The Biology of Thrombosis

For the past decade the concept of a primary role for platelets in the pathogenesis of thrombosis, especially arterial thrombosis, has been a domi­ nant force in research on thrombosis. Several large-scale studies were de­ signed to determine if agents that inhibit platelet aggregation affect clinical arterial ischemic disease. Some of the results were positive, but not as dramatic as might have been anticipated (1, 2). It is possible that agents with a more powerful inhibitory effect and that are directed at platelet adhesion rather than aggregation would have greater therapeutic efficiency. Mean­ while data have been accumulating to indicate that methods for controlling the coagulation system have not been optimally exploited. A prospective study on hemostatic function and cardiovascular death showed that men who subsequently died of cardiovascular causes showed at recruitment significantly higher plasma levels of factors VII and VIII as well as fibrino­ gen and cholesterol. There were no differences in platelet count or adhesive­ ness (3). A recent Dutch trial suggested that dicumarol might reduce mortality by considerably more than the 20% established by earlier trials (4). Several pilot studies of patients with acute myocardial infarction showed that acutely occluded coronary arteries can be recanalized by the intra-coronary injection of streptokinase. This technique has great potential