[Acetylsalicylic acid in unstable angina, after coronary revascularization and in prevention of cardiac thromboembolism]

Abstract

Acetylsalicylic acid (ASA) inhibits platelet function via cyclooxygenase inhibition. The selective inhibition of platelet cyclooxygenase is possible with the use of low doses of ASA due to presystemic acetylation of the platelet enzyme in the portal circulation. The clinical efficacy of ASA has been demonstrated for a number of indications. ASA reduces the rate of myocardial infarctions and cardiovascular deaths in patients with unstable angina. Simultaneous intravenous infusion of heparin has an additional positive effect. The prevention of acute coronary thromboses during PTCA and of early bypass graft occlusion has been convincingly demonstrated, if therapy is initiated immediately after surgery. Neither ASA nor any other drug has been effective in the prevention of late restenosis following PTCA and of late bypass graft occlusions. Thromboembolic complication after implantation of biological valve prostheses is significantly reduced by ASA, if no rheumatic valve disease is present. The rate of peripheral or cerebral thromboembolic events is markedly increased in patients with lone atrial fibrillation. In contrast to the very positive results obtained for anticoagulants, the reports with ASA were contradictory. ASA may be effective in preventing thromboembolic complications in younger patients with a lower risk or in elderly patients with contraindications for anticoagulation. For most clinical indications the efficacy of ASA has been demonstrated for doses of 75-324 mg/d. Following a loading dose of 300 mg on the first day, continuation of therapy with 100 mg/d should combine maximal therapeutic efficacy with a low rate of unwanted drug effects.