ABSTRACT
Located at the juncture between flowing blood and the vessel wall, the vascular endothelium participates in the maintenance of vascular health, and according to the current paradigm, loss of endothelial function is a central mediator of atherogenesis.1 In the normal state the endothelium produces a variety of factors that regulate vasomotor tone, inflammation, coagulation, and the composition of the vascular wall (Table 7.1). The term ‘endothelial dysfunction’ refers to the phenotypic transformation that endothelial cells undergo when exposed to an atherogenic environment.2 The dysfunctional endothelium promotes vasoconstriction, inflammation, thrombosis, and abnormal cellular proliferation; thus, it facilitates the development of atherosclerosis (Figure 7.1). Growing evidence connecting endothelial abnormalities to cardiovascular events has strengthened our appreciation of the clinical significance of this systemic pathophysiologic state.3
