Abstract

Erectile dysfunction (ED) and endothelial dysfunction are common in individuals with multiple cardiovascular risk factors (CRFs) and are longitudinal predictors of cardiovascular events. ED is associated with systemic endothelial cell activation/dysfunction independent from CRFs or from diffuse, unrecognized vascular damage. The pathogenesis of endothelial dysfunction and ED is intimately linked through increased expression and activation of endothelial nitric oxide (NO) synthase and the subsequent physiologic actions of NO. Reduced biologic activity of endothelium-derived NO links human atherosclerosis to ED and underscores the role of altered endothelium in the pathogenesis of both conditions. ED may be the only clinical marker of systemic endothelial damage that is associated with a documented future risk of acute cardiovascular events. Searching for ED might be relevant in men with CRFs and no other clinical atherosclerosis in order to identify patients who could benefit from phosphodiesterase type 5 inhibitors to reduce their cardiovascular risk while treating ED.

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