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This editorial summarizes the mechanisms of platelet aggregation and various antiplatelet approaches, including aspirin, to reduce thrombo-embolic events.
This editorial summarizes the mechanisms of platelet aggregation and various approaches to reducing it.
Platelet aggregation is fundamental to arterial thrombus formation, and antiplatelet agents, i.e., agents that act to reduce platelet aggregation, are of value in improving survival in those at risk of thrombo-embolic events [1]. The antiplatelet agent that is most commonly used as antithrombotic therapy is aspirin, which inhibits the cyclo-oxygenase enzyme and, thereby, inhibits thromboxane synthesis. However, there are many other approaches to interfering with platelet aggregation. What follows is a summary of the mechanisms involved in platelet aggregation and of the numerous approaches to reducing platelet aggregation that have been identified.
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Stan Heptinstall (1995) conducted an editorial in Risk of thrombo-embolic events. Antiplatelet agents was evaluated. This editorial summarizes the mechanisms of platelet aggregation and various antiplatelet approaches, including aspirin, to reduce thrombo-embolic events.
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