Myocardial infarction: pathogenesis
- Lesion
A heart attack is the death of heart muscle when a clot blocks a coronary artery. Which artery is blocked decides which wall dies.
What it is
Most myocardial infarctions follow acute plaque change and thrombosis in a coronary artery. Within a minute of severe ischemia, contraction stops; after about 20 to 40 minutes, injury becomes irreversible, beginning in the subendocardium and spreading as a wavefront toward the epicardium over about 3 to 6 hours. Transmural infarcts usually come from an occlusive thrombus (ST-elevation MI); subendocardial infarcts from partial occlusion, global hypoperfusion or reperfused occlusion (often non-ST-elevation). Reperfusion saves tissue but adds reperfusion injury, haemorrhage and contraction-band necrosis.
Structure
- Gross and microscopic evolution over hours to months: see the infarct timeline page.
- Reperfused infarct: haemorrhagic, with contraction-band necrosis (hypercontracted sarcomeres) at the borders.
- Subendocardial infarct: necrosis of the inner third to half of the wall, often circumferential in global hypoperfusion.
Step by step
- A plaque ruptures and platelets adhere, aggregate and release mediators; the coagulation cascade forms a thrombus.
- The thrombus occludes the artery; within seconds the myocardium switches to anaerobic glycolysis and stops contracting.
- ATP falls and lactate rises; after 20 to 40 minutes injury becomes irreversible in the subendocardium.
- Necrosis advances toward the epicardium; most of the final infarct is complete within about 6 hours.
- Damaged membranes leak troponin and CK-MB into the blood.
- Reperfusion limits the infarct but can cause haemorrhage, calcium overload with contraction bands and oxidative injury.
Which artery infarcts which wall
| Artery | Share of infarcts | Territory |
|---|---|---|
| Left anterior descending | About 40–50 % | Anterior LV wall, apex, anterior two-thirds of septum |
| Right coronary | About 30–40 % | Inferior/posterior LV wall, posterior septum, RV (right-dominant) |
| Left circumflex | About 15–20 % | Lateral LV wall |
Clinical notes
- Typical presentation: crushing chest pain over 30 minutes radiating to the left arm or jaw, sweating, dyspnea; diabetics and older adults may have silent infarcts.
- Type 2 MI: supply–demand mismatch without plaque rupture (anemia, shock, tachyarrhythmia).
Test yourself
Think of the answer, then tap the question to see it.
Which coronary artery is most often occluded in myocardial infarction?
The left anterior descending artery (about 40 to 50 % of infarcts).
Why is the subendocardium the first zone to die?
It is the farthest from the epicardial arteries and is compressed by the high intraventricular pressure, so it is perfused last.
What is contraction-band necrosis, and when is it seen?
Eosinophilic transverse bands of hypercontracted sarcomeres from calcium influx, typical of reperfused infarcts.
Elsewhere in DurgiPedia
- The ECG in ischemia and infarction
- Coronary circulation and myocardial ischemia
- Cardiac muscle: intercalated discs
Connections
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Heart Attack | Myocardial Infarction | MedlinePlus (MedlinePlus, US National Library of Medicine, 2025); Hospital Mortality from Myocardial Infarction in Latin America and the Caribbean: Systematic Review and Meta-Analysis (Arquivos brasileiros de cardiologia, 2023).
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Representative model, for educational purposes only.