Abstract
To the Editor: The concept of antithrombotic treatment with low-dose aspirin has attracted much interest1 since claims that the cyclooxygenase in platelets is more sensitive than vascular cyclooxygenase to the actions of aspirin.2 However, there is still doubt regarding the optimal aspirin dose. Examination of human venous tissue has shown that even a single dose of aspirin (50 mg) inhibits vascular prostacyclin formation.3 , 4 A daily 20-mg dose of aspirin inhibits human serum thromboxane formation but without altering prostacyclin generation, as measured by urinary excretion of its metabolite5 2,3-dinor-6-oxo-prostaglandin f. A recent prospective double-blind trial in 83 patients undergoing . . .