[The role of endothelial dysfunction in the pathogenesis and in clinical practice of atherosclerosis. Current evidences].
Endothelium is not a mere monolayer of cells separating flowing blood and vascular wall, but plays a key role in maintenance of vascular homeostasis. Nitric oxide is the principal mediator of endothelial function; it is a potent vasodilator, it inhibits platelet aggregation, vascular smooth muscle cell migration and proliferation, and monocytes adhesion. Cardiovascular risk factors promote development of endothelial dysfunction, characterized by impairment of endothelium-dependent vasodilation (EDV) and by pro-coagulant/pro-inflammatory endothelial activities. The assessment of EDV is a common parameter for testing endothelial function. EDV in the coronary arteries is angiographically evaluated by measurement of the vessel response to endothelial agonists, such as acetylcholine. A non-invasive technique for the detection of EDV employs the ultrasound evaluation of flow-mediated dilation (FMD) of the brachial artery following reactive hyperemia. A close relation between FMD and coronary vasomotor response to acetylcholine has been demonstrated. Endothelial dysfunction in the coronary circulation may precede development of angiographically evident coronary atherosclerosis; endothelial dysfunction has been also associated with a higher prevalence of coronary artery disease and resulted predictive of future cardiovascular events; recently, it has been associated with a higher risk of restenosis after coronary stent implantation. Endothelial dysfunction is actually considered a reversible phenomenon; drug therapies with ACE-inhibitors, angiotensin receptor blockers, statins, antioxidants agents have shown a beneficial effect on endothelial function.
Patti
Giuseppe
G
Dipartimento di Scienze Cardiovascolari, Università Campus Bio-Medico, Roma. g.disciascio@unicampus.it
Melfi
Rosetta
R
Di Sciascio
Germano
G
D050197:Atherosclerosis / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology*; D002317:Cardiovascular Agents / Q000627:therapeutic use; D003324:Coronary Artery Disease / Q000209:etiology / Q000503:physiopathology; D003331:Coronary Vessels / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism; D012307:Risk Factors; D014664:Vasodilation / Q000187:drug effects
D002317:Cardiovascular Agents; D009569:Nitric Oxide