Abstract
The vascular endothelium comprises a continuous single cell layer of endothelial cells which line the entire cardiovascular system. Impaired endothelial function underlies the pathogenesis and contributes to the progression of atherosclerosis. Oxidative stress, vasoconstriction, inflammation, proliferation and thrombosis occur in dysfunctional endothelium while the latter, is primarily mediated by platelet activation and adherence to vascular wall. Despite the primary action of antiplatelet agents including aspirin, P2Y12 ADP receptor antagonists and glycoprotein IIb/IIIa inhibitors, a growing body of literature suggests that an important mechanism of their action involves complex modulation of endothelial function via platelet-endothelial interactions, modification of the inflammatory cytokine cascade and nitric oxide mediated effects. These agents represent the mainstay in pharmacological treatment of all aspects of cardiovascular disease both in primary and secondary prevention. However beyond these properties, it is important to note that pharmacological modification of endothelial dysfunction has been postulated as a therapeutic target for reduction of cardiovascular events.
Keywords: Endothelial function, antiplatelets, cardiovascular disease, oxidative stress, inflammation.
Current Pharmaceutical Design
Title:The Impact of Antiplatelet Treatment on Endothelial Function
Volume: 22 Issue: 29
Author(s): Emmanuel Androulakis, Karl Norrington, Constantinos Bakogiannis, Eirini Lioudaki, Gerasimos Siasos and Dimitris Tousoulis
Affiliation:
Keywords: Endothelial function, antiplatelets, cardiovascular disease, oxidative stress, inflammation.
Abstract: The vascular endothelium comprises a continuous single cell layer of endothelial cells which line the entire cardiovascular system. Impaired endothelial function underlies the pathogenesis and contributes to the progression of atherosclerosis. Oxidative stress, vasoconstriction, inflammation, proliferation and thrombosis occur in dysfunctional endothelium while the latter, is primarily mediated by platelet activation and adherence to vascular wall. Despite the primary action of antiplatelet agents including aspirin, P2Y12 ADP receptor antagonists and glycoprotein IIb/IIIa inhibitors, a growing body of literature suggests that an important mechanism of their action involves complex modulation of endothelial function via platelet-endothelial interactions, modification of the inflammatory cytokine cascade and nitric oxide mediated effects. These agents represent the mainstay in pharmacological treatment of all aspects of cardiovascular disease both in primary and secondary prevention. However beyond these properties, it is important to note that pharmacological modification of endothelial dysfunction has been postulated as a therapeutic target for reduction of cardiovascular events.
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Cite this article as:
Androulakis Emmanuel, Norrington Karl, Bakogiannis Constantinos, Lioudaki Eirini, Siasos Gerasimos and Tousoulis Dimitris, The Impact of Antiplatelet Treatment on Endothelial Function, Current Pharmaceutical Design 2016; 22 (29) . https://dx.doi.org/10.2174/1381612822666160603020003
DOI https://dx.doi.org/10.2174/1381612822666160603020003 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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