Myocardial Infarction (MI): Overview, ECG Changes, and Treatment

Definition

• Robbins, Cotran & Kumar Pathologic Basis of Disease

Pathogenesis

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

When angiography is performed within 4 hours of MI onset, it demonstrates coronary thrombosis in ~90% of cases. This sequence has direct therapeutic implications: early thrombolysis and/or angioplasty can dramatically limit myocardial necrosis. - Robbins, Cotran & Kumar

Types of MI by Extent

Coronary Artery Territory:

• LAD (Left Anterior Descending) - anterior LV wall, anterior septum (most common; "widow maker")
• LCx (Left Circumflex) - lateral and posterior LV wall
• RCA (Right Coronary Artery) - inferior LV wall, posterior septum, RV
• Robbins, Cotran & Kumar Pathologic Basis of Disease

ECG Changes in MI

Serial ECG Evolution in Anterior MI:

• A - Normal tracing: Baseline
• B - Very early (hours after infarction): ST segment elevation in leads I, aVL, V3-5; reciprocal ST depression in leads II, III, aVF
• C - Later (hours to days): Q waves appear in I, aVL, V5-6; QS complexes in V3-4 (transmural necrosis); ST changes persist but lessen; T waves begin to invert
• D - Days to weeks: Deep T wave inversions; Q waves become more prominent
• E - Weeks to months: Q waves stabilize; T waves may normalize or remain inverted; "electrically silent" scar

Lead Localisation of STEMI:

Other Key ECG Points:

• Reciprocal changes: Leads on the opposite side of the heart show ST depression.
• Q waves: Develop after some days/weeks - electrically silent dead muscle/scar. Abnormal Q = >40ms wide or >25% depth of R wave. Non-Q-wave infarcts tend to be less severe but have high risk of reinfarction.
• Arrhythmias: Common in 3 phases - (1) 0-30 min post-infarction: reentry arrhythmias; (2) relative quiet period; (3) 12h onwards: increased automaticity; (4) 3 days to weeks: reentry again. Risk of ventricular fibrillation is highest.
• NSTEMI/UA: No ST elevation; may show ST depression, T-wave inversions, or a normal ECG; diagnosis requires elevated troponin (NSTEMI) vs. normal troponin (UA).
• Ganong's Review of Medical Physiology, 26th Ed.

Biomarkers

Treatment

Immediate (Acute) Management - MONA + Reperfusion

• Morphine - for pain relief (reduces sympathetic drive, preload; use cautiously)
• Oxygen - for O₂ sat <94% (routine use no longer recommended for all patients)
• Nitrates (sublingual nitroglycerin) - for pain relief and vasodilation; contraindicated in hypotension or RV infarction
• Aspirin (162-325mg, chewed) - immediate antiplatelet effect; reduces mortality

Reperfusion Therapy - The Priority in STEMI

• Goal: door-to-balloon time <90 minutes
• Superior to thrombolysis when performed in a timely manner at a PCI-capable centre
• Mechanical restoration of flow with balloon angioplasty ± stent

• Agents: streptokinase, alteplase (tPA), tenecteplase, reteplase
• Most effective within the first 3 hours ("golden hour")
• Contraindicated if systolic BP >185 mmHg or diastolic >110 mmHg persistently
• Contraindicated in recent stroke, active bleeding, recent major surgery

Antiplatelet and Antithrombotic Therapy

• Dual antiplatelet therapy (DAPT): Aspirin + a P2Y12 inhibitor (clopidogrel, ticagrelor, or prasugrel) - continued for 12 months post-ACS
• Anticoagulation: Heparin (UFH or LMWH), bivalirudin, or fondaparinux - used acutely to prevent further thrombosis

Additional Pharmacotherapy

Summary of In-Hospital Treatment (Fuster's Heart, 15th Ed.):

"Hospitalized patients should be treated with ASA, a platelet P2Y12 receptor inhibitor, antithrombotic therapy, a beta-blocker, an ACE inhibitor, and a high-intensity statin."

Long-term / Secondary Prevention

• Continue DAPT for 12 months
• Lifelong aspirin + statin + ACE inhibitor (if EF reduced)
• Beta-blocker (especially if EF <40%)
• Cardiac rehabilitation
• Risk factor control: smoking cessation, BP and diabetes management, diet, exercise
• ICD implantation if EF remains <35% despite >3 months of optimal medical therapy

Complications of MI

• Robbins, Cotran & Kumar Pathologic Basis of Disease - Pathogenesis, morphology, types
• Ganong's Review of Medical Physiology, 26th Ed. - ECG mechanisms, serial changes, arrhythmias
• Fuster and Hurst's The Heart, 15th Ed. - ACS management, pharmacotherapy
• Goldman-Cecil Medicine - Classification, treatment framework