Department of Mechanical and Materials Engineering, Wright State University, Dayton, USA.
Division of Pediatric Surgery, Department of Surgery, Texas Children's Hospital, Baylor College of Medicine, Houston, USA.
Cardiovasc Eng Technol. 2021 Dec;12(6):559-575. doi: 10.1007/s13239-020-00513-8. Epub 2021 Jan 11.
Discrete subaortic stenosis (DSS) is a left-ventricular outflow tract (LVOT) obstruction caused by a membranous lesion. DSS is associated with steep aortoseptal angles (AoSAs) and is a risk factor for aortic regurgitation (AR). However, the etiology of AR secondary to DSS remains unknown. This study aimed at quantifying computationally the impact of AoSA steepening and DSS on aortic valve (AV) hemodynamics and AR.
An LV geometry reconstructed from cine-MRI data was connected to an AV geometry to generate a unified 2D LV-AV model. Six geometrical variants were considered: unobstructed (CTRL) and DSS-obstructed LVOT (DSS), each reflecting three AoSA variations (110°, 120°, 130°). Fluid-structure interaction simulations were run to compute LVOT flow, AV leaflet dynamics, and regurgitant fraction (RF).
AoSA steepening and DSS generated vortex dynamics alterations and stenotic flow conditions. While the CTRL-110° model generated the highest degree of leaflet opening asymmetry, DSS preferentially altered superior leaflet kinematics, and caused leaflet-dependent alterations in systolic fluttering. LVOT steepening and DSS subjected the leaflets to increasing WSS overloads (up to 94% increase in temporal shear magnitude), while DSS also increased WSS bidirectionality on the inferior leaflet belly (+ 0.30-point in oscillatory shear index). Although AoSA steepening and DSS increased diastolic transvalvular backflow, regurgitant fractions (RF < 7%) remained below the threshold defining clinical mild AR.
The mechanical interactions between AV leaflets and LVOT steepening/DSS hemodynamic derangements do not cause AR. However, the leaflet WSS abnormalities predicted in those anatomies provide new support to a mechanobiological etiology of AR secondary to DSS.
离散型主动脉瓣下狭窄(DSS)是一种由膜性病变引起的左心室流出道(LVOT)梗阻。DSS 与陡峭的主动脉瓣-室间隔夹角(AoSAs)相关,是主动脉瓣反流(AR)的一个危险因素。然而,DSS 引起的 AR 的病因仍不清楚。本研究旨在通过计算的方法来量化 AoSA 变陡和 DSS 对主动脉瓣(AV)血流动力学和 AR 的影响。
从电影 MRI 数据重建的 LV 几何形状与 AV 几何形状相连,生成一个统一的 2D LV-AV 模型。考虑了六种几何变体:无梗阻(CTRL)和 DSS 梗阻的 LVOT(DSS),每个变体反映了三种 AoSA 变化(110°、120°、130°)。进行流体-结构相互作用模拟以计算 LVOT 流量、AV 瓣叶动力学和反流分数(RF)。
AoSA 变陡和 DSS 产生了涡流动力学的改变和狭窄的流动条件。尽管 CTRL-110°模型产生了最大程度的瓣叶开口不对称,但 DSS 优先改变了上瓣叶的运动,并导致了瓣叶依赖的收缩期飘动改变。LVOT 变陡和 DSS 使瓣叶承受越来越大的 WSS 过载(时剪切幅度增加高达 94%),而 DSS 也增加了下瓣叶腹部的 WSS 双向性(振荡剪切指数增加 0.30 点)。尽管 AoSA 变陡和 DSS 增加了舒张期跨瓣反流,但反流分数(RF<7%)仍低于定义临床轻度 AR 的阈值。
AV 瓣叶和 LVOT 变陡/DSS 血流动力学紊乱之间的力学相互作用不会引起 AR。然而,在这些解剖结构中预测的瓣叶 WSS 异常为 DSS 引起的 AR 的机械生物学病因提供了新的支持。