In platelets, the major cyclooxygenase product is thromboxane A2, a labile inducer of platelet aggregation and a potent vasoconstrictor. Aspirin blocks production of thromboxane A2 by acety-lating a Ser residue near the active site of platelet cyclooxygenase (COX-1). Since platelets do not synthesize new proteins, the action of aspirin on platelet cyclooxygenase is permanent, lasting for the life of the platelet (7—10 days). Thus, repeated doses of aspirin produce a cumulative effect on platelet function. Complete inactivation of platelet COX-1 is achieved when 160 mg of aspirin is taken daily. Therefore, aspirin is maximally effective as an antithrombotic agent at doses much lower than those required for other actions of the drug. Numerous trials indicate that aspirin, used as an antithrombotic drug, is maximally effective at doses of50—320 mg/day. Higher doses do not improve efficacy and potentially are less efficacious because of inhibition of prostacyclin production, which can be largely spared by using lower doses of aspirin. Higher doses also increase tox-icity, especially bleeding.
Other nonsteroidal anti-inflammatory drugs (NSAIDs) that are reversible inhibitors of COX-1 have not been shown to have antithrombotic efficacy and in fact may even interfere with low-dose aspirin regimens.
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