In the last two decades, improved treatment of elec-trical disturbances and cardiac pump failure have reduced mortality after the ultimate, irreversible myocardial event of patients suffering from coronary heart disease: myocardial infarction. However, the major challenge in this field, primary prevention of myocardial ischemia, remains unconquered. The traditional belief that myocardial infarction is due to coronary thrombosis might be challenged by the marginal benefit that anticoagulant, antiplatelet, and fibrinolytic agents have provided. However, the classic view linking the pathogenesis of myocardial infarction to thrombotic disorders1 is substantiated by recent findings based on objective arteriographic observations. 2 Moreover, there is increasing evidence that coronary thrombosis also plays a pathogenetic role in sudden deaths in patients suffering from ischemic heart disease without myocardial infarction. 3 In light of these considerations, the discrepancy between the formidable effort to reduce morbidity and mortality from myocardial infarction by various antithrombotic strategies and the results achieved is disappointing. But it is not surprising, perhaps, since thrombosis is multifactorial in origin, with a host of pathologic features and many complicated natural regulatory mechanisms. Considering the complexity of the problem, the progress to date must be regarded as promising, even if far from satisfying.