Evidence map›Paper›PMID 32272230›Full record

ArticleHeart rhythm2020

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

Caroline Mendonca Costa, Aurel Neic, Karli Gillette, Bradley Porter, Justin Gould, Baldeep Sidhu, Zhong Chen, Mark Elliott, Vishal Mehta, Gernot Plank and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Heart rhythm, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.4field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 24 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 2 countries.

Caroline Mendonca CostaKing's College London, London, United Kingdom. Electronic address: caroline.mendonca_costa@kcl.ac.uk.
Aurel NeicMedical University of Graz, Graz, Austria.
Karli GilletteMedical University of Graz, Graz, Austria.
Bradley PorterKing's College London, London, United Kingdom.
Justin GouldKing's College London, London, United Kingdom.
Baldeep SidhuKing's College London, London, United Kingdom.
Zhong ChenKing's College London, London, United Kingdom.
Mark ElliottKing's College London, London, United Kingdom.
Vishal MehtaKing's College London, London, United Kingdom.
Gernot PlankMedical University of Graz, Graz, Austria.
C A RinaldiKing's College London, London, United Kingdom; Guy's and St. Thomas' Hospital, London, United Kingdom.
Martin J BishopKing's College London, London, United Kingdom.
Steven A NiedererKing's College London, London, United Kingdom.
King's College London · GBMedical University of Graz · ATSt Thomas' Hospital · GB

Funding

British Heart Foundation PG/15/91/31812British Heart Foundation PG/16/81/32441British Heart Foundation RE/08/003Department of HealthMedical Research Council MR/N011007/1Wellcome TrustWellcome Trust WT 203148/Z/16/Z
6 · The paper itself

Abstract

backgroundEpicardial 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.

objectiveThe 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.

methodsComputational 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.

resultsPatient-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.

conclusionEndocardial 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.

Indexed as

Computer SimulationCardiac Pacing, ArtificialCicatrixEndocardiumHeart VentriclesHumansTachycardia, VentricularCardiac resynchronization therapyDispersion of repolarizationInfarct scarPatient-specific modelingVentricular tachycardia

Identifiers

PMID32272230
PMCPMC7397521
OpenAlexW3015215780

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.