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Myocyte Remodeling Due to Fibro-Fatty Infiltrations Influences Arrhythmogenicity.

Authors
  • De Coster, Tim1, 2
  • Claus, Piet2
  • Seemann, Gunnar3
  • Willems, Rik2
  • Sipido, Karin R2
  • Panfilov, Alexander V1, 4, 5
  • 1 Department of Physics and Astronomy, Ghent University, Ghent, Belgium. , (Belgium)
  • 2 Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium. , (Belgium)
  • 3 Institute for Experimental Cardiovascular Medicine, University Heart Centre Freiburg • Bad Krozingen, Medical Center - University of Freiburg, and Faculty of Medicine, University of Freiburg, Freiburg, Germany. , (Germany)
  • 4 Laboratory of Experimental Cardiology, Department of Cardiology, Heart Lung Centre Leiden, Leiden University Medical Center, Leiden, Netherlands. , (Netherlands)
  • 5 Laboratory of Computational Biology and Medicine, Ural Federal University, Ekaterinburg, Russia.
Type
Published Article
Journal
Frontiers in Physiology
Publisher
Frontiers Media SA
Publication Date
Jan 01, 2018
Volume
9
Pages
1381–1381
Identifiers
DOI: 10.3389/fphys.2018.01381
PMID: 30344493
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The onset of cardiac arrhythmias depends on the electrophysiological and structural properties of cardiac tissue. Electrophysiological remodeling of myocytes due to the presence of adipocytes constitutes a possibly important pathway in the pathogenesis of atrial fibrillation. In this paper we perform an in-silico study of the effect of such myocyte remodeling on the onset of atrial arrhythmias and study the dynamics of arrhythmia sources-spiral waves. We use the Courtemanche model for atrial myocytes and modify their electrophysiological properties based on published cellular electrophysiological measurements in myocytes co-cultered with adipocytes (a 69-87 % increase in APD 90 and an increase of the RMP by 2.5-5.5 mV). In a generic 2D setup we show that adipose tissue remodeling substantially affects the spiral wave dynamics resulting in complex arrhythmia and such arrhythmia can be initiated under high frequency pacing if the size of the remodeled tissue is sufficiently large. These results are confirmed in simulations with an anatomically accurate model of the human atria.

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