WITHIN a decade of the isolation of salicylate in 1892, aspirin was introduced as an analgesic and antipyretic agent. In 1971, Vane described its inhibition of prostaglandin synthesis from arachidonate in homogenates of guinea pig lung,1 and Smith and Willis demonstrated that aspirin blocks the production of prostaglandin in human platelets.2 During the past decade, it has been shown that platelet aggregation and the formation of thrombi are pathophysiologically important in syndromes of ischemic heart disease. As a result, aspirin is widely used in patients with ischemic heart disease, and its use has recently been advocated in subjects without clinically . . .
Desforges et al. (Thu,) studied this question.