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Front. Physiol. | doi: 10.3389/fphys.2018.01832

Fibrosis Microstructure Modulates Reentry in Non-Ischemic Dilated Cardiomyopathy: Insights from Imaged Guided 2D Computational Modelling

 Gabriel Balaban1*, Brian P. Halliday2,  Caroline Mendonca Costa1, Wenjia Bai3,  Bradley Porter1, 4, Christopher A. Rinaldi4,  Gernot Plank5, Daniel Rueckert3, Sanjay K. Prasad6, 7 and  Martin J. Bishop1
  • 1School of Biomedical Engineering and Imaging Sciences, King’s College London, United Kingdom
  • 2Heart Science, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, United Kingdom
  • 3Imperial College London, United Kingdom
  • 4Guy's and St Thomas' NHS Foundation Trust, United Kingdom
  • 5Medical University of Graz, Austria
  • 6NIHR Royal Brompton Cardiovascular Biomedical Research Unit, United Kingdom
  • 7National Heart and Lung Institute, Faculty of Medicine, Imperial College London, United Kingdom

Aims: Patients who present with non-ischemic dilated cardiomyopathy (NIDCM)
and enhancement on late gadolinium magnetic resonance imaging (LGE-CMR), are at high risk
of sudden cardiac death (SCD). Further risk stratification of these patients based on LGE-CMR
may be improved through better understanding of fibrosis microstructure.
Our aim is to examine variations in fibrosis microstructure based on LGE imaging,
and quantify the effect on reentry inducibility and mechanism. Furthermore,
we examine the relationship between transmural activation time differences and reentry.

Methods and Results: 2D Computational models were created from a single short axis LGE-CMR image,
with 402 variations in fibrosis type (interstitial, replacement) and density,
as well as presence or absence of reduced conductivity (RC).
Transmural activation times (TAT) were measured, as well as reentry incidence and mechanism.
Reentries were inducible above specific density thresholds (0.8, 0.6 for interstitial, replacement fibrosis).
RC reduced these thresholds (0.3, 0.4 for interstitial, replacement fibrosis)
and increased reentry incidence (48 no RC vs. 133 with RC).
Reentries were classified as rotor, micro-reentry, or macro-reentry
and depended on fibrosis micro-structure. Differences in TAT at coupling intervals 210 and 500ms predicted
reentry in the models (sensitivity 89%, specificity 93%).

Conclusions: Computational models of fibrosis micro-structure underlying areas
of LGE in NIDCM provide insight into the mechanisms and inducibility of reentry,
and their dependence upon the type and density of fibrosis.
Transmural activation times can differentiate microstructures which support reentry.

Keywords: nonischemic cardiomiopathy, Compuational Modelling, Late gadolinium enhanced magnetic resonance imaging, Dilated cardiaomypothy, Electrophysiology, reentry, Arrhythmia (any), Ventricular tachycardia (VT)

Received: 11 Sep 2018; Accepted: 06 Dec 2018.

Edited by:

Javier Saiz, Universitat Politècnica de València, Spain

Reviewed by:

Bradley J. Roth, Oakland University, United States
Olivier Bernus, Université de Bordeaux, France  

Copyright: © 2018 Balaban, Halliday, Mendonca Costa, Bai, Porter, Rinaldi, Plank, Rueckert, Prasad and Bishop. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Gabriel Balaban, School of Biomedical Engineering and Imaging Sciences, King’s College London, London, WC2R 2LS, London, United Kingdom,