Pathophysiology of acute myocardial infarction

88 Pathology and therapeuticsInfarctionis tissue death caused by ischaemia. acute myo-cardial infarction (MI) occurs when localized myocardialischaemia causes the development of a defined region of nec-rosis. MI is most often caused by rupture of an atheroscleroticlesion in a coronary artery. This causes the formation of a throm-bus that plugs the artery, stopping it from supplying blood to theregion of the heart that it of thrombosis in MIPivotal studies by DeWood and colleagues showed that coron-ary thrombosisis the critical event resulting in MI. Of patientspresenting within 4 h of symptom onset with ECG evidence of transmural MI, coronary angiography showed that 87% hadcomplete thrombotic occlusion of the infarct-related artery. Theincidence of total occlusion fell to 65% 12 24 h after symptomonset due to spontaneous fibrinolysis. Fresh thrombi on top of ruptured plaques have also been demonstrated in the infarct-related arteries in patients dying of and consequences of plaque ruptureCoronary plaques which are prone to rupture are typically smalland nonobstructive, with a large lipid-rich core covered by a thinfibrous cap.

Pathophysiology of acute myocardial infarction 89 Plaque rupture reveals subendothelial collagen, which serves as a site of platelet adhesion, activation and aggregation.

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  Myocardial, Infractions, Myocardial infarction

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