Antithrombotic Therapy and First Myocardial Infarction in Patients With Atrial Fibrillation.
A conventional tenet of antithrombotic therapy for cardiovascular disease is the use of anticoagulant drugs to prevent formation of fibrin due to activation of the coagulation system in states of hemodynamic stasis, such as occurs in patients with atrial fibrillation (AF). Another is to use antiplatelet drugs to prevent atherothrombotic events, such as myocardial infarction (MI) due to plaque rupture in patients with coronary artery disease. In each situation, the intensity of therapy should be modified in proportion to the risk of thrombotic events. In general, risk is lowest for primary prevention, highest in the early period after an event, and intermediate for long-term secondary prevention during the stable phase of established disease. The use of aspirin for primary prevention of MI and stroke in the general population has been controversial (1), with its role for prevention of coronary events in patients with concomitant AF even more uncertain. Aspirin is also a standard component of therapy for patients with established ischemic heart disease (2). The efficacy of vitamin K antagonists (VKAs) for secondary prevention after MI has also been known for decades (3,4). The combination of VKA plus aspirin has not resulted in lower rates of mortality, reinfarction, or stroke than has been achieved with aspirin alone and increases the risk of bleeding (5,6). Relatively few studies have compared the efficacy of VKA versus antiplatelet therapy for primary prevention of atherothrombotic events. TPT (Thrombosis Prevention Trial) found that low-intensity VKA