Circulation. 2003;108:1917-1923
doi: 10.1161/01.CIR.0000089190.95415.9F
doi: 10.1161/01.CIR.0000089190.95415.9F
(Circulation. 2003;108:1917.)
© 2003 American Heart Association, Inc.
Special Review |
New Markers of Inflammation and Endothelial Cell Activation
Part I
From the Division of Cardiology, University of Calgary, Calgary, Alberta (T.J.A.), and Division of Cardiac Surgery, University of Toronto, Toronto, Ontario (P.E.S., C.-H.W., R.D.W., J.R.d.A., S.V.), Canada.
Correspondence to Subodh Verma, MD, PhD, Division of Cardiac Surgery, Toronto General Hospital, 14EN-215, 200 Elizabeth St, Toronto, Ontario, Canada M5G 2C4. E-mail subodh.verma@sympatico.ca
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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Current views regard atherosclerosis as a dynamic and progressive disease arising from the combination of endothelial dysfunction and inflammation.1–6 The vascular endothelium, located at the interface of blood and tissue, is able to sense changes in hemodynamic forces and bloodborne signals and react by synthesizing and releasing vasoactive substances. Vascular homeostasis is maintained by a balance between endothelium-derived relaxing and contracting factors. With disruption of this balance, mediated by inflammatory and traditional cardiovascular risk factors, the vasculature becomes susceptible to atheroma formation. Inflammatory mediators appear to play a fundamental role in the initiation, progression, and eventual rupture of atherosclerotic plaques. As evidence accumulates linking inflammatory processes to atherogenesis, markers of inflammation and endothelial activation may become useful by providing additional information about a patient’s risk of developing cardiovascular disease, as well as providing new targets for treatment.7,8 This review article is the first part of a two-article series examining emerging markers of inflammation and cardiovascular disease. Part 1 will provide a brief overview of the link between inflammation, endothelial dysfunction, and atherosclerosis and will begin highlighting emerging inflammatory mediators of endothelial cell (EC) activation, a discussion that will be continued in Part 2.
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Endothelial Dysfunction: Setting the Stage for Inflammation |
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Endothelial dysfunction is a broad term that implies diminished production or availability of nitric oxide (NO) and/or an imbalance in the relative contribution of endothelium-derived relaxing and contracting factors, such as endothelin-1 (ET-1), angiotensin, and oxidants.1 NO, generated by the conversion of the amino acid L-arginine to NO and L-citrulline by the enzyme NO synthase,
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