Aspirin and carbasalate calcium
Aspirin and its calcium salt carbasalate calcium inhibit cyclo-oxygenase, an enzyme essential for the conversion of arachidonic acid into thromboxane A2. Thromboxane A2 causes vasoconstriction and platelet activation. Aspirin therefore causes diminished platelet activation. Aspirin binds irreversibly to cyclo-oxygenase and since platelets do not synthesize proteins (enzymes) by themselves, the effect of aspirin lasts for the life of the platelet (7-10 days).
Aspirin is indicated for the secondary prevention of arterial thromboembolism (after a cerebral infarction, TIA, myocardial infarction, unstable angina). Adverse effects of aspirin are increased bleeding (especially gastro-intestinal).
Mr K (58 years old and 90 kg) has gone through a mild myocardial infarction. His medical history mentions frequent episodes of ulcerations in the stomach and diabetes. How would you prophylax for reinfarction?
What is NOT true about thromboxane A2 (TXA2):
Extra info: TXA2 increases the risk of thrombosis as it causes platelet aggregation and vasoconstriction. Thus, COX inhibitors like aspirin and NSAIDs will decrease the production of TXA2 and decrease the risk of thrombosis.