Heart Attack (Myocardial Infarction)

Definition

• Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 511

Causes & Pathogenesis

The Classic Sequence (90% of cases)

1. An atheromatous plaque is eroded or suddenly disrupted by endothelial injury, intraplaque hemorrhage, or mechanical forces - exposing subendothelial collagen and necrotic plaque contents to circulating blood.
2. Platelets adhere, aggregate, and activate, releasing thromboxane A2, ADP, and serotonin - causing further platelet aggregation and vasospasm.
3. Coagulation is activated via tissue factor, adding to the growing thrombus.
4. Within minutes, the thrombus can completely occlude the coronary artery lumen.

Less Common Causes (~10% of cases)

• Vasospasm (with or without atherosclerosis) - triggered by cocaine, ephedrine, or platelet aggregation
• Embolism - from left atrial thrombus (in atrial fibrillation), infective endocarditis vegetations, or prosthetic cardiac material
• Small vessel disease - vasculitis, amyloid deposition
• Hematologic disorders - sickle cell disease, hypercoagulable states

The Progression of Necrosis

• Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 512
• Guyton and Hall Textbook of Medical Physiology

Risk Factors

• Non-modifiable: Age, male sex (females gain similar risk post-menopause due to declining estrogen, rising cholesterol, blood pressure, and inflammatory markers), family history
• Modifiable: Hypertension, hypercholesterolemia, smoking, diabetes, obesity, physical inactivity

Symptoms

• Crushing, pressure-like chest pain - often radiating to the left arm, jaw, or shoulder
• Shortness of breath
• Diaphoresis (sweating), nausea, vomiting
• Sense of impending doom

Diagnosis

ECG Changes

• STEMI (ST-Elevation MI): Full-thickness occlusion - a medical emergency requiring immediate reperfusion
• NSTEMI (Non-ST-Elevation MI): Partial occlusion or subendocardial infarction
• Q waves develop over days-weeks as dead tissue becomes electrically silent

Biomarkers

• Cardiac troponins (cTnI, cTnT): Most sensitive and specific - rise within 2-4 hours, peak at ~24 hours, remain elevated for up to 10-14 days
• CK-MB: Rises within 4-6 hours, returns to normal in ~48-72 hours (useful for detecting reinfarction)

Types of MI

• Type 1 MI: Spontaneous plaque rupture with thrombosis
• Type 2 MI: Supply-demand mismatch without plaque rupture (e.g., tachyarrhythmia, anemia, severe hypertension)

Treatment

Acute Management

• Aspirin immediately (antiplatelet)
• P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel) - dual antiplatelet therapy
• Anticoagulation (heparin, bivalirudin)
• Nitroglycerin (sublingual then IV) - for pain and vasodilation
• Oxygen if SpO2 < 90%
• Morphine for refractory pain

Reperfusion (the core treatment)

• Primary PCI (percutaneous coronary intervention): The preferred strategy for STEMI - goal is door-to-balloon time < 90 minutes. A catheter is used to open the blocked artery with a balloon and stent.
• Fibrinolytic therapy (thrombolytics): Used when PCI is not available within 120 minutes of first medical contact. Examples: alteplase, tenecteplase.
• CABG (coronary artery bypass grafting): Reserved for multivessel disease or anatomical patterns not suitable for PCI.

Long-Term Medications

• Beta-blockers - reduce heart rate, myocardial oxygen demand, and mortality
• ACE inhibitors/ARBs - reduce remodeling, especially if ejection fraction is reduced
• Statins - intensive statin therapy (e.g., atorvastatin 80 mg) to reduce LDL and plaque progression
• Dual antiplatelet therapy - continued for at least 12 months post-stent

Complications

• Guyton and Hall Textbook of Medical Physiology

Prevention

• Smoking cessation
• Blood pressure control (target < 130/80 mmHg)
• Lipid lowering (statin therapy for high-risk individuals)
• Diabetes management
• Regular physical activity
• Healthy diet (Mediterranean-style)
• Aspirin in selected high-risk patients (shared decision-making)

Current Guidelines