Acute myocardial infarction occurs any time that a coronary artery becomes essentially completely obstructed and the segment of myocardium served by that artery loses perfusion and begins to die.
Complete obstruction usually occurs in the setting of fixed obstructive coronary lesions that are the result of coronary atherosclerosis. However, the process of accumulating atherosclerotic plaque in the coronary arteries is slow and gradual. The acute nature of AMI is usually the result of a clot or thrombus forming in the immediate vicinity of an incomplete fixed obstructive lesion.
The cause of clot formation is typically rupture (a split) of an atherosclerotic plaque, which tears the overlying endothelium thereby exposing blood to the lipid-rich interior of the plaque. Many of the substances present in the
Electrocardiographic Hallmarks of STEMI 65
plaque interior stimulate both platelet aggregation and the coagulation cascade, resulting in thrombus formation.
Less than complete obstruction of the coronary arteries can produce ischemia (diminished perfusion) without actual death of tissue, and is the cause of the syndrome called angina.
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