The use of aspirin inhibits COX-1 and hence the production of TXA2. This would prevent the aggregation of platelets. However, inhibition of COX-1 should also inhibit the production of PGI2 which is an antithrombotic prostanoid. How is the overall effect of aspirin leaned towards antithrombotic if it also has prothrombotic effects (inhibits PGI2)? Many thanks in advance!

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