A Mechanism for the Upper Limit of Vulnerability

Overview

Journal Heart Rhythm

Publisher Elsevier

Specialty Cardiology & Vascular Diseases

Date 2009 Mar 3

PMID 19251212

Citations 7

Authors

Nachaat Mazeh

Bradley J Roth

Affiliations

Soon will be listed here.

Abstract

Background: The strongest shock that induces reentry in the heart is the upper limit of vulnerability (ULV). In order to understand defibrillation, one must know what causes the ULV.

Objective: The goal of this study was to examine the mechanism of the upper limit of vulnerability.

Methods: Numerical simulations of cardiac tissue were performed using the bidomain model. An S2 shock was applied during the refractory period of the S1 action potential, and results using a smooth curving fiber geometry were compared with results using a smooth plus random fiber geometry.

Results: When using a smooth fiber geometry only, no ULV was observed. However, when a random fiber geometry was included, the ULV was present. The difference arises from the fate of the shock-induced break wave front when it reaches the edge of the tissue hyperpolarized by the shock (the virtual anode).

Conclusion: Our numerical simulations suggest that local heterogeneities throughout the tissue may be crucial for determining the fate of the shock-induced wave front at the edge of the virtual anode, and therefore play an important role in the mechanism underlying the ULV.

Citing Articles

Bidomain modeling of electrical and mechanical properties of cardiac tissue.

Roth B Biophys Rev (Melville). 2024; 2(4):041301.

PMID: 38504719 PMC: 10903405. DOI: 10.1063/5.0059358.

A Simplified Approach for Simultaneous Measurements of Wavefront Velocity and Curvature in the Heart Using Activation Times.

Mazeh N, Haines D, Kay M, Roth B Cardiovasc Eng Technol. 2014; 4(4):520-534.

PMID: 24772193 PMC: 3998731. DOI: 10.1007/s13239-013-0158-2.

Diastolic field stimulation: the role of shock duration in epicardial activation and propagation.

Woods M, Uzelac I, Holcomb M, Wikswo J, Sidorov V Biophys J. 2013; 105(2):523-32.

PMID: 23870273 PMC: 3714876. DOI: 10.1016/j.bpj.2013.06.009.

Investigating the role of the coronary vasculature in the mechanisms of defibrillation.

Bishop M, Plank G, Vigmond E Circ Arrhythm Electrophysiol. 2011; 5(1):210-9.

PMID: 22157522 PMC: 3378488. DOI: 10.1161/CIRCEP.111.965095.

How hyperpolarization and the recovery of excitability affect propagation through a virtual anode in the heart.

Charteris N, Roth B Comput Math Methods Med. 2011; 2011:375059.

PMID: 21331264 PMC: 3038668. DOI: 10.1155/2011/375059.

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