Editorial: Why aspirin?

Abstract

The rationale for the use of aspirin as an agent for prevention of myocardial infarction depends on the hypothesis that platelet aggregation and release have a role in the pathogenesis of myocardial infarction and/or atherosclerosis. The role of prostaglandin synthesis in platelet physiology and the mechanism by which aspirin interferes with prostaglandin synthesis is presented. Aspirin probably induces a mild defect in platelet function which may increase the threshold for platelet aggregation and release in normal subjects. The very mild nature of the defect induced makes aspirin particularly attractive as an agent to be used as a preventive medicine (i.e., low toxicity). Since aspirin results in permanent inhibition of prostaglandin synthesis, therapy does not require continuous blood levels of the drug, thus making it the most desirable of the drugs which inhibit platelet function by interfering with prostaglandin synthesis. The fact that other prostaglandin synthesis inhibitors can block acetylation of cyclo-oxygenase by aspirin suggests that combinations of agents such as sulfinpyrazone or indomethacin with aspirin would not be expected to be more effective than aspirin alone and might decrease the effectiveness of aspirin by blocking acetylation of cyclo-oxygenase.