Epicardial Fibrosis explains Increased Transmural Conduction in a Computer Model of Atrial Fibrillation

A. Gharaviri*, M. Potse, S. Verheule, R. Krause, A. Auricchio, U. Schotten

*Corresponding author for this work

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

Abstract

Recent work has shown that the transition from persistent to permanent AF in goats coincides with an increase in fibrosis in the outer millimeter of the atrial wall. Macroscopically this leads to reduced electrical conductivity orthogonal to the dominant fiber orientation.We constructed a detailed geometry of the human atria including epicardial layer and all major endocardial bundle structures. The model also includes realistic one to three layers of fiber orientations, corresponding to their location in the atrium.The numbers of waves, phase singularities, and breakthroughs (BTs) were quantified at different degrees of fibrotic tissue. Increase in the "fibrotic" volume from zero (Control) to moderate (50% Fibrotic), and severe (70% Fibrotic) increased both the number of waves and the number of phase singularities. Along with the increase in fibrosis, the endo-epicardial electrical activity dyssynchrony increased.
Original languageEnglish
Title of host publication2016 COMPUTING IN CARDIOLOGY CONFERENCE (CINC), VOL 43
PublisherIEEE
Pages237-240
Number of pages4
Volume43
ISBN (Print)9781509008957
Publication statusPublished - 2016
Event43rd Computing in Cardiology Conference (CinC) - Vancouver, Canada
Duration: 11 Sept 201614 Sept 2016
http://www.cinc2016.org/

Publication series

SeriesComputing in Cardiology Conference
Volume43
ISSN2325-8861

Conference

Conference43rd Computing in Cardiology Conference (CinC)
Abbreviated title CinC 2016
Country/TerritoryCanada
CityVancouver
Period11/09/1614/09/16
Internet address

Keywords

  • PERSISTENT
  • MECHANISMS

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