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J Am Coll Cardiol, 2001; 38:1859-1865
© 2001 by the American College of Cardiology Foundation
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CLINICAL STUDY: ENDOTHELIAL FUNCTION

The relationship between vascular wall shear stress and flow-mediated dilation: endothelial function assessed by phase-contrast magnetic resonance angiography

Harry A. Silber, MD, PhDa, David A. Bluemke, MD, PhDa, Pamela Ouyang, MD, FACCa, Yiping P. Du, PhDa, Wendy S. Post, MD, MS, FACCa and Joao A. C. Lima, MD, FACC*,a

a Johns Hopkins Medical Institutions, Baltimore, Maryland, USA

Manuscript received October 23, 2000; revised manuscript received July 25, 2001, accepted August 20, 2001.

* Reprint requests and correspondence: Dr. Joao A. C. Lima, Division of Cardiology, 568 Carnegie Building 410-614-1284, Johns Hopkins Hospital, 600 North Wolfe Street, Baltimore, Maryland 21287 USA
jlima{at}mri.jhu.edu

OBJECTIVES

We sought: 1) to investigate the relationship between vascular wall shear stress and flow-mediated dilation (FMD) in humans, and 2) to investigate whether this relationship could explain why FMD is greater in small arteries.

BACKGROUND

Arterial wall shear stress (WSS) is considered to be the primary stimulus for the endothelial-dependent FMD response. However, the relationship between WSS and FMD has not been investigated in humans. Furthermore, FMD is greater in small arteries, though the reasons for this phenomenon are unclear.

METHODS

Using phase-contrast magnetic resonance angiography (PMRCA), we measured hyperemic WSS and FMD in 18 healthy volunteers. Peak systolic WSS was calculated assuming a blunted parabolic velocity profile. Diameter by PCMRA and by ultrasound was compared in nine subjects.

RESULTS

Flow-mediated dilation was linearly proportional to hyperemic peak systolic WSS (r = 0.79, p = 0.0001). Flow-mediated dilation was inversely related to baseline diameter (r = 0.62, p = 0.006), but the hyperemic peak WSS stimulus was also inversely related to baseline diameter (r = 0.47, p = 0.049). Phase-contrast magnetic resonance angiography and ultrasound diameters were compared in nine subjects and correlated well (r = 0.84, p < 0.0001), but diameter by PCMRA was greater (4.1 ± 0.7 mm vs. 3.7 ± 0.5 mm, p = 0.009).

CONCLUSIONS

Arterial FMD is linearly proportional to peak hyperemic WSS in normal subjects. Thus, the endothelial response is linearly proportional to the stimulus. Furthermore, the greater FMD response in small arteries is accounted for, at least partially, by a greater hyperemic WSS stimulus in small arteries. By allowing the calculation of vascular WSS, which is the stimulus for FMD, and by imaging a fixed arterial cross-section, thus reducing operator dependence, PCMRA enhances the assessment of vascular endothelial function.

Abbreviations and Acronyms
  A = arterial cross-sectional area at peak systole
  D = arterial lumen diameter at peak systole
  FMD = flow-mediated dilation
  MRI = magnetic resonance imaging
  n = bluntness factor describing a paraboloid flow velocity profile, increasing n means a blunter profile
  PCMRA = phase-contrast magnetic resonance angiography
  VC = blood flow velocity in the center of the arterial cross-section during peak systolic flow
  VSA = blood flow velocity, spatially averaged across the arterial cross-section at peak systole
  WSR = wall shear rate at peak systole
  WSS = wall shear stress at peak systole
  µ = blood viscosity




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