Abstract
Platelets are known to play a fundamental role in acute coronary syndromes. After atherosclerotic plaque rupture, platelets can form pathogenic, occlusive thrombi leading to acute ischemic events. Today there are promising results from recently developed antiplatelet agents. However, morbidity and mortality from acute coronary syndromes remain significant despite the administration of combination therapies (aspirin, thienopyridines). Sharing similar mechanisms, platelets may also form a thin monolayer in areas of damaged endothelium contributing to primary hemostasis. For this reason, administration of antiplatelet drugs is often associated with increased bleeding risk. As a result, currently available antiplatelet therapy cannot be characterized as optimal. The precise mechanisms of platelet activation in acute coronary syndromes are still under investigation. The study of basic mechanisms of platelet adhesion, activation and aggregation after atherosclerotic plaque rupture may help to define new targets for their inhibition. In the future, newer antiplatelet agents may offer more comprehensive platelet inhibition without interfering with primary hemostasis, thus offering greater protection with lower hemorrhagic risk.
Keywords: Activation, acute coronary syndromes, adhesion, aggregation, antiplatelet agents, platelet, receptors, thrombosis, aspirin, thienopyridines
Current Vascular Pharmacology
Title:Mechanisms of Platelet Activation in Acute Coronary Syndromes
Volume: 10 Issue: 5
Author(s): Dimitrios A. Stakos, Dimitrios N. Tziakas and Konstantinos Stellos
Affiliation:
Keywords: Activation, acute coronary syndromes, adhesion, aggregation, antiplatelet agents, platelet, receptors, thrombosis, aspirin, thienopyridines
Abstract: Platelets are known to play a fundamental role in acute coronary syndromes. After atherosclerotic plaque rupture, platelets can form pathogenic, occlusive thrombi leading to acute ischemic events. Today there are promising results from recently developed antiplatelet agents. However, morbidity and mortality from acute coronary syndromes remain significant despite the administration of combination therapies (aspirin, thienopyridines). Sharing similar mechanisms, platelets may also form a thin monolayer in areas of damaged endothelium contributing to primary hemostasis. For this reason, administration of antiplatelet drugs is often associated with increased bleeding risk. As a result, currently available antiplatelet therapy cannot be characterized as optimal. The precise mechanisms of platelet activation in acute coronary syndromes are still under investigation. The study of basic mechanisms of platelet adhesion, activation and aggregation after atherosclerotic plaque rupture may help to define new targets for their inhibition. In the future, newer antiplatelet agents may offer more comprehensive platelet inhibition without interfering with primary hemostasis, thus offering greater protection with lower hemorrhagic risk.
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Cite this article as:
A. Stakos Dimitrios, N. Tziakas Dimitrios and Stellos Konstantinos, Mechanisms of Platelet Activation in Acute Coronary Syndromes, Current Vascular Pharmacology 2012; 10 (5) . https://dx.doi.org/10.2174/157016112801784477
DOI https://dx.doi.org/10.2174/157016112801784477 |
Print ISSN 1570-1611 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6212 |
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