Aspirin has its major effect on hemostasis and thrombosis by inhibiting the synthesis of thromboxane A2 by platelets. This is achieved through the irreversible acetylation of the enzyme, platelet cyclooxygenase. Aspirin also inhibits the synthesis of prostaglandin I2 by the vessel wall cells, but this requires a higher dose; and, compared to its effect on platelets, the inhibitory effect on PGI2 production is short-lived. There is suggestive evidence that aspirin is effective in reducing sudden death in patients who have suffered myocardial infarction and in reducing stroke and death in patients with transient cerebral ischemia. Aspirin, when combined with oral anticoagulants, is more effective than oral anticoagulants alone in preventing systemic embolism in patients with prosthetic heart valves; and, in very low doses, aspirin has been shown to diminish thrombus formation in arteriovenous shunts in patients undergoing chronic hemodialysis.
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