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.
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Published on: 30 June, 2013
Page: [431 - 447]