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(Hypertension. 2004;44:119.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

Shear Stress and Flow-Mediated Dilation

From the University of New South Wales/Victor Chang Cardiac Research Institute/St. Vincent’s Clinic (M.F.O’R.), Sydney, Australia, Department of Medicine and Cardiology (W.W.N.), University of Florida, Gainesville.

Correspondence to Michael O’Rourke, Ste 810, St. Vincent’s Clinic, 438 Victoria Street, Darlinghurst, NSW 2010, Australia. E-mail M.ORourke@unsw.edu.au

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

In this edition of Hypertension, the Framingham Heart Study group reports on the relationship between diastolic shear stress and brachial artery flow mediated dilation (FMD) in 2045 participants of the Framingham Offspring group.¹ Clinical correlates and heritability of FMD in the participants have been published previously.² The new report¹ challenges conventional concepts on endothelial function and on modification of endothelial function by risk factors of cardiovascular disease. The authors conclude that when present, impaired FMD of the brachial artery may be due not to impaired release of NO from the vascular endothelium, but from a lesser stimulus to NO release as a consequence of decreased flow velocity (and shear stress) during reactive hyperemia caused by impaired microvascular response. Are there fewer peripheral vessels capable of responding to local ischemia?

The method used by the authors differed from those previously applied in that they related FMD to systolic dilation to diastolic shear stress (DSS), not to systolic shear stress or to shear stress averaged over the whole cardiac cycle. They calculated shear stress from constant blood viscosity, mean diastolic flow velocity, and baseline end-diastolic diameter, assuming a parabolic velocity profile. Expressed this way, they found a close relationship between DSS and FMD that was not related to most conventional risk factors, including gender. These results¹ add a new twist to the study of endothelial function and NO production, and raise other possibilities as to how disease, drugs, and/or risk factors affect arteries that are not subject to atherosclerosis. Present techniques . . . [Full Text of this Article]

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