Aortic Valve Stenosis Alters Expression of Regional Aortic Wall Shear Stress: New Insights From a 4-Dimensional Flow Magnetic Resonance Imaging Study of 571 Subjects

Abstract

Background: Wall shear stress (WSS) is a stimulus for vessel wall remodeling. Differences in ascending aorta (AAo) 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 AAo 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 AAo whereas right-noncoronary BAV patients showed 30% WSS increase (P<0.001) at the distal portion of the AAo. 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 AAo 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 AAo. 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.

Keywords: aortic disease; aortic valve; aortic valve stenosis; bicuspid aortic valve; magnetic resonance imaging.

Figure 1

Data analysis workflow for the calculation of a cohort specific 3D wall shear stress (WSS) atlas. WSS quantification was performed in the numbered regions of interest: (1) the inner sinotubular junction, (2) the outer sinotubular junction, (3) the inner proximal ascending aorta (AAo), (4) the outer proximal AAo, (5) the inner distal AAo, and (6) the outer distal AAo. 3D indicates 3‐dimensional; 4D, 4‐dimensional; MRI, magnetic resonance imaging.

Figure 2

Representative examples of systolic 3D velocity fields in the aorta obtained by 4D flow MRI, aortic valve morphology (white inset box) and left ventricular outflow based on 2D CINE SSFP MRI for (A) controls, (B) TAV‐TAA without AS, (C) TAV‐TAA with moderate AS, (D) RL‐BAV without AS, (E) RL‐BAV with moderate AS, (F) RN‐BAV without AS and (G) RN‐BAV with moderate AS. 2D indicates 2‐dimensional; 3D, 3‐dimensional; 4D, 4‐dimensional; AAo, ascending aorta; AS, aortic stenosis; AV, aortic valve; BAV, bicuspid aortic valve; LV, left ventricle; MRI, magnetic resonance imaging; RL‐BAV, right and left coronary leaflet fusion BAV; RN‐BAV, right and noncoronary leaflet fusion BAV; RPA, right pulmonary artery; SSFP, steady state free precession; TAV‐TAA, tricuspid aortic valve with aortic dilation. Arrows indicate high‐velocity outflow jets in RL‐BAV and RN‐BAV without AS.

Figure 3

Atlases of WSS for (A) controls, (B) TAV‐TAA without AS, (C) RL‐BAV without AS, (D) RN‐BAV without AS, (E through G) the corresponding patients with mild AS, and (H through J) the corresponding patients with moderate/severe AS. Significant differences in WSS in the 6 regions of interest are marked by a dagger (“^†”) for comparisons to controls, a double dagger (“^‡”) for “within AS group” comparisons to TAV‐TAA, and a section mark (“^§”) for “within AS group” comparisons to RL‐BAV (analysis adjusted for age and sex). Note: “within AS group” refers to those atlases with a similar degree of AS (eg, only atlases in the same rows were compared to one another). AS indicates aortic stenosis; BAV, bicuspid aortic valve; RL‐BAV, right and left coronary leaflet fusion BAV; RN‐BAV, right and noncoronary leaflet fusion BAV; TAV‐TAA, tricuspid aortic valve with aortic dilation; WSS, wall shear stress.

Figure 4

Atlases of WSS interquartile range (IQR) for (A) controls, (B) TAV‐TAA without AS, (C) RL‐BAV without AS, (D) RN‐BAV without AS, (E through G) the corresponding patients with mild AS, and (H through J) the corresponding patients with moderate/severe AS. IQR is expressed as the range between the 75% and 25% quartile of WSS magnitude for all subjects in a given cohort. This represents the regional variability of WSS experienced across the subjects in each group. Controls and patients with no AS (top row) had relatively low WSS variability in the thoracic aorta with mildly elevated WSS IQR in the ascending aorta of BAV patients. In contrast, WSS variability was markedly elevated in the ascending aorta of most AS patient groups (RL‐BAV, RN‐BAV, TAV, and dilated aorta). Color coding=intersubject IQR of WSS magnitude. AS indicates aortic stenosis; BAV, bicuspid aortic valve; RL‐BAV, right and left coronary leaflet fusion BAV; RN‐BAV, right and noncoronary leaflet fusion BAV; TAV‐TAA, tricuspid aortic valve with aortic dilation; WSS, wall shear stress.