Abstract
The incidence of metabolic syndrome is rapidly increasing in the United States. Metabolic syndrome is associated with increased cardiovascular morbidity and mortality, and endothelial dysfunction is an early pathogenetic event in the metabolic syndrome. Endothelial dysfunction of either the coronary, the peripheral, or the cerebral vasculature is a predictor of vascular events and appears to be a marker of uncontrolled atherosclerotic risk that adds to the burden of the genetic predisposition to cardiovascular disease. Clinically and experimentally, endothelial dysfunction can be restored by several agents, including blockers/inhibitors of the renin-angiotensin-aldosterone system, as well as statins. Nevertheless, it would be premature, and most likely inappropriate, to use improvement of endothelial function as a surrogate end point to predict reduction in cardiovascular morbidity and mortality. However, a clear understanding of the mechanisms of endothelial dysfunction in the metabolic syndrome may allow the development of preventive and early therapeutic measures targeting cardiovascular disease.
