The case of low-dose aspirin for the prevention of myocardial infarction: but how low is low?
Although there is firm consensus that aspirin reduces the incidences (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 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.
Förster
W
W
Department of Physiology and Pharmacology, University of Strathclyde, Glasgow, Scotland.
Parratt
J R
JR
D001241:Aspirin / Q000627:therapeutic use*; D003327:Coronary Disease / Q000517:prevention & control; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use*; D004305:Dose-Response Relationship, Drug; D011464:Epoprostenol / Q000096:biosynthesis*; D006801:Humans; D009203:Myocardial Infarction / Q000517:prevention & control*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D013931:Thromboxanes / Q000096:biosynthesis*
D016861:Cyclooxygenase Inhibitors; D010975:Platelet Aggregation Inhibitors; D013931:Thromboxanes; D011464:Epoprostenol; D001241:Aspirin