Abstract
Acute myocardial infarction is caused by coronary thrombosis on an ulcerated atheroma. We now believe that the predominant cause of this intimal disruption is the rupture of the atheroma through the intimal surface, caused by enzymes released by activated macrophages. The subsequent clinical course following atheroma disruption is determined by the rate and size of thrombus formation. Partially occlusive thrombi produce unstable angina; completely occlusive thrombi produce myocardial infarction; clot embolization can produce sudden death. The localized thrombus lyses within days. The healing process, however, is frequently accompanied by rapid local progression of the size of the atheroma at the site of intimal disruption. With healing of the intimal surface, the patient's clinical status stabilizes. Thus coronary disease is a cyclical phenomenon driven by cellular events within the atheroma and by the interaction of the atheroma with circulating blood elements.
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