Purpose

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.

Methods

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).

Results

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.

Conclusions

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.

中文翻译：

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离散主动脉瓣下狭窄瓣膜功能障碍的计算评估：参数研究

目的

离散主动脉瓣下狭窄 (DSS) 是由膜性病变引起的左心室流出道 (LVOT) 阻塞。DSS 与陡主动脉隔角 (AoSA) 相关，是主动脉瓣反流 (AR) 的危险因素。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 变陡和 DSS 对主动脉瓣 (AV) 血流动力学和 AR 的影响。

方法

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。考虑了六种几何变体：无阻塞 (CTRL) 和 DSS 阻塞 LVOT (DSS)，每种都反映了三种 AoSA 变化（110°、120°、130°）。运行流固耦合模拟以计算 LVOT 流量、AV 传单动力学和反流分数 (RF)。

结果

AoSA 变陡和 DSS 产生涡流动力学改变和狭窄流动条件。虽然 CTRL-110° 模型产生了最高程度的小叶开口不对称性，但 DSS 优先改变了优越的小叶运动学，并导致收缩期扑动的小叶依赖性改变。LVOT 变陡和 DSS 使小叶增加 WSS 超载（时间剪切幅度增加高达 94%），而 DSS 还增加了下小叶腹部的 WSS 双向性（振荡剪切指数 + 0.30 点）。尽管 AoSA 变陡和 DSS 增加了舒张期跨瓣膜回流，但返流分数 (RF < 7%) 仍低于定义临床轻度 AR 的阈值。

结论

AV 小叶和 LVOT 变陡/DSS 血流动力学紊乱之间的机械相互作用不会导致 AR。然而，在这些解剖结构中预测的小叶 WSS 异常为 DSS 继发 AR 的机械生物学病因学提供了新的支持。