The coronary arteries are diffusely involved by atherosclerotic plaques in fatal acute myocardial infarction (AMI). The degree of luminal narrowing may vary but plaques are present in practically every millimeter of extramural coronary artery. Usually the lumens of at least two of the three major coronary arteries are narrowed > 75% by old plaques in patients who die suddenly (< 6 hours) from cardiac disease with or without myocardial necrosis. Coronary thrombi occur in about 10% of patients who die suddenly or in whom necrosis is limited to the left ventricular subendocardium, and in about 50% of patients with transmural myocardial necrosis. Coronary thrombi usually indicate the presence of shock or congestive heart failure or both during the development of myocardial necrosis. The infrequency of coronary thrombi in patients dying suddenly of cardiac disease and in those with transmural necrosis who never have shock or congestive heart failure suggests that the thrombi may be consequences rather than causes of AMI.Although it may not precipitate AMI, coronary thrombosis may still be the underlying cause of the atherosclerosis. The finding of fibrin deposits in old atherosclerotic plaques and the findings of atherosclerotic-type lesions (cholesterol clefts, foam cells, pultaceous debris, calcific deposits) in organized known thrombi (as in the left atrium in mitral stenosis) suggest a strong relationship between thrombosis and atherosclerosis.Coronary arterial emboli are not rare; they are located in distal portions of the coronary tree and are present in the small epicardial branches as well as in intramural coronary arteries. In contrast, coronary thrombi are located in proximal portions of major extramural vessels, are infrequent in the small epicardial branches, and are absent in intramural coronary arteries. Coronary atherosclerosis is limited to the extramural coronary arteries and spares the intramural coronary arteries.