摘要: Under pro-atherosclerotic conditions, endothelial cells lose the ability to produce bioactive nitric oxide and demonstrate increased expression of vasoconstrictor, pro-inflammatory, pro-thrombotic factors. The available evidence suggests that these alterations in phenotype contribute formation, progression, rupture atherosclerotic lesions. There currently is great interest understanding mechanisms clinical relevance changes cell biology, because they could lead new approaches for management patients with atherosclerosis. While it clear endothelium regulates many aspects vascular homeostasis, current evaluate local “endothelial function” humans have been limited assessment dependent vasodilation. In addition, investigators measure blood concentrations various derived thrombotic inflammatory factors and, most recently, numbers progenitor cells. The dysfunction cardiovascular disease events strongly supported by studies human coronary circulation showing impaired vasodilation response acetylcholine or shear stress predicts outcome. For example, more severe impairment vasomotor intracoronary infusion identifies individuals risk acute syndromes, death, stroke.1–4 Impaired flow mediated dilation2 a constrictor cold pressor test2,5 also predict future events. These findings apply advanced artery disease2,3 angiographically normal nearly arteries.1,3,5 Although greatest relevance, interesting measures function peripheral arteries predictive value heart disease. …