Abstract
Platelets play an important role in both normal hemostasis and pathological thrombus formation. The key role of platelets in thrombosis is highlighted by the clinical benefit of treatment with antiplatelet drugs. Aspirin, either alone or in combination with clopidogrel in high-risk patients, is the most widely used antiplatelet agent. However, there is an individual response to these agents that may reduce the cardiovascular protection in patients who achieve a lower antiplatelet effect. Recently, P2Y12 receptor antagonists more potent than clopidogrel (e.g., prasugrel and ticagrelor) have been approved for patients with acute coronary syndromes and those undergoing percutaneous coronary interventions; these drugs provide greater platelet inhibition than clopidogrel. However, the increased effectiveness of these treatments has underscored the importance of carefully balancing the risks of ischemia and bleeding to achieve the best clinical outcomes. The increased knowledge of the molecular mechanisms of platelet activation has prompted a search for novel pharmacological targets for the inhibition of platelet reactivity. This article reviews the molecular mechanisms of action and limitations of use of current and emerging antiplatelet agents for treatment of cardiovascular disease.
Keywords: Aspirin resistance, clopidogrel, GPIIbIIIa antagonists, PAR-1 antagonists, phosphodiesterase inhibitors, prasugrel, thromboxane receptor antagonists, ticagrelor.
Current Vascular Pharmacology
Title:Pharmacological Inhibition of Platelet Reactivity. Clinical and Pharmacodynamic Effects
Volume: 11 Issue: 4
Author(s): Juana Valles, Antonio Moscardo, Isabel Madrid and Maria Teresa Santos
Affiliation:
Keywords: Aspirin resistance, clopidogrel, GPIIbIIIa antagonists, PAR-1 antagonists, phosphodiesterase inhibitors, prasugrel, thromboxane receptor antagonists, ticagrelor.
Abstract: Platelets play an important role in both normal hemostasis and pathological thrombus formation. The key role of platelets in thrombosis is highlighted by the clinical benefit of treatment with antiplatelet drugs. Aspirin, either alone or in combination with clopidogrel in high-risk patients, is the most widely used antiplatelet agent. However, there is an individual response to these agents that may reduce the cardiovascular protection in patients who achieve a lower antiplatelet effect. Recently, P2Y12 receptor antagonists more potent than clopidogrel (e.g., prasugrel and ticagrelor) have been approved for patients with acute coronary syndromes and those undergoing percutaneous coronary interventions; these drugs provide greater platelet inhibition than clopidogrel. However, the increased effectiveness of these treatments has underscored the importance of carefully balancing the risks of ischemia and bleeding to achieve the best clinical outcomes. The increased knowledge of the molecular mechanisms of platelet activation has prompted a search for novel pharmacological targets for the inhibition of platelet reactivity. This article reviews the molecular mechanisms of action and limitations of use of current and emerging antiplatelet agents for treatment of cardiovascular disease.
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Cite this article as:
Valles Juana, Moscardo Antonio, Madrid Isabel and Santos Teresa Maria, Pharmacological Inhibition of Platelet Reactivity. Clinical and Pharmacodynamic Effects, Current Vascular Pharmacology 2013; 11 (4) . https://dx.doi.org/10.2174/1570161111311040007
DOI https://dx.doi.org/10.2174/1570161111311040007 |
Print ISSN 1570-1611 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6212 |
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