The case for low-dose aspirin for the prevention of myocardial infarction: But how low is low?

Although there is firm consensus that aspirin reduces the incidence (and severity) of reinfarction if given to patients after a myocardial infarction or in patients with unstable angina, there is disagreement about the optimum dose that should be used. We make the case that it could be considerably lower than the ''medium dose'' (75-320 mg daily) in current usage and put forward the view that a dose of 30 mg daily is sufficient. The arguments are based on the presystemic, exclusively pharmacokinetic inhibition of thromboxane synthesis in platelets by very low-dose aspirin and the importance of maintaining prostacyclin production by endothelial cells. Little attention has been paid in the past to the endogenous myocardial protection that results from prostacyclin generation. Such low doses have the additional advantage of not inducing gastrointestinal ulceration. We conclude that more extensive clinical trials with such ''low-dose'' aspirin preparations are warranted.