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Effects of fibroblast on electromechanical dynamics of human atrial tissue—insights from a 2D discrete element model

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Effects of fibroblast on electromechanical dynamics of human atrial tissue—insights from a 2D discrete element model. / Brocklehurst, Paul; Zhang, Henggui; Ye, Jianqiao.

In: Frontiers in Physiology, Vol. 13, 938497, 26.07.2022.

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@article{2253fc302e674346b942730dadbb4d2a,
title = "Effects of fibroblast on electromechanical dynamics of human atrial tissue—insights from a 2D discrete element model",
abstract = "Roughly 75% of normal myocardial tissue volume is comprised of myocytes, however, fibroblasts by number are the most predominant cells in cardiac tissue. Previous studies have shown distinctive differences in cellular electrophysiology and excitability between myocytes and fibroblasts. However, it is still unclear how the electrical coupling between the two and the increased population of fibroblasts affects the electromechanical dynamics of cardiac tissue. This paper focuses on investigating effects of fibroblast-myocyte electrical coupling (FMEC) and fibroblast population on atrial electrical conduction and mechanical contractility by using a two-dimensional Discrete Element Method (DEM) model of cardiac tissue that is different to finite element method (FEM). In the model, the electro-mechanics of atrial cells are modelled by a biophysically detailed model for atrial electrical action potentials and myofilament kinetics, and the atrial fibroblasts are modelled by an active model that considers four active membrane ionic channel currents. Our simulation results show that the FMEC impairs myocytes{\textquoteright} electrical action potential and mechanical contractibility, manifested by reduced upstroke velocity, amplitude and duration of action potentials, as well as cell length shortening. At the tissue level, the FMEC slows down the conduction of excitation waves, and reduces strain of the tissue produced during a contraction course. These findings provide new insights into understandings of how FMEC impairs cardiac electrical and mechanical dynamics of the heart.",
keywords = "Physiology, fibroblast, cardiac model, discrete element method (DEM), electrical excitation, mechanical contraction, simulation, human atrial action potential model",
author = "Paul Brocklehurst and Henggui Zhang and Jianqiao Ye",
year = "2022",
month = jul,
day = "26",
doi = "10.3389/fphys.2022.938497",
language = "English",
volume = "13",
journal = "Frontiers in Physiology",
issn = "1664-042X",
publisher = "Frontiers Media S.A.",

}

RIS

TY - JOUR

T1 - Effects of fibroblast on electromechanical dynamics of human atrial tissue—insights from a 2D discrete element model

AU - Brocklehurst, Paul

AU - Zhang, Henggui

AU - Ye, Jianqiao

PY - 2022/7/26

Y1 - 2022/7/26

N2 - Roughly 75% of normal myocardial tissue volume is comprised of myocytes, however, fibroblasts by number are the most predominant cells in cardiac tissue. Previous studies have shown distinctive differences in cellular electrophysiology and excitability between myocytes and fibroblasts. However, it is still unclear how the electrical coupling between the two and the increased population of fibroblasts affects the electromechanical dynamics of cardiac tissue. This paper focuses on investigating effects of fibroblast-myocyte electrical coupling (FMEC) and fibroblast population on atrial electrical conduction and mechanical contractility by using a two-dimensional Discrete Element Method (DEM) model of cardiac tissue that is different to finite element method (FEM). In the model, the electro-mechanics of atrial cells are modelled by a biophysically detailed model for atrial electrical action potentials and myofilament kinetics, and the atrial fibroblasts are modelled by an active model that considers four active membrane ionic channel currents. Our simulation results show that the FMEC impairs myocytes’ electrical action potential and mechanical contractibility, manifested by reduced upstroke velocity, amplitude and duration of action potentials, as well as cell length shortening. At the tissue level, the FMEC slows down the conduction of excitation waves, and reduces strain of the tissue produced during a contraction course. These findings provide new insights into understandings of how FMEC impairs cardiac electrical and mechanical dynamics of the heart.

AB - Roughly 75% of normal myocardial tissue volume is comprised of myocytes, however, fibroblasts by number are the most predominant cells in cardiac tissue. Previous studies have shown distinctive differences in cellular electrophysiology and excitability between myocytes and fibroblasts. However, it is still unclear how the electrical coupling between the two and the increased population of fibroblasts affects the electromechanical dynamics of cardiac tissue. This paper focuses on investigating effects of fibroblast-myocyte electrical coupling (FMEC) and fibroblast population on atrial electrical conduction and mechanical contractility by using a two-dimensional Discrete Element Method (DEM) model of cardiac tissue that is different to finite element method (FEM). In the model, the electro-mechanics of atrial cells are modelled by a biophysically detailed model for atrial electrical action potentials and myofilament kinetics, and the atrial fibroblasts are modelled by an active model that considers four active membrane ionic channel currents. Our simulation results show that the FMEC impairs myocytes’ electrical action potential and mechanical contractibility, manifested by reduced upstroke velocity, amplitude and duration of action potentials, as well as cell length shortening. At the tissue level, the FMEC slows down the conduction of excitation waves, and reduces strain of the tissue produced during a contraction course. These findings provide new insights into understandings of how FMEC impairs cardiac electrical and mechanical dynamics of the heart.

KW - Physiology

KW - fibroblast

KW - cardiac model

KW - discrete element method (DEM)

KW - electrical excitation

KW - mechanical contraction

KW - simulation

KW - human atrial action potential model

U2 - 10.3389/fphys.2022.938497

DO - 10.3389/fphys.2022.938497

M3 - Journal article

VL - 13

JO - Frontiers in Physiology

JF - Frontiers in Physiology

SN - 1664-042X

M1 - 938497

ER -