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Emergency and Acute Medicine – Acute Coronary Syndrome: Myocardial Infarction
Overview and Definitions
Myocardial infarction (MI) results from an acute imbalance between myocardial oxygen supply and demand, leading to ischemia and irreversible myocardial injury. It is a core component of acute coronary syndrome (ACS), which includes unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Differentiation among these entities is essential, as management strategies and urgency of reperfusion differ substantially.
Etiology and Pathophysiology
The most common cause of MI is atherosclerotic coronary artery disease with plaque rupture and superallowing thrombus formation, resulting in partial or complete coronary occlusion. Other mechanisms include coronary vasospasm (variant/Prinzmetal angina), microvascular dysfunction, coronary embolism, arteritis (e.g., lupus, Takayasu arteritis, Kawasaki disease), prolonged hypotension, severe anemia, carbon monoxide poisoning, thyroid storm, or structural abnormalities such as aneurysm or ectasia. Cocaine and amphetamine use may precipitate MI through intense vasospasm and thrombosis.
Major risk factors include hypercholesterolemia, diabetes mellitus, hypertension, smoking, male sex, postmenopausal status in women, and a family history of premature coronary artery disease.
Clinical Presentation
Chest pain is the most common presenting symptom. Patients typically describe substernal pressure, heaviness, squeezing, burning, or tightness. Pain may radiate to the arms, shoulders, back, neck, or jaw. Anginal equivalents, particularly common in older adults, women, and patients with diabetes, include dyspnea, diaphoresis, nausea or vomiting, abdominal pain, syncope, or unexplained weakness.
Symptoms often last longer than 30 minutes and may occur at rest or with exertion. Many patients report preceding crescendo angina. Pain is usually not positional or pleuritic and is often only partially relieved by rest or nitroglycerin. A clenched fist over the chest (Levine sign) is suggestive of ischemic pain.
Physical Examination
The physical exam may be normal, especially early. Possible findings include tachycardia, hypertension during pain, S3 or S4 gallop, a new murmur from papillary muscle dysfunction with mitral regurgitation, diminished peripheral pulses, or signs of acute decompensated heart failure.
Essential Emergency Evaluation
History remains the most critical element in differentiating MI from noncardiac causes of chest pain. Rapid assessment and early testing are required to avoid delays in reperfusion therapy.
Electrocardiography
A 12-lead ECG is the cornerstone of diagnosis and must be obtained immediately. ECG findings help distinguish STEMI from NSTEMI and nonischemic causes of ST elevation such as pericarditis, early repolarization, left ventricular hypertrophy with strain, prior infarction with aneurysm, or hyperkalemia.
Diagnostic criteria for STEMI include new ST-segment elevation at the J point in two contiguous leads (with sex- and lead-specific thresholds). ST depression in leads V1–V2 may indicate posterior infarction.
New or presumed new left bundle branch block alone is no longer considered diagnostic of STEMI; however, Sgarbossa criteria can identify MI in patients with LBBB. Echocardiography may reveal regional wall motion abnormalities or mechanical complications.
Laboratory and Imaging Studies
Cardiac biomarkers (troponin I or T, CK-MB) confirm myocardial necrosis and guide risk stratification. Additional testing includes electrolytes, calcium, magnesium, renal function, and digoxin level when relevant. Chest radiography may reveal pulmonary edema, cardiomegaly, or alternative diagnoses such as aortic dissection.
Differential Diagnosis
The differential for MI-like chest pain includes aortic dissection, pulmonary embolism, pericarditis, pneumonia, pneumothorax, esophageal disorders, biliary disease, peptic ulcer disease, anxiety or panic disorder, and musculoskeletal chest pain.
Prehospital and Initial ED Management
Early management includes IV access, cardiac monitoring, oxygen if hypoxic, aspirin administration, and sublingual nitroglycerin for symptom relief. When feasible, a prehospital ECG with advance notification to the receiving facility improves outcomes.
Definitive Emergency Treatment
STEMI is a time-critical emergency requiring immediate reperfusion. Primary percutaneous coronary intervention (PCI) is preferred and should occur within 90 minutes of first medical contact. If PCI is not available within 120 minutes, fibrinolytic therapy should be administered promptly.
All patients without contraindications should receive aspirin. Dual antiplatelet therapy with clopidogrel, prasugrel, or ticagrelor is used based on reperfusion strategy and patient factors. Nitrates are administered if systolic blood pressure is adequate and there is no evidence of right ventricular infarction.
β-blockers are recommended within the first 24 hours unless contraindicated. Anticoagulation with unfractionated heparin, bivalirudin, or low-molecular-weight heparin is used depending on whether PCI or thrombolysis is planned. Morphine may be used judiciously for pain control.
Life-threatening dysrhythmias and conduction disturbances must be managed promptly, with pacing or defibrillation as indicated. Patients in cardiogenic shock require urgent transfer to a catheterization laboratory for revascularization and mechanical circulatory support when necessary.
Disposition and Follow-Up
All patients with confirmed myocardial infarction require hospital admission, typically to a coronary care or intensive care unit. Patients with uncertain diagnoses often benefit from observation with serial ECGs, biomarkers, and advanced testing. No patient with MI should be discharged from the emergency department.
Clinical Pearls and Pitfalls
Rapid recognition and reperfusion save myocardium and lives—time is muscle. Door-to-needle time for thrombolysis should be within 30 minutes when PCI is unavailable. A single normal ECG or negative biomarker does not exclude MI early in the course. New LBBB alone should not be considered diagnostic without supportive findings. Maintain a high index of suspicion in patients with atypical presentations.
Overview and Definitions
Myocardial infarction (MI) results from an acute imbalance between myocardial oxygen supply and demand, leading to ischemia and irreversible myocardial injury. It is a core component of acute coronary syndrome (ACS), which includes unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). Differentiation among these entities is essential, as management strategies and urgency of reperfusion differ substantially.
Etiology and Pathophysiology
The most common cause of MI is atherosclerotic coronary artery disease with plaque rupture and superallowing thrombus formation, resulting in partial or complete coronary occlusion. Other mechanisms include coronary vasospasm (variant/Prinzmetal angina), microvascular dysfunction, coronary embolism, arteritis (e.g., lupus, Takayasu arteritis, Kawasaki disease), prolonged hypotension, severe anemia, carbon monoxide poisoning, thyroid storm, or structural abnormalities such as aneurysm or ectasia. Cocaine and amphetamine use may precipitate MI through intense vasospasm and thrombosis.
Major risk factors include hypercholesterolemia, diabetes mellitus, hypertension, smoking, male sex, postmenopausal status in women, and a family history of premature coronary artery disease.
Clinical Presentation
Chest pain is the most common presenting symptom. Patients typically describe substernal pressure, heaviness, squeezing, burning, or tightness. Pain may radiate to the arms, shoulders, back, neck, or jaw. Anginal equivalents, particularly common in older adults, women, and patients with diabetes, include dyspnea, diaphoresis, nausea or vomiting, abdominal pain, syncope, or unexplained weakness.
Symptoms often last longer than 30 minutes and may occur at rest or with exertion. Many patients report preceding crescendo angina. Pain is usually not positional or pleuritic and is often only partially relieved by rest or nitroglycerin. A clenched fist over the chest (Levine sign) is suggestive of ischemic pain.
Physical Examination
The physical exam may be normal, especially early. Possible findings include tachycardia, hypertension during pain, S3 or S4 gallop, a new murmur from papillary muscle dysfunction with mitral regurgitation, diminished peripheral pulses, or signs of acute decompensated heart failure.
Essential Emergency Evaluation
History remains the most critical element in differentiating MI from noncardiac causes of chest pain. Rapid assessment and early testing are required to avoid delays in reperfusion therapy.
Electrocardiography
A 12-lead ECG is the cornerstone of diagnosis and must be obtained immediately. ECG findings help distinguish STEMI from NSTEMI and nonischemic causes of ST elevation such as pericarditis, early repolarization, left ventricular hypertrophy with strain, prior infarction with aneurysm, or hyperkalemia.
Diagnostic criteria for STEMI include new ST-segment elevation at the J point in two contiguous leads (with sex- and lead-specific thresholds). ST depression in leads V1–V2 may indicate posterior infarction.
New or presumed new left bundle branch block alone is no longer considered diagnostic of STEMI; however, Sgarbossa criteria can identify MI in patients with LBBB. Echocardiography may reveal regional wall motion abnormalities or mechanical complications.
Laboratory and Imaging Studies
Cardiac biomarkers (troponin I or T, CK-MB) confirm myocardial necrosis and guide risk stratification. Additional testing includes electrolytes, calcium, magnesium, renal function, and digoxin level when relevant. Chest radiography may reveal pulmonary edema, cardiomegaly, or alternative diagnoses such as aortic dissection.
Differential Diagnosis
The differential for MI-like chest pain includes aortic dissection, pulmonary embolism, pericarditis, pneumonia, pneumothorax, esophageal disorders, biliary disease, peptic ulcer disease, anxiety or panic disorder, and musculoskeletal chest pain.
Prehospital and Initial ED Management
Early management includes IV access, cardiac monitoring, oxygen if hypoxic, aspirin administration, and sublingual nitroglycerin for symptom relief. When feasible, a prehospital ECG with advance notification to the receiving facility improves outcomes.
Definitive Emergency Treatment
STEMI is a time-critical emergency requiring immediate reperfusion. Primary percutaneous coronary intervention (PCI) is preferred and should occur within 90 minutes of first medical contact. If PCI is not available within 120 minutes, fibrinolytic therapy should be administered promptly.
All patients without contraindications should receive aspirin. Dual antiplatelet therapy with clopidogrel, prasugrel, or ticagrelor is used based on reperfusion strategy and patient factors. Nitrates are administered if systolic blood pressure is adequate and there is no evidence of right ventricular infarction.
β-blockers are recommended within the first 24 hours unless contraindicated. Anticoagulation with unfractionated heparin, bivalirudin, or low-molecular-weight heparin is used depending on whether PCI or thrombolysis is planned. Morphine may be used judiciously for pain control.
Life-threatening dysrhythmias and conduction disturbances must be managed promptly, with pacing or defibrillation as indicated. Patients in cardiogenic shock require urgent transfer to a catheterization laboratory for revascularization and mechanical circulatory support when necessary.
Disposition and Follow-Up
All patients with confirmed myocardial infarction require hospital admission, typically to a coronary care or intensive care unit. Patients with uncertain diagnoses often benefit from observation with serial ECGs, biomarkers, and advanced testing. No patient with MI should be discharged from the emergency department.
Clinical Pearls and Pitfalls
Rapid recognition and reperfusion save myocardium and lives—time is muscle. Door-to-needle time for thrombolysis should be within 30 minutes when PCI is unavailable. A single normal ECG or negative biomarker does not exclude MI early in the course. New LBBB alone should not be considered diagnostic without supportive findings. Maintain a high index of suspicion in patients with atypical presentations.
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