BACKGROUND: Low endothelial shear stress (ESS) elicits endothelial dysfunction. However, the relationship between ESS and arterial remodeling and arterial stiffness is unknown in humans. We developed a 3.0-T MRI protocol to evaluate the contribution of ESS to arterial remodeling and stiffness. METHODS AND RESULTS: Fifteen young (aged 26 ± 3 years) and 15 older (aged 57 ± 3 years) healthy volunteers as well as 15 patients with cardiovascular disease (aged 63 ± 10 years) were enrolled. Phase-contrast MRI of the common carotid arteries was used to derive ESS data from the spatial velocity gradients close to the arterial wall. ESS measurements were performed on 3 occasions and showed excellent reproducibility (intraclass correlation coefficient, 0.79). Multiple linear regression analysis accounting for age and blood pressure revealed that ESS was an independent predictor of the following response variables: carotid wall thickness (regression coefficient [b], -0.19 mm(2) per N/m(2); P=0.02), lumen area (b, -15.5 mm(2) per N/m(2); P<0.001), and vessel size (b, -24.0 mm(2) per N/m(2); P<0.001). Segments of the artery wall exposed to lower ESS were significantly thicker than segments exposed to higher ESS within the same artery (P=0.009). Furthermore, ESS was associated with arterial compliance, accounting for age, blood pressure, and wall thickness (b, -0.003 mm(2)/mm Hg per N/m(2); P=0.04). CONCLUSIONS: Our carotid MRI data show that ESS is an important determinant of arterial remodeling and arterial stiffness in humans. The data warrant further studies to evaluate use of carotid ESS as a noninvasive tool to improve the understanding of individual cardiovascular disease risk and to assess novel drug therapies in cardiovascular disease prevention.
BACKGROUND: Low endothelial shear stress (ESS) elicits endothelial dysfunction. However, the relationship between ESS and arterial remodeling and arterial stiffness is unknown in humans. We developed a 3.0-T MRI protocol to evaluate the contribution of ESS to arterial remodeling and stiffness. METHODS AND RESULTS: Fifteen young (aged 26 ± 3 years) and 15 older (aged 57 ± 3 years) healthy volunteers as well as 15 patients with cardiovascular disease (aged 63 ± 10 years) were enrolled. Phase-contrast MRI of the common carotid arteries was used to derive ESS data from the spatial velocity gradients close to the arterial wall. ESS measurements were performed on 3 occasions and showed excellent reproducibility (intraclass correlation coefficient, 0.79). Multiple linear regression analysis accounting for age and blood pressure revealed that ESS was an independent predictor of the following response variables: carotid wall thickness (regression coefficient [b], -0.19 mm(2) per N/m(2); P=0.02), lumen area (b, -15.5 mm(2) per N/m(2); P<0.001), and vessel size (b, -24.0 mm(2) per N/m(2); P<0.001). Segments of the artery wall exposed to lower ESS were significantly thicker than segments exposed to higher ESS within the same artery (P=0.009). Furthermore, ESS was associated with arterial compliance, accounting for age, blood pressure, and wall thickness (b, -0.003 mm(2)/mm Hg per N/m(2); P=0.04). CONCLUSIONS: Our carotid MRI data show that ESS is an important determinant of arterial remodeling and arterial stiffness in humans. The data warrant further studies to evaluate use of carotid ESS as a noninvasive tool to improve the understanding of individual cardiovascular disease risk and to assess novel drug therapies in cardiovascular disease prevention.
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