Biomechanics of Human Fetal Hearts with Critical Aortic Stenosis
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Annals of Biomedical Engineering ( 2020) https://doi.org/10.1007/s10439-020-02683-x
Original Article
Biomechanics of Human Fetal Hearts with Critical Aortic Stenosis CHI WEI ONG,1 MEIFENG REN,1 HADI WIPUTRA,1 JOY MOJUMDER,2 WEI XUAN CHAN,1 ANDREAS TULZER,3 GERALD TULZER,3 MARTIN LINDSAY BUIST,1 CITRA NURFARAH ZAINI MATTAR,4 LIK CHUAN LEE,2 and CHOON HWAI YAP 5 1
Department of Biomedical Engineering, National University of Singapore, Singapore, Singapore; 2Department of Mechanical Engineering, Michigan State University, East Lansing, United States; 3Department of Pediatric Cardiology, Children’s Heart Center Linz, Kepler University Hospital, Linz, Austria; 4Department of Obstetrics and Gynecology, Yong Loo Lin School of Medicine, National University of Singapore, National University Health System, Singapore, Singapore; and 5Department of Bioengineering, Imperial College London, London, UK (Received 23 July 2020; accepted 26 October 2020) Associate Editor Lakshmi Prasad Dasi oversaw the review of this article.
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 patientspecific 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
Address correspondence to Choon Hwai Yap, Department of Bioengineering, Imperial College London, London, UK. Electronic mail: [email protected]
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