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Pathophysiology of Acute Myocardial Infarction, 1981

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▸Requests for reprints should be addressed to Philip B. Oliva, M.D.; Cardiology Division, Proctor Hospital, 5409 North Knoxville Avenue; Peoria, IL 61614.

Peoria, Illinois

© 1981 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1981;94(2):236-250. doi:10.7326/0003-4819-94-2-236
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Recent observations and discoveries necessitate reassessing the pathophysiology of acute myocardial infarction. Platelet aggregability has been shown to be increased in patients with an acute myocardial infarction, and coronary arterial spasm has been documented by arteriography done just before and during the onset of infarction. These clinical observations have been complemented by the recent discovery of two potent substances; thromboxane A2 and prostacyclin, which affect platelet aggregability and coronary arterial tone. These recent observations and discoveries are blended with older pathologic information to attain a more comprehensive understanding of the pathophysiology of acute myocardial infarction. A dynamic interaction among damaged intima, platelet aggregates, and spasm is postulated to occur as a prelude to thrombosis in acute transmural myocardial infarction. Spasm appears to initiate the infarction process in some instances, but the exact sequence of events has not been established.





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