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Myocardial Infarction for the American Board of Internal Medicine Exam
Overview of Myocardial Infarction
Myocardial infarction (MI), or heart attack, is caused by an acute reduction in coronary blood flow leading to myocardial ischemia and cell death. MIs are classified into ST-segment elevation myocardial infarctions (STEMIs) and non-ST-segment elevation myocardial infarctions (NSTEMIs). MI is a major cause of morbidity and mortality globally and is typically associated with atherosclerosis, where plaque rupture leads to thrombus formation and occlusion of coronary vessels.
Pathophysiology
  • Atherosclerosis: The buildup of plaques in coronary arteries leads to narrowing and restricts blood flow. Atherosclerosis is driven by risk factors such as hyperlipidemia, smoking, hypertension, and diabetes.
  • Plaque Rupture and Thrombus Formation: When an atherosclerotic plaque ruptures, exposure of the lipid-rich core activates platelets and the coagulation cascade, leading to thrombus formation. Thrombus may partially or completely occlude a coronary artery, resulting in reduced oxygen supply to the myocardium.
  • Myocardial Ischemia and Infarction: Prolonged ischemia causes necrosis of myocardial cells. In STEMI, there is full-thickness (transmural) ischemia, while in NSTEMI, ischemia is typically subendocardial.
Risk Factors
  • Non-Modifiable: Age, race, sex, family history of early CAD. Risk is higher in African Americans than in White Americans. Women have higher mortality than men.
  • Modifiable: Smoking, hypertension, hyperlipidemia, diabetes mellitus, obesity, sedentary lifestyle, and high-fat diet.
Clinical Presentation
  • Symptoms:
    • Chest Pain: Most common symptom, typically described as a severe, crushing, or squeezing sensation in the central chest, lasting more than 20 minutes. It may radiate to the left arm, neck, jaw, or back.
    • Associated Symptoms: Dyspnea, diaphoresis, nausea, vomiting, and anxiety.
    • Additional Presentations: Common in older adults, women, and diabetics, including symptoms like fatigue, syncope, and abdominal discomfort.
myocardial infarction signs and symptoms
  • Physical Exam:
    • General Appearance: Distressed, sweating, or pale.
    • Vital Signs: Tachycardia or bradycardia, hypotension (especially in right ventricular infarction), and low-grade fever.
    • Cardiovascular Exam: Possible S3 or S4 gallop, jugular venous distention in right-sided MI, and new murmurs (indicating papillary muscle dysfunction or ventricular septal defect).
Types of Myocardial Infarction
ST-Segment Elevation Myocardial Infarction (STEMI)
  • Definition: Full-thickness infarction characterized by ST-segment elevation on ECG in at least two contiguous leads.
  • Pathophysiology: Complete occlusion of a coronary artery by thrombus following plaque rupture, causing transmural ischemia.
  • Diagnosis:
    • ECG: ST-segment elevation in ≥2 contiguous leads (e.g., anterior MI with ST elevation in V2-V4), new left bundle branch block (LBBB).
    • Biomarkers: Elevated troponins confirm myocardial injury.
  • Management:
    • Reperfusion Therapy:
    • Primary PCI: Preferred within 90 minutes of first medical contact.
    • Fibrinolysis: Alternative if PCI cannot be performed within 120 minutes; administered within 30 minutes if STEMI is confirmed.
    • Medications:
    • Antiplatelets: Aspirin plus a P2Y12 inhibitor (e.g., clopidogrel).
    • Anticoagulants: Unfractionated heparin or bivalirudin during PCI.
    • Adjuncts: Beta-blockers, nitrates, ACE inhibitors, and statins.
Non-ST Segment Elevation Myocardial Infarction (NSTEMI)
  • Definition: Subendocardial infarction without ST-segment elevation, diagnosed by elevated troponins and ischemic symptoms.
  • Pathophysiology: Partial occlusion of a coronary artery by thrombus or high demand relative to coronary flow.
  • Diagnosis:
    • ECG: ST-segment depression, T-wave inversion, or nonspecific changes.
    • Biomarkers: Elevated troponins confirm myocardial necrosis.
  • Management:
    • Antithrombotic Therapy:
    • Antiplatelets: Dual antiplatelet therapy (aspirin and a P2Y12 inhibitor).
    • Anticoagulants: Heparin, enoxaparin, or bivalirudin.
    • Risk Stratification: TIMI or GRACE score to guide invasive management.
    • Invasive Strategy: PCI within 24–72 hours for high-risk patients.
    • Medical Therapy: Beta-blockers, nitrates, ACE inhibitors, and statins.
Diagnostic Modalities
  • Electrocardiogram (ECG): Essential for early diagnosis of STEMI; also used to assess for ischemic changes in NSTEMI.
  • Cardiac Biomarkers: Troponins are highly specific and sensitive for myocardial injury. Elevated levels confirm MI, with serial measurements showing a rise and fall pattern.
  • Echocardiography: Used to assess left ventricular function, wall motion abnormalities, and complications (e.g., ventricular aneurysm or septal rupture).
  • Coronary Angiography: Gold standard for diagnosing coronary artery blockages and guiding revascularization.
Complications of Myocardial Infarction
  • Early Complications (within 24–72 hours):
    • Arrhythmias: Ventricular fibrillation, ventricular tachycardia, atrial fibrillation, and sinus bradycardia.
    • Heart Failure: Due to impaired ventricular function.
    • Cardiogenic Shock: Seen in large infarcts, usually in anterior MI.
  • Mechanical Complications (days to weeks post-MI):
    • Papillary Muscle Rupture: Can lead to acute mitral regurgitation.
    • Ventricular Septal Rupture: Presents with new murmur and hemodynamic instability.
    • Left Ventricular Free Wall Rupture: Leads to cardiac tamponade and is usually fatal.
  • Late Complications:
    • Left Ventricular Aneurysm: Causes persistent ST elevation on ECG and risk of thrombus formation.
    • Dressler’s Syndrome: Post-MI pericarditis, typically 2–6 weeks after infarction.
Secondary Prevention
Long-term management is focused on reducing recurrence risk and improving survival.
  • Lifestyle Modification: Smoking cessation, healthy diet, weight management, and regular physical activity.
  • Pharmacologic Therapy:
    • Antiplatelet Therapy: Aspirin indefinitely and a P2Y12 inhibitor for at least 12 months post-PCI.
    • Beta-Blockers: Decrease mortality and prevent arrhythmias.
    • ACE Inhibitors or ARBs: Recommended for patients with heart failure, left ventricular dysfunction, or diabetes.
    • Statins: High-intensity statins for LDL reduction and plaque stabilization.
Key Points
  • Types of MI:
    • STEMI: Complete coronary artery occlusion, characterized by ST-segment elevation; requires immediate reperfusion with PCI or fibrinolysis.
    • NSTEMI: Partial occlusion; managed with antithrombotic therapy, with PCI indicated in high-risk patients.
  • Diagnosis:
    • ECG: ST-segment elevation in STEMI; ST depression or T-wave inversion in NSTEMI.
    • Biomarkers: Elevated troponins confirm myocardial injury in both STEMI and NSTEMI.
  • Management:
    • STEMI: Immediate PCI within 90 minutes or fibrinolysis if PCI is delayed.
    • NSTEMI: Dual antiplatelet therapy, anticoagulation, and invasive management based on risk.
    • Medications: Include beta-blockers, ACE inhibitors, statins, and nitrates.
  • Complications:
    • Early: Arrhythmias, heart failure, and cardiogenic shock.
    • Mechanical: Papillary muscle or ventricular septal rupture, and free wall rupture.
    • Late: Left ventricular aneurysm and Dressler’s syndrome.
  • Secondary Prevention:
    • Lifestyle: Smoking cessation, exercise, and a heart-healthy diet.
    • Medications: Long-term aspirin, beta-blockers, ACE inhibitors, and statins to reduce recurrence and improve survival.