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 w all shear stress and flow-mediated dilation (FMD) in humans, and 2) to inve stigate 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 relation ship between WSS and FMD has not been investigated in humans. Furthermore, FMD is greater in small arteries, though the reasons for this phenomenon ar e unclear. Methods Using phase-contrast magnetic resonance angiography (PMRCA), we mea sured hyperemic WSS and FMD in 18 healthy volunteers. Peak systolic WSS was calculated assuming a blunted parabolic velocity profile. Diameter by PCMR A 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 relat ed to baseline diameter (r=0.62, p=0.006), but the hyperemic peak WSS stimu lus was also inversely related to baseline diameter (r=0.47, p=0.049). Phas e-contrast magnetic resonance angiography and ultrasound diameters were com pared 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 a ccounted for, at least partially, by a greater hyperemic WSS stimulus in sm all arteries. By allowing the calculation of vascular WSS, which is the sti mulus 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 Co llege of Cardiology.