Computational Assessment of Valvular Dysfunction in Discrete Subaortic Stenosis: A Parametric Study.
Computational Assessment of Valvular Dysfunction in Discrete Subaortic Stenosis: A Parametric Study.
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DOI：
10.1007/s13239-020-00513-8
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发表时间：
2021-12
影响因子：
1.8
通讯作者：
Sucosky P
中科院分区：
文献类型：
--
作者：
Shar JA;Keswani SG;Grande-Allen KJ;Sucosky P
离散性主动脉瓣下狭窄（DSS）是由膜性病变引起的左心室流出道（LVOT）阻塞。DSS与陡峭的主动脉中隔角（AoSA）相关，是主动脉瓣返流（AR）的风险因素。然而，继发于DSS的AR的病因仍然未知。本研究旨在通过计算量化AoSA陡峭化和DSS对主动脉瓣（AV）血流动力学和AR的影响。将从电影-MRI数据重建的LV几何结构连接到AV几何结构以生成统一的2D LV-AV模型。考虑了6种几何变化：无阻塞（CTRL）和DSS阻塞的LVOT（DSS），每种都反映了3种AoSA变化（110°、120°、130°）。运行流体-结构相互作用模拟，以计算LVOT流量、AV瓣叶动力学和阻力分数（RF）。AoSA变陡和DSS产生涡流动力学变化和狭窄流动条件。虽然CTRL-110°模型产生了最高程度的瓣叶开口不对称性，但DSS优先改变了上级瓣叶运动学，并导致了收缩期扑动的瓣叶依赖性改变。LVOT变陡和DSS使瓣叶承受WSS过载增加（时间剪切幅度增加高达94%），而DSS也增加了下瓣叶腹部的WSS双向性（振荡剪切指数+0.30点）。尽管AoSA变陡和DSS增加了舒张期跨瓣返流，但返流分数（RF<7%）仍低于定义临床轻度AR的阈值。AV瓣叶和LVOT陡峭化/DSS血流动力学紊乱之间的机械相互作用不会引起AR。然而，在这些解剖结构中预测的瓣叶WSS异常为继发于DSS的AR的机械生物学病因学提供了新的支持。
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.
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