Left ventricular endocardial pacing is less arrhythmogenic than conventional epicardial pacing when pacing in proximity to scar.

Cardiac resynchronization therapy Dispersion of repolarization Infarct scar Patient-specific modeling Ventricular tachycardia

Journal

Heart rhythm
ISSN: 1556-3871
Titre abrégé: Heart Rhythm
Pays: United States
ID NLM: 101200317

Informations de publication

Date de publication:
08 2020
Historique:
received: 20 12 2019
accepted: 21 03 2020
pubmed: 10 4 2020
medline: 1 9 2021
entrez: 10 4 2020
Statut: ppublish

Résumé

Epicardial pacing increases risk of ventricular tachycardia (VT) in patients with ischemic cardiomyopathy (ICM) when pacing in proximity to scar. Endocardial pacing may be less arrhythmogenic as it preserves the physiological sequences of activation and repolarization. The purpose of this study was to determine the relative arrhythmogenic risk of endocardial compared to epicardial pacing, and the role of the transmural gradient of action potential duration (APD) and pacing location relative to scar on arrhythmogenic risk during endocardial pacing. Computational models of ICM patients (n = 24) were used to simulate left ventricular (LV) epicardial and endocardial pacing 0.2-3.5 cm from a scar. Mechanisms were investigated in idealized models of the ventricular wall and scar. Simulations were run with/without a 20-ms transmural APD gradient in the physiological direction and with the gradient inverted. Dispersion of repolarization was computed as a surrogate of VT risk. Patient-specific models with a physiological APD gradient predict that endocardial pacing decreases VT risk (34%; P <.05) compared to epicardial pacing when pacing in proximity to scar (0.2 cm). Endocardial pacing location does not significantly affect VT risk, but epicardial pacing at 0.2 cm compared to 3.5 cm from scar increases it (P <.05). Inverting the transmural APD gradient reverses this trend. Idealized models predict that propagation in the direction opposite to APD gradient decreases VT risk. Endocardial pacing is less arrhythmogenic than epicardial pacing when pacing proximal to scar and is less susceptible to pacing location relative to scar. The physiological repolarization sequence during endocardial pacing mechanistically explains reduced VT risk compared to epicardial pacing.

Sections du résumé

BACKGROUND
Epicardial pacing increases risk of ventricular tachycardia (VT) in patients with ischemic cardiomyopathy (ICM) when pacing in proximity to scar. Endocardial pacing may be less arrhythmogenic as it preserves the physiological sequences of activation and repolarization.
OBJECTIVE
The purpose of this study was to determine the relative arrhythmogenic risk of endocardial compared to epicardial pacing, and the role of the transmural gradient of action potential duration (APD) and pacing location relative to scar on arrhythmogenic risk during endocardial pacing.
METHODS
Computational models of ICM patients (n = 24) were used to simulate left ventricular (LV) epicardial and endocardial pacing 0.2-3.5 cm from a scar. Mechanisms were investigated in idealized models of the ventricular wall and scar. Simulations were run with/without a 20-ms transmural APD gradient in the physiological direction and with the gradient inverted. Dispersion of repolarization was computed as a surrogate of VT risk.
RESULTS
Patient-specific models with a physiological APD gradient predict that endocardial pacing decreases VT risk (34%; P <.05) compared to epicardial pacing when pacing in proximity to scar (0.2 cm). Endocardial pacing location does not significantly affect VT risk, but epicardial pacing at 0.2 cm compared to 3.5 cm from scar increases it (P <.05). Inverting the transmural APD gradient reverses this trend. Idealized models predict that propagation in the direction opposite to APD gradient decreases VT risk.
CONCLUSION
Endocardial pacing is less arrhythmogenic than epicardial pacing when pacing proximal to scar and is less susceptible to pacing location relative to scar. The physiological repolarization sequence during endocardial pacing mechanistically explains reduced VT risk compared to epicardial pacing.

Identifiants

pubmed: 32272230
pii: S1547-5271(20)30282-4
doi: 10.1016/j.hrthm.2020.03.021
pmc: PMC7397521
pii:
doi:

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1262-1270

Subventions

Organisme : British Heart Foundation
ID : PG/16/81/32441
Pays : United Kingdom
Organisme : Wellcome Trust
ID : WT 203148/Z/16/Z
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RE/08/003
Pays : United Kingdom
Organisme : Department of Health
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/N011007/1
Pays : United Kingdom
Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : British Heart Foundation
ID : PG/15/91/31812
Pays : United Kingdom

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

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Auteurs

Caroline Mendonca Costa (C)

King's College London, London, United Kingdom. Electronic address: caroline.mendonca_costa@kcl.ac.uk.

Aurel Neic (A)

Medical University of Graz, Graz, Austria.

Karli Gillette (K)

Medical University of Graz, Graz, Austria.

Bradley Porter (B)

King's College London, London, United Kingdom.

Justin Gould (J)

King's College London, London, United Kingdom.

Baldeep Sidhu (B)

King's College London, London, United Kingdom.

Zhong Chen (Z)

King's College London, London, United Kingdom.

Mark Elliott (M)

King's College London, London, United Kingdom.

Vishal Mehta (V)

King's College London, London, United Kingdom.

Gernot Plank (G)

Medical University of Graz, Graz, Austria.

C A Rinaldi (CA)

King's College London, London, United Kingdom; Guy's and St. Thomas' Hospital, London, United Kingdom.

Martin J Bishop (MJ)

King's College London, London, United Kingdom.

Steven A Niederer (SA)

King's College London, London, United Kingdom.

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Classifications MeSH