The past 10 years have witnessed major changes in our understanding of the pathophysiologic mechanisms underlying vascular occlusion1,2 and considerable progress in the clinical assessment of aspirin and other antiplatelet agents3–5. The purpose of this review is to describe a rational basis for antithrombotic prophylaxis and treatment with aspirin. Basic information on the molecular mechanism of action of aspirin in inhibiting platelet function will be integrated with the appropriate clinical pharmacologic data and the results of randomized clinical trials. Mechanism of Action Aspirin induces a long-lasting functional defect in platelets, clinically detectable as a prolongation of the . . .