Endothelial function and clinical outcome.

U nder pro-atherosclerotic conditions, endothelial cells lose the ability to produce bioactive nitric oxide and demonstrate increased expression of vasoconstrictor, pro-inflammatory, and pro-thrombotic factors. The available evidence suggests that these alterations in endothelial phenotype contribute to the formation, progression, and rupture of atherosclerotic lesions. There currently is great interest in understanding the mechanisms and clinical relevance of these changes in endothelial cell biology, because they could lead to new approaches for the management of patients with atherosclerosis. While it is clear that the endothelium regulates many aspects of vascular homeostasis, current approaches to evaluate local ‘‘endothelial function’’ in humans have been limited to assessment of endothelium dependent vasodilation. In addition, investigators have the ability to measure blood concentrations of various endothelium derived thrombotic and inflammatory factors and, most recently, numbers of endothelial progenitor cells.