Myocardial Infarction (MI): High-Yield Pathology
Myocardial infarction is a critical clinical event characterized by irreversible necrosis of the heart muscle, almost exclusively caused by acute thrombosis over a ruptured atherosclerotic plaque.
1. Morphological Evolution of Infarct
| Timeframe | Key Pathological Finding |
|---|---|
| 0–4 Hours | None (or early wavy fibers). |
| 4–24 Hours | Coagulative necrosis, contraction bands, and early neutrophilic infiltrate. |
| 1–3 Days | Extensive coagulative necrosis, loss of nuclei, dense neutrophilic infiltrate. |
| 3–7 Days | Macrophage infiltration, phagocytosis of necrotic debris (yellow-soft center). |
| 7–14 Days | Granulation tissue formation at the margins. |
| >2 Weeks | Collagen deposition, fibrous scar formation. |
2. Critical Complications
- Arrhythmia: The most common cause of death in the pre-hospital phase.
- Ventricular Free Wall Rupture (3-7 days): Leads to cardiac tamponade.
- Interventricular Septal Rupture (3-7 days): Leads to a new holosystolic murmur and left-to-right shunt.
- Papillary Muscle Rupture: Typically involving the posteromedial muscle (supplied only by the RCA); leads to acute mitral regurgitation.
- Dressler Syndrome: Autoimmune fibrinous pericarditis occurring weeks after an MI.
3. Exam Must-Knows
Pathology Pearl: The Left Anterior Descending (LAD) artery is the most commonly involved (40-50%), affecting the anterior wall of the LV. The Right Coronary Artery (RCA) affects the posterior wall, and the left circumflex artery (LCX) affects the lateral wall.
- Biomarkers: Troponin I is the gold standard (most sensitive/specific); rises in 4-6 hours, stays elevated for 7-10 days.
- Reperfusion Injury: Occurs when blood flow is restored; it can lead to contraction band necrosis due to calcium influx and reactive oxygen species.