Epicardial fibrosis explains increased transmural conduction in a computer model of atrial fibrillation

Ali Gharaviri; Mark Potse; Sander Verheule; Rolf Krause; Angelo Auricchio; Ulrich Schotten

doi:10.22489/cinc.2016.071-216

Epicardial fibrosis explains increased transmural conduction in a computer model of atrial fibrillation

Ali Gharaviri^*, Mark Potse, Sander Verheule, Rolf Krause, Angelo Auricchio, Ulrich Schotten

^*Corresponding author for this work

Applied Mathematics and Computational Science

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution › peer-review

1 Scopus citations

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 language	English (US)
Title of host publication	Computing in Cardiology Conference, CinC 2016
Editors	Alan Murray
Publisher	IEEE Computer Society
Pages	237-240
Number of pages	4
ISBN (Electronic)	9781509008964
DOIs	https://doi.org/10.22489/cinc.2016.071-216
State	Published - Mar 1 2016
Event	43rd Computing in Cardiology Conference, CinC 2016 - Vancouver, Canada Duration: Sep 11 2016 → Sep 14 2016

Publication series

Name	Computing in Cardiology
Volume	43
ISSN (Print)	2325-8861
ISSN (Electronic)	2325-887X

Conference

Conference	43rd Computing in Cardiology Conference, CinC 2016
Country/Territory	Canada
City	Vancouver
Period	09/11/16 → 09/14/16

Bibliographical note

Publisher Copyright:
© 2016 CCAL.

ASJC Scopus subject areas

General Computer Science
Cardiology and Cardiovascular Medicine

Access to Document

10.22489/cinc.2016.071-216

Cite this

Gharaviri, A., Potse, M., Verheule, S., Krause, R., Auricchio, A., & Schotten, U. (2016). Epicardial fibrosis explains increased transmural conduction in a computer model of atrial fibrillation. In A. Murray (Ed.), Computing in Cardiology Conference, CinC 2016 (pp. 237-240). Article 7868723 (Computing in Cardiology; Vol. 43). IEEE Computer Society. https://doi.org/10.22489/cinc.2016.071-216

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title = "Epicardial fibrosis explains increased transmural conduction in a computer model of atrial fibrillation",

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.",

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Gharaviri, A, Potse, M, Verheule, S, Krause, R, Auricchio, A & Schotten, U 2016, Epicardial fibrosis explains increased transmural conduction in a computer model of atrial fibrillation. in A Murray (ed.), Computing in Cardiology Conference, CinC 2016., 7868723, Computing in Cardiology, vol. 43, IEEE Computer Society, pp. 237-240, 43rd Computing in Cardiology Conference, CinC 2016, Vancouver, Canada, 09/11/16. https://doi.org/10.22489/cinc.2016.071-216

Epicardial fibrosis explains increased transmural conduction in a computer model of atrial fibrillation. / Gharaviri, Ali; Potse, Mark; Verheule, Sander et al.
Computing in Cardiology Conference, CinC 2016. ed. / Alan Murray. IEEE Computer Society, 2016. p. 237-240 7868723 (Computing in Cardiology; Vol. 43).

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution › peer-review

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T1 - Epicardial fibrosis explains increased transmural conduction in a computer model of atrial fibrillation

AU - Gharaviri, Ali

AU - Potse, Mark

AU - Verheule, Sander

AU - Krause, Rolf

AU - Auricchio, Angelo

AU - Schotten, Ulrich

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N2 - 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.

AB - 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.

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Epicardial fibrosis explains increased transmural conduction in a computer model of atrial fibrillation

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