Abstract
Over fifty years ago J. B. Herrick (1, 2) published the papers which eventually became the basis for the classic pathogenetic theory of myocardial infarction. In brief that theory states that myocardial infarction is produced by the sudden occlusion of a coronary artery with subsequent acute ischemia and necrosis of the area supplied by the occluded bessel. Generally thrombosis in a coronary artery was thought to be responsible for the occlusion. Subsequently, anticoagulants were extensively used in order to prevent the thrombosis. | In recent years, however, evidence has begun to accumulate that perhaps the above represents an incomplete explanation of the problem of human myocardial infarction. It is universally acknowledged that coronary atherosclerosis almost invariably accompanies myocardial infarction (3, 4). However, doubts have been raised that an arterial thrombosis is ultimately responsible for the necrosis. Quite often the thrombosis is associated with such an advanced state of atherosclerosis (5) that "the observer frequently cannot help wondering what difference the minimal added insult might have made" (6).