[Action mechanism and clinical indications for thrombocyte aggregation inhibitors]

The mechanisms of action of three most commonly used antiplatelet agents (aspirin, sulfinpyrazone, dipyridamole) are briefly discussed. Aspirin inhibits the prostaglandin synthetase of platelets irreversibly and thereby blocks the production of prostaglandin endoperoxides and thromboxane A2, which stimulate platelet aggregation. A daily aspirin dose of 200--300 mg is sufficient to achieve this effect. Sulfinpyrazone appears to interfere with the adhesion of platelets to subendothelial structures and atherosclerotic plaques. Dipyridamole increases cyclic AMP in platelets and thus reduces platelet response to aggregating agents. A few of the satisfactorily performed studies on the clinical effectiveness of antiplatelet agents are mentioned. Sulfinpyrazone treatment of patients with myocardial infarction (Killip--classification I and II), starting 25--35 days after the acute myocardial infarction, reduces cardiac mortality and incidence of sudden death for a period of two years. The efficacy of aspirin treatment in coronary artery disease is not yet definitely established. In patients with transient ischemic attacks, particularly males with appropriate carotid lesions, aspirin therapy reduces the frequency of transient ischemic attacks and possibly the incidence of stroke and death. Sulfinpyrazone is ineffective in these patients. Sulfinpyrazone and aspirin are of value in the prevention of thrombosis in straight arterio-venous shunts. Aspirin reduces the frequency of deep venous thrombosis after total hip replacement in males but not in females. In patients with recurrent venous thrombosis, sulfinpyrazone treatment is effective in preventing thrombosis.