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Heart Failure I(EY POIilTS leacling to worsening global tV function and dilation. This pro cess is referred to as ventricular remodeling. These deleterious HVC o Stress testing is not routinely recommended in asymp- changes result in a cycle of slowly worsening LV function n ith tomatic patients with diabetes mellitus to detect sub decreasing lorward flow and increasing pulmonary and right clinical coronary artery disease. sided pressures. . [n patients with type 2 diabetes mellitus and clinical Diastolic dysfunction usuirlly is characterized by a stiff atherosclerotic cardiovascular disease, a sodium-glucose ened [V with abnormal relaxation cluring diastole. resulting in cotransporter 2 inhibitor or glucagon-like peptide I an increase 1n 1y preload. t.VFlF classically remains normal in receptor agonist with demonstrated cardiovascular dis- this setting. knort,n as heart failure rvith presened ejection ease benefit should be initiated as part of a glycemic fraction (HFpEF). HFpEF is ctimmonly defined by an LVEF of' control regimen. 50'X, or greater. Hypertension is the most common causer how o Coronary artery bypass grafting is associated with ever, aging. obesity diabetes mellitus. atrial fibrillation. and improved outcomes, including lower rates of repeat CAD are also contributors. Recently. amyloid deposits. due to revascularization and the composite of death, myocar wild type or mutation in the transthyretin gene, have been dial infarction, or stroke, in patients with diabetes mel reported in more than 10'7, olpatients with HFpEF. I itus undergoing revascularization. lleart failure with mid range ejection tiaction (HFmEF) has been proposed as a category to clescribe patients rvith LVEF between 40',1, and 50'){,. HFmEF includes up to 25'1, of all patients with heart failure. There have been fen,clinical trials Heart Failure evaluating therapy outcomes in these patients.

I(EY POIilTS leacling to worsening global tV function and dilation. This pro cess is referred to as ventricular remodeling. These deleterious HVC o Stress testing is not routinely recommended in asymp- changes result in a cycle of slowly worsening LV function n ith tomatic patients with diabetes mellitus to detect sub decreasing lorward flow and increasing pulmonary and right clinical coronary artery disease. sided pressures. . [n patients with type 2 diabetes mellitus and clinical Diastolic dysfunction usuirlly is characterized by a stiff atherosclerotic cardiovascular disease, a sodium-glucose ened [V with abnormal relaxation cluring diastole. resulting in cotransporter 2 inhibitor or glucagon-like peptide I an increase 1n 1y preload. t.VFlF classically remains normal in receptor agonist with demonstrated cardiovascular dis- this setting. knort,n as heart failure rvith presened ejection ease benefit should be initiated as part of a glycemic fraction (HFpEF). HFpEF is ctimmonly defined by an LVEF of' control regimen. 50'X, or greater. Hypertension is the most common causer how o Coronary artery bypass grafting is associated with ever, aging. obesity diabetes mellitus. atrial fibrillation. and improved outcomes, including lower rates of repeat CAD are also contributors. Recently. amyloid deposits. due to revascularization and the composite of death, myocar wild type or mutation in the transthyretin gene, have been dial infarction, or stroke, in patients with diabetes mel reported in more than 10'7, olpatients with HFpEF. I itus undergoing revascularization. lleart failure with mid range ejection tiaction (HFmEF) has been proposed as a category to clescribe patients rvith LVEF between 40',1, and 50'){,. HFmEF includes up to 25'1, of all patients with heart failure. There have been fen,clinical trials Heart Failure evaluating therapy outcomes in these patients. Pathophysiology of Heart Failure t(EY POIilIS Heart failure is a clinical syndrome characterized by signs and . Common causes of heart failure with reduced ejection symptoms of fluid overload and decreased cardiac output. It can fraction include coronary artery disease, hypertension, result tiom any structural or lunctional impairment in ejection obesity, diabetes mellitus, and valvular heart disease. of blood (systolic dysfunction) or ventricular filling and/or relax . Hypertension is the most common cause of heart failure ation (diastolic dysfunction). Systolic and diastolic dysfunction with preserved ejection fraction. both result in increased left ventricular (LV) filling pressures. causing the classic signs and symptoms of heart failure, includ ing dyspnea, paroxysmal nocturnal dyspnea, orthopnea, periph Screening eral edema, crackles, elevated central venous pressure. and an S,. A validated sex and race specific l0 \'ear Pooled Cohort In systolic dysfunction, LV ejection fraction (LVEF) is reduced, Equ:rtion to Prevent Heart F'ailure risk score can be used in termed heart failure with reduced ejection fraction (HFTEF). primary care settings to assist in iclentifying asymptomatic IIFTEF is fbrmally defined by an LVEF of 40"/,, or less. Common patients at increased risk fbr heart failure who may merit causes of HFrEF include coronary artery disease (CAD), hyperten intensive screening and,ror targeted prevention strategies and vahular heart disease. si<-rn, obesity, diabetes mellitus, (http:i,hf risk calculator.surge.shi). In response to a reduced ejection fraction, neurohormo In patients at risk fbr developing heart failure (such as nal systems, including the renin angiotensin aldosterone sys those with hypertension, diabetes. or vascular disease). natriu tem (RAAS) and sympathetic nervous system. are activated. retic peptide biomarker basecl screening can be useful to pre RAAS activation results in the production of angiotensin II and vent the development of IV dysfunction. Small studies have aldosterone. Angiotensin ll causes vasoconstriction, thereby shown that in asymptomatic persons n,ith elevated B hpe increasing blood pressure, and also stimulates thirst; aldoster natriuretic peptide (BNP) or N terminal pro B lvpe natriuretic one increases fluid retention by increasing sodium resorption. peptide (NT proBNP) levels. team based care and aggressive Stimulation of the sympathetic nerv<.rus system results in the guideline based medical therapy involving a cardiovascular release of'epinephrine and norepinephrine, which cause an specialist can help prevent future Ily' dysfunction or new onset increase in heart rate, contractility, and vascular resistance. heart failure; however. there is n<t agreed on standard Ibr sr-rch Enhanced sympathetic activity and increased angiotensin II screening and no certainty as to its cost effectiveness. levels stimulate vasopressin release, causing additional fluicl retention. Initially, this response is adaptive and maintains an adequate cardiac output and blood pressure; however, it Diagnosis and Evaluation becomes chronic and maladaptive in the long term. of Heart Failure (lhronic activation olthe neurohormonal systems in HFrEF Clinical Evaluation not only causes hemodynamic alterations by vasoconstriction Clinical evaluation ofpatients suspected ofhaving heart failure ancl tluid overload but also is responsible fbr structural and should include a comprehensive history and physical exami firnctional changes in the individual myocytes, ultimately nation, tbcusing on potential risk f:rctors and assessment of.

Pathophysiology of Heart Failure t(EY POIilIS Heart failure is a clinical syndrome characterized by signs and . Common causes of heart failure with reduced ejection symptoms of fluid overload and decreased cardiac output. It can fraction include coronary artery disease, hypertension, result tiom any structural or lunctional impairment in ejection obesity, diabetes mellitus, and valvular heart disease. of blood (systolic dysfunction) or ventricular filling and/or relax . Hypertension is the most common cause of heart failure ation (diastolic dysfunction). Systolic and diastolic dysfunction with preserved ejection fraction. both result in increased left ventricular (LV) filling pressures. causing the classic signs and symptoms of heart failure, includ ing dyspnea, paroxysmal nocturnal dyspnea, orthopnea, periph Screening eral edema, crackles, elevated central venous pressure. and an S,. A validated sex and race specific l0 \'ear Pooled Cohort In systolic dysfunction, LV ejection fraction (LVEF) is reduced, Equ:rtion to Prevent Heart F'ailure risk score can be used in termed heart failure with reduced ejection fraction (HFTEF). primary care settings to assist in iclentifying asymptomatic IIFTEF is fbrmally defined by an LVEF of 40"/,, or less. Common patients at increased risk fbr heart failure who may merit causes of HFrEF include coronary artery disease (CAD), hyperten intensive screening and,ror targeted prevention strategies and vahular heart disease. si<-rn, obesity, diabetes mellitus, (http:i,hf risk calculator.surge.shi). In response to a reduced ejection fraction, neurohormo In patients at risk fbr developing heart failure (such as nal systems, including the renin angiotensin aldosterone sys those with hypertension, diabetes. or vascular disease). natriu tem (RAAS) and sympathetic nervous system. are activated. retic peptide biomarker basecl screening can be useful to pre RAAS activation results in the production of angiotensin II and vent the development of IV dysfunction. Small studies have aldosterone. Angiotensin ll causes vasoconstriction, thereby shown that in asymptomatic persons n,ith elevated B hpe increasing blood pressure, and also stimulates thirst; aldoster natriuretic peptide (BNP) or N terminal pro B lvpe natriuretic one increases fluid retention by increasing sodium resorption. peptide (NT proBNP) levels. team based care and aggressive Stimulation of the sympathetic nerv<.rus system results in the guideline based medical therapy involving a cardiovascular release of'epinephrine and norepinephrine, which cause an specialist can help prevent future Ily' dysfunction or new onset increase in heart rate, contractility, and vascular resistance. heart failure; however. there is n<t agreed on standard Ibr sr-rch Enhanced sympathetic activity and increased angiotensin II screening and no certainty as to its cost effectiveness. levels stimulate vasopressin release, causing additional fluicl retention. Initially, this response is adaptive and maintains an adequate cardiac output and blood pressure; however, it Diagnosis and Evaluation becomes chronic and maladaptive in the long term. of Heart Failure (lhronic activation olthe neurohormonal systems in HFrEF Clinical Evaluation not only causes hemodynamic alterations by vasoconstriction Clinical evaluation ofpatients suspected ofhaving heart failure ancl tluid overload but also is responsible fbr structural and should include a comprehensive history and physical exami firnctional changes in the individual myocytes, ultimately nation, tbcusing on potential risk f:rctors and assessment of. 30

Heart Failure flr-rid irnd perfusion status. ileiirl frrilurc r-rrost contr-nonly ltre with increased filling pressures and heart failure (typically scnts with signs and syntptolns of' rrolunte overload u,ith >,100 pglrrl-). \ rhereas BN [' levels are low to normal in paticlrts norr-nal cardiac output. Less cor.r.rntorllyl volume or,erloird is with pulmonary disease (typically <100 pg/ml.). BNP levels acconrpanied by low cardiac olltput, and rarely, patients l.rave tencl to be lower in tlFpFiF than in tlFrEFl, Studies have shor.r,rr Itiw cardiac output without v<tlr"rr-nc overktad. that an elevated BNP level l.ras a sensitivity for heart f'ailure o{' Volume overload is suggestecl ltv svntptoms such as r,reigl-rt 95'X, to 97"/,, and a negative predictive value of 9O'/,, lct L)7'/,. gitin. dyspnea, orthopnea, and pirroxl,sn-ral r-rocturnal dyspnea. l.evels betr.teen 100 pgi n.rL and ,100 pg/ml- are not particulxrly l3enclopnea (shortness of breath n,hen leaning over) is :rssoci sensitive or specific in diagnosing or excluding heart f:rilure. atecl with elevated filling pressr-rr-es. particularly in the setling Other factors that increase BN[) levels include kidney failur-e. of reduced cardiac index. S1'nrptr)n1s typicall),progress fionr older age. sepsis. r.r.redical therapy with an angiotensin exertional dyspnea to orthopnel lncl paroxl,smal nocturnal receptor neprilysin inhibikrr (ARNI), and female sex. BN[' dyspr.rea. Supportive exanrination f)ndings ir-rclude elevated levels are fypically reducecl in patients with an elevated BMl. central venous pressure, cdcnla. lbdonrinal distention fronr Laboratory assessnlent also should inciude a cor-r-rplete asciles, crackles or findings consistent with pleural eflusion on blood count, serum electnrlytes and kidney function tests. lung examination, and an S.,. glucose and lipid levels, liver chenristry tests, and serunr l.o'nv cardiac output is signaled by hypotension, l61ar pulse thyroid stimulating hormone ('l'Stl) level. TSH measurement pressure, cool extremities, irncl reclucecl cogr-rition. Although is indicated to evaluate fbr occult hypothyroidism or hyperthy r,r,orsening kidney or liver fur-rction rlay be a sign of iolr,car nridism as a reversible cause of heart failure. Evaluatior-r ftlr diac output. end organ clystirnction also can be causecl lry other causes. such as hen.tochronratosis, HIV rheun.ratologic virscular congestion. disease. amyloidosis, and pheochromocytoma, should only bc pcrfbrr-r-red u'her-r clinical suspicion warrants, not routitrely. Diagnosis lJchocardiography is the prinrary diagnostic modality fbr Initiirl diagnostic testillg for heart failure includes ECG, chest evaluatior-r of hearl failure. lt provides infbrmation on chanrber radiography, and select laboratory str-rdies. An ECG can be size and thickness, systrilic and diastolic function, and valvular helptul in evaluating for possiblc myocardial infarction, tach pathotogr. Echocardiographic tindings additionally may pK) yarrhythmia. or LV hypertroplry. Ohest radiography may reveal vide clues to the underlying cause of heart failure. Regional fir.rdir.rgs that support he:rrt failure. including cardiomegaly. wall motion abnormalities increase suspicion fbr CAI). vascular congestion. engorged lynrphatics (Kerley B lines) whereas changes in the myoc:rrdium may suggest conditions (Figure 12). and pleural efTusion. or nray exclude alternative such as cardiac amyloidosis. l)rognostic information can bc pulmonary causes of dyspnea. gained from echocardiography. particularly in the setting of In patients presenting ulith dyspnea of'unknou,n etiologi severely depressed tVEF. BN['] or NT proBNP ]evel c:rn eflectively differentiate cardiac Cardiac magnetic resonance (CMR) imaging is fieqr-rer.rtly fiom pulmonary causes. BNP levels are elevated in patier.rts used to assess for myocarditis and intjltrative processes, st-tcl't as her.nochromatosis, sarcoidosis, and amyloidosis. Currcttt guidelines do not reconrnrend routine CMR imaging; it slrttulcl be used only in the search tbr a specific diagnosis. The HTFPEF risk score is a means of assessing the likeli hrxrd of HFpEF and is used to discrin.rinate cardiac versus noncardiac causes of dyspnea. Predictive variables include obesity (2 points). atrial fibrillatior-r (3 points). age older than 60 years (l point). treatnrent rt,ith two or more antihyperten sive drugs (1 point), echocardiographic Ere'ratio greater thrlr 9 (l point), and echocardiographic estimated pultt.tonary artery systolic pressure higher than 35 mm Hg (1 point). l'hc odds of HFpEF double for each l unit score increase, with thc probrrbility of HFpEF <-r1 0.2 at a score ol1 increasing to 0.95 at l score of 7. Evaluation for lschemia CAI) is the leading cause of heart firilure in the United States (>.50',1, of patients) ar.rd should be considered in all patierlts

flr-rid irnd perfusion status. ileiirl frrilurc r-rrost contr-nonly ltre with increased filling pressures and heart failure (typically scnts with signs and syntptolns of' rrolunte overload u,ith >,100 pglrrl-). \ rhereas BN [' levels are low to normal in paticlrts norr-nal cardiac output. Less cor.r.rntorllyl volume or,erloird is with pulmonary disease (typically <100 pg/ml.). BNP levels acconrpanied by low cardiac olltput, and rarely, patients l.rave tencl to be lower in tlFpFiF than in tlFrEFl, Studies have shor.r,rr Itiw cardiac output without v<tlr"rr-nc overktad. that an elevated BNP level l.ras a sensitivity for heart f'ailure o{' Volume overload is suggestecl ltv svntptoms such as r,reigl-rt 95'X, to 97"/,, and a negative predictive value of 9O'/,, lct L)7'/,. gitin. dyspnea, orthopnea, and pirroxl,sn-ral r-rocturnal dyspnea. l.evels betr.teen 100 pgi n.rL and ,100 pg/ml- are not particulxrly l3enclopnea (shortness of breath n,hen leaning over) is :rssoci sensitive or specific in diagnosing or excluding heart f:rilure. atecl with elevated filling pressr-rr-es. particularly in the setling Other factors that increase BN[) levels include kidney failur-e. of reduced cardiac index. S1'nrptr)n1s typicall),progress fionr older age. sepsis. r.r.redical therapy with an angiotensin exertional dyspnea to orthopnel lncl paroxl,smal nocturnal receptor neprilysin inhibikrr (ARNI), and female sex. BN[' dyspr.rea. Supportive exanrination f)ndings ir-rclude elevated levels are fypically reducecl in patients with an elevated BMl. central venous pressure, cdcnla. lbdonrinal distention fronr Laboratory assessnlent also should inciude a cor-r-rplete asciles, crackles or findings consistent with pleural eflusion on blood count, serum electnrlytes and kidney function tests. lung examination, and an S.,. glucose and lipid levels, liver chenristry tests, and serunr l.o'nv cardiac output is signaled by hypotension, l61ar pulse thyroid stimulating hormone ('l'Stl) level. TSH measurement pressure, cool extremities, irncl reclucecl cogr-rition. Although is indicated to evaluate fbr occult hypothyroidism or hyperthy r,r,orsening kidney or liver fur-rction rlay be a sign of iolr,car nridism as a reversible cause of heart failure. Evaluatior-r ftlr diac output. end organ clystirnction also can be causecl lry other causes. such as hen.tochronratosis, HIV rheun.ratologic virscular congestion. disease. amyloidosis, and pheochromocytoma, should only bc pcrfbrr-r-red u'her-r clinical suspicion warrants, not routitrely. Diagnosis lJchocardiography is the prinrary diagnostic modality fbr Initiirl diagnostic testillg for heart failure includes ECG, chest evaluatior-r of hearl failure. lt provides infbrmation on chanrber radiography, and select laboratory str-rdies. An ECG can be size and thickness, systrilic and diastolic function, and valvular helptul in evaluating for possiblc myocardial infarction, tach pathotogr. Echocardiographic tindings additionally may pK) yarrhythmia. or LV hypertroplry. Ohest radiography may reveal vide clues to the underlying cause of heart failure. Regional fir.rdir.rgs that support he:rrt failure. including cardiomegaly. wall motion abnormalities increase suspicion fbr CAI). vascular congestion. engorged lynrphatics (Kerley B lines) whereas changes in the myoc:rrdium may suggest conditions (Figure 12). and pleural efTusion. or nray exclude alternative such as cardiac amyloidosis. l)rognostic information can bc pulmonary causes of dyspnea. gained from echocardiography. particularly in the setting of In patients presenting ulith dyspnea of'unknou,n etiologi severely depressed tVEF. BN['] or NT proBNP ]evel c:rn eflectively differentiate cardiac Cardiac magnetic resonance (CMR) imaging is fieqr-rer.rtly fiom pulmonary causes. BNP levels are elevated in patier.rts used to assess for myocarditis and intjltrative processes, st-tcl't as her.nochromatosis, sarcoidosis, and amyloidosis. Currcttt guidelines do not reconrnrend routine CMR imaging; it slrttulcl be used only in the search tbr a specific diagnosis. The HTFPEF risk score is a means of assessing the likeli hrxrd of HFpEF and is used to discrin.rinate cardiac versus noncardiac causes of dyspnea. Predictive variables include obesity (2 points). atrial fibrillatior-r (3 points). age older than 60 years (l point). treatnrent rt,ith two or more antihyperten sive drugs (1 point), echocardiographic Ere'ratio greater thrlr 9 (l point), and echocardiographic estimated pultt.tonary artery systolic pressure higher than 35 mm Hg (1 point). l'hc odds of HFpEF double for each l unit score increase, with thc probrrbility of HFpEF <-r1 0.2 at a score ol1 increasing to 0.95 at l score of 7. Evaluation for lschemia CAI) is the leading cause of heart firilure in the United States (>.50',1, of patients) ar.rd should be considered in all patierlts urith neu,ly diagnosed heart failure. The decision to evaluate FIGU RE 1 2. Chest radiograph showing evidence o{ decompensated heart failure with pulmonary edema characterized by difluse increased interstitial firr CAD with stress testiltg or coronary angiograllhy opacities, including Kerley B lines; prominent and indistinct pulmonary vasculature; depends on the patient's sylrptoms and risk factors (diabc and tiny pleural efiusions. tes, hypertension, tobacco use, family history, male sex);

urith neu,ly diagnosed heart failure. The decision to evaluate FIGU RE 1 2. Chest radiograph showing evidence o{ decompensated heart failure with pulmonary edema characterized by difluse increased interstitial firr CAD with stress testiltg or coronary angiograllhy opacities, including Kerley B lines; prominent and indistinct pulmonary vasculature; depends on the patient's sylrptoms and risk factors (diabc and tiny pleural efiusions. tes, hypertension, tobacco use, family history, male sex); 31