Antithrombotic therapy in the secondary prevention of myocardial infarction.

There is now convincing evidence that the majority of myocardial infarcts are caused by acute occlusion of the coronary artery with a thrombus, often originating from a ruptured atherosclerotic plaque. The thrombus is composed of both platelets and fibrin, so it is logical to expect that both antiplatelet and anticoagulant therapy would be effective for the prevention of reinfarction and other thrombotic vascular events following myocardial infarction. A review of clinical trials confirms this suggestion. Aspirin is beneficial in that it reduces vascular mortality by about 12% and total vascular events by 25%. Similarly, oral anticoagulants reduce total mortality by up to 20% and vascular events by about 40%. However, relatively few large scale trials of oral anticoagulants after infarction have been carried out, and the confidence intervals are wider than those for the aspirin trials. In practice aspirin is used more widely than oral anticoagulants as it is easier to administer and control. Only one trial (EPSIM) has directly compared oral anticoagulants and aspirin. This trial showed that both drugs had equal efficacy but that compliance with aspirin was better. Finally, the question of giving antiplatelet agents and anticoagulants together, to block both platelet aggregation and fibrin formation, is considered. A preliminary trial in prosthetic heart-valve patients has been encouraging but more large, long-term trials are required before recommendations can be made, as the use of both drugs together carries an increased risk of severe hemorrhage.