Key result
Anti-platelet therapies, including cyclooxygenase, phosphodiesterase, P2Y12, and glycoprotein IIb/IIIa inhibitors, reduce cardiovascular adverse events but may increase bleeding risk.
This review outlines the mechanisms, clinical uses, and bleeding risks of current and emerging anti-platelet therapies for cardiovascular disease.
Balances CV benefits against bleeding in selection; leaves open optimization of emerging agents.
A variety of orally and intravenously administered agents have been made available for anti-platelet therapy. Clinical trials in patients with acute manifestations of cardiovascular disease have shown that the combined administration of substances which inhibit different steps of platelet adhesion and aggregation reduce cardiovascular adverse events. However, the risk of bleeding may increase depending on the patient’s comorbidity, age and the agents that are used for concomitant anticoagulation. Therefore, ongoing efforts are made to develop highly effective inhibitors of platelet function with an excellent controllability and the lowest acceptable risk of bleeding events. The current pharmacological strategies for the inhibition of platelet function are i) the inhibition of the cyclooxygenase, ii) inhibition of the phosphodiesterase, iii) blockade of the platelet P2Y12 ADP receptor, and iv) blockade of the platelet glycoprotein IIb/IIIa. In the following review, the mechanisms of action and the clinical use of approved anti-platelet agents will be described. Furthermore, substances for the future that are under development are discussed.
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Ahrens et al. (2007) conducted a review in Cardiovascular disease. Anti-platelet therapy was evaluated. Anti-platelet therapies, including cyclooxygenase, phosphodiesterase, P2Y12, and glycoprotein IIb/IIIa inhibitors, reduce cardiovascular adverse events but may increase bleeding risk.
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