of disease. it cannot determine the recommendation). Ticagrelor (lB0 mg at presentation lol clegree o1'obstruction. In addition, CAC scoring has no use in lor,ved by 90 n1g twice daily) is more e{Iective than cktpidogrel patients already receiving statin therapy CAC scor:ing will pro (300-600 mg at prcsentation followed by 75 mg/d) and pre- vide no benefit to this patient with acute, refiactory ischemia. f'crred in patients rtithout increased bleeding risk. Horterer. This patient's chest pain w"rrants inraging of the cor ticagrelor is associated rtith higher rates ot'bleeding than clcr onary arteries, rvhich could be accomplisl.red by coronary pidogel and is associatcd with an increasecl incidence of dys- CT angiography (Option B). Ilowever, the acuity of this pre- pnea and bradycardia. 'l his patient has oxygen dependent COPD, sentation indicates a high likelil-rood ol requiring coronary r,r,hich may limit her ability to tderutc ticagelor therapy: 'lhere inten€ntion, '"r,hich nrould be delayed by pursuing another fbre. clopidogrcl is the rnost reasonable option fbr this paticnt. imaging test beforehand. In addition, coK)nary CT angiogra Prasugrel (Option ts) is an cftective antiplatelet agent in phy assessnrent of atherosclercltic occlusions may be limited patients with ACS but is resenred ltlr use after coronary stent b1r the presence of accompanying calcification. placement and not at presentation. Prasugrel is also contra Transthoracic echocardiography (T'lE) (Option D) can indicatecl in p:rtients rged 75 years or older and those with evaluate right ancl lctt chamber size, thickness, and func previous transient ischemic attack or stroke; it also must be tion, including wall motion. TTE also provides infbrnration t rusecl rvitl-t crution in underr.teight patients. on valr,ular pathology, diastolic function. hernodynam Thronrbolytic therapyi such as reteplase (Option C), ics, and tl.re pericarclium. New wa1l rnotion abnonr.ralities has not been shown 1o be benelicial in patients without might suggest the presence ol ischemic disease, but cor- ST ele'uation myocardial infarction (STEMI) or STEMI cquiv onary ar.rgiography can establish a precise anatomic diag- alcnts (e.g., ner,r,, bundle branch block) and is r.rot indicated nosis and has the potential b be fbllowecl immediately by lbr this patient. rcvasculari zation.

elevation acute coronary syndrome with dual antiplatelet appropriate imaging test to evaluate this patient's chest therapy. : pain. This procedure is indicated for patients with acute ( All patients u,ith non ST-elevation acute coK)nary synclrome chest pain who arc highly synptomatic with abnormal (NSTE-ACS) sl-rould be treated with aspirin and a P2Y,, inlrib- findings on stress testing or lbr selected patients with an itor. such as clopidogrel (Option A). regarclless of reperfusion acute coronary synclrome. Coronary angiographl, should strateS/. Cun-ent Anrerican Hearl Association,'American Col also be considered fbr patients with ischemic symptoms lege of Cardiologz guidelines recommend aclnrinistration of that are relractory to medication, such as tl-ris patient with mpirin (162 :125 mg at presentation. fbllowecl by 81 162 rng/d) unstable angina refractory to rnedical therapy. If culprit lnci P2\',, inl.ribitior.r cornbined n'ith earl1, inrasive irngiog lesions arnenable to intervention are identilied cluring L raphy rtithin 2,1 hours of presentation in hemodynamically diagnostic coronary angiography, percutaneous revascu stable paticnts who have evidence of NSI'U ACS and elevated larization can be perfbrmed. I risk as determined by prognostic irssessmer.rt with risk scores. Calcification of the coronary arteries indicates athero- such as'flMI and GRACE risk moclels. Clopidogrel or ticagre sclerosis and may be quantified with CT. Although coronary ; lor is indicated at presentation in patients with acute coronary ar1ery calcium (CAC) scoring (Option A) provides inlirrnration syndroure managed with an early inrrasivc strates/ (class 1 regarding the burden of disease. it cannot determine the recommendation). Ticagrelor (lB0 mg at presentation lol clegree o1'obstruction. In addition, CAC scoring has no use in lor,ved by 90 n1g twice daily) is more e{Iective than cktpidogrel patients already receiving statin therapy CAC scor:ing will pro (300-600 mg at prcsentation followed by 75 mg/d) and pre- vide no benefit to this patient with acute, refiactory ischemia. f'crred in patients rtithout increased bleeding risk. Horterer. This patient's chest pain w"rrants inraging of the cor ticagrelor is associated rtith higher rates ot'bleeding than clcr onary arteries, rvhich could be accomplisl.red by coronary pidogel and is associatcd with an increasecl incidence of dys- CT angiography (Option B). Ilowever, the acuity of this pre- pnea and bradycardia. 'l his patient has oxygen dependent COPD, sentation indicates a high likelil-rood ol requiring coronary r,r,hich may limit her ability to tderutc ticagelor therapy: 'lhere inten€ntion, '"r,hich nrould be delayed by pursuing another fbre. clopidogrcl is the rnost reasonable option fbr this paticnt. imaging test beforehand. In addition, coK)nary CT angiogra Prasugrel (Option ts) is an cftective antiplatelet agent in phy assessnrent of atherosclercltic occlusions may be limited patients with ACS but is resenred ltlr use after coronary stent b1r the presence of accompanying calcification. placement and not at presentation. Prasugrel is also contra Transthoracic echocardiography (T'lE) (Option D) can indicatecl in p:rtients rged 75 years or older and those with evaluate right ancl lctt chamber size, thickness, and func previous transient ischemic attack or stroke; it also must be tion, including wall motion. TTE also provides infbrnration t rusecl rvitl-t crution in underr.teight patients. on valr,ular pathology, diastolic function. hernodynam Thronrbolytic therapyi such as reteplase (Option C), ics, and tl.re pericarclium. New wa1l rnotion abnonr.ralities has not been shown 1o be benelicial in patients without might suggest the presence ol ischemic disease, but cor- ST ele'uation myocardial infarction (STEMI) or STEMI cquiv onary ar.rgiography can establish a precise anatomic diag- alcnts (e.g., ner,r,, bundle branch block) and is r.rot indicated nosis and has the potential b be fbllowecl immediately by lbr this patient. rcvasculari zation. 209

Answers and Critiques XEY POIlIT Bibliography . Coronary angiography is indicated for patients with Guglin N{. Zucker l\{J. Borlaug BA, et al: ACC Hean l,ailure and'l'ransplant l\'lember Section and Leadership Council. E\€luation tbr heart transplanta acute chest pain who are highly symptomatic with tion and L\AD implantation: JACC Council Perspectives. J Ant Coll Cardiol. 2020r75:1-171 1487. IPMII): 32216916) doi:10.1016,'j.jlcc.2020.01.03.1 abnormal findings on stress testing, selected patients with acute coronary syndrome, and patients with ischemic symptoms that are refractory to medication. Item 107 Answer: A Educational Objective: Treat a patient with atrial fibril- Bibliography lation and coronary artery disease. Amsterdam EA, Wenger NK, Brindis RG, et al. 201,1 AHA/ ACC guideline fbr the management of prtients with non ST elevation acute coronary syn The most appropriate management is to discontinue aspirin dromes, a report of the American College of Cardiolog, American Heart Association Task Force on Practice Cuidelines. I Am Coll Cardiol.20l1: (Option A). This patient is currently treated with triple ther 64:e139 e228. IPMID: 25260718] doi:10.1016 j.jacc.20l.1.09.O17 apy with an oral anticoagulant and dual antiplatelet therapy UI to prevent stroke in atrial fibrillation (AF) and recurrent E o Item 106 Answer: C acute coronary syndrome, respectively. Each of these drugs is UI the cornerstone of preventive therapy lor the respective dis q, Educational Objective: Manage advanced heart failure ease processes; however, together they significantly increase with a left ventricular assist device. CL the risk for bleeding. This patient is being evaluated 7 months n The most appropriate management is left ventricular assist after coronary stent placement, and she has a history ofgas device (LVAD) placement (Option C). LVADs are reasonable trointestinal bleeding. lt is reasonable to discontinue aspirin .lI to reduce the risk for bleeding associated lt,ith triple therapy, either as a bridge to heart transplant or as primary therapy .D as several trials have demonstrated the safety and efficacy of UI in patients with advanced heart failure. Survival at 1 year is near the survival after heart transplant, and an LVAD would double therapy with an oral anticoagulant and a second- or be worth considering in patients who have several markers third generation P2Y,, inhibitor. such as clopidogrel. of increased mortality. This patient has advanced heart failure This patient's CHATDS2 VASc score is 4 (1 point each with several risk factors for an increase in mofiality over the for age 65 74 years, female sex, hypertension, and coronary next 2 years. These risk factors include several heart fail artery disease), putting her at substantial risk for AF'related ure hospitalizations, worsening kidney function, low semm stroke. Although dual antiplatelet therapy may be sufficient sodium level, high diuretic dosage, and inability to toler to prevent recurrent acute coronary syndrome, it is insuffi ate usual heart failure medications because of symptomatic cient therapy to prevent stroke. lherefore, discontinuation of hypotension. Based on these risk factors, a discussion with rivaroxaban (Option B) is inappropriate. the patient about his $'ishes fbr end ofllife care and thoughts Although switching from rivaroxaban to reduced dose about advanced heart failure therapies would be appropriate. apixaban (Option C) may reduce this patient's risk for bleed This patient is not a candidate for heart transplant ing, this strates/ has two drawbacks. First, triple therapy (Option A) based on his age and recent colon cancer. Most with reduced dose apixaban may not be associated with a centers have an age cutoff of 65 years, although some may lower bleeding risk than dual therapy with rivaroxaban plus extend the cutoff past that age. With the exception of skin clopidogrel. Second, the reduced dose ofapixaban fbr stroke cancer, most programs require that a patient be cancer lree prevention in AF is indicated among patients with at least for at least 5 years before being considered for heart transplant. two of the fbllowing three criteria: age B0 years or older, The decision to hospitalize a patient with heart failure weight less than 60 kg (132.3 lb), and serum creatinine level (Option B) is usually based on evidence of acute decompen of 1 .5 mgldl or higher (>-tZZ.6 pmol/L). She does not fulflll sation with elevated neck veins and symptomatic heart lail these criteria and will not be adequately treated to prevent ure. This patient has New York Heart Association functional AF related stroke with reduced dose apixaban. class III to IV symptoms but does not appear to have volume Switching rivaroxaban to warfarin (Option D) is more overload on examination. Therefore, his symptoms are most likely to increase her bleeding risk, not decrease it, "t,ithout likely unrelated to acute volume overload and instead are a signiflcant improvement in clinical benefit in terms of stroke sign of his progressive heart failure. prevention. Of more importance, switching from one anti This patient's p blocker (carvedilol) was stopped because of coagulant to another does not address the burden oF triple slmptomatic hypotension. There is no absolute blood pressure therapy in this patient. cutofffor initiating a p blocker, but starting a p blocker (Option D) XEY POIilT in a patient who has not tolerated one in the past, especially with this patient's low blood pressure, is not appropriate. . Among patients with atrial fibrillation who have under- gone percutaneous coronary intervention for acute coro- I(EY POITI nary syndrome, double therapy with clopidogrel or o Left ventricular assist devices, either as a bridge to ticagrelor plus a direct oral anticoagulant is recommended heart transplant or as primary therapy, are reasonable over triple therapy with an oral anticoagulant, aspirin, and in patients with advanced heart failure. P2Y,, inhibitor to reduce the risk for bleeding.

XEY POIlIT Bibliography . Coronary angiography is indicated for patients with Guglin N{. Zucker l\{J. Borlaug BA, et al: ACC Hean l,ailure and'l'ransplant l\'lember Section and Leadership Council. E\€luation tbr heart transplanta acute chest pain who are highly symptomatic with tion and L\AD implantation: JACC Council Perspectives. J Ant Coll Cardiol. 2020r75:1-171 1487. IPMII): 32216916) doi:10.1016,'j.jlcc.2020.01.03.1 abnormal findings on stress testing, selected patients with acute coronary syndrome, and patients with ischemic symptoms that are refractory to medication. Item 107 Answer: A Educational Objective: Treat a patient with atrial fibril- Bibliography lation and coronary artery disease. Amsterdam EA, Wenger NK, Brindis RG, et al. 201,1 AHA/ ACC guideline fbr the management of prtients with non ST elevation acute coronary syn The most appropriate management is to discontinue aspirin dromes, a report of the American College of Cardiolog, American Heart Association Task Force on Practice Cuidelines. I Am Coll Cardiol.20l1: (Option A). This patient is currently treated with triple ther 64:e139 e228. IPMID: 25260718] doi:10.1016 j.jacc.20l.1.09.O17 apy with an oral anticoagulant and dual antiplatelet therapy UI to prevent stroke in atrial fibrillation (AF) and recurrent E o Item 106 Answer: C acute coronary syndrome, respectively. Each of these drugs is UI the cornerstone of preventive therapy lor the respective dis q, Educational Objective: Manage advanced heart failure ease processes; however, together they significantly increase with a left ventricular assist device. CL the risk for bleeding. This patient is being evaluated 7 months n The most appropriate management is left ventricular assist after coronary stent placement, and she has a history ofgas device (LVAD) placement (Option C). LVADs are reasonable trointestinal bleeding. lt is reasonable to discontinue aspirin .lI to reduce the risk for bleeding associated lt,ith triple therapy, either as a bridge to heart transplant or as primary therapy .D as several trials have demonstrated the safety and efficacy of UI in patients with advanced heart failure. Survival at 1 year is near the survival after heart transplant, and an LVAD would double therapy with an oral anticoagulant and a second- or be worth considering in patients who have several markers third generation P2Y,, inhibitor. such as clopidogrel. of increased mortality. This patient has advanced heart failure This patient's CHATDS2 VASc score is 4 (1 point each with several risk factors for an increase in mofiality over the for age 65 74 years, female sex, hypertension, and coronary next 2 years. These risk factors include several heart fail artery disease), putting her at substantial risk for AF'related ure hospitalizations, worsening kidney function, low semm stroke. Although dual antiplatelet therapy may be sufficient sodium level, high diuretic dosage, and inability to toler to prevent recurrent acute coronary syndrome, it is insuffi ate usual heart failure medications because of symptomatic cient therapy to prevent stroke. lherefore, discontinuation of hypotension. Based on these risk factors, a discussion with rivaroxaban (Option B) is inappropriate. the patient about his $'ishes fbr end ofllife care and thoughts Although switching from rivaroxaban to reduced dose about advanced heart failure therapies would be appropriate. apixaban (Option C) may reduce this patient's risk for bleed This patient is not a candidate for heart transplant ing, this strates/ has two drawbacks. First, triple therapy (Option A) based on his age and recent colon cancer. Most with reduced dose apixaban may not be associated with a centers have an age cutoff of 65 years, although some may lower bleeding risk than dual therapy with rivaroxaban plus extend the cutoff past that age. With the exception of skin clopidogrel. Second, the reduced dose ofapixaban fbr stroke cancer, most programs require that a patient be cancer lree prevention in AF is indicated among patients with at least for at least 5 years before being considered for heart transplant. two of the fbllowing three criteria: age B0 years or older, The decision to hospitalize a patient with heart failure weight less than 60 kg (132.3 lb), and serum creatinine level (Option B) is usually based on evidence of acute decompen of 1 .5 mgldl or higher (>-tZZ.6 pmol/L). She does not fulflll sation with elevated neck veins and symptomatic heart lail these criteria and will not be adequately treated to prevent ure. This patient has New York Heart Association functional AF related stroke with reduced dose apixaban. class III to IV symptoms but does not appear to have volume Switching rivaroxaban to warfarin (Option D) is more overload on examination. Therefore, his symptoms are most likely to increase her bleeding risk, not decrease it, "t,ithout likely unrelated to acute volume overload and instead are a signiflcant improvement in clinical benefit in terms of stroke sign of his progressive heart failure. prevention. Of more importance, switching from one anti This patient's p blocker (carvedilol) was stopped because of coagulant to another does not address the burden oF triple slmptomatic hypotension. There is no absolute blood pressure therapy in this patient. cutofffor initiating a p blocker, but starting a p blocker (Option D) XEY POIilT in a patient who has not tolerated one in the past, especially with this patient's low blood pressure, is not appropriate. . Among patients with atrial fibrillation who have under- gone percutaneous coronary intervention for acute coro- I(EY POITI nary syndrome, double therapy with clopidogrel or o Left ventricular assist devices, either as a bridge to ticagrelor plus a direct oral anticoagulant is recommended heart transplant or as primary therapy, are reasonable over triple therapy with an oral anticoagulant, aspirin, and in patients with advanced heart failure. P2Y,, inhibitor to reduce the risk for bleeding. 210

Answers and Critiques Bibliography Bibliography January CT, Wann LS. Calkins II. et al. 2019 AHA'ACC/ IIRS focused update Otto CM, Nishimura RA. Bonorv RO. et al. 2020 AC(irAHA guideline tbr the of the 201.1 AHA,ACC,'llRS guideline tbr the management ol patients management of patients u'ith v;rlvular heart disease: a report of the h,ith atrial fibrillation: 0 report of the American College of Cardiolog, r American College of Cirrdiolopy,'American IIeart Association Joint American I leart Association Task Firrce on Clinical Practice Guidelines Committec on Clinical Practice (iuidelines. CircuLltion. 2021 ;l4lj:e7'2 and the llcart Rhythm Sociery J Am Coll Cardiol.2019;74:104 132. e227. IPl\4 Il): 333321s01 doi:10.1161 1cl R.00000000o0000923 IPMID: 307031311 doi:10. l0l6/j.jacc.2019.01.011

Bibliography Bibliography January CT, Wann LS. Calkins II. et al. 2019 AHA'ACC/ IIRS focused update Otto CM, Nishimura RA. Bonorv RO. et al. 2020 AC(irAHA guideline tbr the of the 201.1 AHA,ACC,'llRS guideline tbr the management ol patients management of patients u'ith v;rlvular heart disease: a report of the h,ith atrial fibrillation: 0 report of the American College of Cardiolog, r American College of Cirrdiolopy,'American IIeart Association Joint American I leart Association Task Firrce on Clinical Practice Guidelines Committec on Clinical Practice (iuidelines. CircuLltion. 2021 ;l4lj:e7'2 and the llcart Rhythm Sociery J Am Coll Cardiol.2019;74:104 132. e227. IPl\4 Il): 333321s01 doi:10.1161 1cl R.00000000o0000923 IPMID: 307031311 doi:10. l0l6/j.jacc.2019.01.011 Item 109 Answer: A Item 108 Answer: E Educational Objective: Monitor an asymptomatic patient Ed u cati ona I O bj ective : Avoid inappropriate endocarditis with severe aortic regurgitation. prophylaxis. 'lhe most appropriate next step in management is reevalua- This patient requires no endocarditis prophylaxis (Option E). tion with clinical examination and echocardiography in 6 to Endocarditis prophylaris is recommended for a specific group tt 12 months (Option A), or earlier as dictated by a change in 6, of patients before dental procedures that involve manipula clinical status or examination findings concerning for heart ET tion ofgingival tissue or the periapical region ofthe teeth, or failure. This patient's examination flndings (widened pulse .?- perforation of the oral mucosa. The highest risk for infective pressure, murmur, and bounding pulses) are consistent with L' endocarditis (lE) is in patients with a prosthetic val'ue, previous severe aortic regurgitation (AR). With all regurgitant lesions, 'E E IE, or congenital heart disease with residual flow disturbances. indications for invasive intervention are based on either the .U ra Current indications for endocarditis prophylaxis include (1) a negative impact of valvular regurgitation on ventricular size/ o history of IE; (2) cardiac transplantation with valve regurgita contractility or the emergence of symptoms due to valvular UI tion due to a structurally abnormal valve; (3) a prosthetic valve; regurgitation or heart failure. ln symptomatic patients with = (4) prosthetic material used for cardiac valve repair, including severe AR, aorlic valve surgery is indicated regardless of left annuloplasty rings and chords; (5) unrepaired cyanotic congen ventricular (LV) systolic function. In asymptomatic patients ital heart disease; (6) repaired congenital cyanotic heart disease with chronic severe AR and LV systolic dysfunction (LV ejec with residual defects at the site or adjacent to the site of a pros tion fraction <557,), aortic valve surgery is indicated ifl no thetic patch or device; and (7) a defect that has been repaired other cause for systolic dysfunction is identifled. In asymp (surgical or catheter based) with prosthetic material within the tomatic patients with severe AR and normal LV systolic previous 6 months. None of these indications is present in this function (LV ejection fraction >55'/"), aortic valve surgery patient, and antibiotic prophylaxis is unnecessary is reasonable if the left ventricle is severely enlarged (LV In patients with valvular heart disease who are at high risk end systolic dimension >50 mm). fbr IE, antibiotic prophylaris (Options A-D) is not recommended This patient does not require surgical aortic valve for nondental procedures, such as transesophageal echocardiog replacement now (Option B). He is asymptomatic, and raphy, esophagogastroduodenoscopy, colonoscopy, or cystoscopy, quantitative echocardiographic evaluation conflrms severe in the absence of active infection. Drug resistant organisms, AR with a normal LV ejection fraction and without signif Clostridioides dfficile colitis, unnecessary expense, and drug icant ventricular dilation. He should be followed closely toxici$/ may result from indiscriminate antibiotic prescribing. with clinical examination and echocardiography every 6 to If the patient had an indication for endocarditis pro 12 months. phylaxis, amoxicillin (2 g once orally 60 minutes befbre the Current guidelines recommend that patients with iso cleaning) would be the most appropriate therapy. Azithro lated severe AR who have indications for surgical aortic valve mycin and clindamycin should be reserved for patients able replacement and are candidates for surgery not undergo to take oral antibiotics who have a penicillin allergz. lntra transcatheter aortic valre implantation (Option C), because venous ceftriaxone should be used for endocarditis prophy- it is rarely feasible and has potential harms. laxis only in patients unable to take oral antibiotics. Transesophageal echocardiography (Option D) may be I(EY POITTS used to assess AR. However, in native valve AR, it rarely provides incremental diagnostic information beyond what . Endocarditis prophylaxis is indicated only for patients is obtained by transthoracic echocardiography with good at high risk for infective endocarditis who are about to image quality. undergo gingival manipulation or other procedures that break the oral mucosa. rEY POIl{TS . The highest risk for infective endocarditis (lE) is in . In symptomatic patients with severe aortic regurgitation, patients with a prosthetic valve, previous IE, or congenital aortic valve surgery is indicated regardless ofleft ventric heart disease (repaired or unrepaired) with residual flow ular systolic function. disturbances; other indications include cardiac transplan r In asymptomatic patients with chronic severe aortic tation vah.ulopathy, prosthetic material used for cardiac regurgitation and left ventricular systolic dysfunction lalve repair, and a cardiac defect that has been repaired (ejection fraction <55%), aortic valve surgery is indi- with prosthetic material within the previous 6 months. cated.

Item 109 Answer: A Item 108 Answer: E Educational Objective: Monitor an asymptomatic patient Ed u cati ona I O bj ective : Avoid inappropriate endocarditis with severe aortic regurgitation. prophylaxis. 'lhe most appropriate next step in management is reevalua- This patient requires no endocarditis prophylaxis (Option E). tion with clinical examination and echocardiography in 6 to Endocarditis prophylaris is recommended for a specific group tt 12 months (Option A), or earlier as dictated by a change in 6, of patients before dental procedures that involve manipula clinical status or examination findings concerning for heart ET tion ofgingival tissue or the periapical region ofthe teeth, or failure. This patient's examination flndings (widened pulse .?- perforation of the oral mucosa. The highest risk for infective pressure, murmur, and bounding pulses) are consistent with L' endocarditis (lE) is in patients with a prosthetic val'ue, previous severe aortic regurgitation (AR). With all regurgitant lesions, 'E E IE, or congenital heart disease with residual flow disturbances. indications for invasive intervention are based on either the .U ra Current indications for endocarditis prophylaxis include (1) a negative impact of valvular regurgitation on ventricular size/ o history of IE; (2) cardiac transplantation with valve regurgita contractility or the emergence of symptoms due to valvular UI tion due to a structurally abnormal valve; (3) a prosthetic valve; regurgitation or heart failure. ln symptomatic patients with = (4) prosthetic material used for cardiac valve repair, including severe AR, aorlic valve surgery is indicated regardless of left annuloplasty rings and chords; (5) unrepaired cyanotic congen ventricular (LV) systolic function. In asymptomatic patients ital heart disease; (6) repaired congenital cyanotic heart disease with chronic severe AR and LV systolic dysfunction (LV ejec with residual defects at the site or adjacent to the site of a pros tion fraction <557,), aortic valve surgery is indicated ifl no thetic patch or device; and (7) a defect that has been repaired other cause for systolic dysfunction is identifled. In asymp (surgical or catheter based) with prosthetic material within the tomatic patients with severe AR and normal LV systolic previous 6 months. None of these indications is present in this function (LV ejection fraction >55'/"), aortic valve surgery patient, and antibiotic prophylaxis is unnecessary is reasonable if the left ventricle is severely enlarged (LV In patients with valvular heart disease who are at high risk end systolic dimension >50 mm). fbr IE, antibiotic prophylaris (Options A-D) is not recommended This patient does not require surgical aortic valve for nondental procedures, such as transesophageal echocardiog replacement now (Option B). He is asymptomatic, and raphy, esophagogastroduodenoscopy, colonoscopy, or cystoscopy, quantitative echocardiographic evaluation conflrms severe in the absence of active infection. Drug resistant organisms, AR with a normal LV ejection fraction and without signif Clostridioides dfficile colitis, unnecessary expense, and drug icant ventricular dilation. He should be followed closely toxici$/ may result from indiscriminate antibiotic prescribing. with clinical examination and echocardiography every 6 to If the patient had an indication for endocarditis pro 12 months. phylaxis, amoxicillin (2 g once orally 60 minutes befbre the Current guidelines recommend that patients with iso cleaning) would be the most appropriate therapy. Azithro lated severe AR who have indications for surgical aortic valve mycin and clindamycin should be reserved for patients able replacement and are candidates for surgery not undergo to take oral antibiotics who have a penicillin allergz. lntra transcatheter aortic valre implantation (Option C), because venous ceftriaxone should be used for endocarditis prophy- it is rarely feasible and has potential harms. laxis only in patients unable to take oral antibiotics. Transesophageal echocardiography (Option D) may be I(EY POITTS used to assess AR. However, in native valve AR, it rarely provides incremental diagnostic information beyond what . Endocarditis prophylaxis is indicated only for patients is obtained by transthoracic echocardiography with good at high risk for infective endocarditis who are about to image quality. undergo gingival manipulation or other procedures that break the oral mucosa. rEY POIl{TS . The highest risk for infective endocarditis (lE) is in . In symptomatic patients with severe aortic regurgitation, patients with a prosthetic valve, previous IE, or congenital aortic valve surgery is indicated regardless ofleft ventric heart disease (repaired or unrepaired) with residual flow ular systolic function. disturbances; other indications include cardiac transplan r In asymptomatic patients with chronic severe aortic tation vah.ulopathy, prosthetic material used for cardiac regurgitation and left ventricular systolic dysfunction lalve repair, and a cardiac defect that has been repaired (ejection fraction <55%), aortic valve surgery is indi- with prosthetic material within the previous 6 months. cated. 211

Answers and Critiques Bibliography Item 111 Answer: A Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: a report of the Educational Objective: Treat heart failure with cardiac American College of Cardiolo$//American Heart Association Joint resynchronization therapy. Committee on Clinical Practice Guidelines. Circulation. 2021 143:e72 e227. IPMID: 33332150] doi:10.1161/CIR.O00000OO0oooo923 Cardiac resynchronization therapy (CRT) (Option A) is the most appropriate treatment. This patient with heart fail-

Bibliography Item 111 Answer: A Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease: a report of the Educational Objective: Treat heart failure with cardiac American College of Cardiolo$//American Heart Association Joint resynchronization therapy. Committee on Clinical Practice Guidelines. Circulation. 2021 143:e72 e227. IPMID: 33332150] doi:10.1161/CIR.O00000OO0oooo923 Cardiac resynchronization therapy (CRT) (Option A) is the most appropriate treatment. This patient with heart fail- tr Item 11O Answer: B Educational Objective: Discontinue flecainide in a ure with reduced ejection fraction is on optimal guideline- directed medical therapy. CRT is indicated in patients with a left ventricular ejection fraction (LVEF) of 35% or less, patient with ischemic heart disease. New York Heart Association (NYHA) functional class II to IV The most appropriate management is to discontinue fle symptoms despite guideline-directed medical therapy. sinus cainide (Option B). This patient has ischenric l.reart disease rhythm, and left bundle branch block with a QRS complex of and previously diagnosed paroxysmal atrial fibrillation (AF). 150 ms or longer (class 1 recommendation). In such patients, ut Amioclarone. dof'etilide. flecainide. propafenone. sotalol. CRT is associated with improved LVEF, reduced symptoms, € (D and dronedaK)ne may be used to maintain sir.rus rhythrn in and improved survival rates. Many patients who meet the UT patients '-t ith Ali Antiarrhyhmic drug selectiou is guided by indication for CRT also meet indications for implantable q, cardioverter-deflbrillator (lCD) therapy. ICD therapy reduces the patient's comorbid conditions and safet-v considerirtior-rs. =L C Flecainide is a class IC antiarrhyhmic agent and, along \,\,ith mortality in patients with NYHA class I to III heart failure n propafblrone. is absolutely contraindicated in patients rvith symptoms and LVEF less than 35'/o on optimal medical ther- ischemic heart disease, gir€n the increased risk for ventricular apy. This patient meets the criteria for ICD placement, but lt=. c.D arrhythmias in this population. This patient also has evidence she may experience substantial improvement in ejection la of left r,entricular (LV) dysfirnction on a post m),"ocardia} fraction with CRT and may not require or beneflt from ICD infarction echocardiograrr.r. r,r,l.rich n.ray be due to infarcted (as insertion. opposed to stunned) myocardium and nlay lead to increased In patients with LVEF of 35% or less who are in sinus long term risk fbr ventricular arrhl.thmias. Furlhermore. his rhythm with a heart rate of at least 7Olmin and taking ECG shows widening of the QRS intenal, $rhich may reflect maximally tolerated doses of a p-blocker, the sinoatrial adverse ellects of flecainide. 'lhis drug, thereflore, is not safe in node modulator ivabradine (Option B) reduces heart tl-ris patient; it should be discontinued ar-rd not restarted. failure-associated hospitalizations and the combined Although ambulatory ECG morritoring (Option A) at end point of mortality and heart failure hospitalization. discharge nray be helpful to assess AF burden, rates. and Ivabradine is not indicated in this patient with a heart symptoms, it should not be used to guide flecainide theripl' rate of 58/min. in this patient, given his contraindications, which arnbula- The mitral valve clip (Option C) is designed to approx tory ECG mollitoring r,r,ill not address. imate mitral valve leaflets and reduce mitral regurgitation. There is no reason to stop metoprolol (Option C). This Mitral valve clip placement is reasonable for patients with patient's heaft rate is only mildly bradycardic. does not appear severe secondary mitral regurgitation with heart failure to be causing adrerse effects, and is unlikely to be aft'ecting symptoms and a left ventricular end systolic dimension his right bundle branch block. Aggressive p blockade is r,tar Iess than 70 mm and pulmonary artery pressure less than ranted, given his recent myocardial infarction, coronary artery 70 mm Hg. CRT is more likely to improve symptoms and is disease, and LV dysfunction. Furlhermore. he will likell'need the most appropriate step for this patient before considering metoprolol for rate control, if or when he relerls to AE a mitral valve clip. In the revascularized patient nith stable or absent Transcatheter aortic valve implantation (16y1) (aption D) ischemic symptoms. there is no role lor predischarge stress is usually reserved for patients with symptomatic severe testing (Option D). Although exercise stress testing is some aortic stenosis. Factors that increase procedural risk include tinres used to assess the QRS duration during exercise in reduced ejection fraction, another reason not to proceed patients treated with class IC antiarrhythmic drugs, it will with TAVI in this patient. not change management in this patier.rt. This patient already has QRS prolongation at rest and an absolute contraindica t(lY POrXr tion to flecainide because of his coronary artery disease. o Cardiac resynchronization therapy is indicated for patients with ejection fraction of 35% or less with left XEY POIXI bundle branch block, QRS duration of 150 ms or r Flecainide and other class IC antiarrhythmic agents greater, and New York Heart Association functional are contraindicated in patients with ischemic heart class II to IV symptoms despite guideline-directed disease. medical therapy.

tr Item 11O Answer: B Educational Objective: Discontinue flecainide in a ure with reduced ejection fraction is on optimal guideline- directed medical therapy. CRT is indicated in patients with a left ventricular ejection fraction (LVEF) of 35% or less, patient with ischemic heart disease. New York Heart Association (NYHA) functional class II to IV The most appropriate management is to discontinue fle symptoms despite guideline-directed medical therapy. sinus cainide (Option B). This patient has ischenric l.reart disease rhythm, and left bundle branch block with a QRS complex of and previously diagnosed paroxysmal atrial fibrillation (AF). 150 ms or longer (class 1 recommendation). In such patients, ut Amioclarone. dof'etilide. flecainide. propafenone. sotalol. CRT is associated with improved LVEF, reduced symptoms, € (D and dronedaK)ne may be used to maintain sir.rus rhythrn in and improved survival rates. Many patients who meet the UT patients '-t ith Ali Antiarrhyhmic drug selectiou is guided by indication for CRT also meet indications for implantable q, cardioverter-deflbrillator (lCD) therapy. ICD therapy reduces the patient's comorbid conditions and safet-v considerirtior-rs. =L C Flecainide is a class IC antiarrhyhmic agent and, along \,\,ith mortality in patients with NYHA class I to III heart failure n propafblrone. is absolutely contraindicated in patients rvith symptoms and LVEF less than 35'/o on optimal medical ther- ischemic heart disease, gir€n the increased risk for ventricular apy. This patient meets the criteria for ICD placement, but lt=. c.D arrhythmias in this population. This patient also has evidence she may experience substantial improvement in ejection la of left r,entricular (LV) dysfirnction on a post m),"ocardia} fraction with CRT and may not require or beneflt from ICD infarction echocardiograrr.r. r,r,l.rich n.ray be due to infarcted (as insertion. opposed to stunned) myocardium and nlay lead to increased In patients with LVEF of 35% or less who are in sinus long term risk fbr ventricular arrhl.thmias. Furlhermore. his rhythm with a heart rate of at least 7Olmin and taking ECG shows widening of the QRS intenal, $rhich may reflect maximally tolerated doses of a p-blocker, the sinoatrial adverse ellects of flecainide. 'lhis drug, thereflore, is not safe in node modulator ivabradine (Option B) reduces heart tl-ris patient; it should be discontinued ar-rd not restarted. failure-associated hospitalizations and the combined Although ambulatory ECG morritoring (Option A) at end point of mortality and heart failure hospitalization. discharge nray be helpful to assess AF burden, rates. and Ivabradine is not indicated in this patient with a heart symptoms, it should not be used to guide flecainide theripl' rate of 58/min. in this patient, given his contraindications, which arnbula- The mitral valve clip (Option C) is designed to approx tory ECG mollitoring r,r,ill not address. imate mitral valve leaflets and reduce mitral regurgitation. There is no reason to stop metoprolol (Option C). This Mitral valve clip placement is reasonable for patients with patient's heaft rate is only mildly bradycardic. does not appear severe secondary mitral regurgitation with heart failure to be causing adrerse effects, and is unlikely to be aft'ecting symptoms and a left ventricular end systolic dimension his right bundle branch block. Aggressive p blockade is r,tar Iess than 70 mm and pulmonary artery pressure less than ranted, given his recent myocardial infarction, coronary artery 70 mm Hg. CRT is more likely to improve symptoms and is disease, and LV dysfunction. Furlhermore. he will likell'need the most appropriate step for this patient before considering metoprolol for rate control, if or when he relerls to AE a mitral valve clip. In the revascularized patient nith stable or absent Transcatheter aortic valve implantation (16y1) (aption D) ischemic symptoms. there is no role lor predischarge stress is usually reserved for patients with symptomatic severe testing (Option D). Although exercise stress testing is some aortic stenosis. Factors that increase procedural risk include tinres used to assess the QRS duration during exercise in reduced ejection fraction, another reason not to proceed patients treated with class IC antiarrhythmic drugs, it will with TAVI in this patient. not change management in this patier.rt. This patient already has QRS prolongation at rest and an absolute contraindica t(lY POrXr tion to flecainide because of his coronary artery disease. o Cardiac resynchronization therapy is indicated for patients with ejection fraction of 35% or less with left XEY POIXI bundle branch block, QRS duration of 150 ms or r Flecainide and other class IC antiarrhythmic agents greater, and New York Heart Association functional are contraindicated in patients with ischemic heart class II to IV symptoms despite guideline-directed disease. medical therapy. Bibliography Echt DS. Ruskin JN. Use of flecainide for the treatment of atrial fibrillation. Bibliography Am J Cardiol. 2020;125:1123 33. [PMID: 320440371 doi:10.1016/j.ami Wu A. Heart failure. Ann Intern Med. 2o18;168:lTC8l ITC96. [PMID: card.2019.l 2.041 2986881 6l doi:10.7326lAITC201806os0

Bibliography Echt DS. Ruskin JN. Use of flecainide for the treatment of atrial fibrillation. Bibliography Am J Cardiol. 2020;125:1123 33. [PMID: 320440371 doi:10.1016/j.ami Wu A. Heart failure. Ann Intern Med. 2o18;168:lTC8l ITC96. [PMID: card.2019.l 2.041 2986881 6l doi:10.7326lAITC201806os0 212

Answers and Critiques Item 112 Answer: B Bibliography JH, DChMCT GJ, Et AI. ACC/AATS/AHA/ASI]/ASNC/SCAI/ PATEI MR, CiTIhOON Educational Objective: Assess the benefit ofcoronary SCCT/STS 2017 appropriate use criteria fbr coronary revascularization in artery bypass grafting in a patient with chronic stable patients with stable ischemic heaft disease: a report of the American College ol Cardiolory Appropriate Use Criteria Task Force, American angina. Association tbr Thoracic Surgery. American Heart Association. American Society of llchocardiography, American Society of Nuclear Cardiologl, The anticipated benefit of coronary artery bypass grafting Society frrr Cardiovascular Angiography and Interventions, Society of (CABG) in this patient with stable coronary artery disease is Cardiovascular Cr)mputed n)mography, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2017;69:2212 41. [PMID: 282916631 doi:10.1016/j. an improvement in symptoms (Option B). The relative ben- iacc.20U.02.00l eflt of revascularization depends on a patient's underlying clinical and anatomic features. The goal of revasculariza tion in stable syndromes is generally to relieve angina and Item 1 13 Answer: A improve quality of life. This patient has stable but persistent Educational Objective: Diagnose atrial septal defect. symptoms in the setting of documented moderate ischemia U! An atrial septal defect (ASD) (Option A) is the most likely 6, and two vessel coronary artery disease with preserved left diagnosis in this patient. An ASD is a defect in the atrial ET ventricular function. Revascularization with CABG (or per septum resulting in a left to right shunt with eventual cutaneous coronary intervention) and continued medical right-sided cardiac chamber dilatation in most patients. fYt therapy have the potential to improve symptoms and would .E, Adults with an ASD most often present with dyspnea, atrial be the primary reason to proceed with revascularization in .E arrhythmias, and/or right heart enlargement detected on this patient with persistent symptoms despite maximally aa cardiac imaging. Characteristic clinical flndings include ele (l, tolerated medical therapy. CABG with optimal medical ther vated central venous pressure, a right ventricular lift, and apy is generally recommended for patients with multivessel U! = flxed splitting ofthe Sr. A large left to right shunt causes a E coronary artery disease, particularly in the setting of left pulmonary midsystolic flow murmur and a tricuspid dia- ventricular dysfunction and/or diabetes mellitus, because it stolic flow rumble owing to increased flow This patient's results in decreased recurrence ofangina and lower rates of ECG shows right axis deviation, incomplete right bundle major cardiovascular events compared with percutaneous branch block, and right ventricular hypertrophy, flndings intervention or medical therapy alone. consistent with secundum ASD. Antiplatelet therapy and other cardioprotective medi Aortic regurgitation due to a bicuspid aortic valve cations, such as statins, are required in all patients with cor (Option B) causes a diastolic murmur at the left sternal bor onary heart disease, including those who have undergone der. The central venous pressure is generally normal, and a CABG. Discontinuation of cardioprotective medications (Option A) is not a beneflt of coronary artery revascular right ventricular impulse would not be expected. A systolic ejection click is often heard in patients with bicuspid aor ization. tic valve, but flxed splifiing of the S, is not heard. The ECG CABG may be considered an option to increase survival (Option C) in patients with signiflcant (>70'1,) stenosis of two typically demonstrates a normal axis and features of left ventricular hypertrophy. or more major coronary arteries in the setting of extensive Patients with mitral stenosis (Option C) often present myocardial ischemia, especially with involvement of the proximal left anterior descending coronary artery and/or with dyspnea and atrial arrhythmias. The central venous pressure is often elevated, with associated pulmonary marked left ventricular dysfunction. This patient does not hypertension or tricuspid regurgitation. A right ventricu meet these criteria. In this patient with a stable coronary syndrome receiv lar impulse may occur. An opening snap might be heard, ing optimal medical therapy and secondary prevention strat loilowed by a diastolic murmur; this is generally best heard egies, there is no expectation for reduced risk for myocardial at the apex. Fixed splitting of the S, is not heard. The ECG infarction (Option D) or death following surgical or percu typically demonstrates left atrial enlargement. Patients with a small (restrictive) ventricular septal defect taneous revascularization. Early symptomatic improvement (VSD) (Option D) are usually asymptomatic and demonstrate would be the primary goal of revascularization. a loud holosystolic murmur along the left sternal border that XEY POIIITS often obliterates the Sr. A thrill may be noted at the left stemal . Coronary artery bypass grafting can reduce angina in border. A right ventricular impulse would not be present. The ECG in patients with a small VSD is typically normal. patients with chronic stable angina. . Coronary artery bypass grafting may be considered as rtY P0l1{Tt an option to increase survival in patients with signifi o Characteristic clinical findings of an atrial septal defect cant (>7O%) stenosis of two or more major coronary include a parasternal impulse, fixed splitting of the 52, arteries in the setting ofextensive myocardial and a pulmonary outflow murmur. ischemia, especially with involvement of the proximal . In patients with an ostium secundum atrial septal left anterior descending coronary artery and/or defect, the ECG demonstrates right axis deviation and marked left ventricular dysfunction. incomplete right bundle branch block.

Item 112 Answer: B Bibliography JH, DChMCT GJ, Et AI. ACC/AATS/AHA/ASI]/ASNC/SCAI/ PATEI MR, CiTIhOON Educational Objective: Assess the benefit ofcoronary SCCT/STS 2017 appropriate use criteria fbr coronary revascularization in artery bypass grafting in a patient with chronic stable patients with stable ischemic heaft disease: a report of the American College ol Cardiolory Appropriate Use Criteria Task Force, American angina. Association tbr Thoracic Surgery. American Heart Association. American Society of llchocardiography, American Society of Nuclear Cardiologl, The anticipated benefit of coronary artery bypass grafting Society frrr Cardiovascular Angiography and Interventions, Society of (CABG) in this patient with stable coronary artery disease is Cardiovascular Cr)mputed n)mography, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2017;69:2212 41. [PMID: 282916631 doi:10.1016/j. an improvement in symptoms (Option B). The relative ben- iacc.20U.02.00l eflt of revascularization depends on a patient's underlying clinical and anatomic features. The goal of revasculariza tion in stable syndromes is generally to relieve angina and Item 1 13 Answer: A improve quality of life. This patient has stable but persistent Educational Objective: Diagnose atrial septal defect. symptoms in the setting of documented moderate ischemia U! An atrial septal defect (ASD) (Option A) is the most likely 6, and two vessel coronary artery disease with preserved left diagnosis in this patient. An ASD is a defect in the atrial ET ventricular function. Revascularization with CABG (or per septum resulting in a left to right shunt with eventual cutaneous coronary intervention) and continued medical right-sided cardiac chamber dilatation in most patients. fYt therapy have the potential to improve symptoms and would .E, Adults with an ASD most often present with dyspnea, atrial be the primary reason to proceed with revascularization in .E arrhythmias, and/or right heart enlargement detected on this patient with persistent symptoms despite maximally aa cardiac imaging. Characteristic clinical flndings include ele (l, tolerated medical therapy. CABG with optimal medical ther vated central venous pressure, a right ventricular lift, and apy is generally recommended for patients with multivessel U! = flxed splitting ofthe Sr. A large left to right shunt causes a E coronary artery disease, particularly in the setting of left pulmonary midsystolic flow murmur and a tricuspid dia- ventricular dysfunction and/or diabetes mellitus, because it stolic flow rumble owing to increased flow This patient's results in decreased recurrence ofangina and lower rates of ECG shows right axis deviation, incomplete right bundle major cardiovascular events compared with percutaneous branch block, and right ventricular hypertrophy, flndings intervention or medical therapy alone. consistent with secundum ASD. Antiplatelet therapy and other cardioprotective medi Aortic regurgitation due to a bicuspid aortic valve cations, such as statins, are required in all patients with cor (Option B) causes a diastolic murmur at the left sternal bor onary heart disease, including those who have undergone der. The central venous pressure is generally normal, and a CABG. Discontinuation of cardioprotective medications (Option A) is not a beneflt of coronary artery revascular right ventricular impulse would not be expected. A systolic ejection click is often heard in patients with bicuspid aor ization. tic valve, but flxed splifiing of the S, is not heard. The ECG CABG may be considered an option to increase survival (Option C) in patients with signiflcant (>70'1,) stenosis of two typically demonstrates a normal axis and features of left ventricular hypertrophy. or more major coronary arteries in the setting of extensive Patients with mitral stenosis (Option C) often present myocardial ischemia, especially with involvement of the proximal left anterior descending coronary artery and/or with dyspnea and atrial arrhythmias. The central venous pressure is often elevated, with associated pulmonary marked left ventricular dysfunction. This patient does not hypertension or tricuspid regurgitation. A right ventricu meet these criteria. In this patient with a stable coronary syndrome receiv lar impulse may occur. An opening snap might be heard, ing optimal medical therapy and secondary prevention strat loilowed by a diastolic murmur; this is generally best heard egies, there is no expectation for reduced risk for myocardial at the apex. Fixed splitting of the S, is not heard. The ECG infarction (Option D) or death following surgical or percu typically demonstrates left atrial enlargement. Patients with a small (restrictive) ventricular septal defect taneous revascularization. Early symptomatic improvement (VSD) (Option D) are usually asymptomatic and demonstrate would be the primary goal of revascularization. a loud holosystolic murmur along the left sternal border that XEY POIIITS often obliterates the Sr. A thrill may be noted at the left stemal . Coronary artery bypass grafting can reduce angina in border. A right ventricular impulse would not be present. The ECG in patients with a small VSD is typically normal. patients with chronic stable angina. . Coronary artery bypass grafting may be considered as rtY P0l1{Tt an option to increase survival in patients with signifi o Characteristic clinical findings of an atrial septal defect cant (>7O%) stenosis of two or more major coronary include a parasternal impulse, fixed splitting of the 52, arteries in the setting ofextensive myocardial and a pulmonary outflow murmur. ischemia, especially with involvement of the proximal . In patients with an ostium secundum atrial septal left anterior descending coronary artery and/or defect, the ECG demonstrates right axis deviation and marked left ventricular dysfunction. incomplete right bundle branch block. 213

Answers and Critiques Bibliography Bibliography Stout KK. Daniels CJ. Aboulhosn JA. et al. 2018 AHA ACC guideline fbr the Januar} CL U'ann LS. Calkins I I. ct al. 2019 AHA ACC I IRS tbcused update management of adults \\'ith congenital heart disease: a report of the of the 201,1 AHA ACC llRS guicleline firr the management ol pirtients American College ofCardiolopS American Heart Association Task Rrrce u'ith atrial fibrillation: a report ot the American College of Cardiolop5, on Clinical Practice Guidelines. J Am Coll Cardiol. 2019:73:e81 e192. American Heart Association Task I.brce on Clinical Practice Guidelines IPMID: 301212391 doi:10.1016 j.iacc.2018.08.1029 and the Heart Rh1'thm Societ-r' in Collaboration With the Socielv ot' Thoracic Surgeons. Circulation. 2019;l{O:el25-e151. [PMID: 306860{ll doi:10.1161, CIR.0000000000000665

Bibliography Bibliography Stout KK. Daniels CJ. Aboulhosn JA. et al. 2018 AHA ACC guideline fbr the Januar} CL U'ann LS. Calkins I I. ct al. 2019 AHA ACC I IRS tbcused update management of adults \\'ith congenital heart disease: a report of the of the 201,1 AHA ACC llRS guicleline firr the management ol pirtients American College ofCardiolopS American Heart Association Task Rrrce u'ith atrial fibrillation: a report ot the American College of Cardiolop5, on Clinical Practice Guidelines. J Am Coll Cardiol. 2019:73:e81 e192. American Heart Association Task I.brce on Clinical Practice Guidelines IPMID: 301212391 doi:10.1016 j.iacc.2018.08.1029 and the Heart Rh1'thm Societ-r' in Collaboration With the Socielv ot' Thoracic Surgeons. Circulation. 2019;l{O:el25-e151. [PMID: 306860{ll doi:10.1161, CIR.0000000000000665 Item 114 Answer: D Educational Objective: Treat parorysmal atrial fibrilla- Item 115 tion with heart failure with rhythm control. Answer: D Educational Objective: Diagnose acute aortic regurgita tr The most appropriate treatment is rhyhm control (Option D). tion complicating ascending aortic dissection. Atrial flbrilation (AF) complicates nearly 40'l. of heart failure D cases, and the combination of AF and heart failure dramatically Thc rnost appropriate cliiignostic tests are transthoracic (a yorsens outcomes. Several clinical trials have demonstrated that cchocardiographl, ancl CT angiographl' of the aorta € o (Option D). This patient's presenting symptom ol acute aggressive efforts to achiere rhlthm control in patients with AF t^ and concomitant heart failure decrease morbidity and mortality. anterior chest pain suggests acute coronary syndromc, o, pulnronary embolisnr. or aortic clissection. In this patient, In patients with heart failure with reduced ejection fraction, CL aortic dissection is most likely because of the significant n recent clinical trials have shown that catheter ablation of AF is difierences in systolic bloocl pressures between the right associated with a favorable eflect on morbidity and mortality ,lt compared with medical therapy. Amiodarone is another option and left arms. In acldition, thc grade 3/6 decrescenclo (D for rhythm control. Although amiodarone carries a risk for diastolic murmur at the left stcrnal border indicates the (, presence ofaortic regurgitation (AR). In the setting ol sus toxicity, this patient's lifetime exposure to the drug is likely to be relatively low given her age, comorbid conditions, and probable pccted aortic dissection. t he prcscnce of new or lr,orsenecl amiodarone dosage, which is generally lower for AF than lor AR suggests aortic root involvemcnt, rt'hich constitutes a ventricular arrhyhmias. Monitored appropriately, it can be used snrgical emergency. Transthoracic echocardiogruphy or safely and eflectively in patients her age. transesophageal echocarcliographl' ('fEE) is indicatecl lo Atrioventricular node ablation with permanent pacemaker confirtt the presence. scvcrit),, and etiology of acute AR. implantation (Option A) is an option for patients with AF who C'l angiography is indicrrled in patients with acute aor have continued symptomatic tachycardia despite rate and tic dissection because it is highly accurate and rapidly rhlthm control therapy. Therapeutic ablation of the atrioven irvailable. TEE n.ray be used wlren CT imaging is unavail tricular node requires implantation of a permanent pacemaker. iible and is helpful in asscssntent of aortic valve f'unction befbre and after the surgicirl intcrvention. These patients remain in AF and still require anticoagulation. Management with rh1'thm control should be attempted flrst' i\cute coronarl' slnclronte, particularly ST elevtrtiorl An implantable cardiorerter deflbrillator (lCD) (Option B) m1'ocardial infarction lnd high risk non ST-elevation improves sun'ir,al lvhen used for both primary and second rn1'ocardial inf'arction, ntav be managed lvith cardiac ary pre\€ntion of sudden cardiac death (SCD). Patients with catheterization (Option A). Hor'r'ever, aortic dissection sustained ventricular arrhythmias (>30 seconds) or cardiac is a nruch more likell' diagnosis based on the presencc arrest',t,ithout a reversible cause have a class 1 recommen- ol blood pressure discrepancl'' in the arms, AR murmur. nondiagnostic ECG finclings. ancl indeterminate tropc) dation for secondary prevention ICD placement. ICD place ment is recommended for the primary prevention of SCD nin measurement. Carcliac cirtheterization is relatively contraindicated in acrtte ltortic dissection because <ll'the in patients with ischemic or nonischemic cardiomyopathy, possibilitl' of propagatitlg the dissection. Furthernlorc. ejection fraction less than 35'7,, and New York Heart Associ coronar\' :lrtery catheterization rvill not address aortic ation functional class II or Ill heart failure. This patient with clissection. Thus. if aortic clissection is being considercd, AF and an ejection fraction of 45')(, does not ha\e an indica O'l angiography is prelcrred to coronary artery catheter tion for ICD theraPY. ization. In patients with AF who are at high risk for stroke In patients in lr'hom aortic dissection is suspected. C1' and have contraindications to anticoagulation therapy' left ar.rgiographf is pref.erred to inr"asive aortography (Option B). atrial appendage occlusion (Option C) to prevent stroke and Aortograph!'is less sensitive than either TEE or CT angiog systemic thromboembolism may be considered' Left atrial rapl.rf in the diagr-rosis o1'aortic dissection. Invasive aortog appendage occlusion will not help control her arrhl'thmia raphy should be considerecl only when the diagnosis cannot and is not indicated. be determined by noninvasivc imaging. N,{agnetic resonance angiography (Option C) is rarely fEY POITI usecl in the acute settillg t<l diagnose aortic dissection . Aggfessive efforts to achieve rhythm control in because of patient instabilitl irnd the need for prolongecl patients with atrial fibrillation and concomitant heart sclnnit.tg times. I-imitecl availabilitl' on an emergencl' basis failure decrease morbidity and mortality' also r.nakes it less desirable thirn CT angiograph)l

Item 114 Answer: D Educational Objective: Treat parorysmal atrial fibrilla- Item 115 tion with heart failure with rhythm control. Answer: D Educational Objective: Diagnose acute aortic regurgita tr The most appropriate treatment is rhyhm control (Option D). tion complicating ascending aortic dissection. Atrial flbrilation (AF) complicates nearly 40'l. of heart failure D cases, and the combination of AF and heart failure dramatically Thc rnost appropriate cliiignostic tests are transthoracic (a yorsens outcomes. Several clinical trials have demonstrated that cchocardiographl, ancl CT angiographl' of the aorta € o (Option D). This patient's presenting symptom ol acute aggressive efforts to achiere rhlthm control in patients with AF t^ and concomitant heart failure decrease morbidity and mortality. anterior chest pain suggests acute coronary syndromc, o, pulnronary embolisnr. or aortic clissection. In this patient, In patients with heart failure with reduced ejection fraction, CL aortic dissection is most likely because of the significant n recent clinical trials have shown that catheter ablation of AF is difierences in systolic bloocl pressures between the right associated with a favorable eflect on morbidity and mortality ,lt compared with medical therapy. Amiodarone is another option and left arms. In acldition, thc grade 3/6 decrescenclo (D for rhythm control. Although amiodarone carries a risk for diastolic murmur at the left stcrnal border indicates the (, presence ofaortic regurgitation (AR). In the setting ol sus toxicity, this patient's lifetime exposure to the drug is likely to be relatively low given her age, comorbid conditions, and probable pccted aortic dissection. t he prcscnce of new or lr,orsenecl amiodarone dosage, which is generally lower for AF than lor AR suggests aortic root involvemcnt, rt'hich constitutes a ventricular arrhyhmias. Monitored appropriately, it can be used snrgical emergency. Transthoracic echocardiogruphy or safely and eflectively in patients her age. transesophageal echocarcliographl' ('fEE) is indicatecl lo Atrioventricular node ablation with permanent pacemaker confirtt the presence. scvcrit),, and etiology of acute AR. implantation (Option A) is an option for patients with AF who C'l angiography is indicrrled in patients with acute aor have continued symptomatic tachycardia despite rate and tic dissection because it is highly accurate and rapidly rhlthm control therapy. Therapeutic ablation of the atrioven irvailable. TEE n.ray be used wlren CT imaging is unavail tricular node requires implantation of a permanent pacemaker. iible and is helpful in asscssntent of aortic valve f'unction befbre and after the surgicirl intcrvention. These patients remain in AF and still require anticoagulation. Management with rh1'thm control should be attempted flrst' i\cute coronarl' slnclronte, particularly ST elevtrtiorl An implantable cardiorerter deflbrillator (lCD) (Option B) m1'ocardial infarction lnd high risk non ST-elevation improves sun'ir,al lvhen used for both primary and second rn1'ocardial inf'arction, ntav be managed lvith cardiac ary pre\€ntion of sudden cardiac death (SCD). Patients with catheterization (Option A). Hor'r'ever, aortic dissection sustained ventricular arrhythmias (>30 seconds) or cardiac is a nruch more likell' diagnosis based on the presencc arrest',t,ithout a reversible cause have a class 1 recommen- ol blood pressure discrepancl'' in the arms, AR murmur. nondiagnostic ECG finclings. ancl indeterminate tropc) dation for secondary prevention ICD placement. ICD place ment is recommended for the primary prevention of SCD nin measurement. Carcliac cirtheterization is relatively contraindicated in acrtte ltortic dissection because <ll'the in patients with ischemic or nonischemic cardiomyopathy, possibilitl' of propagatitlg the dissection. Furthernlorc. ejection fraction less than 35'7,, and New York Heart Associ coronar\' :lrtery catheterization rvill not address aortic ation functional class II or Ill heart failure. This patient with clissection. Thus. if aortic clissection is being considercd, AF and an ejection fraction of 45')(, does not ha\e an indica O'l angiography is prelcrred to coronary artery catheter tion for ICD theraPY. ization. In patients with AF who are at high risk for stroke In patients in lr'hom aortic dissection is suspected. C1' and have contraindications to anticoagulation therapy' left ar.rgiographf is pref.erred to inr"asive aortography (Option B). atrial appendage occlusion (Option C) to prevent stroke and Aortograph!'is less sensitive than either TEE or CT angiog systemic thromboembolism may be considered' Left atrial rapl.rf in the diagr-rosis o1'aortic dissection. Invasive aortog appendage occlusion will not help control her arrhl'thmia raphy should be considerecl only when the diagnosis cannot and is not indicated. be determined by noninvasivc imaging. N,{agnetic resonance angiography (Option C) is rarely fEY POITI usecl in the acute settillg t<l diagnose aortic dissection . Aggfessive efforts to achieve rhythm control in because of patient instabilitl irnd the need for prolongecl patients with atrial fibrillation and concomitant heart sclnnit.tg times. I-imitecl availabilitl' on an emergencl' basis failure decrease morbidity and mortality' also r.nakes it less desirable thirn CT angiograph)l 214

Answers and Critiques o Echocardiography and CT angiography ofthe aorta are o Echocardiography is an essential tool in the diagnosis indicated in patients with suspected aortic dissection of cardiac tamponade because it defines the presence, associated with acute aortic regurgitation. distribution, and relative volume of pericardial fluid. o Aortic dissection with aortic root involvement, Bibliography including acute aortic regurgitation, constitutes a Imazio M, De Ferrari CM. Cardiac tamponade: an educational review. Eur surgical emergency. Heart J Acute Cardiovasc Care. 2020:2048872620939341. [PMID: 326280381 doi:LO.1177 I 2O48872620939341 Bibtiography otto cM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the Item 117 Answer: A management of patients with valvular heart disease: a report of the American College of Cardiologl/American Heart Association Joint Educational Objective: Treat a patient with heart failure UI Committee on Clinical Practice Guidelines. Circulation. 2o2l:743 rc7 2 and diabetes mellitus with a sodium-glucose cotransporter (l, e227. IPMID: 33332150] doi:10.1161/CIR.0000000000000923 2 inhibitor. ET

Bibtiography otto cM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the Item 117 Answer: A management of patients with valvular heart disease: a report of the American College of Cardiologl/American Heart Association Joint Educational Objective: Treat a patient with heart failure UI Committee on Clinical Practice Guidelines. Circulation. 2o2l:743 rc7 2 and diabetes mellitus with a sodium-glucose cotransporter (l, e227. IPMID: 33332150] doi:10.1161/CIR.0000000000000923 2 inhibitor. ET Item 116 Answer: E The most appropriate treatment is to add dapagliflozin (Option A). This patient has heart failure, tlpe 2 diabe- (J Ed ucatio na I O bjective: Diagnose pericardial effusion E tes mellitus, and kidney disease. Evidence shows that the with tamponade. .E sodium-glucose cotransporter 2 (SGLI2) inhibitors dapagli- rA Transthoracic echocardiography (TTE) (Option E) is the flozin, empagliflozin, canagliflozin, and ertugliflozin are (l, most appropriate diagnostic test. Symptoms of progressive associated with a reduction in cardiovascular death or hos- ta = dyspnea may be caused by underlying pulmonary or car- pitalization for heart failure in patients with type 2 diabetes, diac disorders, but this patient's physical flndings, including and dapagliflozin and empagliflozin are effective in patients a signiflcant pulsus paradoxus (24 mm Hg), tachycardia, without diabetes. In addition, for patients with type 2 diabe distant heart sounds. and crackles. as well as an enlarged tes, an SGLI2 inhibitor reduces progression ofdiabetic kid- cardiac silhouette on chest radiograph, suggest the ney disease. SGLI2 inhibitors should not be used in patients life-threatening diagnosis of cardiac tamponade. Pulsus with type 1 diabetes, increased risk for type 2 diabetic keto- paradoxus represents exaggerated ventricular interdepen acidosis, or rapidly declining or changing kidney function. dence and is a key clinical feature of cardiac tamponade. It Glimepiride (Option B) is a second-generation sulfonylurea. is characterized by a fall in systolic pressure of greater than Although the rezults of many studies have been inconclusive, it 10 mm Hg during inspiration. Pulsus paradoxus is not spe seems that the second-generation agents most likely do not have cific for tamponade and must be interpreted in conjunction any adverse cardiac eflects but also have no cardiac beneflt. with other clinical and echocardiographic features. If the Among patientswith tlpe 2 diabeteswho have established fluid has accumulated slowly, the cardiac silhouette is typ atherosclerotic cardiovascular disease (ASCVD) or established ically enlarged on chest radiograph. This patient's findings kidney disease, the American Diabetes Association and the should prompt urgent evaluation for cardiac tamponade American College of Cardiologz recommend an SGLT2 inhib- and treatment if present. Echocardiography to evaluate fbr itor or glucagonJike peptide 1 receptor agonist with demon the presence, distribution, and relative volume of pericardial strated cardiovascular beneflt. In patients with type 2 diabetes fluid is important to establish the diagnosis. and ASCVD, Iiraglutide, semaglutide (injectable), and dula- Right heart catheterization (Option A) might conflrm glutide have been shown to decrease cardiovascular death. hemodynamic findings consistent with tamponade, and peri However, liraglutide (Option C) has no effect on heart failure cardiocentesis could be performed within the cardiac cathe outcomes in patients with established heart failure. terization laboratory. TTE to evaluate for a pericardial effusion Saxagliptin (Option D) is a dipeptidyl peptidase-4 inhib- and tamponade should precede any invasive evaluation or itor, a class of drug that has been shown to have no diflerence therapeutic procedure because it is safe and readily available. in cardiovascular outcomes compared with placebo. However, 'Ihis patient has a lung mass that is likely malignant. with depending on the study, there was either a trend toward more associated malignant pericardial effusion. CI directed needle heart failure hospitalizations (saxagliptin) or an increased inci- biopsy (Option B), fiberoptic bronchoscopy (Option C), and/ dence of heart failure (alogliptin). Because of this increased or PET/CT (Option D) may all be indicated to refine the diag incidence of heart failure hospitalizations, adding saxagliptin nosis and guide treatment after the patient is stabilized, but as a second line agent would not be appropriate. echocardiographic evaluation is needed immediately.

Item 116 Answer: E The most appropriate treatment is to add dapagliflozin (Option A). This patient has heart failure, tlpe 2 diabe- (J Ed ucatio na I O bjective: Diagnose pericardial effusion E tes mellitus, and kidney disease. Evidence shows that the with tamponade. .E sodium-glucose cotransporter 2 (SGLI2) inhibitors dapagli- rA Transthoracic echocardiography (TTE) (Option E) is the flozin, empagliflozin, canagliflozin, and ertugliflozin are (l, most appropriate diagnostic test. Symptoms of progressive associated with a reduction in cardiovascular death or hos- ta = dyspnea may be caused by underlying pulmonary or car- pitalization for heart failure in patients with type 2 diabetes, diac disorders, but this patient's physical flndings, including and dapagliflozin and empagliflozin are effective in patients a signiflcant pulsus paradoxus (24 mm Hg), tachycardia, without diabetes. In addition, for patients with type 2 diabe distant heart sounds. and crackles. as well as an enlarged tes, an SGLI2 inhibitor reduces progression ofdiabetic kid- cardiac silhouette on chest radiograph, suggest the ney disease. SGLI2 inhibitors should not be used in patients life-threatening diagnosis of cardiac tamponade. Pulsus with type 1 diabetes, increased risk for type 2 diabetic keto- paradoxus represents exaggerated ventricular interdepen acidosis, or rapidly declining or changing kidney function. dence and is a key clinical feature of cardiac tamponade. It Glimepiride (Option B) is a second-generation sulfonylurea. is characterized by a fall in systolic pressure of greater than Although the rezults of many studies have been inconclusive, it 10 mm Hg during inspiration. Pulsus paradoxus is not spe seems that the second-generation agents most likely do not have cific for tamponade and must be interpreted in conjunction any adverse cardiac eflects but also have no cardiac beneflt. with other clinical and echocardiographic features. If the Among patientswith tlpe 2 diabeteswho have established fluid has accumulated slowly, the cardiac silhouette is typ atherosclerotic cardiovascular disease (ASCVD) or established ically enlarged on chest radiograph. This patient's findings kidney disease, the American Diabetes Association and the should prompt urgent evaluation for cardiac tamponade American College of Cardiologz recommend an SGLT2 inhib- and treatment if present. Echocardiography to evaluate fbr itor or glucagonJike peptide 1 receptor agonist with demon the presence, distribution, and relative volume of pericardial strated cardiovascular beneflt. In patients with type 2 diabetes fluid is important to establish the diagnosis. and ASCVD, Iiraglutide, semaglutide (injectable), and dula- Right heart catheterization (Option A) might conflrm glutide have been shown to decrease cardiovascular death. hemodynamic findings consistent with tamponade, and peri However, liraglutide (Option C) has no effect on heart failure cardiocentesis could be performed within the cardiac cathe outcomes in patients with established heart failure. terization laboratory. TTE to evaluate for a pericardial effusion Saxagliptin (Option D) is a dipeptidyl peptidase-4 inhib- and tamponade should precede any invasive evaluation or itor, a class of drug that has been shown to have no diflerence therapeutic procedure because it is safe and readily available. in cardiovascular outcomes compared with placebo. However, 'Ihis patient has a lung mass that is likely malignant. with depending on the study, there was either a trend toward more associated malignant pericardial effusion. CI directed needle heart failure hospitalizations (saxagliptin) or an increased inci- biopsy (Option B), fiberoptic bronchoscopy (Option C), and/ dence of heart failure (alogliptin). Because of this increased or PET/CT (Option D) may all be indicated to refine the diag incidence of heart failure hospitalizations, adding saxagliptin nosis and guide treatment after the patient is stabilized, but as a second line agent would not be appropriate. echocardiographic evaluation is needed immediately. o Sodium-glucose cotransporter 2 inhibitors reduce risk o Findings suggesting cardiac tamponade include pulsus for worsening heart failure and cardiovascular death paradoxus, tachycardia, distant heart sounds, and occa- in patients with heart failure with reduced ejection sionally an enlarged silhouette on chest radiograph. fraction with or without type 2 diabetes mellitus. (Continued) (Continued)

o Sodium-glucose cotransporter 2 inhibitors reduce risk o Findings suggesting cardiac tamponade include pulsus for worsening heart failure and cardiovascular death paradoxus, tachycardia, distant heart sounds, and occa- in patients with heart failure with reduced ejection sionally an enlarged silhouette on chest radiograph. fraction with or without type 2 diabetes mellitus. (Continued) (Continued) 215

Answers and Critiques IEI POIXIS (orfiilrcd) in functional capacity or symptoms in patients with PAD. . Among patients with type 2 diabetes mellitus who ACE inhibitors and angiotensin receptor blockers may be effective in reducing cardiac events in patients with PAD, have established atherosclerotic cardiovascular dis- and there are no data showing preference for one over the ease or established kidney disease, a sodium-glucose others. Switching from olmesartan to ramipril (Option D) cotransporter 2 inhibitor or glucagon-like peptide 1 is not indicated. receptor agonist with demonstrated cardiovascular disease benefit is recommended. XEY POIXT' . Revascularization is indicated in patients with inter Bibliography mittent claudication and severe disability who have Wilcox T, De Block C, Schwartzbard AZ. et al. Diabetic agents, fiom met not improved with optimal medical therapy and formin to SCLI2 inhibitors and GLP1 receptor agonists: JACC focus semi nar. J Am Coll Cardiol. 2020;75:1956 1974. [PMID: 32327107] doi:10.1016,' structured exercise programs. j.jacc.2020.02.056 r Canagliflozin and ertugliflozin should be used with Ut caution in patients with severe peripheral artery disease E lD Item 118 Answer: B because of an increased risk for amputation. t^ o, Ed ucati ona I O bjeAive : Treat intermittent claudication with revascularization. Bibliography EL l.l Gerhard Herman MD, Gornik tJL, Barrett C, et al. 2016 AHA/ACC guideline The most appropriate treatment is revascularization (Option B). on the management of patients with lower extremity peripheral artery disease: executive summary: a report of the American College of .a This patient with peripheral artery disease (PAD) has quit Cardiobs//American Heart Association Task Force on Clinical Practice .D smoking, been adherent to a supervised exercise program, Guidelines. J Am Coll Cardiol. 2Ol7:69:1465 1508. [PMID: 27851991] UI doi:10.1016/j.jacc.2016.11.0O8 and been treated with aspirin, cilostazol, and atorvasta tin; despite these interventions, she remains symptom atic, with lifestyle-limiting claudication. She is therefore a candidate for revascularization, and because she has worse symptoms and a lower ankle-brachial index on the Item 1 19 Answer: D Educational Objective: Evaluate a patient with chest tr pain and left ventricular hypertrophy with exercise left, revascularization should be targeted to the left leg. myocardial perfusion imaging. Experienced vascular specialists can accomplish recanal- ization with angioplasty, atherectomy, stenting, and/or a Thc most appropriate cliagnostic test is exercise ntyocardial combination of techniques. Aortobifemoral bypass surgery perfusion in,aging (Option D). 'Ihis patient presents with is reserved for patients with severe aortoiliac stenoses. cl.rest pain that is concerning ftrr ischemic hcart disease. and Aortoiliac disease most typically manifests as buttock, hip, carcliac stress testing is indicated. Stress testing to evaluate and, in some cases, thigh claudication. f<rr con-rnary artery disease should aln,:rys be perforn'red u'ith Historically, pentoxifylline (Option A) was used in exercise, unless exercisc is contraindicated or the paticnt patients with intermittent claudication; however, this med is unable. Exercise capacit-v is a polterlul predictor of out ication has a high adverse-effect proflle, is not effective, and comes: individuals unable to achicve 5 nretabolic equiv is no longer recommended by guidelines. alents. or the first stage of a Bruce protocol. have higher In patients with tlpe 2 diabetes mellitus, sodium glucose all cause nrortalitl,. Stress testing with imaging is indicated cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide 1 in patients u,ith an inability to exercise, baseline ECG abnor receptor agonists reduce the rates of acute myocardial infarc- malities that limit intcrpretation of the exercise ECG, or tion, stroke, cardiovascular death, and, in the case ofSGLI2 indeterminate findings ot-t the exercise EC(1. Exercise myo inhibitors, heart lailure hospitalizations. These classes of cardial perfusion imaging provides a visual assessment of drugs are recommended as part of the glucose lowering reg relatir,e my'ticardial blood flow (using a radionuclide tracer) imen in patients with atherosclerotic cardiovascular disease bl,comparing images in the resting and stressed states. Jhis (ASCVD) or at high risk for ASCVD. The American College test is thc most appropriate option lbr this patient !\.ith lell of Cardiologr recommends that canagliflozin be used with ventricular hypertrophy r,r'ith a strain pattern on baseline caution in patients with prior amputation, severe periph E(.G that u'ill impair the interpretation of an exercisc ECG. eral neuropathy, severe peripheral vascular disease, or active Exercise is preferred over pharmacologic stressors. diabetic foot infections. In this patient, revascularization Dobutanrine. like exercise. increascs ml,ocardial oxygen will improve her symptoms, whereas stopping canagliflozin dernand and elicits ischemia because of insulficient perlu (Option C) is neither necessary nor helpful. sion to the aff'ected myocardium. Exercise rnvocardial per A small study showed that patients with intermittent firsion imaging is preferred to a d<tbutamine based strcss claudication treated with ramipril had an improvement in tcst u.ith either echocardiography or tnyocardial perfusion pain free walking time and maximal walking time com- imaging (Options A, B). pared with patients treated with usual care. However, there Exercise ECG (Option C) is the test of choice fbr most have not been additional studies that have shown ramipril patients ur-rdergoing ir.ritial evaluation for chest pain thought or other ACE inhibitors to be associated with improvements to be of cardiac origin, unless there are c<lntraindicatiot.ts.

IEI POIXIS (orfiilrcd) in functional capacity or symptoms in patients with PAD. . Among patients with type 2 diabetes mellitus who ACE inhibitors and angiotensin receptor blockers may be effective in reducing cardiac events in patients with PAD, have established atherosclerotic cardiovascular dis- and there are no data showing preference for one over the ease or established kidney disease, a sodium-glucose others. Switching from olmesartan to ramipril (Option D) cotransporter 2 inhibitor or glucagon-like peptide 1 is not indicated. receptor agonist with demonstrated cardiovascular disease benefit is recommended. XEY POIXT' . Revascularization is indicated in patients with inter Bibliography mittent claudication and severe disability who have Wilcox T, De Block C, Schwartzbard AZ. et al. Diabetic agents, fiom met not improved with optimal medical therapy and formin to SCLI2 inhibitors and GLP1 receptor agonists: JACC focus semi nar. J Am Coll Cardiol. 2020;75:1956 1974. [PMID: 32327107] doi:10.1016,' structured exercise programs. j.jacc.2020.02.056 r Canagliflozin and ertugliflozin should be used with Ut caution in patients with severe peripheral artery disease E lD Item 118 Answer: B because of an increased risk for amputation. t^ o, Ed ucati ona I O bjeAive : Treat intermittent claudication with revascularization. Bibliography EL l.l Gerhard Herman MD, Gornik tJL, Barrett C, et al. 2016 AHA/ACC guideline The most appropriate treatment is revascularization (Option B). on the management of patients with lower extremity peripheral artery disease: executive summary: a report of the American College of .a This patient with peripheral artery disease (PAD) has quit Cardiobs//American Heart Association Task Force on Clinical Practice .D smoking, been adherent to a supervised exercise program, Guidelines. J Am Coll Cardiol. 2Ol7:69:1465 1508. [PMID: 27851991] UI doi:10.1016/j.jacc.2016.11.0O8 and been treated with aspirin, cilostazol, and atorvasta tin; despite these interventions, she remains symptom atic, with lifestyle-limiting claudication. She is therefore a candidate for revascularization, and because she has worse symptoms and a lower ankle-brachial index on the Item 1 19 Answer: D Educational Objective: Evaluate a patient with chest tr pain and left ventricular hypertrophy with exercise left, revascularization should be targeted to the left leg. myocardial perfusion imaging. Experienced vascular specialists can accomplish recanal- ization with angioplasty, atherectomy, stenting, and/or a Thc most appropriate cliagnostic test is exercise ntyocardial combination of techniques. Aortobifemoral bypass surgery perfusion in,aging (Option D). 'Ihis patient presents with is reserved for patients with severe aortoiliac stenoses. cl.rest pain that is concerning ftrr ischemic hcart disease. and Aortoiliac disease most typically manifests as buttock, hip, carcliac stress testing is indicated. Stress testing to evaluate and, in some cases, thigh claudication. f<rr con-rnary artery disease should aln,:rys be perforn'red u'ith Historically, pentoxifylline (Option A) was used in exercise, unless exercisc is contraindicated or the paticnt patients with intermittent claudication; however, this med is unable. Exercise capacit-v is a polterlul predictor of out ication has a high adverse-effect proflle, is not effective, and comes: individuals unable to achicve 5 nretabolic equiv is no longer recommended by guidelines. alents. or the first stage of a Bruce protocol. have higher In patients with tlpe 2 diabetes mellitus, sodium glucose all cause nrortalitl,. Stress testing with imaging is indicated cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide 1 in patients u,ith an inability to exercise, baseline ECG abnor receptor agonists reduce the rates of acute myocardial infarc- malities that limit intcrpretation of the exercise ECG, or tion, stroke, cardiovascular death, and, in the case ofSGLI2 indeterminate findings ot-t the exercise EC(1. Exercise myo inhibitors, heart lailure hospitalizations. These classes of cardial perfusion imaging provides a visual assessment of drugs are recommended as part of the glucose lowering reg relatir,e my'ticardial blood flow (using a radionuclide tracer) imen in patients with atherosclerotic cardiovascular disease bl,comparing images in the resting and stressed states. Jhis (ASCVD) or at high risk for ASCVD. The American College test is thc most appropriate option lbr this patient !\.ith lell of Cardiologr recommends that canagliflozin be used with ventricular hypertrophy r,r'ith a strain pattern on baseline caution in patients with prior amputation, severe periph E(.G that u'ill impair the interpretation of an exercisc ECG. eral neuropathy, severe peripheral vascular disease, or active Exercise is preferred over pharmacologic stressors. diabetic foot infections. In this patient, revascularization Dobutanrine. like exercise. increascs ml,ocardial oxygen will improve her symptoms, whereas stopping canagliflozin dernand and elicits ischemia because of insulficient perlu (Option C) is neither necessary nor helpful. sion to the aff'ected myocardium. Exercise rnvocardial per A small study showed that patients with intermittent firsion imaging is preferred to a d<tbutamine based strcss claudication treated with ramipril had an improvement in tcst u.ith either echocardiography or tnyocardial perfusion pain free walking time and maximal walking time com- imaging (Options A, B). pared with patients treated with usual care. However, there Exercise ECG (Option C) is the test of choice fbr most have not been additional studies that have shown ramipril patients ur-rdergoing ir.ritial evaluation for chest pain thought or other ACE inhibitors to be associated with improvements to be of cardiac origin, unless there are c<lntraindicatiot.ts. 216

Answers and g-']-t!gy9: FFI (lt.rntrainclications include an inability to exercise ancl nitroglycerin. Typical qualities of angina include squeezing, lll 1',rr"1i,'," ECG abnornralities (e.g., S'f segment clepression tightness, pressure, constriction, fullness, heaviness, and c0NT >l nrnr, lelt bunclle brarrch block. left ventricular hypertro weight. Angina typically resolves when the inciting factor ph1,. paced rhythnr. or preexcitation). 'lhis patient's chesl is removed. Most episodes of stable angina last 2 to 5 min plin in lhe presence of left ventricular hypertrophy will be utes, not seconds or 20 to 30 minutes. The degree to which belter ilssessed r,r,ith exercise myocardial perfusion inragir.rg a patient's symptoms match these components reflects the becuuse the tiCG chilrges associaterl with left vetrtricular pretest likelihood of coronary artery disease (CAD) as the hypertrophy r,vill obscurc the presence ol llCG ischcnric underlying cause of the symptoms. Although she meets chunges. two criteria for typical angina (quality and duration of dis- comfort, provocation by exertional or emotional stress), her TEY POI]IIS symptoms resolve without rest; therefore, she has atypical o Stress testing to evaluate for coronary artery disease chest pain, with an intermediate pretest probability of CAD should always be performed with exercise, unless as the cause of her symptoms. UI (u exercise is contraindicated or the patient is unable. Patients with only one or none of the features of typical ET . Stress testing with imaging is indicated in patients with stable angina pectoris are classified as having nonanginal an inability to exercise, baseline ECG abnormalities or noncardiac chest pain (Option B). Such patients have a L' that limit interpretation of the exercise ECG, or inde corresponding low likelihood of symptomatic CAD. Patients are classifled as having tlpical angina (Option C), =, terminate findings on the exercise ECG. .E with an associated high likelihood of CAD, if all three com- t

FFI (lt.rntrainclications include an inability to exercise ancl nitroglycerin. Typical qualities of angina include squeezing, lll 1',rr"1i,'," ECG abnornralities (e.g., S'f segment clepression tightness, pressure, constriction, fullness, heaviness, and c0NT >l nrnr, lelt bunclle brarrch block. left ventricular hypertro weight. Angina typically resolves when the inciting factor ph1,. paced rhythnr. or preexcitation). 'lhis patient's chesl is removed. Most episodes of stable angina last 2 to 5 min plin in lhe presence of left ventricular hypertrophy will be utes, not seconds or 20 to 30 minutes. The degree to which belter ilssessed r,r,ith exercise myocardial perfusion inragir.rg a patient's symptoms match these components reflects the becuuse the tiCG chilrges associaterl with left vetrtricular pretest likelihood of coronary artery disease (CAD) as the hypertrophy r,vill obscurc the presence ol llCG ischcnric underlying cause of the symptoms. Although she meets chunges. two criteria for typical angina (quality and duration of dis- comfort, provocation by exertional or emotional stress), her TEY POI]IIS symptoms resolve without rest; therefore, she has atypical o Stress testing to evaluate for coronary artery disease chest pain, with an intermediate pretest probability of CAD should always be performed with exercise, unless as the cause of her symptoms. UI (u exercise is contraindicated or the patient is unable. Patients with only one or none of the features of typical ET . Stress testing with imaging is indicated in patients with stable angina pectoris are classified as having nonanginal an inability to exercise, baseline ECG abnormalities or noncardiac chest pain (Option B). Such patients have a L' that limit interpretation of the exercise ECG, or inde corresponding low likelihood of symptomatic CAD. Patients are classifled as having tlpical angina (Option C), =, terminate findings on the exercise ECG. .E with an associated high likelihood of CAD, if all three com- t ponents of stable angina are present. 6, Bibliography u! Fihn SD, Blankenship JC, Alexander KB et al. 2014 ACC/AHA/AATS/PCNA/ This patient's ongoing and unvarying exertional symp- = SCAI/STS focused update ofthe guideline Ibr the diagnosis and manage toms are not consistent with a classiflcation of unstable ment of patients with stable ischemic hearl disease: a report of the angina (Option D), which is characterized by angina that American College of Cardiologr/American Heart Association Task Force on Practice Cuidelines. and the American Association for Thoracic is new in onset, occurs at rest or with little exertion, or is Surgery Preventive Cardiovascular Nurses Association, Society fbr worsening in severig or frequency. Unstable angina is asso- Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2014;1301749-67. [PMID: 25070666] doi:1o.1161/ ciated with increased short-term risk for acute myocardial cl R.0000000000000095 infarction. XEY POIXI Item 120 Answer: A o Stable angina pectoris can be classified according to Educational Objective: Diagnose atypical chest pain. three components: 1) the quality and duration of dis This patient's symptoms are most consistent with atypical comfort, 2) provocation by exertion or emotional angina (Option A). The structured evaluation of patients stress, and 3) reliefwith rest or nitroglycerin, and the with chest pain includes a focused history regarding the degree to which symptoms match these components duration, type, and associated characteristics of discomfort. reflects the likelihood ofcoronary artery disease being Stable angina pectoris, deflned as reproducible discomfort the underlying cause. of the chest, neck, or arms of at least 2 months' duration, can be further classifled according to three components: Bibliography 1) the quality and duration of discomfort, 2) provocation Katz D, Gavin MC. Stable ischemic heart disease. Ann Intern Med. 2019: by exertion or emotional stress, and 3) relief with rest or 17t:lTCt7 ITC32. IPMID: stlAzZes] doi:10.7326lAITC2ol908o60

ponents of stable angina are present. 6, Bibliography u! Fihn SD, Blankenship JC, Alexander KB et al. 2014 ACC/AHA/AATS/PCNA/ This patient's ongoing and unvarying exertional symp- = SCAI/STS focused update ofthe guideline Ibr the diagnosis and manage toms are not consistent with a classiflcation of unstable ment of patients with stable ischemic hearl disease: a report of the angina (Option D), which is characterized by angina that American College of Cardiologr/American Heart Association Task Force on Practice Cuidelines. and the American Association for Thoracic is new in onset, occurs at rest or with little exertion, or is Surgery Preventive Cardiovascular Nurses Association, Society fbr worsening in severig or frequency. Unstable angina is asso- Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2014;1301749-67. [PMID: 25070666] doi:1o.1161/ ciated with increased short-term risk for acute myocardial cl R.0000000000000095 infarction. XEY POIXI Item 120 Answer: A o Stable angina pectoris can be classified according to Educational Objective: Diagnose atypical chest pain. three components: 1) the quality and duration of dis This patient's symptoms are most consistent with atypical comfort, 2) provocation by exertion or emotional angina (Option A). The structured evaluation of patients stress, and 3) reliefwith rest or nitroglycerin, and the with chest pain includes a focused history regarding the degree to which symptoms match these components duration, type, and associated characteristics of discomfort. reflects the likelihood ofcoronary artery disease being Stable angina pectoris, deflned as reproducible discomfort the underlying cause. of the chest, neck, or arms of at least 2 months' duration, can be further classifled according to three components: Bibliography 1) the quality and duration of discomfort, 2) provocation Katz D, Gavin MC. Stable ischemic heart disease. Ann Intern Med. 2019: by exertion or emotional stress, and 3) relief with rest or 17t:lTCt7 ITC32. IPMID: stlAzZes] doi:10.7326lAITC2ol908o60 217

t t Index Note: Page numbers followed by fand t denote figure and table, respectively. Aortic atheromas. l02 Test questions are indicated by Q. Aortic regurgitation, 62t, 64t,67-68, Q78, Q109, Q115 Aortic root dilation, Q87 A Aortic stenosis, 62t, 63 67 , 64t, 651 Abdominal aortic aneurysm (AAA),1O1 1O2, i01t, Q42 aortic valve replacement for, 66, Q8 ACE inhibitors diagnosis of, 63-66. Q53 for ACS, 24, 25t, 27 low flow, low gradient, Q90 angioedema and, 32 radiation related. 112 cough induced by, 32 Aortic valve replacement, 66, Q72 for heart failure, 32-34, Q70 Aortogmphy, l00t during pregnancy, 71 6, 777 t Apixaban,53,53t, l17t for stable angina, 16 Arrhythmias, 43- 61. See olso Atrial fibrillation; Bradycardia; Palpitations; Aclarubicin, cardiotoxicity of, 1131 Vent ricu lar arrhythmias Acute aortic syndromes, 102 106, 102f diagnostic testing for, 10 13 Acute coronary syndrome (ACS), 17-28 implantable electronic devices, 45t care after, 28 Arrhlthmogenic ri ght ventricular cardiomyopathy/dysplasia (ARVC/D), diagnosis of, 18f 57. 58t general considerations, 17-18 Arsenic, cardiotoxicity of. 1131 medical therapy for, 24-26, 25t Arterial insufficiency ulcers, 107f non ST elevation, S, Q20 Ascites, 38 without obstructive CAD. 27 28 Aspirin Acute decompensated heart failure, 38-40 for ACS, 24, 25t Acute limb ischemia, 111, Q46 after coronary revascularization, 17 Acutemyocarditis,41 42 after percutaneous coronary intervention, Q36 Acute pericarditis, 84-86, 851 111-112 in diabetes, 29 Adenosine, 47t, 116, l17t for PAD, 110, Q33 Advanced refractory heart faiure,40 41 during pregnancy, 1l7t Alcohol septal ablation, 80 for stable angina pectoris, 14 Aldosterone antagonists Atenolol, 25t, 47t, 116, 177 t for ACS, 25t. 27 Atherosclerotic cardiovascular disease (ASCVD) contraindications to. 116 diabetes and, Q79, Q93 for heart failure, 34, Q38 risk of, 2, Q19 for HFpEE, 38 testing for, 3 l0 side effects of. 34 Atherosclerotic ulcers, lo3, l04f Aliskiren during pregnancy, 117t Athlete heart, diagnosis of. 78, 78t, Q75 Alteplase in STEMI, 21 Atorvastatin. 14 Amiodarone, 47t, 57 , llTt Atrial fibrillation, 50 55,51f AmJodipine for hean failure.35 anticoagulation therapy for, 17, 52 54, 53t Ampicillin in infective endocarditis, 76t chemotherapy related. ll3l Andexanet alfa. 53 embolic stroke and, Q99 Angina. See olso Stable angina pectoris hypertrophic cardiomyopathy and, 77 coronary revascularization for, 16-17 ibrutinib-related, Q97 evaluation of, 13, Q88 management of, 51 55, Q11, Q107 Angioedema, 32,41 nonpharmacologic approaches, 54 Angiography paroxysmal, Ql14 coronary 5t,9, Q24, Q105 in restrictive cardiomyopathy, 82 83 cT, 3, st,100t, Q4, Q42, Q101 stroke prevention in. Q83 with FFR,9 stroke rates and. 52t magnetic resonance, 1001 suDcllnlcat.54 55 radionucleotide. 11t Atrial flutter, 55, 551, Q32 Angiosarcomas, S3 84,841 Ql4 Atrial myxomas, 83, 831; Q80 Angiotensin receptor neprilysin inhibitor (ARNI), 32 33, Q1 Atrial septal aneurysm, 9l Angiotensin receptor blockers, 251, 27 ,32-35,116, llTl Atrial septal defects (ASDs), 63t,91-94,92f, Q56, Q1i3 Ankle brachial index, 108, 108t, 1091 Q28 Atrioventricular block,22.43,43f, 441 45, 80, 113t Anthracycline toxicity, 112 113 Atrioventricular nodal reentrant tachycardia (AVNRT), 49, Q25 Antianginal medications, 16, 26 27 ,26t Atrioventricular reciprocating tachycardia (AVRT), 49-50 Antiarrhythmic drugs, 46-48, 47t Atropine,45, Q4.1 Anticoagulation therapy. See olso Specific Anticoagulants Azithromycin, 76t for ACS, 26 in acute limb ischemia, Q46 B after coronary revascularization, 17 B-type natriuretic peptide (BNP), 30-31, 37-39 for atrial fibrillation, 17, 52-54, 53t Belinostat, cardiok)xicity ol 1131 mechanical mitral valves and, Ql00 Bendopnea,3l for peripheral artery disease, Q33 Benign flow murmur,63t during pregnanry, 116-118, 1181 p-Blockers Antiplatelet agents for ACS, 24,25t,26 forACS,24,25t,26 28 Anxiery cardiovascular disease and, 1 contraindications to, l6 Aorta dosages, 34t coarctation, 931, 96-97, 96f function of. 16 diseases of. 99-106 heart rate control and,42 dissection,103,105f,116, Q16, Q62, Q78, Q115 for HFTEF. 33- 34, 34t

Note: Page numbers followed by fand t denote figure and table, respectively. Aortic atheromas. l02 Test questions are indicated by Q. Aortic regurgitation, 62t, 64t,67-68, Q78, Q109, Q115 Aortic root dilation, Q87 A Aortic stenosis, 62t, 63 67 , 64t, 651 Abdominal aortic aneurysm (AAA),1O1 1O2, i01t, Q42 aortic valve replacement for, 66, Q8 ACE inhibitors diagnosis of, 63-66. Q53 for ACS, 24, 25t, 27 low flow, low gradient, Q90 angioedema and, 32 radiation related. 112 cough induced by, 32 Aortic valve replacement, 66, Q72 for heart failure, 32-34, Q70 Aortogmphy, l00t during pregnancy, 71 6, 777 t Apixaban,53,53t, l17t for stable angina, 16 Arrhythmias, 43- 61. See olso Atrial fibrillation; Bradycardia; Palpitations; Aclarubicin, cardiotoxicity of, 1131 Vent ricu lar arrhythmias Acute aortic syndromes, 102 106, 102f diagnostic testing for, 10 13 Acute coronary syndrome (ACS), 17-28 implantable electronic devices, 45t care after, 28 Arrhlthmogenic ri ght ventricular cardiomyopathy/dysplasia (ARVC/D), diagnosis of, 18f 57. 58t general considerations, 17-18 Arsenic, cardiotoxicity of. 1131 medical therapy for, 24-26, 25t Arterial insufficiency ulcers, 107f non ST elevation, S, Q20 Ascites, 38 without obstructive CAD. 27 28 Aspirin Acute decompensated heart failure, 38-40 for ACS, 24, 25t Acute limb ischemia, 111, Q46 after coronary revascularization, 17 Acutemyocarditis,41 42 after percutaneous coronary intervention, Q36 Acute pericarditis, 84-86, 851 111-112 in diabetes, 29 Adenosine, 47t, 116, l17t for PAD, 110, Q33 Advanced refractory heart faiure,40 41 during pregnancy, 1l7t Alcohol septal ablation, 80 for stable angina pectoris, 14 Aldosterone antagonists Atenolol, 25t, 47t, 116, 177 t for ACS, 25t. 27 Atherosclerotic cardiovascular disease (ASCVD) contraindications to. 116 diabetes and, Q79, Q93 for heart failure, 34, Q38 risk of, 2, Q19 for HFpEE, 38 testing for, 3 l0 side effects of. 34 Atherosclerotic ulcers, lo3, l04f Aliskiren during pregnancy, 117t Athlete heart, diagnosis of. 78, 78t, Q75 Alteplase in STEMI, 21 Atorvastatin. 14 Amiodarone, 47t, 57 , llTt Atrial fibrillation, 50 55,51f AmJodipine for hean failure.35 anticoagulation therapy for, 17, 52 54, 53t Ampicillin in infective endocarditis, 76t chemotherapy related. ll3l Andexanet alfa. 53 embolic stroke and, Q99 Angina. See olso Stable angina pectoris hypertrophic cardiomyopathy and, 77 coronary revascularization for, 16-17 ibrutinib-related, Q97 evaluation of, 13, Q88 management of, 51 55, Q11, Q107 Angioedema, 32,41 nonpharmacologic approaches, 54 Angiography paroxysmal, Ql14 coronary 5t,9, Q24, Q105 in restrictive cardiomyopathy, 82 83 cT, 3, st,100t, Q4, Q42, Q101 stroke prevention in. Q83 with FFR,9 stroke rates and. 52t magnetic resonance, 1001 suDcllnlcat.54 55 radionucleotide. 11t Atrial flutter, 55, 551, Q32 Angiosarcomas, S3 84,841 Ql4 Atrial myxomas, 83, 831; Q80 Angiotensin receptor neprilysin inhibitor (ARNI), 32 33, Q1 Atrial septal aneurysm, 9l Angiotensin receptor blockers, 251, 27 ,32-35,116, llTl Atrial septal defects (ASDs), 63t,91-94,92f, Q56, Q1i3 Ankle brachial index, 108, 108t, 1091 Q28 Atrioventricular block,22.43,43f, 441 45, 80, 113t Anthracycline toxicity, 112 113 Atrioventricular nodal reentrant tachycardia (AVNRT), 49, Q25 Antianginal medications, 16, 26 27 ,26t Atrioventricular reciprocating tachycardia (AVRT), 49-50 Antiarrhythmic drugs, 46-48, 47t Atropine,45, Q4.1 Anticoagulation therapy. See olso Specific Anticoagulants Azithromycin, 76t for ACS, 26 in acute limb ischemia, Q46 B after coronary revascularization, 17 B-type natriuretic peptide (BNP), 30-31, 37-39 for atrial fibrillation, 17, 52-54, 53t Belinostat, cardiok)xicity ol 1131 mechanical mitral valves and, Ql00 Bendopnea,3l for peripheral artery disease, Q33 Benign flow murmur,63t during pregnanry, 116-118, 1181 p-Blockers Antiplatelet agents for ACS, 24,25t,26 forACS,24,25t,26 28 Anxiery cardiovascular disease and, 1 contraindications to, l6 Aorta dosages, 34t coarctation, 931, 96-97, 96f function of. 16 diseases of. 99-106 heart rate control and,42 dissection,103,105f,116, Q16, Q62, Q78, Q115 for HFTEF. 33- 34, 34t 219

lndex p-Blockers (Continuedl Cloxacillin. T6t in peripheral artery disease, 109 110 Clubbing,95,98 during pregnancy, U6, 1l7t Complete heart block, 22,43 for premature ventricular contractions, Q55 Congenital heart disease for stable angina, 16 adult,90-99 titration in HFTEF, Q45 c,"notic, 98-99, Q73 Betrixaban during pregnancy, lut Connective tissue disorders. 99t Bevacizumab,114 constrictive pericarditis, 851, 88-90, 90f, Q58 Bicuspid aortic valve disease, 68, 99, Q34, Q101 Continuous positive airway pressure (CPAP), 36 Biguanides,3St Contraceptives, 91 Bisoprolol, 16, 25t,34,34t, 47t Contrast media, risks ol 9 Black patients. See olso Ethnicity, cardiovascular disease and Coronary angiography, 5t. See olso Angiography amyloidosis in, 81 in ischemic chest pain, Q1O5 heart failure in,41 microvascular dysfunction on, Q24 isosorbide dinitrate-hydralazine in, 34, Q31 risks of. 9 peripartum cardiomyopathy in, 115-116 in stable angina pectoris, 16, Q41 Bortezomib, cardiotoxicity of, u3t Coronary arteries, visualization ol 8 9 Bradycardia,43 45,113t, Q2, Q44 Coronary artery bypass graft (CABC) surgery 17, Q6, Ql12 Breastfeeding, 116 Coronary artery calcium (CAC) scoring,3, 5t, 9 Bruce protocol, 6 Coronary artery disease (CAD), 13-30, 14f Brugada syndrome, 57, 58t,591 Q71 atherosclerotic, 3-10, Q19 alrial nbrillation and. Ql07 c diagnosis ol 3 9,13,14f, Q67 CAD. See Coronary artery disease (CAD) evaluation of, Q85 Calcium channel blockers, 16, 261, 35, 68 multivessel, Q6 Canagliflozin for heart failure, 35 premafure,2 Capecitabine, cardiotoxicity of, l13t pretest likelihood of, 13, 13t Captopril, 22, 1171 radiation associated, 112, Q76 Cardiac amyloidosis, 10, 81-82, 81f, 81t risk ofdiagnostic testing, 9 10 Cardiac catheterization, 111, 23, 89, Q85 stress testing for, 3-9, 31-32 Cardiac magnetic resonance (CMR) imaging, 5t,8, 111, 31 Coronary revascularization, 16-17 , Q29 in infiltrative cardiac disease, 81, Q7 Coronary vasospasm, 27, 29, Q95 mitral regurgitation evaluation with, Q84 Crackles, 38 in structural cardiac disease, 10 CT angiography, 5t, llt, Q4. See olso Angiogaphy ventricular tachycardia evaluation with, Q89 AAA localization using, Q42 Cardiac rehabilitation, 28, 37, Q86 bicuspid valve examination using, Q101 Cardiac resynchronization therapy (CRT), 36,45t, Q77, Q111 thoracic aortic imaging, l00t Cardiac syndrome X, 27 qanotic congenital heart disease, 98-99, Q73 Cardiac tamponade, 85t, 86-88, 87f Clclophosphamide, 1131 Cardiac tumors. 83 84 Cyclosporine,4l Cardiogenic shock, 22, 39-40, 39t, Q98 Qrtomegalovirus (CMV), 41 Cardiomyopathies, 41 42 peripartum, 115-116 D Cardiorenal syndrome, 38 Dabigatran, 53, 531, 1171 Cardiovascular disease (CVD) Dapagliflozin for heart failure, 35, Q117 calculating the risk of 2 Decompensated heart failure, 38 40, Q15 cost of 1 Delta wave, 49f epidemiologl of, 1-3 Depression, CVD and, 1 risk factors for, I 2 Dexrazoxane. 114 Cardioversion, 51-52 Diabetes mellitus Carfi lzomib, cardiotoxicity ol 113t atherosclerotic cardiovascular disease and, Q79 Carvedilol, 16, 251, 34t, 47t, 80, Q45 CAD in.29-30 Catecholaminergic polymorphic VT, 58t cardiovascular disease risk and, 2 Catheter ablation, 49,54, 55, Q32 heart failure prevention and, 37, 41 Cefazolin. T6t in peripheral artery disease, 109 Cephalexin, T6t risk reduction, 1 Cerebral aneurysm, 96 Diastolic dysfunction, 30 Chemotherapy, cardiotoxicity ol 112-114, 1l3t Diastolic heart sounds, 89t Chest CT with contrast. l1t Digoxin, 35, 471, 117t Chest pain Diltiazem, 16, 47t, 117 t atypical, Ql20 Dipyridamole, T, 117t coronary cT angiography in, Q4 Direct oral anticoagulant (DOAC), 17, 52 53, 53t, evaluation ol 13, Q57 117t,118 ischemic, Ql05 Direct renin inhibitors, u6 microvascular dysfunction and, Q24 Disopyramide,80, lut myocardial perfusion imaging in, Q1l9 Diuretic therapy Chest radiogaphy, 31, 311 85t, 871 89, 89f clinical traiectories, 39f Cholesterol levels, 1, 14, 15 for heart failure, 34, 37-38 Chronic limb threatening ischemia (CLil), 106-107, Q1O2 during pregnancy, 1171 Cilostazol,110, Q3 for pulmonary vascular congestion, 22 Cisplatin, cardiotoxicity of, 113t Dobutamine.39t Clarithromycin, 16, 76t Dobutamine cardiac magnetic resonance imaging, 5t Clopidogrel Dobutamine echocardiography, 4t, 10 for ACS, 251, 26 Dobutamine myocardial perfusion imaging, 4t after percutaneous intervention, Q36 Docetaxel, cardiotoxicity of, 1131 in aspirin intolerance, Q12 Dofetilide, 471, 48 characteristics of, 21t Dopamine,39t discontinuing, Q65 Doxorubicin. ll3t for PAD, u0, Q33 DPP-4 receptor antagonists, 35t during pregnancy, lut Dronedarone, 47t, 48 for stable angina pectoris, 14, Q12 Dual antiplatelet rherapy (DAPT). 17, 26, Q36, Ql04 in STEMI.2I Duke Treadmill Score. 6

p-Blockers (Continuedl Cloxacillin. T6t in peripheral artery disease, 109 110 Clubbing,95,98 during pregnancy, U6, 1l7t Complete heart block, 22,43 for premature ventricular contractions, Q55 Congenital heart disease for stable angina, 16 adult,90-99 titration in HFTEF, Q45 c,"notic, 98-99, Q73 Betrixaban during pregnancy, lut Connective tissue disorders. 99t Bevacizumab,114 constrictive pericarditis, 851, 88-90, 90f, Q58 Bicuspid aortic valve disease, 68, 99, Q34, Q101 Continuous positive airway pressure (CPAP), 36 Biguanides,3St Contraceptives, 91 Bisoprolol, 16, 25t,34,34t, 47t Contrast media, risks ol 9 Black patients. See olso Ethnicity, cardiovascular disease and Coronary angiography, 5t. See olso Angiography amyloidosis in, 81 in ischemic chest pain, Q1O5 heart failure in,41 microvascular dysfunction on, Q24 isosorbide dinitrate-hydralazine in, 34, Q31 risks of. 9 peripartum cardiomyopathy in, 115-116 in stable angina pectoris, 16, Q41 Bortezomib, cardiotoxicity of, u3t Coronary arteries, visualization ol 8 9 Bradycardia,43 45,113t, Q2, Q44 Coronary artery bypass graft (CABC) surgery 17, Q6, Ql12 Breastfeeding, 116 Coronary artery calcium (CAC) scoring,3, 5t, 9 Bruce protocol, 6 Coronary artery disease (CAD), 13-30, 14f Brugada syndrome, 57, 58t,591 Q71 atherosclerotic, 3-10, Q19 alrial nbrillation and. Ql07 c diagnosis ol 3 9,13,14f, Q67 CAD. See Coronary artery disease (CAD) evaluation of, Q85 Calcium channel blockers, 16, 261, 35, 68 multivessel, Q6 Canagliflozin for heart failure, 35 premafure,2 Capecitabine, cardiotoxicity of, l13t pretest likelihood of, 13, 13t Captopril, 22, 1171 radiation associated, 112, Q76 Cardiac amyloidosis, 10, 81-82, 81f, 81t risk ofdiagnostic testing, 9 10 Cardiac catheterization, 111, 23, 89, Q85 stress testing for, 3-9, 31-32 Cardiac magnetic resonance (CMR) imaging, 5t,8, 111, 31 Coronary revascularization, 16-17 , Q29 in infiltrative cardiac disease, 81, Q7 Coronary vasospasm, 27, 29, Q95 mitral regurgitation evaluation with, Q84 Crackles, 38 in structural cardiac disease, 10 CT angiography, 5t, llt, Q4. See olso Angiogaphy ventricular tachycardia evaluation with, Q89 AAA localization using, Q42 Cardiac rehabilitation, 28, 37, Q86 bicuspid valve examination using, Q101 Cardiac resynchronization therapy (CRT), 36,45t, Q77, Q111 thoracic aortic imaging, l00t Cardiac syndrome X, 27 qanotic congenital heart disease, 98-99, Q73 Cardiac tamponade, 85t, 86-88, 87f Clclophosphamide, 1131 Cardiac tumors. 83 84 Cyclosporine,4l Cardiogenic shock, 22, 39-40, 39t, Q98 Qrtomegalovirus (CMV), 41 Cardiomyopathies, 41 42 peripartum, 115-116 D Cardiorenal syndrome, 38 Dabigatran, 53, 531, 1171 Cardiovascular disease (CVD) Dapagliflozin for heart failure, 35, Q117 calculating the risk of 2 Decompensated heart failure, 38 40, Q15 cost of 1 Delta wave, 49f epidemiologl of, 1-3 Depression, CVD and, 1 risk factors for, I 2 Dexrazoxane. 114 Cardioversion, 51-52 Diabetes mellitus Carfi lzomib, cardiotoxicity ol 113t atherosclerotic cardiovascular disease and, Q79 Carvedilol, 16, 251, 34t, 47t, 80, Q45 CAD in.29-30 Catecholaminergic polymorphic VT, 58t cardiovascular disease risk and, 2 Catheter ablation, 49,54, 55, Q32 heart failure prevention and, 37, 41 Cefazolin. T6t in peripheral artery disease, 109 Cephalexin, T6t risk reduction, 1 Cerebral aneurysm, 96 Diastolic dysfunction, 30 Chemotherapy, cardiotoxicity ol 112-114, 1l3t Diastolic heart sounds, 89t Chest CT with contrast. l1t Digoxin, 35, 471, 117t Chest pain Diltiazem, 16, 47t, 117 t atypical, Ql20 Dipyridamole, T, 117t coronary cT angiography in, Q4 Direct oral anticoagulant (DOAC), 17, 52 53, 53t, evaluation ol 13, Q57 117t,118 ischemic, Ql05 Direct renin inhibitors, u6 microvascular dysfunction and, Q24 Disopyramide,80, lut myocardial perfusion imaging in, Q1l9 Diuretic therapy Chest radiogaphy, 31, 311 85t, 871 89, 89f clinical traiectories, 39f Cholesterol levels, 1, 14, 15 for heart failure, 34, 37-38 Chronic limb threatening ischemia (CLil), 106-107, Q1O2 during pregnancy, 1171 Cilostazol,110, Q3 for pulmonary vascular congestion, 22 Cisplatin, cardiotoxicity of, 113t Dobutamine.39t Clarithromycin, 16, 76t Dobutamine cardiac magnetic resonance imaging, 5t Clopidogrel Dobutamine echocardiography, 4t, 10 for ACS, 251, 26 Dobutamine myocardial perfusion imaging, 4t after percutaneous intervention, Q36 Docetaxel, cardiotoxicity of, 1131 in aspirin intolerance, Q12 Dofetilide, 471, 48 characteristics of, 21t Dopamine,39t discontinuing, Q65 Doxorubicin. ll3t for PAD, u0, Q33 DPP-4 receptor antagonists, 35t during pregnancy, lut Dronedarone, 47t, 48 for stable angina pectoris, 14, Q12 Dual antiplatelet rherapy (DAPT). 17, 26, Q36, Ql04 in STEMI.2I Duke Treadmill Score. 6 220

lndex t Dyslipidemia, 1, 109 Heart failure with preservecl ejection fraction (HFpEF), 37-38, e3t, e82 Dyspnea, causes ol 31 Heart failure with reduced €jection tiaction (HFTEF). 30,32 36,33f, el, e4S Heart rate control. 52 i t Heart sounds, 89t t Echocardiography, 1O, 11t Heart transplant, Q22, Q66 in aortic stenosis. 661 t evaluation of palpitations using, Q30 for cardiac amyloidosis, 81, 8l t tbr heart failure, 32t, 36-37. 40 41. 116 in heart failure, 31, 36 infections and. 74 t pericardial effusion on, 84 for m),ocarditis, 42 screening for myocardial dysfunction, e40 i for restrictive cardiomyopathy. 82, Q66 Edoxaban,53t t Heparin for ACS, 26 Ehlers Danlos syndrome, 99 HIV CAD risk in, 3 t Eisenmenger syndrome, 93t, 94, 9g 99 \ Elderly patients, CAD in, 28 29 Holter monitors, 10, 12t Hydralazine during pregnancy, 1171 Electrical alternans. 85r, 87, 87f \ Electrocardiography, 4t, 6, 10, 121. See olso Specilic conditions Electrophysiolory study, 12t Hypercalcemia, Hyperkalemia,34 19

lndex t Dyslipidemia, 1, 109 Heart failure with preservecl ejection fraction (HFpEF), 37-38, e3t, e82 Dyspnea, causes ol 31 Heart failure with reduced €jection tiaction (HFTEF). 30,32 36,33f, el, e4S Heart rate control. 52 i t Heart sounds, 89t t Echocardiography, 1O, 11t Heart transplant, Q22, Q66 in aortic stenosis. 661 t evaluation of palpitations using, Q30 for cardiac amyloidosis, 81, 8l t tbr heart failure, 32t, 36-37. 40 41. 116 in heart failure, 31, 36 infections and. 74 t pericardial effusion on, 84 for m),ocarditis, 42 screening for myocardial dysfunction, e40 i for restrictive cardiomyopathy. 82, Q66 Edoxaban,53t t Heparin for ACS, 26 Ehlers Danlos syndrome, 99 HIV CAD risk in, 3 t Eisenmenger syndrome, 93t, 94, 9g 99 \ Elderly patients, CAD in, 28 29 Holter monitors, 10, 12t Hydralazine during pregnancy, 1171 Electrical alternans. 85r, 87, 87f \ Electrocardiography, 4t, 6, 10, 121. See olso Specilic conditions Electrophysiolory study, 12t Hypercalcemia, Hyperkalemia,34 19 j Hypertension L Empagliflozin, 35, Q10, Q93 cardiovascular risk and, I -2 Enalapril,25t, 33, 117t, Q70 chemotherapy related. lt3t Endocarditis i heart failure prevention and, 37 antibiotic therapy, 76t Hypertrophic cardiomyopathy (HCM),57,77 81. Q50. QI03 I infective, 74-76, Q18, Q72 diagnosis of, 4t, 10, 77 78, Q23 L prophylaxis, 75-76, 761, Q108 ECG findings in, 77, 781' t Endovascular revascularization, 110 111 evaluation of, 63t, 77 78 \ Enoxaparin, 21, 26 Epirubicin, cardiotoxicity of , ll3t imaging of, 79f I presentation, 77 I Eplerenone,2T, 34 I Erlotinib, cardiotoxicity ot, 113t risk stratification. 78 79 sudden cardiac death and, 58t, 78, 79t i Esmolol during pregnancy, 117t t Etaracizumab, cardiotoxicity ol 113t I I Ethnicity, cardiovascular disease and, 2-3 Ibrutinib, 1131, Q97 t Exercise electrocardiography, 4t, 6, 6t, 72I, Q43, Q67 Extracorporeal membrane oxygenation (ECMO), 22 Idarubicin, cardiotoxicity ol, I l3t ldarucizumab. S3 I ldiopathic pericarditis, 86 \ F Ifosfamide, cardiotoxicity ol; I I 3t 4-factor prothrombin complex concentrate, 53 i lmplantable cardioverter delibrillators (lCDs), 22, 36, 45t, 7tt 79, Q9, Q103 \ Felodipine for heart failure, 35 Inappropriate sinus tachycardia (lST), 48 Figure 3 sign, 96, 96f ; Infections Flecainide, 46-4a,47t I endocarditis, 7 4 -7 6, 7 6t, Ql 8, Q72 discontinuing, Ql10 implantable cardiac devices. 61, Q64 I during pregnancy, llTt lnfective endocarditis (l E), 74-76 ) toxicity,46f i Duke criteria. 75t Fluid overload, 30, 38-40 I evaluation of, Q18 h Fluid retention, 30 treatment ol 76t, Q72 5 Fluorouracil. 113t Insulin in heart failure, 35( I Fondaparinux, 21, 26 t Fractional flow reserve (FFR), angiography with, 3, 5t, 9 Intermittent claudicatkrn. 106-107, 110, Q3, Q86, QtlS lntra-aortic balloon pump (IABP), 22, 7l Frailty, definition of, 61 i lntramural hematoma, 103, 103f, 104 Furosemide,34, Q15 lodinated contrast material. 9 i Iron deficiency, 35, Q73 I G Cadolinium contrast, 9, 86f Iron therapy for hearl lrrilure. 35 Gemcitabine, cardiotoxicity ol 1131 lschemia I i Gentamicin in infective endocarditis, 76t chemotherapy related. ll3t Giant cell myocarditis, 42 evaluation for. 31 32 on exercise ECG. 6 7 i Glucagon-like peptide I (GLP 1) receptor antagonists, 29, 35t, Q79 Glucocorticoids, for recurrent pericarditis, 86, Q35 limb threatening, 106 108, Ql02 :

j Hypertension L Empagliflozin, 35, Q10, Q93 cardiovascular risk and, I -2 Enalapril,25t, 33, 117t, Q70 chemotherapy related. lt3t Endocarditis i heart failure prevention and, 37 antibiotic therapy, 76t Hypertrophic cardiomyopathy (HCM),57,77 81. Q50. QI03 I infective, 74-76, Q18, Q72 diagnosis of, 4t, 10, 77 78, Q23 L prophylaxis, 75-76, 761, Q108 ECG findings in, 77, 781' t Endovascular revascularization, 110 111 evaluation of, 63t, 77 78 \ Enoxaparin, 21, 26 Epirubicin, cardiotoxicity of , ll3t imaging of, 79f I presentation, 77 I Eplerenone,2T, 34 I Erlotinib, cardiotoxicity ot, 113t risk stratification. 78 79 sudden cardiac death and, 58t, 78, 79t i Esmolol during pregnancy, 117t t Etaracizumab, cardiotoxicity ol 113t I I Ethnicity, cardiovascular disease and, 2-3 Ibrutinib, 1131, Q97 t Exercise electrocardiography, 4t, 6, 6t, 72I, Q43, Q67 Extracorporeal membrane oxygenation (ECMO), 22 Idarubicin, cardiotoxicity ol, I l3t ldarucizumab. S3 I ldiopathic pericarditis, 86 \ F Ifosfamide, cardiotoxicity ol; I I 3t 4-factor prothrombin complex concentrate, 53 i lmplantable cardioverter delibrillators (lCDs), 22, 36, 45t, 7tt 79, Q9, Q103 \ Felodipine for heart failure, 35 Inappropriate sinus tachycardia (lST), 48 Figure 3 sign, 96, 96f ; Infections Flecainide, 46-4a,47t I endocarditis, 7 4 -7 6, 7 6t, Ql 8, Q72 discontinuing, Ql10 implantable cardiac devices. 61, Q64 I during pregnancy, llTt lnfective endocarditis (l E), 74-76 ) toxicity,46f i Duke criteria. 75t Fluid overload, 30, 38-40 I evaluation of, Q18 h Fluid retention, 30 treatment ol 76t, Q72 5 Fluorouracil. 113t Insulin in heart failure, 35( I Fondaparinux, 21, 26 t Fractional flow reserve (FFR), angiography with, 3, 5t, 9 Intermittent claudicatkrn. 106-107, 110, Q3, Q86, QtlS lntra-aortic balloon pump (IABP), 22, 7l Frailty, definition of, 61 i lntramural hematoma, 103, 103f, 104 Furosemide,34, Q15 lodinated contrast material. 9 i Iron deficiency, 35, Q73 I G Cadolinium contrast, 9, 86f Iron therapy for hearl lrrilure. 35 Gemcitabine, cardiotoxicity ol 1131 lschemia I i Gentamicin in infective endocarditis, 76t chemotherapy related. ll3t Giant cell myocarditis, 42 evaluation for. 31 32 on exercise ECG. 6 7 i Glucagon-like peptide I (GLP 1) receptor antagonists, 29, 35t, Q79 Glucocorticoids, for recurrent pericarditis, 86, Q35 limb threatening, 106 108, Ql02 : Glycemic control, 29 lschemic cardiomyopathy, 57 I Glycoprotein IIb/llla inhibitors, 26 Isosorbide dinitrate hydralazine, ll4, Q31 GRACE risk score, 23 Isosorbide mononitrate. 34 Guideline-directed medical therapy (GDMT), Q26, Q33 lvabradine for heart failure. il4 for heart failure, 331 35-36, 57, 66 for stable angina, 14, l5l l7 J for ventricular dyslunction, 72 Jugular venous distention. 38

Glycemic control, 29 lschemic cardiomyopathy, 57 I Glycoprotein IIb/llla inhibitors, 26 Isosorbide dinitrate hydralazine, ll4, Q31 GRACE risk score, 23 Isosorbide mononitrate. 34 Guideline-directed medical therapy (GDMT), Q26, Q33 lvabradine for heart failure. il4 for heart failure, 331 35-36, 57, 66 for stable angina, 14, l5l l7 J for ventricular dyslunction, 72 Jugular venous distention. 38 H x H2FPEF risk score, 3l Kerley B lines, 31 Heart block, transient, Q81 Kidney disease, risks ofcontrast media in, 9 Heart failure (HF), 30 42 Kussmaul sign, 82, 89 ACE inhibitors for, Q70 aldosterone antagonists fbr, Q38 L atrial fibrillation treatment in, Q114 hbetalol during pregnancy, llTt diagnosis of, 30 32 lactation, drugs during, ll6. llTt heart transplantation for, Q22 Leadless pacemakers, 45t, 46f' management of,32-41, Q52, Q1o6 Left bundle branch block. 6,7, 36. 56f. Q57 new-onset, Q85 Left ventricular assist devices (LVADs), 22, .10, Ql06 pathophysiolos/ of, 30 Left ventricular ejection fiaction (t.VEF). 30 in pregnancy, 116 Left ventricular hypertrophlr .5t. 6. .531, 81, Q119 right sided,88 Left ventricular outflow tract obstructlon, 77. 77t I screening tbr, 30 Left ventricular free wall rupture, 22 severity ol 32, 32t Left ventricular wall thickness, 78t SGLT2 inhibitor for, Q10, Q117 Leucovorin, cardiotoxicity of, ll3t treatment with CRT, Q77, Q111 Lidocaine,4Tt, u7t

H x H2FPEF risk score, 3l Kerley B lines, 31 Heart block, transient, Q81 Kidney disease, risks ofcontrast media in, 9 Heart failure (HF), 30 42 Kussmaul sign, 82, 89 ACE inhibitors for, Q70 aldosterone antagonists fbr, Q38 L atrial fibrillation treatment in, Q114 hbetalol during pregnancy, llTt diagnosis of, 30 32 lactation, drugs during, ll6. llTt heart transplantation for, Q22 Leadless pacemakers, 45t, 46f' management of,32-41, Q52, Q1o6 Left bundle branch block. 6,7, 36. 56f. Q57 new-onset, Q85 Left ventricular assist devices (LVADs), 22, .10, Ql06 pathophysiolos/ of, 30 Left ventricular ejection fiaction (t.VEF). 30 in pregnancy, 116 Left ventricular hypertrophlr .5t. 6. .531, 81, Q119 right sided,88 Left ventricular outflow tract obstructlon, 77. 77t I screening tbr, 30 Left ventricular free wall rupture, 22 severity ol 32, 32t Left ventricular wall thickness, 78t SGLT2 inhibitor for, Q10, Q117 Leucovorin, cardiotoxicity of, ll3t treatment with CRT, Q77, Q111 Lidocaine,4Tt, u7t 221

lndex Lifestyle, cardiovascular risk and, 1 Paclitaxel, cardiotoxicity oi 113t Limb ischemia, 106, 110, 111, Q46 PAD. See Peripheral artery disease (PAD) Lipid lowering ther^py, 14, 27 Palpitations, 1o. Q30, Q60 Lisinopril, 25t, 117t Papillary fibroelastomas, 83 Long QT syndrome, 57, 581 58t,113t PARADIGM HF trial,33, Ql Loop diuretics for heart failure, 34, 38, 39f Patent ductus arteriosus (PDA), 95, Q27 Looping event recorders, 10, 12t, 13 Patent lbramen ovale (PFO), 91, 9lf, 93t, Q48 Low cardiac output, 31 Patient triggered event recorders, l2t Percutaneous coronary intervention (PCI), 17, 20-21 m Pericardial calcifi cation, 891 Magnetic resonance angiography, 100t, l08t Pericardial disease, 84 90, 84t, 85t Marfan syndrome, 99-101, 106, 116, Q87 Pericardial efTusion, 84. 86-88, 88f, Q116 Mechanical circulatory support, 40 Pericardial friction rub. 84 Metabolic syndrome, 2 Pericardial thickening, 90 Metformin in heart failure. 35t Pericardiocentesis. 86 Metoprolol, 16, 34t. 47 I, 117 I Pericarditis,84 86 Mexiletine.4Tt acute,84 86,851 1ll 112, Q94 Microvascular dysfunction, 27, 29, Q24 constrictive, 851, 88-90, 90f, Q58 Milrinone,39t idiopathic, 86 MINOCA (MI in the absence of obstructive CAD). 27 recurrent, Q35 Mitoxantrone, cardiotoxicity ol, 1131 restrictrive, 89f Mitral inflow velocity, 88f Peripartum cardiomyopathy, ll5 l16, Q13, Q70 Mitral regurgitation. 62t, 641. 7 O 72, 7 2t Peripheral artery disease (PAD), 106 ll1 CMR imaging in, Q84 asymptomatic. Q69 mitral valve repair in, Q63 cardiovascular risk reduction in, Q21 treatment ol Q26 cilostazol fbr intermittent claudication, Q3 Mitral stenosis, 62t, 64t, 68-7O, 69f. Q43 clinical presentation, 106-107 Mitral valve clipping, 73f diagnosis of. Q28 Mitral valve prolapse, 70, 71f imaging, loSt Mitral valve repair, 72, Q63 interventional therapy, 110 lll Mitral valves, mechanical. 73, Q100 medicaltherapy, 109 110 Mobile cardiac outpatient telemetry 12t physical examination in, 107t Multi-Ethnic Study of Atherosclerosis, 2 revascularization in, Q118 Multifocal atrial tachycardia, 50, 50f statin therapy in, Q54 Myocardial disease, 77 8,1 treatment with GDMT, Q33 Myocardial fibrosis, radiation and, 112 Peripheral edema, 38 Myocardial infarction (MI), 17 28 PET/CT,5t,9 heart block after, Q81 Phenytoin during pregnancy, 117t hereditary factors in, 2 Platypnea-orthodeoxia syndrome. 91 non ST elevation,23 24, Q98 Plebotomy,98 in pregnancy, 116 Pooled Cohort Equations (PCE), 2 with right ventricular involvement. Q51 Postural orthostatic tachycardia syndrome (POTS). 48 49 ST elevation. 18 23 Prasugrel, 21t.25t,26 Myocardial injury interpretation ol 18f Pregnancy Myocardial interstitial librosis, 63 anticoagulation therapy during, 116-118 Myocardial perlusion imaging (l\{PI).7, Q88, Q119 p blockers during. l16 Myocardial viability study, T 8,8t cardiovascular disease and. 114 118 Myocarditis,4l ,12 drugs during, 1171 Marfan syndrome and, Q87 il normal signs in, 1151 Nadolol.4Tt pathobgic signs in, l15t Neprilysin, inhibition of, 32-33 peripartum cardiomyopathy, Qi3, Q70 Nitrates, 16, 24, 26-27, Q96 pulmonary stenosis and. 96 Nitroglycerin, 16, 26t, 39t warfarin during, Q68 Nivolumab, cardiotoxicity of, 113t Premature atrial contractions (PACs), 50 Nocturnal bradycardia, 43 Premature ventricular contractions (PVCs), 55 57, Ql7, Q55 Nondihydropyridine calcium channel blockers, 26t, 35, 47t, 48 Presyncope, diagnostic testing in, 10 Non ST elevation acute coronary syndrome (NSTE ACS).17 l8 Procainamide during pregnancy, i17t 23 24,23t,Q2O Propafenone, 16 48, 47t, 48f , 117t management of, Q59 Propranol,4Tt, 117t, Q55. See olso p-Blockers risk stratiflcation in, 23 Prosthetic valves, 73 74, Q68 treatment of, 23 24,24f,Q1O4 Pseudoclaudication. 107t Non ST elevation myocardial infarction,23 24, Q98 Pulmonary balloon valvuloplasty, 95-96 Nonsteroidal antiinflammatory drugs, 86, Q35 Pulmonary regurgitation, 621, 97, Q92 Noonan syndrome,96 Pulmonary stenosis (PS). 62t, 95 96 Norepinephrine. 39t Pulmonary vascular congestion, 22

Lifestyle, cardiovascular risk and, 1 Paclitaxel, cardiotoxicity oi 113t Limb ischemia, 106, 110, 111, Q46 PAD. See Peripheral artery disease (PAD) Lipid lowering ther^py, 14, 27 Palpitations, 1o. Q30, Q60 Lisinopril, 25t, 117t Papillary fibroelastomas, 83 Long QT syndrome, 57, 581 58t,113t PARADIGM HF trial,33, Ql Loop diuretics for heart failure, 34, 38, 39f Patent ductus arteriosus (PDA), 95, Q27 Looping event recorders, 10, 12t, 13 Patent lbramen ovale (PFO), 91, 9lf, 93t, Q48 Low cardiac output, 31 Patient triggered event recorders, l2t Percutaneous coronary intervention (PCI), 17, 20-21 m Pericardial calcifi cation, 891 Magnetic resonance angiography, 100t, l08t Pericardial disease, 84 90, 84t, 85t Marfan syndrome, 99-101, 106, 116, Q87 Pericardial efTusion, 84. 86-88, 88f, Q116 Mechanical circulatory support, 40 Pericardial friction rub. 84 Metabolic syndrome, 2 Pericardial thickening, 90 Metformin in heart failure. 35t Pericardiocentesis. 86 Metoprolol, 16, 34t. 47 I, 117 I Pericarditis,84 86 Mexiletine.4Tt acute,84 86,851 1ll 112, Q94 Microvascular dysfunction, 27, 29, Q24 constrictive, 851, 88-90, 90f, Q58 Milrinone,39t idiopathic, 86 MINOCA (MI in the absence of obstructive CAD). 27 recurrent, Q35 Mitoxantrone, cardiotoxicity ol, 1131 restrictrive, 89f Mitral inflow velocity, 88f Peripartum cardiomyopathy, ll5 l16, Q13, Q70 Mitral regurgitation. 62t, 641. 7 O 72, 7 2t Peripheral artery disease (PAD), 106 ll1 CMR imaging in, Q84 asymptomatic. Q69 mitral valve repair in, Q63 cardiovascular risk reduction in, Q21 treatment ol Q26 cilostazol fbr intermittent claudication, Q3 Mitral stenosis, 62t, 64t, 68-7O, 69f. Q43 clinical presentation, 106-107 Mitral valve clipping, 73f diagnosis of. Q28 Mitral valve prolapse, 70, 71f imaging, loSt Mitral valve repair, 72, Q63 interventional therapy, 110 lll Mitral valves, mechanical. 73, Q100 medicaltherapy, 109 110 Mobile cardiac outpatient telemetry 12t physical examination in, 107t Multi-Ethnic Study of Atherosclerosis, 2 revascularization in, Q118 Multifocal atrial tachycardia, 50, 50f statin therapy in, Q54 Myocardial disease, 77 8,1 treatment with GDMT, Q33 Myocardial fibrosis, radiation and, 112 Peripheral edema, 38 Myocardial infarction (MI), 17 28 PET/CT,5t,9 heart block after, Q81 Phenytoin during pregnancy, 117t hereditary factors in, 2 Platypnea-orthodeoxia syndrome. 91 non ST elevation,23 24, Q98 Plebotomy,98 in pregnancy, 116 Pooled Cohort Equations (PCE), 2 with right ventricular involvement. Q51 Postural orthostatic tachycardia syndrome (POTS). 48 49 ST elevation. 18 23 Prasugrel, 21t.25t,26 Myocardial injury interpretation ol 18f Pregnancy Myocardial interstitial librosis, 63 anticoagulation therapy during, 116-118 Myocardial perlusion imaging (l\{PI).7, Q88, Q119 p blockers during. l16 Myocardial viability study, T 8,8t cardiovascular disease and. 114 118 Myocarditis,4l ,12 drugs during, 1171 Marfan syndrome and, Q87 il normal signs in, 1151 Nadolol.4Tt pathobgic signs in, l15t Neprilysin, inhibition of, 32-33 peripartum cardiomyopathy, Qi3, Q70 Nitrates, 16, 24, 26-27, Q96 pulmonary stenosis and. 96 Nitroglycerin, 16, 26t, 39t warfarin during, Q68 Nivolumab, cardiotoxicity of, 113t Premature atrial contractions (PACs), 50 Nocturnal bradycardia, 43 Premature ventricular contractions (PVCs), 55 57, Ql7, Q55 Nondihydropyridine calcium channel blockers, 26t, 35, 47t, 48 Presyncope, diagnostic testing in, 10 Non ST elevation acute coronary syndrome (NSTE ACS).17 l8 Procainamide during pregnancy, i17t 23 24,23t,Q2O Propafenone, 16 48, 47t, 48f , 117t management of, Q59 Propranol,4Tt, 117t, Q55. See olso p-Blockers risk stratiflcation in, 23 Prosthetic valves, 73 74, Q68 treatment of, 23 24,24f,Q1O4 Pseudoclaudication. 107t Non ST elevation myocardial infarction,23 24, Q98 Pulmonary balloon valvuloplasty, 95-96 Nonsteroidal antiinflammatory drugs, 86, Q35 Pulmonary regurgitation, 621, 97, Q92 Noonan syndrome,96 Pulmonary stenosis (PS). 62t, 95 96 Norepinephrine. 39t Pulmonary vascular congestion, 22 0 Obesity, CVD risk and, 2 Quinidine during pregnancy, 1171 Ostium primum ASD,91, 93t Ostium secundum ASD, 91, 93t, Q56 R Oxacillin. T6t Radiation therapy, 111, 111t, Q76 Oxiplatin, cardiotoxicity ol, 1l3t Radionucleotide angiography (MUCA), 11t Oxygen. supplem ental, 24, 26 Ranolazine. 16 Renin-angiotensin aldosterone system (RAAS), 30, 32 P Restrictive cardiomyopathy. 82 83. 9Of, Q66 P2Yu inhibitors, 2lt, Q36 Reteplase in STEMI, 21 Pacemakers.45t Retroperitoneal hemorrhage, 9 infections, Q64 Reynolds risk score, 2 leadless, 45t,46f Rheumatoid arthritis, 3 for symptomatic bradycardia, Q2 Rhythm control,42, 54-55, 80, 82, Q11, Q114 transvenous. 45t Rifampin, T6t

0 Obesity, CVD risk and, 2 Quinidine during pregnancy, 1171 Ostium primum ASD,91, 93t Ostium secundum ASD, 91, 93t, Q56 R Oxacillin. T6t Radiation therapy, 111, 111t, Q76 Oxiplatin, cardiotoxicity ol, 1l3t Radionucleotide angiography (MUCA), 11t Oxygen. supplem ental, 24, 26 Ranolazine. 16 Renin-angiotensin aldosterone system (RAAS), 30, 32 P Restrictive cardiomyopathy. 82 83. 9Of, Q66 P2Yu inhibitors, 2lt, Q36 Reteplase in STEMI, 21 Pacemakers.45t Retroperitoneal hemorrhage, 9 infections, Q64 Reynolds risk score, 2 leadless, 45t,46f Rheumatoid arthritis, 3 for symptomatic bradycardia, Q2 Rhythm control,42, 54-55, 80, 82, Q11, Q114 transvenous. 45t Rifampin, T6t t 222

lndex Right ventricular infarction, 22 Thiazide diuretics. 34 Rivaroxaban, 53, 531, 54, 110, 1171, Q21 Thiazolidinediones, 35t Rosuvastatin, 14, 251, 35 Thoracic aortic aneurysm (TAA), 99-101, 991, 1001, Q91 Thoracic endovascular aortic repair (TEVAR), 101-102, 104 s Thoracic irradiation, U1, l1lt, 112f Sarcoidosis.42 Three-dimensional echocardiography, l1t Septal myectomy, 80 Thrombolytic therapy. lgf , 21, 22t Septal reduction therapy (SRT), 80, Q50 Ticagrelor, 211, 251, 26, 53, Q36 Sexual activity after ACS, 28 Tobacco use, CVD and, 1 Shone syndrome, 96 Torsades de pointes, 1131 Silent myocardial ischemia, 28 Transcatheter aortic valve implantation (TAVI). 66, 67f, Q8 Sinus bradycardia, 43, Q2 Transesophageal echocardiography (TEE), 10, lof, llt, 67,74,91, Sinus tachycardia, 48-49 100t, Q18 Sinus venosus ASD, 91, 93t Transthoracic echocardiography (TTE), 10, 11t Sleep disordered breathing, 36 in aortic regurgitation, 67-68 Smoking cessation, 37, 109, Q39 in bicuspid aortic valve disease, 69 Sodium nitroprusside, 391, 117t in cardiac tamponade, 87, Ql16 Sodium-glucose cotransporter 2 (SGL12) inhibitors in hypertrophic cardiomyopathy, 77 78 for ASCVD, 29, Q93 in infective endocarditis, T4 75 for heart failure, 35, 351, Qlo, Ql17 in mitral regurgitation,To 72 Sorafenib, cardiotoxicity of, l13t murmur evaluated using, Q49 Sotalol,47t,48, 1ut in thoracic aortic disease, 10ot SPECT imaging, Tf Transthyretin amyloid (ATTR) amyloidosis, 10, 81, 811: Q7 myocardial perfusion, 4t, 7t Tranwenous pacemaker, 45t risks of, 9 Trastuzumab, 113t, 114, Q40 Spironolactone for heart failure, 34, 38 Tricuspid regurgiralion, 62t, 72 7 3 Spontaneous coronary artery dissection (SCAD), 27,116, Q47 Tricuspid stenosis, 621, 73 Stable angina pectoris, 13-17, 13t Tricuspid valve disease, T2 73 CABG beneflts in, Q112 Troponin levels, 8, 17, 181 39 diagnosis ol 13 14 Tuberculosis.85 86 treatment ol 14-16, 15f, Q12, Q41 Tumor plop, 83 Statin therapy, 74,24, 25t,27 ,28, 35,109, Q54 Turner syndrome, 96 ST elevation myocardial infarction (STEMI), u-23 complications of, 21 23 ECGfindingsin,fi la,2of Unfractionated heparin, 21, 26, 111, Q46 management of, 19t, 20 21, Q29 recognition of, 18-20 U thrombolytic therapy, 21, Q7 4 Valsartan sacubitril,32 33,38, Ql Stress echocardiography, 41, 7, 7t, Q90 Vahular heart disease (VHD), 61 76, 62t,63r,641 Stress testing, 3, 4t, 5 8, 31-32 Vancomycin, T6t in aortic stenosis. 65 Vandetanib, ll3t contraindications to. 9 Vasculitis. 99t interpretation of, 7t Vasodilator myocardial perfusion imaging, 4t, 9, Q57 risks of, 9 Vasodilator single-photon emission CT, Q57 Stroke Vasopressin, 39t anticoagulation for prevention ol 52 54, Q83 Venous I h romboembolism. l13t atrial fibrillation and. 50 51 Ventricular arrhlthmias, 55 57 embolic, Q99 Ventricular fibrillation, 22, 60f patent formen ovale and, Q48 Ventricular septal defect (VSD), 23, 63t, 931, 94, 94f, Q5 risk stratiflcation, 52 Ventricular tachycardia, 46, 56-57 Structural heart disease, 10, Q49 after reperfusion, 22 Sudden cardiac arrest, 59, 60f, 61 chemotherapy related. I l3t Sudden cardiac death, 28, 36, 57 -61,7a 79,79t, Q9, Q103 diagnosis of, Q37 Sulfonylureas in heart failure. 35t evaluation of, Q89 Sunitinib, 1131,114 during MI, 22 Supraventricular tachycardias (SVTs), 19-20. 49-50, 116, Q25 Verapamil, 16, 26t, 35, 47t, 57, 80, 1171 Syncope, diagnostic testing in, 10 Volume overload, signs ol 31, 38 Systemic inflammation, CAD risk in,3 Volume status, assessment ol 38-40 Systemic lupus erythematosus, 3 Systolic dysfunction, 7, 30, 115 w Systolic murmur, 10, 621, Q5 Warfarin, 52, 53, 53t in atrial fibrillation, 17, 52, 53, 53t T mechanical mitral valves and, 74, Qi00 Tachycardia mediated cardiomyopathy, 42 in peripheral artery disease, 110 Tachycardias, 45-50 during pregnancy, 116-118, 118t Tacrolimus,4l Water boftle heart, 85t, 87f Takotsubo cardiomyopath]: 27 28 , 41 , 42f, Q67 Weight loss, heart failure prevention and, 37 Tamponade, cardiac, 85t, 86-88, 871 Q1l6 Wenckebach heart block, 22.43,43f 99m-Technetium pyrophosphate scintigraphy, 10, 11t, 81, 81f Women Tenecteplase in STEMI, 21 CAD in,29 Tetralos/ of Fallot,93t,97 98,97f, Q92 CAD risk in, 3 Thalidomide, cardiotoxicity of, 113t congenital heart disease in,90 91

Right ventricular infarction, 22 Thiazide diuretics. 34 Rivaroxaban, 53, 531, 54, 110, 1171, Q21 Thiazolidinediones, 35t Rosuvastatin, 14, 251, 35 Thoracic aortic aneurysm (TAA), 99-101, 991, 1001, Q91 Thoracic endovascular aortic repair (TEVAR), 101-102, 104 s Thoracic irradiation, U1, l1lt, 112f Sarcoidosis.42 Three-dimensional echocardiography, l1t Septal myectomy, 80 Thrombolytic therapy. lgf , 21, 22t Septal reduction therapy (SRT), 80, Q50 Ticagrelor, 211, 251, 26, 53, Q36 Sexual activity after ACS, 28 Tobacco use, CVD and, 1 Shone syndrome, 96 Torsades de pointes, 1131 Silent myocardial ischemia, 28 Transcatheter aortic valve implantation (TAVI). 66, 67f, Q8 Sinus bradycardia, 43, Q2 Transesophageal echocardiography (TEE), 10, lof, llt, 67,74,91, Sinus tachycardia, 48-49 100t, Q18 Sinus venosus ASD, 91, 93t Transthoracic echocardiography (TTE), 10, 11t Sleep disordered breathing, 36 in aortic regurgitation, 67-68 Smoking cessation, 37, 109, Q39 in bicuspid aortic valve disease, 69 Sodium nitroprusside, 391, 117t in cardiac tamponade, 87, Ql16 Sodium-glucose cotransporter 2 (SGL12) inhibitors in hypertrophic cardiomyopathy, 77 78 for ASCVD, 29, Q93 in infective endocarditis, T4 75 for heart failure, 35, 351, Qlo, Ql17 in mitral regurgitation,To 72 Sorafenib, cardiotoxicity of, l13t murmur evaluated using, Q49 Sotalol,47t,48, 1ut in thoracic aortic disease, 10ot SPECT imaging, Tf Transthyretin amyloid (ATTR) amyloidosis, 10, 81, 811: Q7 myocardial perfusion, 4t, 7t Tranwenous pacemaker, 45t risks of, 9 Trastuzumab, 113t, 114, Q40 Spironolactone for heart failure, 34, 38 Tricuspid regurgiralion, 62t, 72 7 3 Spontaneous coronary artery dissection (SCAD), 27,116, Q47 Tricuspid stenosis, 621, 73 Stable angina pectoris, 13-17, 13t Tricuspid valve disease, T2 73 CABG beneflts in, Q112 Troponin levels, 8, 17, 181 39 diagnosis ol 13 14 Tuberculosis.85 86 treatment ol 14-16, 15f, Q12, Q41 Tumor plop, 83 Statin therapy, 74,24, 25t,27 ,28, 35,109, Q54 Turner syndrome, 96 ST elevation myocardial infarction (STEMI), u-23 complications of, 21 23 ECGfindingsin,fi la,2of Unfractionated heparin, 21, 26, 111, Q46 management of, 19t, 20 21, Q29 recognition of, 18-20 U thrombolytic therapy, 21, Q7 4 Valsartan sacubitril,32 33,38, Ql Stress echocardiography, 41, 7, 7t, Q90 Vahular heart disease (VHD), 61 76, 62t,63r,641 Stress testing, 3, 4t, 5 8, 31-32 Vancomycin, T6t in aortic stenosis. 65 Vandetanib, ll3t contraindications to. 9 Vasculitis. 99t interpretation of, 7t Vasodilator myocardial perfusion imaging, 4t, 9, Q57 risks of, 9 Vasodilator single-photon emission CT, Q57 Stroke Vasopressin, 39t anticoagulation for prevention ol 52 54, Q83 Venous I h romboembolism. l13t atrial fibrillation and. 50 51 Ventricular arrhlthmias, 55 57 embolic, Q99 Ventricular fibrillation, 22, 60f patent formen ovale and, Q48 Ventricular septal defect (VSD), 23, 63t, 931, 94, 94f, Q5 risk stratiflcation, 52 Ventricular tachycardia, 46, 56-57 Structural heart disease, 10, Q49 after reperfusion, 22 Sudden cardiac arrest, 59, 60f, 61 chemotherapy related. I l3t Sudden cardiac death, 28, 36, 57 -61,7a 79,79t, Q9, Q103 diagnosis of, Q37 Sulfonylureas in heart failure. 35t evaluation of, Q89 Sunitinib, 1131,114 during MI, 22 Supraventricular tachycardias (SVTs), 19-20. 49-50, 116, Q25 Verapamil, 16, 26t, 35, 47t, 57, 80, 1171 Syncope, diagnostic testing in, 10 Volume overload, signs ol 31, 38 Systemic inflammation, CAD risk in,3 Volume status, assessment ol 38-40 Systemic lupus erythematosus, 3 Systolic dysfunction, 7, 30, 115 w Systolic murmur, 10, 621, Q5 Warfarin, 52, 53, 53t in atrial fibrillation, 17, 52, 53, 53t T mechanical mitral valves and, 74, Qi00 Tachycardia mediated cardiomyopathy, 42 in peripheral artery disease, 110 Tachycardias, 45-50 during pregnancy, 116-118, 118t Tacrolimus,4l Water boftle heart, 85t, 87f Takotsubo cardiomyopath]: 27 28 , 41 , 42f, Q67 Weight loss, heart failure prevention and, 37 Tamponade, cardiac, 85t, 86-88, 871 Q1l6 Wenckebach heart block, 22.43,43f 99m-Technetium pyrophosphate scintigraphy, 10, 11t, 81, 81f Women Tenecteplase in STEMI, 21 CAD in,29 Tetralos/ of Fallot,93t,97 98,97f, Q92 CAD risk in, 3 Thalidomide, cardiotoxicity of, 113t congenital heart disease in,90 91 223