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