Effects of Electroporation on the Transmembrane Potential Distribution in a Two‐Dimensional Bidomain Model of Cardiac Tissue

Aguel, Felipe; DeBruin, Katherine A.; Krassowska, Wanda; Trayanova, Natalia A.

doi:10.1111/j.1540-8167.1999.tb00247.x

Cited by 36 publications

(17 citation statements)

References 37 publications

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“…There are exceptions. For example, Aguel et al, 31 Skouibine et al, 32 and Ashihara et al 33 included electroporation in their simulations, and found significant quantitative effects. Similarly, Bray and I 34 found that electroporation did indeed keep V m from becoming extremely large near an electrode.…”

Section: Invalid Assumptions In the Simulationsmentioning

confidence: 99%

Artifacts, assumptions, and ambiguity: Pitfalls in comparing experimental results to numerical simulations when studying electrical stimulation of the heart

Roth

2002

Chaos: An Interdisciplinary Journal of Nonlinear Science

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Insidious experimental artifacts and invalid theoretical assumptions complicate the comparison of numerical predictions and observed data. Such difficulties are particularly troublesome when studying electrical stimulation of the heart. During unipolar stimulation of cardiac tissue, the artifacts include nonlinearity of membrane dyes, optical signals blocked by the stimulating electrode, averaging of optical signals with depth, lateral averaging of optical signals, limitations of the current source, and the use of excitation-contraction uncouplers. The assumptions involve electroporation, membrane models, electrode size, the perfusing bath, incorrect model parameters, the applicability of a continuum model, and tissue damage. Comparisons of theory and experiment during far-field stimulation are limited by many of these same factors, plus artifacts from plunge and epicardial recording electrodes and assumptions about the fiber angle at an insulating boundary. These pitfalls must be overcome in order to understand quantitatively how the heart responds to an electrical stimulus. (c) 2002 American Institute of Physics.

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Section: Invalid Assumptions In the Simulationsmentioning

confidence: 99%

Artifacts, assumptions, and ambiguity: Pitfalls in comparing experimental results to numerical simulations when studying electrical stimulation of the heart

Roth

2002

Chaos: An Interdisciplinary Journal of Nonlinear Science

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“…These effects are important to defibrillation success and to the susceptibility for further arrhythmias (34), and they are critical for the accuracy of computational models of defibrillation (1,3,11,27). However, longer-term effects have not been studied in intact hearts, but should be considered, since electroporation can be irreversible.…”

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confidence: 99%

Electroporation induced by internal defibrillation shock with and without recovery in intact rabbit hearts

Wang

Efimov

Cheng

2012

American Journal of Physiology-Heart and Circulatory Physiology

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Wang YT, Efimov IR, Cheng Y. Electroporation induced by internal defibrillation shock with and without recovery in intact rabbit hearts. Am J Physiol Heart Circ Physiol 303: H439 -H449, 2012. First published June 22, 2012; doi:10.1152/ajpheart.01121.2011.-Defibrillation shocks from implantable cardioverter defibrillators can be lifesaving but can also damage cardiac tissues via electroporation. This study characterizes the spatial distribution and extent of defibrillation shock-induced electroporation with and without a 45-min postshock period for cell membranes to recover. Langendorff-perfused rabbit hearts (n ϭ 31) with and without a chronic left ventricular (LV) myocardial infarction (MI) were studied. Mean defibrillation threshold (DFT) was determined to be 161.4 Ϯ 17.1 V and 1.65 Ϯ 0.44 J in MI hearts for internally delivered 8-ms monophasic truncated exponential (MTE) shocks during sustained ventricular fibrillation (Ͼ20 s, SVF). A single 300-V MTE shock (twice determined DFT voltage) was used to terminate SVF. Shock-induced electroporation was assessed by propidium iodide (PI) uptake. Ventricular PI staining was quantified by fluorescent imaging. Histological analysis was performed using Masson's Trichrome staining. Results showed PI staining concentrated near the shock electrode in all hearts. Without recovery, PI staining was similar between normal and MI groups around the shock electrode and over the whole ventricles. However, MI hearts had greater total PI uptake in anterior (P Ͻ 0.01) and posterior (P Ͻ 0.01) LV epicardial regions. Postrecovery, PI staining was reduced substantially, but residual staining remained significant with similar spacial distributions. PI staining under SVF was similar to previously studied paced hearts. In conclusion, electroporation was spatially correlated with the active region of the shock electrode. Additional electroporation occurred in the LV epicardium of MI hearts, in the infarct border zone. Recovery of membrane integrity postelectroporation is likely a prolonged process. Short periods of SVF did not affect electroporation injury. membrane recovery; myocardial infarction; propidium iodide; sustained ventricular fibrillation DEFIBRILLATION IS THE MOST effective and immediate treatment for sustained ventricular fibrillation (SVF), a major cause of sudden cardiac death (SCD) (30). However, while life-saving, defibrillation has adverse effects. These include impaired myocardial contraction and relaxation (50), decreased cardiac output (36) and cardiac index (46), increased pacing threshold (49), and permanent tissue damage (43). This injury may increase the risk of developing heart failure (HF) or exacerbate its symptoms (6,16,44). With the increasing use of implantable cardioverter defibrillators (ICDs) to prevent SCD (28), it is increasingly important to understand the deleterious effects of defibrillation therapy.Electroporation, the disruption of cell membranes by an electric shock, may play a role in these adverse effects. Cardiac studies have shown that electrop...

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“…In the absence of a better strategy, strong electrical shocks have remained the only reliable treatment for cardiac fibrillation. Over the years, biophysically-detailed multi-scale models of defibrillation [3,6,105,107] have made major contributions to understanding how defibrillation shocks used in clinical practice interact with cardiac tissue [7,9,11,29,50,78,103,104,115,118]; these models have been validated by comparing to the results of optimal mapping experiments [20,24,25]. Computer modeling of whole-heart defibrillation has been instrumental in the development of the virtual electrode polarization (VEP) theory for defibrillation.…”

Section: Simulation Of Cardiac Arrhythmia Terminationmentioning

confidence: 99%

Cardiac Arrhythmias: Mechanistic Knowledge and Innovation from Computer Models

Trayanova

Boyle

2015

MS&A

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Computational simulation is increasingly recognized as an integral aspect of modern cardiovascular research. Realistic and biophysically detailed models of the cardio-circulatory system can help interpret complex experimental observations, dissect underlying mechanisms, and explain emerging organ-scale phenomena resulting from subtle changes at the tissue, cellular, and/or sub-cellular scales. This chapter provides an overview of recent advances in the simulation of cardiac electrical behavior, focusing specifically on detailed models of the initiation, perpetuation, and termination of ventricular arrhythmias, including fibrillation. The development and validation of such models has opened several noteworthy avenues of research, including close scrutiny of arrhythmia dynamics in healthy and diseased hearts, dissection of arrhythmogenic and cardioprotective properties of specialized cardiac tissue regions such as the Purkinje system, and exploration of emerging paradigms for anti-arrhythmia treatment, such as optogenetics. Excitingly, the clinical community is currently taking the first steps towards using patient-specific ventricular models to stratify arrhythmia risk, personalize treatment planning, and optimize device placement for difficult or unusual procedures.

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Effects of Electroporation on the Transmembrane Potential Distribution in a Two‐Dimensional Bidomain Model of Cardiac Tissue

Abstract: These results indicate that electroporation of the cardiac membrane plays an important role in the distribution of Vm induced by defibrillation strength shocks.

Cited by 36 publications

References 37 publications

Artifacts, assumptions, and ambiguity: Pitfalls in comparing experimental results to numerical simulations when studying electrical stimulation of the heart

Artifacts, assumptions, and ambiguity: Pitfalls in comparing experimental results to numerical simulations when studying electrical stimulation of the heart

Electroporation induced by internal defibrillation shock with and without recovery in intact rabbit hearts

Cardiac Arrhythmias: Mechanistic Knowledge and Innovation from Computer Models

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