Assessing the ability of substrate mapping techniques to guide ventricular tachycardia ablation using computational modelling.

Arrhythmia Catheter ablation Computer simulation Electroanatomical mapping Myocardial infarction

Journal

Computers in biology and medicine
ISSN: 1879-0534
Titre abrégé: Comput Biol Med
Pays: United States
ID NLM: 1250250

Informations de publication

Date de publication:
03 2021
Historique:
received: 05 08 2020
revised: 05 01 2021
accepted: 05 01 2021
pubmed: 22 1 2021
medline: 3 7 2021
entrez: 21 1 2021
Statut: ppublish

Résumé

Identification of targets for ablation of post-infarction ventricular tachycardias (VTs) remains challenging, often requiring arrhythmia induction to delineate the reentrant circuit. This carries a risk for the patient and may not be feasible. Substrate mapping has emerged as a safer strategy to uncover arrhythmogenic regions. However, VT recurrence remains common. To use computer simulations to assess the ability of different substrate mapping approaches to identify VT exit sites. A 3D computational model of the porcine post-infarction heart was constructed to simulate VT and paced rhythm. Electroanatomical maps were constructed based on endocardial electrogram features and the reentry vulnerability index (RVI - a metric combining activation (AT) and repolarization timings to identify tissue susceptibility to reentry). Since scar transmurality in our model was not homogeneous, parameters derived from all signals (including dense scar regions) were used in the analysis. Potential ablation targets obtained from each electroanatomical map during pacing were compared to the exit site detected during VT mapping. Simulation data showed that voltage cut-offs applied to bipolar electrograms could delineate the scar, but not the VT circuit. Electrogram fractionation had the highest correlation with scar transmurality. The RVI identified regions closest to VT exit site but was outperformed by AT gradients combined with voltage cut-offs. The performance of all metrics was affected by pacing location. Substrate mapping could provide information about the infarct, but the directional dependency on activation should be considered. Activation-repolarization metrics have utility in safely identifying VT targets, even with non-transmural scars.

Sections du résumé

BACKGROUND
Identification of targets for ablation of post-infarction ventricular tachycardias (VTs) remains challenging, often requiring arrhythmia induction to delineate the reentrant circuit. This carries a risk for the patient and may not be feasible. Substrate mapping has emerged as a safer strategy to uncover arrhythmogenic regions. However, VT recurrence remains common.
GOAL
To use computer simulations to assess the ability of different substrate mapping approaches to identify VT exit sites.
METHODS
A 3D computational model of the porcine post-infarction heart was constructed to simulate VT and paced rhythm. Electroanatomical maps were constructed based on endocardial electrogram features and the reentry vulnerability index (RVI - a metric combining activation (AT) and repolarization timings to identify tissue susceptibility to reentry). Since scar transmurality in our model was not homogeneous, parameters derived from all signals (including dense scar regions) were used in the analysis. Potential ablation targets obtained from each electroanatomical map during pacing were compared to the exit site detected during VT mapping.
RESULTS
Simulation data showed that voltage cut-offs applied to bipolar electrograms could delineate the scar, but not the VT circuit. Electrogram fractionation had the highest correlation with scar transmurality. The RVI identified regions closest to VT exit site but was outperformed by AT gradients combined with voltage cut-offs. The performance of all metrics was affected by pacing location.
CONCLUSIONS
Substrate mapping could provide information about the infarct, but the directional dependency on activation should be considered. Activation-repolarization metrics have utility in safely identifying VT targets, even with non-transmural scars.

Identifiants

pubmed: 33476992
pii: S0010-4825(21)00008-1
doi: 10.1016/j.compbiomed.2021.104214
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

104214

Subventions

Organisme : British Heart Foundation
ID : PG/16/81/32441
Pays : United Kingdom
Organisme : British Heart Foundation
ID : PG/18/74/34077
Pays : United Kingdom
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Department of Health
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/N011007/1
Pays : United Kingdom

Informations de copyright

Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.

Auteurs

Fernando O Campos (FO)

School of Biomedical Engineering and Imaging Sciences, Rayne Institute, 4th Floor, Lambeth Wing, St. Thomas' Hospital, Westminster Bridge Road, London, SE1 7EH, United Kingdom. Electronic address: fernando.campos@kcl.ac.uk.

Michele Orini (M)

Institute of Cardiovascular Science, University College London, London, United Kingdom; Electrophysiology Department, Barts Heart Centre, St Bartholomew's Hospital, London, United Kingdom.

Robert Arnold (R)

Gottfried Schatz Research Center (for Cell Signaling, Metabolism and Aging), Division of Biophysics, Graz, Austria.

John Whitaker (J)

School of Biomedical Engineering and Imaging Sciences, Rayne Institute, 4th Floor, Lambeth Wing, St. Thomas' Hospital, Westminster Bridge Road, London, SE1 7EH, United Kingdom.

Mark O'Neill (M)

School of Biomedical Engineering and Imaging Sciences, Rayne Institute, 4th Floor, Lambeth Wing, St. Thomas' Hospital, Westminster Bridge Road, London, SE1 7EH, United Kingdom.

Reza Razavi (R)

School of Biomedical Engineering and Imaging Sciences, Rayne Institute, 4th Floor, Lambeth Wing, St. Thomas' Hospital, Westminster Bridge Road, London, SE1 7EH, United Kingdom.

Gernot Plank (G)

Gottfried Schatz Research Center (for Cell Signaling, Metabolism and Aging), Division of Biophysics, Graz, Austria.

Ben Hanson (B)

Department of Mechanical Engineering, University College London, London, United Kingdom.

Bradley Porter (B)

School of Biomedical Engineering and Imaging Sciences, Rayne Institute, 4th Floor, Lambeth Wing, St. Thomas' Hospital, Westminster Bridge Road, London, SE1 7EH, United Kingdom; Department of Cardiology, Guys and St Thomas' NHS Trust, London, United Kingdom.

Christopher Aldo Rinaldi (CA)

Department of Cardiology, Guys and St Thomas' NHS Trust, London, United Kingdom.

Jaswinder Gill (J)

School of Biomedical Engineering and Imaging Sciences, Rayne Institute, 4th Floor, Lambeth Wing, St. Thomas' Hospital, Westminster Bridge Road, London, SE1 7EH, United Kingdom; Department of Cardiology, Guys and St Thomas' NHS Trust, London, United Kingdom.

Pier D Lambiase (PD)

Institute of Cardiovascular Science, University College London, London, United Kingdom; Electrophysiology Department, Barts Heart Centre, St Bartholomew's Hospital, London, United Kingdom.

Peter Taggart (P)

Institute of Cardiovascular Science, University College London, London, United Kingdom; Electrophysiology Department, Barts Heart Centre, St Bartholomew's Hospital, London, United Kingdom.

Martin J Bishop (MJ)

School of Biomedical Engineering and Imaging Sciences, Rayne Institute, 4th Floor, Lambeth Wing, St. Thomas' Hospital, Westminster Bridge Road, London, SE1 7EH, United Kingdom.

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