Purpose: To assess the accuracy and precision of a volumetric wall shear stress (WSS) calculation method applied to cine phase contrast magnetic resonance imaging (PC‐MRI) data.Materials and Methods: Volumetric WSS vectors were calculated in software phantoms. WSS algorithm parameters were optimized and the influence of spatial resolution and segmentation was evaluated. Subsequently, 2D cine PC‐MRI data in the carotid and the aorta at varying spatial resolutions were obtained (n = 2) and compared with the simulations. Finally, volumetric WSS was calculated in 3D cine PC‐MRI data of the carotid bifurcation and the aorta (n = 6).Results: We found that at least 8 voxels across the diameter are required to obtain a WSS accuracy of 5% and a precision of 20% in software phantoms. Systematic WSS quantification errors up to 40% were found in the case of segmentation errors. The in vivo measurements using 2D cine PC‐MRI exhibited WSS increase at increasing spatial resolutions, similar to the results in software phantoms. Volumetric WSS vectors were successfully calculated in three healthy carotid bifurcations and aortas.Conclusion: The effects of resolution and segmentation on the accuracy and precision of the WSS algorithm were quantified. We were able to calculate volumetric WSS in the carotid bifurcation and the aorta. J. Magn. Reson. Imaging 2015;41:505–516.© 2013 Wiley Periodicals, Inc.

Purpose: To present a theoretical basis for noninvasively characterizing in vivo fluid‐mechanical energy losses and to apply it in a pilot study of patients known to express abnormal aortic flow patterns.Methods: Four‐dimensional flow MRI was used to characterize laminar viscous energy losses in the aorta of normal controls (n = 12, age = 37 ± 10 yr), patients with aortic dilation (n = 16, age = 52 ± 8 yr), and patients with aortic valve stenosis matched for age and aortic size (n = 14, age = 46 ± 15 yr), using a relationship between the three‐dimensional velocity field and viscous energy dissipation.Results: Viscous energy loss was elevated significantly in the thoracic aorta in patients with dilated aorta (3.6 ± 1.3 mW, P = 0.024) and patients with aortic stenosis (14.3 ± 8.2 mW, P < 0.001) compared with healthy volunteers (2.3 ± 0.9 mW). The same pattern of significant differences was seen in the ascending aorta, where viscous energy losses in patients with dilated aortas (2.2 ± 1.1 mW, P = 0.021) and patients with aortic stenosis (10.9 ± 6.8 mW, P < 0.001) were elevated compared with healthy volunteers (1.2 ± 0.6 mW).Conclusion: This technique provides a capability to quantify the contribution of abnormal laminar blood flow to increased ventricular afterload. In this pilot study, viscous energy loss in patient cohorts was significantly elevated and indicates that cardiac afterload is increased due to abnormal flow. Magn Reson Med 72:620–628, 2014.

Background: Wall shear stress ( WSS ) is a stimulus for vessel wall remodeling. Differences in ascending aorta ( AA o) hemodynamics have been reported between bicuspid aortic valve ( BAV ) and tricuspid aortic valve patients with aortic dilatation, but the confounding impact of aortic valve stenosis ( AS ) is unknown. Methods and Results: Five hundred seventy‐one subjects underwent 4‐dimensional flow magnetic resonance imaging in the thoracic aorta (210 right‐left BAV cusp fusions, 60 right‐noncoronary BAV cusp fusions, 245 tricuspid aortic valve patients with aortic dilatation, and 56 healthy controls). There were 166 of 515 (32%) patients with AS . WSS atlases were created to quantify group‐specific WSS patterns in the AA o as a function of AS severity. In BAV patients without AS , the different cusp fusion phenotypes resulted in distinct differences in eccentric WSS elevation: right‐left BAV patients exhibited increased WSS by 9% to 34% ( P <0.001) at the aortic root and along the entire outer curvature of the AA o whereas right‐noncoronary BAV patients showed 30% WSS increase ( P <0.001) at the distal portion of the AA o. WSS in tricuspid aortic valve patients with aortic dilatation patients with no AS was significantly reduced by 21% to 33% ( P <0.01) in 4 of 6 AA o regions. In all patient groups, mild, moderate, and severe AS resulted in a marked increase in regional WSS ( P <0.001). Moderate‐to‐severe AS further increased WSS magnitude and variability in the AA o. Differences between valve phenotypes were no longer apparent. Conclusions: AS significantly alters aortic hemodynamics and WSS independent of aortic valve phenotype and over‐rides previously described flow patterns associated with BAV and tricuspid aortic valve with aortic dilatation. Severity of AS must be considered when investigating valve‐mediated aortopathy.