The impact of myocardial compressibility on organ-level simulations of the normal and infarcted heart

Abstract Myocardial infarction (MI) rapidly impairs cardiac contractile function and instigates maladaptive remodeling leading to heart failure. Patient-specific models are a maturing technology for developing and determining therapeutic modalities for MI that require accurate descriptions of myocar...

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Autores principales:	Hao Liu, João S. Soares, John Walmsley, David S. Li, Samarth Raut, Reza Avazmohammadi, Paul Iaizzo, Mark Palmer, Joseph H. Gorman, Robert C. Gorman, Michael S. Sacks
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/82d45691d36245a6ae9cd5b612ac0300
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spelling	oai:doaj.org-article:82d45691d36245a6ae9cd5b612ac03002021-12-02T16:31:53ZThe impact of myocardial compressibility on organ-level simulations of the normal and infarcted heart10.1038/s41598-021-92810-y2045-2322https://doaj.org/article/82d45691d36245a6ae9cd5b612ac03002021-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-92810-yhttps://doaj.org/toc/2045-2322Abstract Myocardial infarction (MI) rapidly impairs cardiac contractile function and instigates maladaptive remodeling leading to heart failure. Patient-specific models are a maturing technology for developing and determining therapeutic modalities for MI that require accurate descriptions of myocardial mechanics. While substantial tissue volume reductions of 15–20% during systole have been reported, myocardium is commonly modeled as incompressible. We developed a myocardial model to simulate experimentally-observed systolic volume reductions in an ovine model of MI. Sheep-specific simulations of the cardiac cycle were performed using both incompressible and compressible tissue material models, and with synchronous or measurement-guided contraction. The compressible tissue model with measurement-guided contraction gave best agreement with experimentally measured reductions in tissue volume at peak systole, ventricular kinematics, and wall thickness changes. The incompressible model predicted myofiber peak contractile stresses approximately double the compressible model (182.8 kPa, 107.4 kPa respectively). Compensatory changes in remaining normal myocardium with MI present required less increase of contractile stress in the compressible model than the incompressible model (32.1%, 53.5%, respectively). The compressible model therefore provided more accurate representation of ventricular kinematics and potentially more realistic computed active contraction levels in the simulated infarcted heart. Our findings suggest that myocardial compressibility should be incorporated into future cardiac models for improved accuracy.Hao LiuJoão S. SoaresJohn WalmsleyDavid S. LiSamarth RautReza AvazmohammadiPaul IaizzoMark PalmerJoseph H. GormanRobert C. GormanMichael S. SacksNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-15 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Hao Liu João S. Soares John Walmsley David S. Li Samarth Raut Reza Avazmohammadi Paul Iaizzo Mark Palmer Joseph H. Gorman Robert C. Gorman Michael S. Sacks The impact of myocardial compressibility on organ-level simulations of the normal and infarcted heart
description	Abstract Myocardial infarction (MI) rapidly impairs cardiac contractile function and instigates maladaptive remodeling leading to heart failure. Patient-specific models are a maturing technology for developing and determining therapeutic modalities for MI that require accurate descriptions of myocardial mechanics. While substantial tissue volume reductions of 15–20% during systole have been reported, myocardium is commonly modeled as incompressible. We developed a myocardial model to simulate experimentally-observed systolic volume reductions in an ovine model of MI. Sheep-specific simulations of the cardiac cycle were performed using both incompressible and compressible tissue material models, and with synchronous or measurement-guided contraction. The compressible tissue model with measurement-guided contraction gave best agreement with experimentally measured reductions in tissue volume at peak systole, ventricular kinematics, and wall thickness changes. The incompressible model predicted myofiber peak contractile stresses approximately double the compressible model (182.8 kPa, 107.4 kPa respectively). Compensatory changes in remaining normal myocardium with MI present required less increase of contractile stress in the compressible model than the incompressible model (32.1%, 53.5%, respectively). The compressible model therefore provided more accurate representation of ventricular kinematics and potentially more realistic computed active contraction levels in the simulated infarcted heart. Our findings suggest that myocardial compressibility should be incorporated into future cardiac models for improved accuracy.
format	article
author	Hao Liu João S. Soares John Walmsley David S. Li Samarth Raut Reza Avazmohammadi Paul Iaizzo Mark Palmer Joseph H. Gorman Robert C. Gorman Michael S. Sacks
author_facet	Hao Liu João S. Soares John Walmsley David S. Li Samarth Raut Reza Avazmohammadi Paul Iaizzo Mark Palmer Joseph H. Gorman Robert C. Gorman Michael S. Sacks
author_sort	Hao Liu
title	The impact of myocardial compressibility on organ-level simulations of the normal and infarcted heart
title_short	The impact of myocardial compressibility on organ-level simulations of the normal and infarcted heart
title_full	The impact of myocardial compressibility on organ-level simulations of the normal and infarcted heart
title_fullStr	The impact of myocardial compressibility on organ-level simulations of the normal and infarcted heart
title_full_unstemmed	The impact of myocardial compressibility on organ-level simulations of the normal and infarcted heart
title_sort	impact of myocardial compressibility on organ-level simulations of the normal and infarcted heart
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/82d45691d36245a6ae9cd5b612ac0300
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The impact of myocardial compressibility on organ-level simulations of the normal and infarcted heart

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