Anticoagulation in myocardial infarction: modern approach to an old problem

The role of routine anticogulation in acute myocardial infarction continues to be a source of controversy. There is currently strong evidence to suggest that conventional anticoagulation will prevent the formation of most deep vein thrombi and subsequent pulmonary embolization. Anticoagulant agents also appear to reduce the incidence of emboli from cardiac mural thrombi to peripheral arteries. Patients without a predisposition to bleeding are unlikely to have hemorrhagic complications in the hospital after usual doses of anticoagulant drugs. In patients with severe hypertension, prior gastrointestinal bleeding, carcinoma or advanced age, small dose heparin therapy appears to reduce the incidence of venous thrombosis and probably of pulmonary emboli as well. Its value in preventing peripheral arterial embolization has not been defined. Anticoagulation with standard "large" doses is an effective means of preventing the risks of pulmonary and peripheral emboli during the in-patient phase of acute myocardial infarction. Small dose heparin therapy provides an excellent alternative to conventional anticoagulation when there is more than a negligible risk of hemorrhage. There is little evidence at this time to support the use of long-term anticoagulation beyond the acute phase of myocardial infarction.