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(Stroke. 1996;27:585-587.)
© 1996 American Heart Association, Inc.

Articles

Aspirin Wars

The Optimal Dose of Aspirin to Prevent Stroke

Robert G. Hart, MD Michael J.G. Harrison, MD

From the Department of Medicine (Neurology), University of Texas Health Science Center, San Antonio, Texas (R.G.H.), and the Reta Lila Weston Institute of Neurological Studies, University College London Medical School, London, England (M.J.G.H.).

Correspondence to Robert G. Hart, MD, Department of Medicine (Neurology), University of Texas Health Science Center, 7703 Floyd Curl Dr, San Antonio, TX 78284-7883.

Key Words: aspirin • platelet aggregation • stroke prevention

	Introduction

 
In 1899, Farbenfabriken Bayer introduced acetylsalicylic acid (brand name, aspirin) for the treatment of fever and rheumatism, assuring consumers that it had no effect on the heart.¹ At that time, the more commercially promising product of this respected pharmaceutical firm was the recently synthesized heroin, successfully marketed as a cough suppressant and for colic of infants.¹ Times have changed.

Interestingly, the clinical antithrombotic effects of aspirin were not widely recognized until the 1970s.² Aspirin reduces the risk of myocardial infarct, ischemic stroke, and vascular death for many patients.³ In this issue of Stroke, Patrono and Roth⁴ argue persuasively that the optimal dose of aspirin to prevent stroke is the same as that to prevent myocardial infarction and need not exceed 75 mg/d. Their conclusion is based on careful scrutiny of existing clinical data and on the maximal inhibition of platelet thromboxane synthesis by low doses of aspirin,⁵ the presumed major mediator of the clinical antithrombotic effect of aspirin.

The strongest clinical support for their contention comes from two randomized trials that directly compared different doses of aspirin in patients with transient ischemic attack (TIA) or minor ischemic stroke.^{6 7} These well-executed trials showed that an aspirin dose of 283 mg/d is unlikely to be more than 5% better than 30 mg/d⁷ and that 1200 mg/d is unlikely to be more than 25% better than 300 mg/d⁶ for stroke prevention, with small nonsignificant trends favoring the lower doses. Some have argued that recruits to these trials were not typical of patients . . . [Full Text of this Article]

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