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Fluid–structure interaction in a fully coupled three-dimensional mitral–atrium–pulmonary model
This paper aims to investigate detailed mechanical interactions between the pulmonary haemodynamics and left heart function in pathophysiological situations (e.g. atrial fibrillation and acute mitral regurgitation). This is achieved by developing a complex computational framework for a coupled pulmo...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Berlin Heidelberg
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8298265/ https://www.ncbi.nlm.nih.gov/pubmed/33770307 http://dx.doi.org/10.1007/s10237-021-01444-6 |
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author | Feng, Liuyang Gao, Hao Qi, Nan Danton, Mark Hill, Nicholas A. Luo, Xiaoyu |
author_facet | Feng, Liuyang Gao, Hao Qi, Nan Danton, Mark Hill, Nicholas A. Luo, Xiaoyu |
author_sort | Feng, Liuyang |
collection | PubMed |
description | This paper aims to investigate detailed mechanical interactions between the pulmonary haemodynamics and left heart function in pathophysiological situations (e.g. atrial fibrillation and acute mitral regurgitation). This is achieved by developing a complex computational framework for a coupled pulmonary circulation, left atrium and mitral valve model. The left atrium and mitral valve are modelled with physiologically realistic three-dimensional geometries, fibre-reinforced hyperelastic materials and fluid–structure interaction, and the pulmonary vessels are modelled as one-dimensional network ended with structured trees, with specified vessel geometries and wall material properties. This new coupled model reveals some interesting results which could be of diagnostic values. For example, the wave propagation through the pulmonary vasculature can lead to different arrival times for the second systolic flow wave (S2 wave) among the pulmonary veins, forming vortex rings inside the left atrium. In the case of acute mitral regurgitation, the left atrium experiences an increased energy dissipation and pressure elevation. The pulmonary veins can experience increased wave intensities, reversal flow during systole and increased early-diastolic flow wave (D wave), which in turn causes an additional flow wave across the mitral valve (L wave), as well as a reversal flow at the left atrial appendage orifice. In the case of atrial fibrillation, we show that the loss of active contraction is associated with a slower flow inside the left atrial appendage and disappearances of the late-diastole atrial reversal wave (AR wave) and the first systolic wave (S1 wave) in pulmonary veins. The haemodynamic changes along the pulmonary vessel trees on different scales from microscopic vessels to the main pulmonary artery can all be captured in this model. The work promises a potential in quantifying disease progression and medical treatments of various pulmonary diseases such as the pulmonary hypertension due to a left heart dysfunction. |
format | Online Article Text |
id | pubmed-8298265 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Springer Berlin Heidelberg |
record_format | MEDLINE/PubMed |
spelling | pubmed-82982652021-07-23 Fluid–structure interaction in a fully coupled three-dimensional mitral–atrium–pulmonary model Feng, Liuyang Gao, Hao Qi, Nan Danton, Mark Hill, Nicholas A. Luo, Xiaoyu Biomech Model Mechanobiol Original Paper This paper aims to investigate detailed mechanical interactions between the pulmonary haemodynamics and left heart function in pathophysiological situations (e.g. atrial fibrillation and acute mitral regurgitation). This is achieved by developing a complex computational framework for a coupled pulmonary circulation, left atrium and mitral valve model. The left atrium and mitral valve are modelled with physiologically realistic three-dimensional geometries, fibre-reinforced hyperelastic materials and fluid–structure interaction, and the pulmonary vessels are modelled as one-dimensional network ended with structured trees, with specified vessel geometries and wall material properties. This new coupled model reveals some interesting results which could be of diagnostic values. For example, the wave propagation through the pulmonary vasculature can lead to different arrival times for the second systolic flow wave (S2 wave) among the pulmonary veins, forming vortex rings inside the left atrium. In the case of acute mitral regurgitation, the left atrium experiences an increased energy dissipation and pressure elevation. The pulmonary veins can experience increased wave intensities, reversal flow during systole and increased early-diastolic flow wave (D wave), which in turn causes an additional flow wave across the mitral valve (L wave), as well as a reversal flow at the left atrial appendage orifice. In the case of atrial fibrillation, we show that the loss of active contraction is associated with a slower flow inside the left atrial appendage and disappearances of the late-diastole atrial reversal wave (AR wave) and the first systolic wave (S1 wave) in pulmonary veins. The haemodynamic changes along the pulmonary vessel trees on different scales from microscopic vessels to the main pulmonary artery can all be captured in this model. The work promises a potential in quantifying disease progression and medical treatments of various pulmonary diseases such as the pulmonary hypertension due to a left heart dysfunction. Springer Berlin Heidelberg 2021-03-26 2021 /pmc/articles/PMC8298265/ /pubmed/33770307 http://dx.doi.org/10.1007/s10237-021-01444-6 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Original Paper Feng, Liuyang Gao, Hao Qi, Nan Danton, Mark Hill, Nicholas A. Luo, Xiaoyu Fluid–structure interaction in a fully coupled three-dimensional mitral–atrium–pulmonary model |
title | Fluid–structure interaction in a fully coupled three-dimensional mitral–atrium–pulmonary model |
title_full | Fluid–structure interaction in a fully coupled three-dimensional mitral–atrium–pulmonary model |
title_fullStr | Fluid–structure interaction in a fully coupled three-dimensional mitral–atrium–pulmonary model |
title_full_unstemmed | Fluid–structure interaction in a fully coupled three-dimensional mitral–atrium–pulmonary model |
title_short | Fluid–structure interaction in a fully coupled three-dimensional mitral–atrium–pulmonary model |
title_sort | fluid–structure interaction in a fully coupled three-dimensional mitral–atrium–pulmonary model |
topic | Original Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8298265/ https://www.ncbi.nlm.nih.gov/pubmed/33770307 http://dx.doi.org/10.1007/s10237-021-01444-6 |
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