Erectile dysfunction (ED) shares the same vascular risk factors (VRFs) with coronary arteries disease (CAD). A reduced biological activity of endothelium-derived nitric oxide links human atherosclerosis to ED and underscores the role of an altered endothelium in the pathogenesis of both conditions. ED is associated to a systemic endothelial cell activation/dysfunction independent from VRFs or from a diffuse vascular damage, indicating that ED is a marker of an early systemic endothelial damage, a relevant determinant of atherosclerosis. A diffuse vascular damage of carotid arteries indicative of pre-clinical atherosclerosis is significantly associated to an increased risk of severe ED in men with VRFs but without clinical atherosclerosis and ED was the most efficient predictor of angiographically verified silent CAD among different VRFs in uncomplicated type 2 diabetes. In conclusion, ED may be the only clinical correlate of a diffuse, unrecognized vascular damage that is associated to a documented future risk of acute vascular events. Searching ED might be of relevance in men with VRFs but no other clinical atherosclerosis to identify patients that should aggressively reduce their VRFs while treating ED.

Vascular Etiology of Erectile Dysfunction

FRANCAVILLA, Sandro;NECOZIONE, STEFANO;FRANCAVILLA, Felice
2005-01-01

Abstract

Erectile dysfunction (ED) shares the same vascular risk factors (VRFs) with coronary arteries disease (CAD). A reduced biological activity of endothelium-derived nitric oxide links human atherosclerosis to ED and underscores the role of an altered endothelium in the pathogenesis of both conditions. ED is associated to a systemic endothelial cell activation/dysfunction independent from VRFs or from a diffuse vascular damage, indicating that ED is a marker of an early systemic endothelial damage, a relevant determinant of atherosclerosis. A diffuse vascular damage of carotid arteries indicative of pre-clinical atherosclerosis is significantly associated to an increased risk of severe ED in men with VRFs but without clinical atherosclerosis and ED was the most efficient predictor of angiographically verified silent CAD among different VRFs in uncomplicated type 2 diabetes. In conclusion, ED may be the only clinical correlate of a diffuse, unrecognized vascular damage that is associated to a documented future risk of acute vascular events. Searching ED might be of relevance in men with VRFs but no other clinical atherosclerosis to identify patients that should aggressively reduce their VRFs while treating ED.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11697/11795
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