Determination of adequate defibrillation of ventricular tachycardia using computer simulation of electroporation aftershock effects on human cardiomyocytes

Po Yuan Chen, Wei Hua Tang, Min Hung Chen, Ching Hsing Luo

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Electric defibrillation is a life-saving therapy for clinically dangerous ventricular arrhythmias. Unfortunately, direct-current (DC) shock treatment often induces or worsens other tachyarrhythmias. The adverse effects of electric shock delivered to human ventricular cardiomyocytes are not fully understood. This study thus uses computer simulation to investigate the pathogenesis of the electrophoresis in epicardial and endocardial human tissue. The O'Hara-Rudy dynamic human ventricular cell model incorporated with Ohuchi's mathematical DC shock model is used. The effect of electroporation is described as a transmembrane pore, mimicking the reversible breakdown of the cell membrane. The aftershock effects on epiardial and endocardial ventricular cardiomyocytes are evaluated. The effects of delivering shock from the endocardium and epicardium using a multicellular one-dimensional strand model are also investigated. Ventricular tachycardia can be terminated by a low-strength shock to endocardial cardiomyocytes. However, an excessively strong shock to epicardial cardiomyocytes induces early afterdepolarization and is arrhythmogenic. The aftershock effect of the electroporation is serious for epicardial ventricular myocytes. The optimization of defibrillation energy delivery to the maximum membrane potential and the pathogenesis of the aftershock effect during ventricular tachycardia are also investigated. The aftershock effect of electroporation is more serious in epicardial cells than it is in endocardial cells. It is suggested that the DC shock be delivered to endocardium cells before the maximum membrane potential of the epicardial cell in a multicellular one-dimensional strand model is reached, which is before the electrocardiogram R wave spike.

Original languageEnglish
Pages (from-to)597-605
Number of pages9
JournalJournal of Medical and Biological Engineering
Volume33
Issue number6
DOIs
Publication statusPublished - 2013 Dec 1

Fingerprint

Electroporation
Ventricular Tachycardia
Cardiac Myocytes
Computer Simulation
Shock
Computer simulation
Endocardium
Membranes
Membrane Potentials
Cell membranes
Electrophoresis
Electrocardiography
Electric Countershock
Tissue
Pericardium
Tachycardia
Muscle Cells
Cardiac Arrhythmias
Cell Membrane
Therapeutics

All Science Journal Classification (ASJC) codes

  • Biomedical Engineering

Cite this

@article{443fcb017ec740afbd4f068a6fee6b37,
title = "Determination of adequate defibrillation of ventricular tachycardia using computer simulation of electroporation aftershock effects on human cardiomyocytes",
abstract = "Electric defibrillation is a life-saving therapy for clinically dangerous ventricular arrhythmias. Unfortunately, direct-current (DC) shock treatment often induces or worsens other tachyarrhythmias. The adverse effects of electric shock delivered to human ventricular cardiomyocytes are not fully understood. This study thus uses computer simulation to investigate the pathogenesis of the electrophoresis in epicardial and endocardial human tissue. The O'Hara-Rudy dynamic human ventricular cell model incorporated with Ohuchi's mathematical DC shock model is used. The effect of electroporation is described as a transmembrane pore, mimicking the reversible breakdown of the cell membrane. The aftershock effects on epiardial and endocardial ventricular cardiomyocytes are evaluated. The effects of delivering shock from the endocardium and epicardium using a multicellular one-dimensional strand model are also investigated. Ventricular tachycardia can be terminated by a low-strength shock to endocardial cardiomyocytes. However, an excessively strong shock to epicardial cardiomyocytes induces early afterdepolarization and is arrhythmogenic. The aftershock effect of the electroporation is serious for epicardial ventricular myocytes. The optimization of defibrillation energy delivery to the maximum membrane potential and the pathogenesis of the aftershock effect during ventricular tachycardia are also investigated. The aftershock effect of electroporation is more serious in epicardial cells than it is in endocardial cells. It is suggested that the DC shock be delivered to endocardium cells before the maximum membrane potential of the epicardial cell in a multicellular one-dimensional strand model is reached, which is before the electrocardiogram R wave spike.",
author = "Chen, {Po Yuan} and Tang, {Wei Hua} and Chen, {Min Hung} and Luo, {Ching Hsing}",
year = "2013",
month = "12",
day = "1",
doi = "10.5405/jmbe.1203",
language = "English",
volume = "33",
pages = "597--605",
journal = "Journal of Medical and Biological Engineering",
issn = "1609-0985",
publisher = "Biomedical Engineering Society",
number = "6",

}

TY - JOUR

T1 - Determination of adequate defibrillation of ventricular tachycardia using computer simulation of electroporation aftershock effects on human cardiomyocytes

AU - Chen, Po Yuan

AU - Tang, Wei Hua

AU - Chen, Min Hung

AU - Luo, Ching Hsing

PY - 2013/12/1

Y1 - 2013/12/1

N2 - Electric defibrillation is a life-saving therapy for clinically dangerous ventricular arrhythmias. Unfortunately, direct-current (DC) shock treatment often induces or worsens other tachyarrhythmias. The adverse effects of electric shock delivered to human ventricular cardiomyocytes are not fully understood. This study thus uses computer simulation to investigate the pathogenesis of the electrophoresis in epicardial and endocardial human tissue. The O'Hara-Rudy dynamic human ventricular cell model incorporated with Ohuchi's mathematical DC shock model is used. The effect of electroporation is described as a transmembrane pore, mimicking the reversible breakdown of the cell membrane. The aftershock effects on epiardial and endocardial ventricular cardiomyocytes are evaluated. The effects of delivering shock from the endocardium and epicardium using a multicellular one-dimensional strand model are also investigated. Ventricular tachycardia can be terminated by a low-strength shock to endocardial cardiomyocytes. However, an excessively strong shock to epicardial cardiomyocytes induces early afterdepolarization and is arrhythmogenic. The aftershock effect of the electroporation is serious for epicardial ventricular myocytes. The optimization of defibrillation energy delivery to the maximum membrane potential and the pathogenesis of the aftershock effect during ventricular tachycardia are also investigated. The aftershock effect of electroporation is more serious in epicardial cells than it is in endocardial cells. It is suggested that the DC shock be delivered to endocardium cells before the maximum membrane potential of the epicardial cell in a multicellular one-dimensional strand model is reached, which is before the electrocardiogram R wave spike.

AB - Electric defibrillation is a life-saving therapy for clinically dangerous ventricular arrhythmias. Unfortunately, direct-current (DC) shock treatment often induces or worsens other tachyarrhythmias. The adverse effects of electric shock delivered to human ventricular cardiomyocytes are not fully understood. This study thus uses computer simulation to investigate the pathogenesis of the electrophoresis in epicardial and endocardial human tissue. The O'Hara-Rudy dynamic human ventricular cell model incorporated with Ohuchi's mathematical DC shock model is used. The effect of electroporation is described as a transmembrane pore, mimicking the reversible breakdown of the cell membrane. The aftershock effects on epiardial and endocardial ventricular cardiomyocytes are evaluated. The effects of delivering shock from the endocardium and epicardium using a multicellular one-dimensional strand model are also investigated. Ventricular tachycardia can be terminated by a low-strength shock to endocardial cardiomyocytes. However, an excessively strong shock to epicardial cardiomyocytes induces early afterdepolarization and is arrhythmogenic. The aftershock effect of the electroporation is serious for epicardial ventricular myocytes. The optimization of defibrillation energy delivery to the maximum membrane potential and the pathogenesis of the aftershock effect during ventricular tachycardia are also investigated. The aftershock effect of electroporation is more serious in epicardial cells than it is in endocardial cells. It is suggested that the DC shock be delivered to endocardium cells before the maximum membrane potential of the epicardial cell in a multicellular one-dimensional strand model is reached, which is before the electrocardiogram R wave spike.

UR - http://www.scopus.com/inward/record.url?scp=84891601042&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84891601042&partnerID=8YFLogxK

U2 - 10.5405/jmbe.1203

DO - 10.5405/jmbe.1203

M3 - Article

AN - SCOPUS:84891601042

VL - 33

SP - 597

EP - 605

JO - Journal of Medical and Biological Engineering

JF - Journal of Medical and Biological Engineering

SN - 1609-0985

IS - 6

ER -