Published online before print July 12, 2004, doi: 10.1161/01.HYP.0000137301.99716.e8
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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{at}unsw.edu.au
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 of measuring FMD are time consuming, have low reproducibility, and are imprecise (because dilation is so small, averaging just 2.3% in the males of this series). If a fault lies in the peripheral circulation, then more attention should be given to absolute flow in the smaller vessels, using old-fashioned, conventional venous occlusive plethysmography. Many investigators have done this previously; Irace et al3 concluded that endothelial function could be reliably evaluated by plethysmography or by FMD and that the 2 methods correlated. Alternatively, one might consider other techniques of pulse waveform analysis,4,5 which evaluate global endothelial function, but also appear to correlate with the conventional measures.
In the present study, FMD was related to DSS, whereas others have related FMD to maximal (systolic) shear stress. Flow is much higher in systole than in diastole, but the relationship varies with cardiac and vascular disease6,7 and with aging. It is not established whether conventionally measured peak (systolic) or diastolic shear stress is the stimulus to NO production and to FMD. Further, investigators assumed laminar flow and a parabolic velocity profile when measuring wall stress. This is not strictly correct. The flow velocity varies across the vessel lumen during the cardiac cycle so that wall stress varies in a complex way with time during pulsatile flow. This was calculated by McDonald and Womersley, whose velocity profiles are shown in the Figure for an artery of similar caliber to the brachial artery in humans and concur with those measured experimentally.8,9
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are summed together with a parabola (axial velocity 30 cm/s) representing the steady forward flow. The maximum forward velocity occurs in the axis because here the harmonic components are in phase, but the maximum backward velocity lies between 
=0.3 and 0.4 at 180°. The reversal of flow beginning near the wall is clearly seen. (Reprinted with permission from Nichols WW, O’Rourke MF. McDonald’s Blood Flow in Arteries. London; Edward Arnold;1998:40).Clearly, this field remains controversial and requires new and different approaches. The beauty of the present study is that it was conducted in a large, well characterized group of normal subjects as part of an extensive screening process during a half-day period. It was also conducted under modest circumstances. Framingham is famous for its frugality as well as its inventiveness and has shown that major advances do not require expensive premises and budget, just adequate funding, good planning and supervision, readiness to innovate, cooperation and coordination between staff and community, and above all, perseverance.
Footnotes
The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.
References
1. Mitchell GF, Parise H, Vita JA, Larson MG, Warner E, Keaney JF, Keyes MJ, Levy D, Vasan RS, Benjamin EJ. Local shear stress and brachial artery flow-mediates dilation: the Framingham Heart Study. Hypertension. 2004; 44: 134–139.
2. Benjamin EJ, Larson MG, Keyes MJ, Mitchell GF, Vasan RS, Keaney JF, Lehman Jr.,BT, Fan S, Osypiuk E, Vita JA. Clinical correlates and heritability of flow-mediated dilation in the community: the Framingham Heart Study. Circulation. 2004; 109: 613–619.
3. Irace C, Ceravolo R, Notarangelo L, Crescenzo A, Ventura G, Tamburrini O, Perticone F, Gnasso A. Comparison of endothelial function evaluated by strain gauge plethysmography and brachial artery ultrasound. Atherosclerosis. 2001; 158: 53–59.[CrossRef][Medline] [Order article via Infotrieve]
4. Wilkinson IB, Hall IR, MacCallum H, Mackenzie IS, McEniery CM, van der Arend BJ, Shu Y-E, MacKay LS, Webb DJ, Cockcroft JR. Pulse-wave analysis: clinical evaluation of a noninvasive, widely applicable method for assessing endothelial function. Arterioscler Thromb Vasc Biol. 2002; 22: 147–152.
5. Hayward CS, Kraidly M, Webb CM, Collins P. Assessment of endothelial function using peripheral waveform analysis: a clinical application. J Am Coll Cardiol. 2002; 40: 521–528.
6. Gault JH, Ross J, Mason DT. Patterns of brachial arterial blood flow in conscious human subjects with and without cardiac dysfunction. Circulation. 1996; 34: 833–848.
7. Nichols WW, O’Rourke MF. McDonald’s Blood Flow in Arteries. London; Edward Arnold; 1998.
8. Simon AC, Levenson J, Flaud P. Pulsatile flow and oscillating wall shear stress in the brachial artery of normotensive and hypertensive subjects. Cardiovasc Res. 1990; 24: 129–136.
9. Tortoli P, Bambi G, Guidi F, Muchada R. Toward a better quantitative measurement of aortic flow. Ultrasound Med Biol. 2002; 28: 249–257.[CrossRef][Medline] [Order article via Infotrieve]
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