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Investigation of Low-Voltage Defibrillation by Standing Waves in Human Ventricular Tissue Models

Research output: Chapter in Book/Report/Conference proceedingConference paperpeer-review

Original languageEnglish
Title of host publication2021 Computing in Cardiology, CinC 2021
PublisherIEEE Computer Society
ISBN (Electronic)9781665479165
DOIs
Published2021
Event2021 Computing in Cardiology, CinC 2021 - Brno, Czech Republic
Duration: 13 Sep 202115 Sep 2021

Publication series

NameComputing in Cardiology
Volume2021-September
ISSN (Print)2325-8861
ISSN (Electronic)2325-887X

Conference

Conference2021 Computing in Cardiology, CinC 2021
Country/TerritoryCzech Republic
CityBrno
Period13/09/202115/09/2021

Bibliographical note

Funding Information: This work was supported by the Wellcome/EPSRC Centre for Medical Engineering [WT 203148/Z/16/Z]. Publisher Copyright: © 2021 Creative Commons.

King's Authors

Abstract

Ventricular fibrillation (VF) is one of the main causes of sudden cardiac death. Strong electric shocks remain the only reliable mechanism for successful termination of VF, but often lead to post-injuries. This study aims to explore whether low-voltage shocks at certain frequencies could result in successful defibrillation of human ventricular tissue. 1 D and 2D ventricular tissue models were based on the Ten Tusscher et al. myocyte model combined with an extended version of the bidomain model with an external bath, to which the electric shocks were delivered. Sinusoidal low-voltage (10-50 Hz, 20-40 V) shocks were applied at opposite sides of 1D tissue strands and 2D square tissues of variable sizes; in 2D models, VF was induced in form of a single re-entrant wave. In 1 D models, standing waves were observed at all frequencies in short ventricular strands (1-2 cm, comparable to the transmural distance in the human ventricles), but not in long strands (5-10 cm). Accordingly, in 2D tissue models of 5-10 cm2, standing waves failed to form and terminate re-entry; otherwise, electrical waves originating from the shock application sites led to the generation of additional reentries. In summary, the formation of standing waves due to periodic low-voltage stimulation of human ventricular tissue can lead to defibrillation of transmural re-entrant waves, but not of rotors on the ventricular surface.

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