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(Circulation. 2007;115:2373-2375.)
© 2007 American Heart Association, Inc.

Editorial

Prognostic Significance of Brachial Flow-Mediated Vasodilation

Todd J. Anderson, MD

From the Department of Cardiovascular Sciences and the Libin Cardiovascular Institute, University of Calgary, Calgary, Alberta, Canada.

Correspondence to T.J. Anderson, MD, 1403 29th Street NW, Calgary, AB, T2N 2T9. E-mail todd.anderson@calgaryhealthregion.ca

Key Words: Editorials • atherosclerosis • endothelium • risk factors

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
There is currently much research devoted to the study of vascular biology in intact humans. These efforts aim to translate findings from the basic science arena to a better understanding of the pathophysiology of atherosclerosis and its complications. Markers of vascular risk have been used as surrogate end points in treatment studies. More recently, long-term studies have emerged that speak to the prognostic significance of these novel markers with a goal of refining risk stratification approaches. C-reactive protein is an excellent example of such a marker, with many others being evaluated.¹

Article p 2390

The vascular endothelium is in a unique position to serve as a metric of atherosclerotic risk. The healthy endothelium is antiatherogenic through favorable paracrine effects on vasodilation, inhibition of leukocyte adhesion, platelet aggregation and coagulation, and promotion of healing via progenitor cells.² However, because of its position in the vascular wall, it is also the target of hemodynamic and biochemical perturbations. This leads to endothelial dysfunction early in the course of the disease, a property that could be exploited for risk evaluation.

	Endothelial Function

 
Endothelium-dependent vasodilation is a nitric oxide–dependent process that has been well studied in humans. There are many methods of assessing conduit and resistance vessel function. Conduit vessel responses can be evaluated by measuring the change in vessel diameter in response to physiological (shear stress) or pharmacological (acetylcholine) stimuli. Ludmer and colleagues³ were among the first to describe the differences in coronary responses to acetylcholine between healthy subjects and those with vascular dysfunction. Although the . . . [Full Text of this Article]

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