Biomechanics of Human Fetal Hearts with Critical Aortic Stenosis

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, w...

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Bibliographic Details
Published in:Annals of biomedical engineering 2021-05, Vol.49 (5), p.1364-1379
Main 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
Format: Article
Language:English
Subjects:
Aorta
Aortic stenosis
Biochemistry
Biological and Medical Physics
Biomechanics
Biomedical and Life Sciences
Biomedical Engineering and Bioengineering
Biomedicine
Biophysics
Cardiovascular diseases
Classical Mechanics
Coronary artery disease
Fetuses
Finite element method
Flow velocity
Heart diseases
Hypertrophy
Model testing
Modelling
Muscle contraction
Original
Original Article
Pressure
Regurgitation
Rheumatic heart disease
Stenosis
Stiffness
Stresses
Stroke
Stroke volume
Ultrasound
Ventricle
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Summary: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.
ISSN:0090-6964
1573-9686
DOI:10.1007/s10439-020-02683-x