Appropriate Assessment of the Functional Consequences of Platelet Cyclooxygenase-1 Inhibition by Aspirin in vivo

Abstract

Chronic use of low dose aspirin (acetylsalicylic acid) is generally an effective and relatively low cost strategy for preventing and treating cardiovascular disease [1]. John Vane reported the inhibition of prostaglandin synthesis as a mechanism of action of aspirin-like drugs in 1971 by demonstrating a dose-dependent inhibition of prostaglandin synthesis by aspirin, sodium salicylate and indomethacin [2]. Thromboxane A2 (TxA2) was subsequently identified by Samuelsson’s group as the potent vasoconstrictor and platelet agonist the synthesis of which was inhibited by aspirin [3].