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A Lumped Two-Compartment Model for Simulation of Ventricular Pump and Tissue Mechanics in Ischemic Heart Disease

Introduction: Computational modeling of cardiac mechanics and hemodynamics in ischemic heart disease (IHD) is important for a better understanding of the complex relations between ischemia-induced heterogeneity of myocardial tissue properties, regional tissue mechanics, and hemodynamic pump function...

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Autores principales: Koopsen, Tijmen, Van Osta, Nick, Van Loon, Tim, Van Nieuwenhoven, Frans A., Prinzen, Frits W., Van Klarenbosch, Bas R., Kirkels, Feddo P., Teske, Arco J., Vernooy, Kevin, Delhaas, Tammo, Lumens, Joost
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9130776/
https://www.ncbi.nlm.nih.gov/pubmed/35634163
http://dx.doi.org/10.3389/fphys.2022.782592
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author Koopsen, Tijmen
Van Osta, Nick
Van Loon, Tim
Van Nieuwenhoven, Frans A.
Prinzen, Frits W.
Van Klarenbosch, Bas R.
Kirkels, Feddo P.
Teske, Arco J.
Vernooy, Kevin
Delhaas, Tammo
Lumens, Joost
author_facet Koopsen, Tijmen
Van Osta, Nick
Van Loon, Tim
Van Nieuwenhoven, Frans A.
Prinzen, Frits W.
Van Klarenbosch, Bas R.
Kirkels, Feddo P.
Teske, Arco J.
Vernooy, Kevin
Delhaas, Tammo
Lumens, Joost
author_sort Koopsen, Tijmen
collection PubMed
description Introduction: Computational modeling of cardiac mechanics and hemodynamics in ischemic heart disease (IHD) is important for a better understanding of the complex relations between ischemia-induced heterogeneity of myocardial tissue properties, regional tissue mechanics, and hemodynamic pump function. We validated and applied a lumped two-compartment modeling approach for IHD integrated into the CircAdapt model of the human heart and circulation. Methods: Ischemic contractile dysfunction was simulated by subdividing a left ventricular (LV) wall segment into a hypothetical contractile and noncontractile compartment, and dysfunction severity was determined by the noncontractile volume fraction ( [Formula: see text] ). Myocardial stiffness was determined by the zero-passive stress length ( [Formula: see text] and nonlinearity ( [Formula: see text] ) of the passive stress-sarcomere length relation of the noncontractile compartment. Simulated end-systolic pressure volume relations (ESPVRs) for 20% acute ischemia were qualitatively compared between a two- and one-compartment simulation, and parameters of the two-compartment model were tuned to previously published canine data of regional myocardial deformation during acute and prolonged ischemia and reperfusion. In six patients with myocardial infarction (MI), the [Formula: see text] was automatically estimated using the echocardiographic LV strain and volume measurements obtained acutely and 6 months after MI. Estimated segmental [Formula: see text] values at the baseline and 6-month follow-up were compared with percentage late gadolinium enhancement (LGE) at 6-month follow-up. Results: Simulation of 20% of [Formula: see text] shifted the ESPVR rightward while moderately reducing the slope, while a one-compartment simulation caused a leftward shift with severe reduction in the slope. Through tuning of the [Formula: see text] , [Formula: see text] , and [Formula: see text] , it was found that manipulation of the [Formula: see text] alone reproduced the deformation during acute ischemia and reperfusion, while additional manipulations of [Formula: see text] and [Formula: see text] were required to reproduce deformation during prolonged ischemia and reperfusion. Out of all segments with LGE>25% at the follow-up, the majority (68%) had higher estimated [Formula: see text] at the baseline than at the follow-up. Furthermore, the baseline [Formula: see text] correlated better with percentage LGE than [Formula: see text] did at the follow-up. Conclusion: We successfully used a two-compartment model for simulation of the ventricular pump and tissue mechanics in IHD. Patient-specific optimizations using regional myocardial deformation estimated the [Formula: see text] in a small cohort of MI patients in the acute and chronic phase after MI, while estimated [Formula: see text] values closely approximated the extent of the myocardial scar at the follow-up. In future studies, this approach can facilitate deformation imaging–based estimation of myocardial tissue properties in patients with cardiovascular diseases.
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spelling pubmed-91307762022-05-26 A Lumped Two-Compartment Model for Simulation of Ventricular Pump and Tissue Mechanics in Ischemic Heart Disease Koopsen, Tijmen Van Osta, Nick Van Loon, Tim Van Nieuwenhoven, Frans A. Prinzen, Frits W. Van Klarenbosch, Bas R. Kirkels, Feddo P. Teske, Arco J. Vernooy, Kevin Delhaas, Tammo Lumens, Joost Front Physiol Physiology Introduction: Computational modeling of cardiac mechanics and hemodynamics in ischemic heart disease (IHD) is important for a better understanding of the complex relations between ischemia-induced heterogeneity of myocardial tissue properties, regional tissue mechanics, and hemodynamic pump function. We validated and applied a lumped two-compartment modeling approach for IHD integrated into the CircAdapt model of the human heart and circulation. Methods: Ischemic contractile dysfunction was simulated by subdividing a left ventricular (LV) wall segment into a hypothetical contractile and noncontractile compartment, and dysfunction severity was determined by the noncontractile volume fraction ( [Formula: see text] ). Myocardial stiffness was determined by the zero-passive stress length ( [Formula: see text] and nonlinearity ( [Formula: see text] ) of the passive stress-sarcomere length relation of the noncontractile compartment. Simulated end-systolic pressure volume relations (ESPVRs) for 20% acute ischemia were qualitatively compared between a two- and one-compartment simulation, and parameters of the two-compartment model were tuned to previously published canine data of regional myocardial deformation during acute and prolonged ischemia and reperfusion. In six patients with myocardial infarction (MI), the [Formula: see text] was automatically estimated using the echocardiographic LV strain and volume measurements obtained acutely and 6 months after MI. Estimated segmental [Formula: see text] values at the baseline and 6-month follow-up were compared with percentage late gadolinium enhancement (LGE) at 6-month follow-up. Results: Simulation of 20% of [Formula: see text] shifted the ESPVR rightward while moderately reducing the slope, while a one-compartment simulation caused a leftward shift with severe reduction in the slope. Through tuning of the [Formula: see text] , [Formula: see text] , and [Formula: see text] , it was found that manipulation of the [Formula: see text] alone reproduced the deformation during acute ischemia and reperfusion, while additional manipulations of [Formula: see text] and [Formula: see text] were required to reproduce deformation during prolonged ischemia and reperfusion. Out of all segments with LGE>25% at the follow-up, the majority (68%) had higher estimated [Formula: see text] at the baseline than at the follow-up. Furthermore, the baseline [Formula: see text] correlated better with percentage LGE than [Formula: see text] did at the follow-up. Conclusion: We successfully used a two-compartment model for simulation of the ventricular pump and tissue mechanics in IHD. Patient-specific optimizations using regional myocardial deformation estimated the [Formula: see text] in a small cohort of MI patients in the acute and chronic phase after MI, while estimated [Formula: see text] values closely approximated the extent of the myocardial scar at the follow-up. In future studies, this approach can facilitate deformation imaging–based estimation of myocardial tissue properties in patients with cardiovascular diseases. Frontiers Media S.A. 2022-05-11 /pmc/articles/PMC9130776/ /pubmed/35634163 http://dx.doi.org/10.3389/fphys.2022.782592 Text en Copyright © 2022 Koopsen, Van Osta, Van Loon, Van Nieuwenhoven, Prinzen, Van Klarenbosch, Kirkels, Teske, Vernooy, Delhaas and Lumens. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Physiology
Koopsen, Tijmen
Van Osta, Nick
Van Loon, Tim
Van Nieuwenhoven, Frans A.
Prinzen, Frits W.
Van Klarenbosch, Bas R.
Kirkels, Feddo P.
Teske, Arco J.
Vernooy, Kevin
Delhaas, Tammo
Lumens, Joost
A Lumped Two-Compartment Model for Simulation of Ventricular Pump and Tissue Mechanics in Ischemic Heart Disease
title A Lumped Two-Compartment Model for Simulation of Ventricular Pump and Tissue Mechanics in Ischemic Heart Disease
title_full A Lumped Two-Compartment Model for Simulation of Ventricular Pump and Tissue Mechanics in Ischemic Heart Disease
title_fullStr A Lumped Two-Compartment Model for Simulation of Ventricular Pump and Tissue Mechanics in Ischemic Heart Disease
title_full_unstemmed A Lumped Two-Compartment Model for Simulation of Ventricular Pump and Tissue Mechanics in Ischemic Heart Disease
title_short A Lumped Two-Compartment Model for Simulation of Ventricular Pump and Tissue Mechanics in Ischemic Heart Disease
title_sort lumped two-compartment model for simulation of ventricular pump and tissue mechanics in ischemic heart disease
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9130776/
https://www.ncbi.nlm.nih.gov/pubmed/35634163
http://dx.doi.org/10.3389/fphys.2022.782592
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