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      Effect of myocardial heterogeneity on ventricular electro-mechanical responses: a computational study

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          Abstract

          Background

          The heart wall exhibits three layers of different thicknesses: the outer epicardium, mid-myocardium, and inner endocardium. Among these layers, the mid-myocardium is typically the thickest. As indicated by preliminary studies, heart-wall layers exhibit various characteristics with regard to electrophysiology, pharmacology, and pathology. Construction of an accurate three-dimensional (3D) model of the heart is important for predicting physiological behaviors. However, the wide variability of myocardial shapes and the unclear edges between the epicardium and soft tissues are major challenges in the 3D model segmentation approach for identifying the boundaries of the epicardium, mid-myocardium, and endocardium. Therefore, this results in possible variations in the heterogeneity ratios between the epicardium, mid-myocardium, and endocardium. The objective of this study was to observe the effects of different thickness ratios of the epicardium, mid-myocardium, and endocardium on cardiac arrhythmogenesis, reentry instability, and mechanical responses during arrhythmia.

          Methods

          We used a computational method and simulated three heterogeneous ventricular models: Model 1 had the thickest M cell layer and thinnest epicardium and endocardium. Model 2 had intermediate layer thicknesses. Model 3 exhibited the thinnest mid-myocardium and thickest epicardium and endocardium. Electrical and mechanical simulations of the three heterogeneous models were performed under normal sinus rhythm and reentry conditions.

          Results

          Model 1 exhibited the highest probability of terminating reentrant waves, and Model 3 exhibited to experience greater cardiac arrhythmia. In the reentry simulation, at 8 s, Model 3 generated the largest number of rotors (eight), while Models 1 and 2 produced five and seven rotors, respectively. There was no significant difference in the cardiac output obtained during the sinus rhythm. Under the reentry condition, the highest cardiac output was generated by Model 1 (19 mL/s), followed by Model 2 (9 mL/s) and Model 3 (7 mL/s).

          Conclusions

          A thicker mid-myocardium led to improvements in the pumping efficacy and contractility and reduced the probability of cardiac arrhythmia. Conversely, thinner M cell layers generated more unstable reentrant spiral waves and hindered the ventricular pumping.

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          Most cited references22

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          Coupling of a 3D finite element model of cardiac ventricular mechanics to lumped systems models of the systemic and pulmonic circulation.

          In this study we present a novel, robust method to couple finite element (FE) models of cardiac mechanics to systems models of the circulation (CIRC), independent of cardiac phase. For each time step through a cardiac cycle, left and right ventricular pressures were calculated using ventricular compliances from the FE and CIRC models. These pressures served as boundary conditions in the FE and CIRC models. In succeeding steps, pressures were updated to minimize cavity volume error (FE minus CIRC volume) using Newton iterations. Coupling was achieved when a predefined criterion for the volume error was satisfied. Initial conditions for the multi-scale model were obtained by replacing the FE model with a varying elastance model, which takes into account direct ventricular interactions. Applying the coupling, a novel multi-scale model of the canine cardiovascular system was developed. Global hemodynamics and regional mechanics were calculated for multiple beats in two separate simulations with a left ventricular ischemic region and pulmonary artery constriction, respectively. After the interventions, global hemodynamics changed due to direct and indirect ventricular interactions, in agreement with previously published experimental results. The coupling method allows for simulations of multiple cardiac cycles for normal and pathophysiology, encompassing levels from cell to system.
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            Direct delineation of myocardial infarction without contrast agents using a joint motion feature learning architecture

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              Electromechanical models of the ventricles.

              Computational modeling has traditionally played an important role in dissecting the mechanisms for cardiac dysfunction. Ventricular electromechanical models, likely the most sophisticated virtual organs to date, integrate detailed information across the spatial scales of cardiac electrophysiology and mechanics and are capable of capturing the emergent behavior and the interaction between electrical activation and mechanical contraction of the heart. The goal of this review is to provide an overview of the latest advancements in multiscale electromechanical modeling of the ventricles. We first detail the general framework of multiscale ventricular electromechanical modeling and describe the state of the art in computational techniques and experimental validation approaches. The powerful utility of ventricular electromechanical models in providing a better understanding of cardiac function is then demonstrated by reviewing the latest insights obtained by these models, focusing primarily on the mechanisms by which mechanoelectric coupling contributes to ventricular arrythmogenesis, the relationship between electrical activation and mechanical contraction in the normal heart, and the mechanisms of mechanical dyssynchrony and resynchronization in the failing heart. Computational modeling of cardiac electromechanics will continue to complement basic science research and clinical cardiology and holds promise to become an important clinical tool aiding the diagnosis and treatment of cardiac disease.
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                Author and article information

                Contributors
                dusturianida@kumoh.ac.kr
                swchoe@kangwon.ac.kr
                kssong10@kumoh.ac.kr
                +82544787780 , kmlim@kumoh.ac.kr
                Journal
                Biomed Eng Online
                Biomed Eng Online
                BioMedical Engineering OnLine
                BioMed Central (London )
                1475-925X
                14 March 2019
                14 March 2019
                2019
                : 18
                : 23
                Affiliations
                [1 ]ISNI 0000 0004 0532 9817, GRID grid.418997.a, Department of IT Convergence Engineering, , Kumoh National Institute of Technology, ; 61 Daehak-ro, Gumi, Gyeongbuk 39253 Republic of Korea
                [2 ]ISNI 0000 0001 0707 9039, GRID grid.412010.6, Department of Mechanical and Biomedical Engineering, , Kangwon National University, ; Chuncheon, Republic of Korea
                [3 ]ISNI 0000 0004 0532 9817, GRID grid.418997.a, Department of Medical IT Convergence Engineering, , Kumoh National Institute of Technology, ; Gumi, Republic of Korea
                Author information
                http://orcid.org/0000-0001-6729-8129
                Article
                640
                10.1186/s12938-019-0640-7
                6419335
                30871548
                e7b32d44-a283-4829-97e9-1c5349df5a91
                © The Author(s) 2019

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 20 September 2018
                : 6 March 2019
                Funding
                Funded by: Information Technology Research Center (KR)
                Award ID: IITP-2018-2014-0-00639
                Award Recipient :
                Funded by: National Research Foundation (KR)
                Award ID: 2016R1D1A1B0101440
                Award Recipient :
                Funded by: EDISON
                Award ID: NRF-2011-0020576
                Award Recipient :
                Categories
                Research
                Custom metadata
                © The Author(s) 2019

                Biomedical engineering
                cardiac arrhythmia,endocardium,epicardium,heterogeneous ventricular models,mid-myocardium

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