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

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<plus/minus>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. (J Am Coll Cardiol 2001; 38:1859-65) (C) 2001 by the American College of Cardiology.