Myocardial Infarction - Comprehensive Review

1. Definition & Epidemiology

2. Pathogenesis

Coronary Arterial Occlusion (the typical 90% pathway)

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 blood.
2. Platelets adhere, aggregate, and are activated, releasing thromboxane A2, ADP, and serotonin - causing further platelet aggregation and vasospasm.
3. Coagulation is activated by tissue factor and other mechanisms, adding to the growing thrombus.
4. Within minutes, the thrombus can completely occlude the coronary lumen.

Atypical causes (~10% of MIs)

• Vasospasm with or without atherosclerosis (cocaine, ephedrine, catecholamines)
• Embolism (left atrial mural thrombus from AF, endocarditis vegetations, prosthetic material, PFO)
• Small-vessel disease (vasculitis, sickle cell, amyloid deposition)
• MINOCA (myocardial infarction with nonobstructive coronary arteries)

3. Myocardial Response to Ischemia

4. Infarct Distribution by Coronary Artery

5. Morphological Changes Over Time

6. Clinical Features

• Prolonged chest pain (>30 minutes) - described as crushing, squeezing, or stabbing, often radiating to the left arm, jaw, or shoulder
• Diaphoresis (profuse sweating)
• Nausea and vomiting (especially inferior MI with vagal activation)
• Dyspnea from impaired LV contractility and pulmonary congestion
• Rapid, weak pulse
• Silent MI: In up to 25% of patients (especially diabetics with neuropathy), onset is entirely asymptomatic and discovered only by ECG or biomarkers
• Robbins, Cotran & Kumar, p. 516

7. ECG Changes

STEMI Criteria

• ≥ 0.1 mV in most leads
• ≥ 0.2 mV in V2-V3 in men ≥40 years
• ≥ 0.25 mV in V2-V3 in men <40 years
• ≥ 0.15 mV in V2-V3 in women
• Frameworks for Internal Medicine, p. 33

Evolution of ECG Changes

8. Biomarkers

• Cardiac troponin I and T (cTnI, cTnT) - most clinically useful; proteins that normally regulate calcium-mediated contraction, released when sarcolemmal integrity is lost. Rise within 3-6 hours, peak at 24-48 hours, remain elevated for up to 7-14 days (troponin T) or 5-7 days (troponin I).
• CK-MB - rises at 4-8 hours, peaks at 18-24 hours, returns to normal at 36-48 hours (useful for detecting reinfarction)
• An elevated troponin without ST elevation = NSTEMI; with ST elevation = STEMI; elevated troponin without symptoms/ECG changes = type 2 MI or myocardial injury
• Robbins, Cotran & Kumar, p. 517

9. Classification: STEMI vs. NSTEMI

10. Management

Immediate Goals

• Identify reperfusion candidates and initiate reperfusion immediately
• Relieve ischemic pain
• Recognize and treat hypotension, pulmonary edema, and arrhythmia
• Mortality is directly related to ischemia time - the benefit of reperfusion is inversely proportional to time to reperfusion
• Washington Manual of Medical Therapeutics

Upstream Medications

• Washington Manual of Medical Therapeutics

Reperfusion Strategy (STEMI)

• Primary PCI: Preferred if available within 90 minutes of first medical contact - directly opens the culprit artery
• Thrombolytics (fibrinolytics): Used if PCI not available within 120 minutes; then transfer to PCI-capable center
• Calcium channel blockers are not beneficial acutely; short-acting dihydropyridines may increase mortality - Harrison's Principles of Internal Medicine, 22nd Edition

Morphine (analgesic)

• Given 2-4 mg IV, repeated every 5 minutes for pain control
• Caution: may reduce cardiac output by venous pooling; vagotonic effect can cause bradycardia (treat with atropine 0.5 mg IV)
• Harrison's Principles of Internal Medicine, 22nd Edition, p. 2162

11. Complications

Complications Summary

12. Secondary Prevention (Post-MI)

• Dual antiplatelet therapy (aspirin + P2Y12 inhibitor) for at least 12 months post-ACS
• High-intensity statin (e.g., atorvastatin 40-80 mg)
• ACE inhibitor or ARB (especially with reduced EF or diabetes)
• Beta-blocker (strong evidence in patients with reduced EF; evidence in preserved EF patients is more nuanced - see below)
• Cardiac rehabilitation (home-based or center-based - both shown effective per Cochrane review, 2023)
• Risk factor modification: smoking cessation, BP control, glycemic control, dietary changes

13. Key Diagnostic Algorithm

Chest Pain / Suspected MI
        ↓
12-lead ECG within 10 min of arrival
        ↓
  ┌─────┴─────┐
STEMI        No ST elevation
  ↓              ↓
Immediate    Serial ECGs + Troponins
reperfusion      ↓
(primary PCI   Elevated Troponin?
 <90 min)      ↓          ↓
            NSTEMI     Normal → UA / alternative dx
               ↓
      Risk stratify → early invasive strategy

• Robbins, Cotran & Kumar Pathologic Basis of Disease - pathogenesis, morphology, complications
• Ganong's Review of Medical Physiology, 26th Ed. - ECG mechanisms
• Frameworks for Internal Medicine - STEMI/NSTEMI classification, ECG criteria
• Harrison's Principles of Internal Medicine, 22nd Ed. - pain management, reperfusion strategy
• Washington Manual of Medical Therapeutics - medications and protocol
• Fuster & Hurst's The Heart, 15th Ed. - epidemiology, reperfusion
• 2025 ACC/AHA ACS Guideline - current clinical practice