Video narration
How does a slowly narrowing coronary artery suddenly become a heart attack? Normally, coronary arteries deliver oxygen-rich blood to the myocardium. Over time, atherosclerosis develops: lipids accumulate within the arterial wall, inflammation follows, and a plaque gradually narrows the lumen. This chronic stenosis can limit reserve, but narrowing alone is not yet myocardial infarction. The mechanism flips when a vulnerable fibrous cap ruptures. Thrombogenic material is exposed. Platelets adhere, activate, and aggregate, forming a platelet thrombus that rapidly enlarges at the rupture site. Flow now falls critically-or stops. Downstream myocardium becomes ischemic. Early ischemia is reversible, but if severe reduction in coronary perfusion persists, cardiomyocytes sustain irreversible injury and die: necrosis. So how does plaque become a heart attack? Rupture converts chronic atherosclerotic narrowing into acute thrombosis, abruptly cutting oxygen delivery. Prolonged ischemia then produces irreversible myocardial cell death-myocardial infarction.