Critical aortic stenosis (AS) of the fetal heart causes a drastic change in the cardiac biomechanical environment. Consequently, a substantial proportion of such cases will lead to a single-ventricular birth outcome. However, the biomechanics of the disease is not well understood. To address this, we performed Finite Element (FE) modelling of the healthy fetal left ventricle (LV) based on patient-specific 4D ultrasound imaging, and simulated various disease features observed in clinical fetal AS to understand their biomechanical impact. These features included aortic stenosis, mitral regurgitation (MR) and LV hypertrophy, reduced contractility, and increased myocardial stiffness. AS was found to elevate LV pressures and myocardial stresses, and depending on severity, can drastically decrease stroke volume and myocardial strains. These effects are moderated by MR. AS alone did not lead to MR velocities above 3 m/s unless LV hypertrophy was included, suggesting that hypertrophy may be involved in clinical cases with high MR velocities. LV hypertrophy substantially elevated LV pressure, valve flow velocities and stroke volume, while reducing LV contractility resulted in diminished LV pressure, stroke volume and wall strains. Typical extent of hypertrophy during fetal AS in the clinic, however, led to excessive LV pressure and valve velocity in the FE model, suggesting that reduced contractility is typically associated with hypertrophy. Increased LV passive stiffness, which might represent fibroelastosis, was found to have minimal impact on LV pressures, stroke volume, and wall strain. This suggested that fibroelastosis could be a by-product of the disease progression and does not significantly impede cardiac function. Our study demonstrates that FE modelling is a valuable tool for elucidating the biomechanics of congenital heart disease and can calculate parameters which are difficult to measure, such as intraventricular pressure and myocardial stresses.

胎儿心脏的严重主动脉瓣狭窄 (AS) 会导致心脏生物力学环境发生剧烈变化。因此，很大一部分此类病例将导致单心室分娩结果。然而，该疾病的生物力学还不是很清楚。为了解决这个问题，我们基于患者特定的 4D 超声成像对健康胎儿左心室 (LV) 进行了有限元 (FE) 建模，并模拟了在临床胎儿 AS 中观察到的各种疾病特征，以了解其生物力学影响。这些特征包括主动脉瓣狭窄、二尖瓣关闭不全 (MR) 和 LV 肥大、收缩力降低和心肌僵硬增加。发现 AS 会升高 LV 压力和心肌应力，并且根据严重程度，可以显着降低每搏输出量和心肌应变。这些影响由 MR 缓和。除非将 LV 肥大包括在内，否则单独的 AS 不会导致 MR 速度超过 3 m/s，这表明肥厚可能与高 MR 速度的临床病例有关。LV 肥大显着提高了 LV 压力、瓣膜流速和每搏输出量，同时降低 LV 收缩力导致 LV 压力、每搏输出量和壁应变减少。然而，临床上胎儿 AS 期间典型的肥大程度导致 FE 模型中的 LV 压力和瓣膜速度过高，这表明收缩力降低通常与肥大有关。发现可能代表弹性纤维变性的 LV 被动刚度增加对 LV 压力、每搏输出量和壁应变的影响最小。这表明弹性纤维变性可能是疾病进展的副产品，不会显着阻碍心脏功能。我们的研究表明，有限元建模是阐明先天性心脏病生物力学的宝贵工具，可以计算难以测量的参数，例如心室内压和心肌应力。