THE CONCEPT of inadequate coronary blood flow resulting from chronic atherosclerotic narrowing of the coronary arteries as a cause of myocardial infarction without acute occlusion has become rather generally recognized.1 Among the first pathologic observations of acute myocardial infarction without the presence of an acute coronary occlusion were the studies of Büchner.2 Blumgart, Schlesinger, and Zoll3 have stressed the fact that coronary thrombosis or occlusion does not always produce myocardial infarction and, conversely, that acute myocardial infarction may occur in the absence of acute coronary occlusion. They have demonstrated this particularly by the technic of studying the coronary arteries after injection of radiopaque compounds. Experimentally, both the severity and the duration of the hypoxia of the myocardium occurring with coronary insufficiency would seem to determine whether the changes will be transient and reversible or be characterized by necrosis of the myocardium.4
The primary purpose of this