doi: 10.1161/01.CIR.0000023452.26135.34
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(Circulation. 2002;106:164.)
© 2002 American Heart Association, Inc.
Editorial |
Shouldering the Risk Factor Burden
Infection, Atherosclerosis, and the Vascular Endothelium
From Evans Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Mass.
Correspondence to Joseph A. Vita, MD, Section of Cardiology, Boston Medical Center, 88 East Newton St, Boston, MA 02118. E-mail jvita@bu.edu
Key Words: Editorials • risk factors • infection • atherosclerosis • endothelium
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The 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.
See p 184
In addition to its role in advanced disease, there is strong evidence that endothelial dysfunction is important in the early stages of atherogenesis.5 For example, pharmacological inhibition of nitric oxide synthesis promotes atherogenesis,6 and the endothelial nitric oxide synthase null mouse is more susceptible to lesion formation than its wild type counterpart.7 Endothelial dysfunction is present in patients with coronary risk factors before the development of coronary atherosclerosis, as detected by angiography or intracoronary ultrasound.1,8 Endothelium-dependent flow-mediated dilation is impaired in young children with hypercholesterolemia before any clinical evidence of disease is seen.9 In general, the degree of endothelial dysfunction correlates with the number and severity of coronary risk factors.1,8 Thus,
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