Shouldering the Risk Factor Burden

he healthy endothelium maintains vascular homeostasis via production of paracrine factors that promote vasodilation and inhibit thrombosis, inflammation, and cellular proliferation in the blood vessel. 1 Atherosclerosis is associated with a loss of the biological activity of endothelium-derived nitric oxide and other alterations of endothelial phenotype that may contribute to plaque rupture and subsequent thrombosis and vasospasm.2 Indeed, the severity of impairment of endothelium-dependent vasodilation in the coronary circulation predicts the risk for future cardiovascular disease events.3,4 The ability to reverse endothelial dysfunction is a common property of otherwise diverse interventions that have been proven to reduce cardiovascular risk, including lipid lowering therapy, angiotensin converting enzyme inhibition, smoking cessation, and exercise.1 These observations support the concepts that endothelial dysfunction contributes to the clinical expression of cardiovascular disease and is a clinically useful surrogate for cardiovascular disease risk.