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.
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