Question
Discuss in detail the pathogenesis of acute myocardial infarction. Discuss the gross and microscopic features of myocardial infarction. Add a note on the complications (4+3+3)
Answer
Pathogenesis: Acute myocardial infarction (MI) results from sudden loss of blood supply to a region of myocardium, most commonly due to acute coronary artery thrombosis at the site of a ruptured or eroded atherosclerotic plaque. Plaque rupture exposes thrombogenic subendothelial collagen and lipid core contents, triggering platelet activation, aggregation, and the coagulation cascade, forming an occlusive thrombus. Sustained ischaemia (typically >20–40 minutes) causes irreversible myocyte injury, beginning in the subendocardium (most vulnerable to ischaemia due to lower perfusion pressure) and progressing outward (“wavefront” of necrosis) to become transmural if occlusion persists. Cell death occurs via coagulative necrosis, driven by ATP depletion, calcium influx, membrane damage, and free radical injury on reperfusion.
Gross features (time-dependent):
- 0–12 hrs: Usually no visible change.
- 12–24 hrs: Pallor, sometimes with dark mottling.
- 1–3 days: Sharply defined, yellow-tan, soft infarct.
- 3–7 days: Yellow, softened centre with a hyperaemic (red) border — period of maximal risk of rupture.
- 7–10 days: Maximally yellow, depressed, red-tan granulation margin.
- 2–8 weeks: Progressive grey-white scarring.
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2 months: Complete grey-white fibrous scar.
Microscopic features (time-dependent):
- 4–12 hrs: Early coagulative necrosis, oedema, haemorrhage.
- 1–3 days: Coagulative necrosis (loss of nuclei/striations), extensive neutrophilic infiltration (peak days 2–3).
- 3–7 days: Macrophage infiltration begins, phagocytosis of dead cells, early granulation tissue at margins.
- 10 days–2 weeks: Well-developed granulation tissue.
- 2–8 weeks: Progressive collagen deposition/fibrosis.
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2 months: Dense, well-formed collagenous scar.
Complications:
- Arrhythmias (most common cause of early death)
- Cardiogenic shock/congestive heart failure
- Myocardial rupture (free wall, septum, papillary muscle) — highest risk days 3–7
- Fibrinous pericarditis (2–4 days)
- Mural thrombus with systemic embolization
- Ventricular aneurysm (late complication)
- Dressler syndrome (autoimmune pericarditis, weeks later)