The frequency and significance of coronary arterial thrombi and other observations in fatal acute myocardial infarction: A study of 107 necropsy patients

Abstract

Observations made from histologie study of the entire extramural coronary arterial tree are described in 107 patients who died of acute ischemie heart disease: seventy-four had transmural left ventricular myocardial infarction, nine had necrosis limited to the inner one half of the left ventricular myocardium (acute subendocardial infarcts) and twenty-four died suddenly (less than six hours from onset of symptoms of myocardial ischemia) without histologically detectable myocardial necrosis. Old atherosclerotic plaquing was diffuse and extensive in the extramural coronary arteries in 104 of the 107 patients. The lumens of at least two of the three major extramural coronary arteries (right, left anterior descending and left circumflex) were narrowed more than 75 per cent by old atherosclerotic plaques in 101 of the 107 patients.Coronary arterial thrombi were found in forty (54 per cent) of the seventy-four patients with transmural necrosis, in none of the nine with only subendocardial necrosis and in two (8 per cent) of the twenty-four who died suddenly. In thirty-seven of the forty-two patients with antemortem coronary arterial clots the lumen of the vessel containing the thrombus was already narrowed more than 75 per cent by old atherosclerotic plaques at or distal to the thrombus. The infrequency of coronary thrombi in patients who died of acute cardiovascular collapse without myocardial necrosis, in those in whom necrosis was limited to the subendocardium, in those who died without cardiogenic shock or congestive cardiac failure, and their occurrence at, or proximal to, sites already severely narrowed by old atherosclerotic plaques suggest that coronary thrombi are consequences rather than causes of acute myocardial infarction. The occurrence of components of thrombi, i.e., fibrin and platelets, in old atherosclerotic plaques and the finding of components of old atherosclerotic plaques, i.e., foam cells, cholesterol clefts, pultaceous debris and calcific deposits, in known thrombi (for example, those located in the left atrium of patients with mitral stenosis) strongly suggest, however, that old atherosclerotic plaques are derived, at least in part, from organization of thrombi.