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An acute ST-segment elevation myocardial infarction (STEMI) arises from the occlusion of 1 or more coronary arteries, causing transmural myocardial ischemia and subsequent myocardial injury or necrosis. Risk factors for STEMI include hypertension, hyperlipidemia, smoking, and diabetes, which contribute to the development of atherosclerosis and increase the likelihood of plaque instability. The pathogenic mechanism typically involves plaque rupture and thrombus formation within the coronary artery, though other processes may also lead to STEMI. Diagnosis of STEMI is confirmed by characteristic findings on electrocardiography, including ST-segment elevation in specific leads. Blood tests, such as elevated cardiac troponins, further support the diagnosis. Immediate treatment involves restoring blood flow to the affected area through reperfusion therapy, typically via percutaneous coronary intervention. Early management is critical to limit myocardial damage, and adjunctive therapies, including antiplatelets and anticoagulants, are often used to prevent further thrombus formation. This activity for healthcare professionals reviews the etiology, epidemiology, risk factors, pathogenic mechanisms, clinical presentation, evaluation, and management of STEMI and underscores the integral role of the interprofessional team in improving outcomes for patients with this type of myocardial infarction. Objectives: Identify the signs and symptoms suggesting acute ST-elevation myocardial infarction. Create a clinically guided diagnostic plan for patients with suspected acute ST-segment elevation myocardial infarction. Implement evidence-based, individualized management protocols for patients with acute ST-segment elevation myocardial infarction. Collaborate with the interprofessional team to educate, treat, and monitor individuals with acute ST-segment elevation myocardial infarction to improve health outcomes. Access free multiple choice questions on this topic.

Acute coronary syndrome (ACS) encompasses conditions characterized by a sudden decrease in myocardial perfusion, presenting as ST-segment elevation myocardial infarction (STEMI), non–ST-segment elevation myocardial infarction (NSTEMI), or unstable angina. Globally, over 7 million individuals are diagnosed with ACS annually, with more than 1 million cases requiring hospitalization in the United States each year. STEMI results from the complete blockage of a coronary artery and represents about 30% of all ACS cases. An acute STEMI is marked by transmural myocardial ischemia resulting in myocardial injury or necrosis.[1] The current 2018 clinical definition of myocardial infarction requires confirming the presence of ischemic myocardial injury with abnormal cardiac biomarker levels.[2] STEMI is a clinical syndrome involving myocardial ischemia, electrocardiography (ECG) changes, and chest pain (see Image. Electrocardiogram Tracing for a Case of Proximal Left Anterior Descending Occlusion). If electrocardiography indicates STEMI, prompt reperfusion through primary percutaneous coronary intervention (PCI) within 120 minutes can lower mortality from 9% to 7% (see Image. ST-segment Elevation Myocardial Infarction on Electrocardiogram).[3] In cases where PCI within this timeframe is not feasible, full-dose fibrinolytic therapy with alteplase, reteplase, or tenecteplase should be administered to patients younger than 75 and without contraindications to medical intervention. Individuals 75 and older should receive half the normal dose of fibrinolytic therapy. Alternatively, full-dose streptokinase may be considered when cost is a concern. Following fibrinolytic treatment, patients should be transferred to a facility capable of performing PCI within the next 24 hours.

Myocardial infarction, in general, can be classified into types 1 to 5 based on etiology and pathogenesis.[4] Recent advances in cardiovascular imaging, revised ECG criteria, and high-sensitivity cardiovascular biomarker assays have enhanced the ability to classify the different causes of myocardial infarction more precisely. The underlying pathophysiology of type 1 myocardial infarction differs from that of types 2 through 5. Type 1 myocardial infarction is primarily associated with intracoronary atherothrombosis, whereas the other types may result from various mechanisms, some of which may involve an atherosclerotic component. Type 2 myocardial infarction is characterized by an imbalance in myocardial oxygen supply and demand unrelated to acute coronary atherothrombosis. Types 1 and 2 occur spontaneously, while types 4 and 5 are linked to medical procedures. Type 3 is only identified postmortem. Most types 1 and 2 myocardial infarction cases present as NSTEMI, but some manifest as STEMI (see Image. Acute Myocardial Infarction Types).[5] A STEMI occurs from the occlusion of 1 or more coronary arteries supplying the heart with blood. The cause of this abrupt disruption of blood flow is usually plaque rupture, erosion, fissuring, or dissection of coronary arteries with obstructive thrombus. The major STEMI risk factors are dyslipidemia, diabetes, hypertension, smoking, and a family history of coronary artery disease.[6][7]

Cardiovascular disease (CVD) is the leading cause of death and disability worldwide, with low- and middle-resource countries experiencing a disproportionate share of this burden. ACS frequently serves as the initial presentation of CVD. Approximately 5.8 million new cases of ischemic heart disease were reported across the 57 member countries of the European Society of Cardiology (ESC) in 2019. The median age-standardized incidence rate was 293.3 per 100,000 people, with an interquartile range of 195.8 to 529.5. CVD continues to be the primary cause of death in ESC countries, contributing to nearly 2.2 million fatalities in women and over 1.9 million deaths in men, according to the latest data. Ischemic heart disease remains the leading cause of CVD mortality, accounting for 38% of deaths in women and 44% in men.[8] The estimated annual incidence of myocardial infarction in the United States includes 550,000 new cases and 200,000 recurrent cases. In 2013, 116,793 persons in the United States experienced a fatal myocardial infarction, with 57% occurring in men and 43% in women. The average age of incidence of a first myocardial infarction is 65.1 for men and 72 for women. Approximately 38% of patients who present to the hospital with ACS have a STEMI.[9]

An acute thrombotic coronary event leads to ST-segment elevation on a surface ECG after complete and persistent blood flow occlusion. Coronary atherosclerosis and the presence of a high-risk thin-cap fibroatheroma can result in sudden-onset plaque rupture.[10] This event results in vascular endothelium changes, producing a cascade of platelet adhesion, activation, and aggregation, ultimately leading to thrombosis.[11] Coronary artery occlusion in animal models shows a "wave-front" of myocardial injury that spreads from the subendocardial myocardium to the subepicardial myocardium, resulting in a transmural infarction that produces ST-segment elevation on surface ECG.[12] Myocardial damage occurs when the blood flow is interrupted, warranting immediate management. Sudden-onset acute ischemia can result in severe microvascular dysfunction.

Acute chest discomfort, which patients may describe as pain, pressure, tightness, heaviness, or a burning sensation, is the most common symptom that leads healthcare professionals to consider the diagnosis of ACS and initiate appropriate diagnostic testing. Diagnostic delays or errors can occur from an incomplete patient history or challenges in obtaining a clear description of symptoms. Therefore, thorough patient history and detailed communication are essential to understand the complexity of ACS-related symptoms, potentially enabling a prompt and accurate diagnosis. Obtaining a focused medical history and identifying the presenting symptoms is essential to quickly guide the patient along the appropriate care pathway. A targeted physical examination should involve evaluating all major pulses, measuring blood pressure in both arms, auscultating heart and lung sounds, and assessing for any signs of heart failure or circulatory compromise. Patients should be asked about the characteristics of the pain and associated symptoms, risk factors or history of cardiovascular disease, and recent drug use.[13] STEMI risk factors include age, gender, family history of premature coronary artery disease, tobacco use, dyslipidemia, diabetes, hypertension, abdominal obesity, sedentary lifestyle, a diet low in fruits and vegetables, and psychosocial stressors.[14] Cocaine use can cause STEMI regardless of risk factors.[15] Obtaining a history of known congenital abnormalities can be useful during evaluation.[16] Familial hypercholesterolemia is linked to an increased risk of early-onset atherosclerotic disease. In patients hospitalized with acute myocardial infarction, familial hypercholesterolemia correlates with a higher incidence of both STEMI and NSTEMI, fewer cases of type 2 myocardial infarction, and Takotsubo cardiomyopathy, and a greater need for multiple stents, coronary bypass surgery, and mechanical circulatory support devices.[17]

Electrocardiogram The resting 12-lead ECG is the primary diagnostic tool for evaluating patients with suspected ACS. An ECG should be performed immediately upon first medical contact and interpreted by a qualified emergency medical technician or physician within 10 minutes. Repeat ECGs may be necessary, mainly if symptoms have subsided during first medical contact. Patients with suspected ACS are typically categorized into 2 main diagnostic groups based on the initial ECG findings.[18] Patients with acute chest pain or equivalent symptoms and persistent ST-segment elevation or its ECG equivalents are given a working diagnosis of STEMI. Most of these patients experience myocardial necrosis and elevated troponin levels, meeting the criteria for myocardial infarction, although not all will have a final diagnosis of STEMI. Patients with acute chest pain or equivalent symptoms without persistent ST-segment elevation or its ECG equivalents are categorized under non–ST-elevation ACS (NSTE-ACS). Guidelines from the American Heart Association, American College of Cardiology, European Society of Cardiology, and World Heart Federation Evaluating patients with acute onset of chest pain should begin with an ECG and troponin levels. The American College of Cardiology (ACC), American Heart Association (AHA), ESC, and the World Heart Federation (WHF) committee established the following ECG criteria for STEMI: New ST-segment elevation occurs at the J point in 2 contiguous leads, with a threshold greater than 0.1 mV in all leads except V2 and V3. In leads V2 and V3, the threshold is greater than 0.2 mV for men older than 40, greater than 0.25 mV for men under 40, and greater than 0.15 mV for women.[19]

Evaluating patients with acute onset of chest pain should begin with an ECG and troponin levels. The American College of Cardiology (ACC), American Heart Association (AHA), ESC, and the World Heart Federation (WHF) committee established the following ECG criteria for STEMI: New ST-segment elevation occurs at the J point in 2 contiguous leads, with a threshold greater than 0.1 mV in all leads except V2 and V3. In leads V2 and V3, the threshold is greater than 0.2 mV for men older than 40, greater than 0.25 mV for men under 40, and greater than 0.15 mV for women.[19] Promptly identifying occlusion myocardial infarction (OMI) in patients with acute chest pain is crucial to enable rapid revascularization. In left bundle branch block (LBBB) cases, interpreting the ECG can be particularly challenging due to ST-segment changes associated with this pattern. The Sgarbossa criteria were developed to enhance the detection of acute myocardial infarction in patients with LBBB, relying on the concordance between the QRS complex and the ST segment.[20] Typically, in an ECG with LBBB without OMI, the "principle of appropriate discordance" applies. The ST segment is oriented opposite to the QRS complex, which means that in leads where the QRS is predominantly positive, the ST segment is negative. Conversely, the ST segment is elevated in leads with a predominantly negative QRS complex. In OMI cases, the ST segment may show "concordant" changes with the QRS or exhibit "excessive" discordant elevation. The Sgarbossa criteria include this excessively discordant ST elevation (greater than 0.5 mV) as a 3rd criterion, along with concordant ST-segment changes. While these criteria are highly specific, their sensitivity for detecting OMI is limited.[21] Patients with a preexisting LBBB can be further evaluated using the Sgarbossa criteria: ST-segment elevation of 1 mm or more that is concordant with or in the same direction as the QRS complex ST-segment depression of 1 mm or more in lead V1, V2, or V3 ST-segment elevation of 5 mm or more (that is discordant with or in the opposite direction of the QRS complex)[22]

Patients with a preexisting LBBB can be further evaluated using the Sgarbossa criteria: ST-segment elevation of 1 mm or more that is concordant with or in the same direction as the QRS complex ST-segment depression of 1 mm or more in lead V1, V2, or V3 ST-segment elevation of 5 mm or more (that is discordant with or in the opposite direction of the QRS complex)[22] The ACC, AHA, and Society for Cardiovascular Angiography & Interventions (SCAI) have issued class I recommendations based on recent evidence.[23] For patients experiencing STEMI with ischemic symptoms lasting less than 12 hours, PCI is recommended to enhance survival outcomes. In cases of STEMI where reperfusion following fibrinolytic therapy is unsuccessful, performing rescue PCI on the infarct-related artery is advised to improve clinical outcomes. Primary PCI is recommended for patients with STEMI who present with cardiogenic shock or acute severe heart failure, regardless of the time elapsed since the onset of the myocardial infarction.[23] Cardiac Biomarkers Once STEMI and very high-risk NSTE-ACS are ruled out, biomarkers become essential for confirming the diagnosis, assessing risk, and managing suspected cases of ACS. Measuring a biomarker of cardiomyocyte injury, such as high-sensitivity cardiac troponin (hs-cTn), is recommended for all patients with suspected ACS. If the clinical presentation aligns with myocardial ischemia, an elevation or decrease in hs-cTn levels above the 99th percentile of a healthy population supports the diagnosis of myocardial infarction, according to the 4th universal definition of this condition.[24] Hs-cTn assays offer greater sensitivity and diagnostic precision for detecting myocardial infarction upon presentation, allowing for a shorter interval between the first and second troponin measurements. Timely serial measurements lead to faster diagnosis and reduce emergency department stays, healthcare costs, and patient diagnostic uncertainty.[25] The preferred approach is the 0-hour/1-hour algorithm, with the 0-hour/2-hour algorithm as an alternative. These algorithms have been developed and validated through extensive multicenter diagnostic studies using centralized adjudication of the final diagnosis for all currently available hs-cTn assays.[26] Transthoracic Echocardiogram

Hs-cTn assays offer greater sensitivity and diagnostic precision for detecting myocardial infarction upon presentation, allowing for a shorter interval between the first and second troponin measurements. Timely serial measurements lead to faster diagnosis and reduce emergency department stays, healthcare costs, and patient diagnostic uncertainty.[25] The preferred approach is the 0-hour/1-hour algorithm, with the 0-hour/2-hour algorithm as an alternative. These algorithms have been developed and validated through extensive multicenter diagnostic studies using centralized adjudication of the final diagnosis for all currently available hs-cTn assays.[26] Transthoracic Echocardiogram For patients with suspected ACS where the diagnosis is uncertain, transthoracic echocardiography (TTE) can help identify signs indicative of ongoing ischemia or previous myocardial infarction. However, the use of TTE should not cause significant delays in transferring the patient to the cardiac catheterization laboratory if an acute coronary artery occlusion is suspected. Additionally, TTE can help identify other potential causes of chest pain, such as acute aortic disease and right ventricular signs associated with pulmonary embolism. Computed Tomography Computed tomography (CT) is frequently the preferred diagnostic tool when excluding other potentially life-threatening conditions that may mimic ACS, such as pulmonary embolism and aortic dissection. An ECG-gated contrast CT angiogram covering the entire thoracic aorta and proximal head and neck vessels is recommended in these cases. However, CT is generally not indicated for patients suspected of having an ongoing acute coronary occlusion, where immediate invasive coronary angiography is the priority.

After diagnosing acute STEMI, intravenous access should be obtained, and cardiac monitoring should be started. Timely treatment is crucial for patients classified under the STEMI pathway. Key factors include the total ischemic time, sources of delays in initial management, and the choice of reperfusion strategy for patients with STEMI. The efficiency and quality of care a system provides for individuals with suspected STEMI are reflected in these treatment times. Patients who are hypoxemic or at risk for hypoxemia benefit from oxygen therapy. However, results from recent studies show possible harmful effects in patients who are normoxic.[27][28] Patients should undergo PCI within 90 minutes of presentation at a PCI-capable hospital or within 120 minutes if transfer to a PCI-capable hospital is required. If PCI is not possible within 120 minutes of first medical contact, fibrinolytic therapy should be initiated within 30 minutes of the patient's arrival at the hospital.[29] Patients should be promptly transferred to a PCI center after starting lytic therapy. If fibrinolysis fails or signs of reocclusion or reinfarction, such as recurring ST-segment elevation, emerge, immediate angiography and rescue PCI is necessary.[30] Further administration of fibrinolytic is not recommended in such cases. Even when fibrinolysis appears successful, as indicated by significant resolution of ST-segment elevation (ie, >50% at 60–90 minutes), typical reperfusion arrhythmias, and relief of chest pain, early angiography within 2 to 24 hours is still advised.[31] Conditions that can mimic ACS, such as acute aortic dissection and pulmonary embolism, must be ruled out. Manual thrombus aspiration before PCI in patients with STEMI is a quick and cost-effective technique to reduce microvascular obstruction following PCI.[32] While the TAPAS study (Thrombus Aspiration During Percutaneous Coronary Intervention in Acute Myocardial Infarction) initially suggested that thrombus aspiration before PCI could offer clinical benefits compared to PCI alone, subsequent research and meta-analyses did not significantly improve clinical outcomes.[33]

Manual thrombus aspiration before PCI in patients with STEMI is a quick and cost-effective technique to reduce microvascular obstruction following PCI.[32] While the TAPAS study (Thrombus Aspiration During Percutaneous Coronary Intervention in Acute Myocardial Infarction) initially suggested that thrombus aspiration before PCI could offer clinical benefits compared to PCI alone, subsequent research and meta-analyses did not significantly improve clinical outcomes.[33] Additionally, concerns about patient safety have emerged, with evidence demonstrating a higher risk of stroke in those undergoing thrombus aspiration compared to PCI alone, both at 1 month and 1 year postprocedure.[34][35] Reflecting these findings, the 2023 ESC guidelines for managing ACS advise against routine thrombus aspiration (Class III, Level of Evidence A). However, the guidelines suggest that thrombus aspiration may be considered in certain STEMI cases, particularly those with a high thrombotic burden following PCI. Pharmacological Therapy Nitroglycerin administration can reduce anginal pain. However, this drug should be avoided in patients who have used phosphodiesterase-inhibiting medication within the last 24 hours and in cases of right ventricular infarction. Morphine can be given for further pain relief to patients who continue to report discomfort after nitroglycerin administration. However, reasonable use is not recommended, as it may adversely affect outcomes.[36]

Nitroglycerin administration can reduce anginal pain. However, this drug should be avoided in patients who have used phosphodiesterase-inhibiting medication within the last 24 hours and in cases of right ventricular infarction. Morphine can be given for further pain relief to patients who continue to report discomfort after nitroglycerin administration. However, reasonable use is not recommended, as it may adversely affect outcomes.[36] All patients with an acute myocardial infarction should be started on a beta blocker, high-intensity statin, aspirin, and a P2Y12 inhibitor as soon as possible, with certain exceptions. Aspirin therapy for ACS begins with a loading dose administered as early as possible, followed by a maintenance dose of 75 to 100 mg once daily.[37] Based on the results from the PLATO (PLATlet inhibition and patient Outcomes) and TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasurgrel-Thrombolysis in Myocardial Infarction 38) studies, dual antiplatelet therapy combining aspirin with a potent P2Y12 receptor inhibitor, such as prasugrel or ticagrelor, is the recommended strategy for most individuals with ACS.[38] Clopidogrel, which has less potent and more variable effects on platelet inhibition, should be reserved for cases where prasugrel and ticagrelor are contraindicated or unavailable or in patients with a high bleeding risk, defined as those meeting 1 major or 2 minor Antithrombotic Treatment for High Bleeding Risk criteria.[39] Clopidogrel may also be considered in patients aged 70 or older.[40]

All patients with an acute myocardial infarction should be started on a beta blocker, high-intensity statin, aspirin, and a P2Y12 inhibitor as soon as possible, with certain exceptions. Aspirin therapy for ACS begins with a loading dose administered as early as possible, followed by a maintenance dose of 75 to 100 mg once daily.[37] Based on the results from the PLATO (PLATlet inhibition and patient Outcomes) and TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasurgrel-Thrombolysis in Myocardial Infarction 38) studies, dual antiplatelet therapy combining aspirin with a potent P2Y12 receptor inhibitor, such as prasugrel or ticagrelor, is the recommended strategy for most individuals with ACS.[38] Clopidogrel, which has less potent and more variable effects on platelet inhibition, should be reserved for cases where prasugrel and ticagrelor are contraindicated or unavailable or in patients with a high bleeding risk, defined as those meeting 1 major or 2 minor Antithrombotic Treatment for High Bleeding Risk criteria.[39] Clopidogrel may also be considered in patients aged 70 or older.[40] P2Y-inhibiting antiplatelet medication choice depends on whether the patient underwent PCI or fibrinolytic therapy. Due to results from recent trials showing superiority, ticagrelor and prasugrel are preferred over clopidogrel in patients who undergo PCI.[41] Individuals undergoing fibrinolytic therapy should be started on clopidogrel.[42] The relative contraindications of P2Y12 inhibitors should always be considered. Prasugrel is contraindicated in patients with a history of transient ischemic attack and stroke. Anticoagulation should also be started alongside unfractionated heparin, low-molecular-weight heparin, bivalirudin, or fondaparinux.[43] Lipid-lowering therapy must be initiated as soon as possible following an ACS event, as the treatment is crucial for improving long-term prognosis and enhancing patient adherence after discharge. High-intensity statins, such as atorvastatin and rosuvastatin, should be started early, ideally before any planned PCI, and prescribed at the highest tolerated dose to achieve target low-density lipoprotein-C levels.[44]

P2Y-inhibiting antiplatelet medication choice depends on whether the patient underwent PCI or fibrinolytic therapy. Due to results from recent trials showing superiority, ticagrelor and prasugrel are preferred over clopidogrel in patients who undergo PCI.[41] Individuals undergoing fibrinolytic therapy should be started on clopidogrel.[42] The relative contraindications of P2Y12 inhibitors should always be considered. Prasugrel is contraindicated in patients with a history of transient ischemic attack and stroke. Anticoagulation should also be started alongside unfractionated heparin, low-molecular-weight heparin, bivalirudin, or fondaparinux.[43] Lipid-lowering therapy must be initiated as soon as possible following an ACS event, as the treatment is crucial for improving long-term prognosis and enhancing patient adherence after discharge. High-intensity statins, such as atorvastatin and rosuvastatin, should be started early, ideally before any planned PCI, and prescribed at the highest tolerated dose to achieve target low-density lipoprotein-C levels.[44] Recent studies support β-blocker benefits in patients with reduced left ventricular ejection fraction (LVEF) after ACS. However, the evidence for using these drugs in patients with LVEF greater than 40% following uncomplicated ACS is less definitive.[45] Except for the results from the CAPRICORN trial (CArvedilol Post-infaRct survIval COntRolled evaluatioN), which focused on patients with LVEF less than or equal to 40%, most large randomized controlled trials evaluating postmyocardial infarction β-blocker therapy were conducted before the widespread use of reperfusion therapies.[46]

Recent studies support β-blocker benefits in patients with reduced left ventricular ejection fraction (LVEF) after ACS. However, the evidence for using these drugs in patients with LVEF greater than 40% following uncomplicated ACS is less definitive.[45] Except for the results from the CAPRICORN trial (CArvedilol Post-infaRct survIval COntRolled evaluatioN), which focused on patients with LVEF less than or equal to 40%, most large randomized controlled trials evaluating postmyocardial infarction β-blocker therapy were conducted before the widespread use of reperfusion therapies.[46] Angiotensin-converting enzyme (ACE) inhibitors have been shown to improve postmyocardial infarction outcomes in patients with conditions such as heart failure, LVEF less than or equal to 40%, diabetes, chronic kidney disease, and hypertension.[47] Historical trials of ACE inhibitors in STEMI have indicated a modest but significant reduction in 30-day mortality, particularly in cases of anterior myocardial infarction.[48] Sodium-glucose cotransporter 2 (SGLT2) inhibitors improve glycemic control and reduce weight and blood pressure by inducing glycosuria and lowering plasma glucose levels without causing hypoglycemia.[49] In patients with type 2 diabetes and established atherosclerotic cardiovascular disease, trials of empagliflozin, canagliflozin, and dapagliflozin have demonstrated notable cardiovascular benefits.[50]

Other pathologies that can cause ST-segment elevation include myocarditis, pericarditis, stress cardiomyopathy (Takotsubo), benign early repolarization, acute vasospasm (Prinzmetal), spontaneous coronary artery dissection, LBBB, various channelopathies, and electrolyte abnormalities. Takotsubo cardiomyopathy, often referred to as "broken heart syndrome," is a distinct cardiac condition that has garnered increased interest in recent years.[51] Originally identified in Japan in the early 1990s, this syndrome is marked by abrupt and profound dysfunction of the left ventricle, frequently precipitated by intense emotional stress or major life events. Unlike a conventional myocardial infarction caused by blocked coronary arteries, Takotsubo cardiomyopathy occurs without significant coronary obstructions, setting it apart as a unique and perplexing cardiac disorder.[52] Prinzmetal angina, or vasospastic angina (VSA), arises from spontaneous coronary artery spasms, which can result in serious complications, particularly in individuals with increased coronary vasoconstriction and reduced vasodilation.[53] Early identification of patients at risk is crucial to prevent severe or fatal outcomes. While the exact prevalence of VSA remains uncertain, a study in Japan found that it may affect around 40% of individuals with angina, possibly higher than in White populations due to differences in clinical testing methods.[54] The primary treatment strategy involves using vasodilators and managing risk factors, such as smoking, hypertension, diabetes, lipid levels, stress, and alcohol consumption. VSA may also be linked to migraines.

Prinzmetal angina, or vasospastic angina (VSA), arises from spontaneous coronary artery spasms, which can result in serious complications, particularly in individuals with increased coronary vasoconstriction and reduced vasodilation.[53] Early identification of patients at risk is crucial to prevent severe or fatal outcomes. While the exact prevalence of VSA remains uncertain, a study in Japan found that it may affect around 40% of individuals with angina, possibly higher than in White populations due to differences in clinical testing methods.[54] The primary treatment strategy involves using vasodilators and managing risk factors, such as smoking, hypertension, diabetes, lipid levels, stress, and alcohol consumption. VSA may also be linked to migraines. Spontaneous coronary artery dissection (SCAD) is characterized by a tear in the epicardial coronary arteries, neither caused by medical procedures nor related to trauma or atherosclerosis.[55] Unlike the intraluminal thrombosis or plaque rupture that typically leads to ACS, SCAD-induced ACS results from myocardial damage from coronary artery obstruction following intimal disruption or the formation of an intramural hematoma, which creates a false lumen. SCAD predominantly affects individuals who lack traditional atherosclerotic cardiovascular risk factors and is more frequently observed in younger women without underlying atherosclerotic disease.[56] Symptoms can vary widely, from chest pain to sudden cardiac death. Despite greater awareness and advancements in intravascular imaging, SCAD remains frequently underdiagnosed or misdiagnosed, often being mistaken for atherosclerotic disease.

The Thrombolysis in Myocardial Infarction (TIMI) risk score is a straightforward tool that uses 8 prognostic factors to evaluate the risk associated with STEMI at the bedside. The TIMI risk score is the most commonly used scoring system for 30-day mortality.[57] This scoring system incorporates: Age older than 75 is assigned 3 points. Age between 64 and 74 is assigned 2 points. Diabetes, hypertension, or a history of angina is assigned 1 point. A systolic blood pressure less than 100 mm Hg is assigned 3 points. A heart rate greater than 100 beats per minute is assigned 2 points. Killip class II to IV is assigned 2 points. A body weight less than 150 lbs is assigned 1 point. The TIMI score ranges from 0 to 14, with each point representing a different level of risk based on the patient’s condition.[58] This scoring system helps predict mortality within the first 30 days following STEMI and is reliable for forecasting outcomes in patients receiving fibrinolytic therapy.[59] Studies have applied the TIMI score to estimate mortality rates in anterior wall STEMI cases. The TIMI score can help classify patients based on risk categories. Risk levels are categorized as low for scores ranging from 0 to 4, medium for scores between 5 and 9, and high for scores above 9. Mortality rates at 30 days for patients presenting with STEMI are between 2.5% and 10%.[60][61][62]

Myocardial infarction has 3 life-threatening mechanical complications: ventricular free wall rupture, interventricular septum rupture, and acute mitral regurgitation. Ventricular free wall rupture occurs within 5 days in half the cases and 2 weeks in 90% of cases, with an overall mortality rate of greater than 80%.[63][64] Interventricular septum rupture is reported about half as often as free wall rupture and typically occurs in 3 to 5 days, with an overall mortality rate greater than 70%.[65][66] Prompt surgery reduces the mortality rate in both conditions. Acute mitral regurgitation following a myocardial infarction is most commonly due to ischemic papillary muscle displacement, left ventricular dilatation, or rupture of the papillary muscle or chordae. In STEMI, the degree of mitral regurgitation is usually severe and associated with a 30-day survival of 24%.[67] Inflammation of the pericardium, known as pericarditis, and pericardial effusion resulting from pericardial injury are collectively referred to as postcardiac injury syndrome. This syndrome includes conditions such as postmyocardial infarction, pericarditis (Dressler syndrome), postpericardiotomy syndrome, and posttraumatic pericarditis. Even minor injuries, like those from PCI, cardiac implantable electronic device placement, or radiofrequency ablation, can provoke cardiac injury. These conditions share a common trigger of pericardial or pleural damage, leading to a pleuropericardial syndrome characterized by pericarditis with pericardial effusion and pleural effusion.[68]

Critical considerations in managing STEMI include the following: Chest pain or discomfort: This symptom is the primary trigger for the diagnostic and treatment processes in acute coronary syndrome. Coordination between emergency medical services and hospitals: Effective STEMI management relies on the seamless coordination between emergency medical services (EMS) and hospitals, facilitated by standardized written protocols. EMS should notify the PCI center as soon as a reperfusion strategy is decided, and the patient should be directly transferred to the PCI center, bypassing the emergency department. Invasive strategy: An invasive approach is advised for patients with ACS due to the condition's time-sensitive nature. Immediate invasive intervention is strongly recommended for STEMI.

A door-to-balloon time of less than 90 minutes is the goal of a PCI-capable facility. This parameter is one of the core measures of the Joint Commission on Accreditation of Healthcare Organizations.[69] The door-to-balloon time is the time between the patient's arrival in the emergency department and the crossing of the culprit lesion by a guide wire in the cardiac catheterization laboratory. Teamwork between EMS, emergency department physicians, and interventional cardiologists sets the groundwork for optimal door-to-balloon times. The median door-to-balloon time in 2010 was 64 minutes, with 91% of patients receiving PCI in under 90 minutes and 70% in under 75 minutes.[70]