Please use this identifier to cite or link to this item: https://doi.org/10.1007/s10439-020-02683-x
Title: Biomechanics of Human Fetal Hearts with Critical Aortic Stenosis
Authors: Ong, Chi Wei
Ren, Meifeng
Wiputra, Hadi 
Mojumder, Joy
Chan, Wei Xuan
Tulzer, Andreas
Tulzer, Gerald
Buist, Martin Lindsay 
Mattar, Citra Nurfarah Zaini 
Lee, Lik Chuan
Yap, Choon Hwai
Keywords: Evolving hypoplastic left heart syndrome
Fetal aortic stenosis
Fetal heart biomechanics
Fetal left ventricle
Fetal mitral regurgitation
Finite element method
Issue Date: 11-Nov-2020
Publisher: Springer
Citation: Ong, Chi Wei, Ren, Meifeng, Wiputra, Hadi, Mojumder, Joy, Chan, Wei Xuan, Tulzer, Andreas, Tulzer, Gerald, Buist, Martin Lindsay, Mattar, Citra Nurfarah Zaini, Lee, Lik Chuan, Yap, Choon Hwai (2020-11-11). Biomechanics of Human Fetal Hearts with Critical Aortic Stenosis. Annals of Biomedical Engineering 49 (5) : 1364-1379. ScholarBank@NUS Repository. https://doi.org/10.1007/s10439-020-02683-x
Rights: Attribution 4.0 International
Abstract: 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. © 2020, The Author(s).
Source Title: Annals of Biomedical Engineering
URI: https://scholarbank.nus.edu.sg/handle/10635/233320
ISSN: 0090-6964
DOI: 10.1007/s10439-020-02683-x
Rights: Attribution 4.0 International
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