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Aspirin acetylates the cyclooxygenase (COX)-1 enzyme, thereby preventing the conversion of arachidonate to thromboxane A2 (TxA2), a powerful platelet-aggregating agent. Based on this and other antithrombotic properties of aspirin (attenuation of fibrin cross-linking and augmentation of clot permeability and lysis), this agent has become a mainstay in the management of patients with atherothrombotic disorders. However, disturbing reports of aspirin resistance have weakened confidence in the effectiveness of this inexpensive and readily accessible drug. Patients are considered resistant to aspirin if ex vivo tests of platelet function show lack of inhibition, if production of TxA2 continues during aspirin therapy, or if thrombosis recurs. Yet…