Pathogenesis of Acute Myocardial Infarction

Acute myocardial infarction had generally been considered to be the result of thrombotic occlusion of a major extramural coronary artery until postmortem observations of the infrequency of coronary thrombi began to accumulate in patients who died of extensive myocardial infarction. Roberts and Buja' found coronary artery thrombi in 40 (54%) of 74 patients with transmural necrosis, in none of 9 with only subendocardial necrosis, and in 2 (8%) of 24 who died suddenly. On the basis of their own data and of the literature, which reported the frequency of coronary thrombosis in fatal acute myocardial infarction as ranging from 21% to 91%, they claimed that coronary thrombi are consequences rather than causes of acute myocardial infarction. Similar conclusions were reached by other investigators.2-5 In a workshop on the role of coronary thrombosis in the pathogenesis of acute myocardial infarction, no unanimous conclusion was obtained as to whether the thrombus precedes infarction as a primary lesion or follows infarction as a secondary effect. The report of the workshop stated that although most evidence continues to affirm myocardial infarction to be caused by thrombotic occlusion of a coronary artery, the idea of coronary thrombosis as a secondary event after infarction is also provocative and deserves serious consideration.6 Most of our knowledge of the lesions associated with transmural infarction before 1980 was derived from autopsy studies. These studies were performed in patients who died days to weeks after the infarction or in patients who died suddenly (less than 6 hours after the onset of symptoms). It is generally accepted that postmortem studies on victims of sudden death often reveal multivessel coronary atherosclerosis but only rarely evidence of an acute coronary event or myocardial necrosis.78 However, an autopsy study in which the time interval between the onset of symptoms and death was less than 24 hours and was accurately ascertained