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Editorial
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An editorial discussing the established efficacy of aspirin in secondary prevention of myocardial infarction and stroke, and introducing further analyses by the Antithrombotic Trialists' Collaboration.
Papers p 71 Education and debate p 103 The efficacy of aspirin in the secondary prevention of myocardial infarction and stroke is widely accepted. The evidence which supports this perception includes its identification as an inhibitor of cyclo-oxygenase and platelet aggregation; identification of the major product of platelet cyclo-oxygenase as thromboxane A2, a vasoconstrictor and platelet agonist; the discovery that aspirin irreversibly acetylates cyclo-oxygenase, permitting cumulative inhibition by low doses of thromboxane A2 formation in the presystemic circulation; the discovery that thromboxane A2 biosynthesis is increased during ischaemic episodes of unstable angina; and the demonstration in individual, controlled, prospective double blind trials that aspirin reduces both myocardial infarction and death in unstable angina by 50%, whether given at 75 mg, 324 mg, or 1300 mg/day. 1 2 Following these discoveries Collins, Peto, Baigent, and their colleagues in Oxford organised the Antithrombotic Trialists' Collaboration to share data and permit overview analyses of controlled trials of antiplatelet drugs. At the time of the initial reports, these trials mainly involved aspirin and confirmed its efficacy in syndromes of acute vascular occlusion such as unstable angina, while suggesting a net benefit in the secondary prevention of stroke.3–5 Today, Baigent and colleagues report further analyses (p 71),6 though a critic …
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Reilly et al. (2002) studied this question.
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