Evidence map›Paper›PMID 39576793›Full record

ArticlePloS one2024

Prevalence of endoepicardial asynchrony and breakthrough patterns in a bilayer computational model of heterogeneous endoepicardial dissociation in the left atrium.

Elham Zakeri Zafarghandi, Vincent Jacquemet

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Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Elham Zakeri ZafarghandiDepartment of Pharmacology and Physiology, Faculty of Medicine, Université de Montréal, Montreal, Quebec, Canada.ORCID 0000-0001-7241-3347
Vincent JacquemetDepartment of Pharmacology and Physiology, Faculty of Medicine, Université de Montréal, Montreal, Quebec, Canada.ORCID 0000-0002-8485-8738

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTransmural propagation and endoepicardial delays in activation observed in patients with atrial fibrillation are hypothesized to be associated with structural remodeling and endoepicardial dissociation. We aim to explore in a computational model how the distribution of delays and the rate of endo- and epicardial breakthrough activation patterns are affected by fibrosis and heterogeneous layer dissociation.

methodsA bilayer interconnected cable model of the left atrium was used to simulate a total of 4,800 episodes of atrial fibrillation on 960 different arrhythmogenic substrates with up to 30% epicardium-only diffuse fibrosis. Endoepicardial connections were heterogeneously distributed following random spatial patterns (characteristic length scale from 1.6 to 11.4 mm). Intermediate nodes were introduced in the transmural connections to enable the simulation of weaker coupling. This heterogeneous interlayer dissociation divided the atrial bilayer into connected and disconnected regions (from 27 to 48,000 connected regions). Activation time series were extracted in both layers to compute endoepicardial delays and detect breakthrough patterns.

resultsBecause of epicardial fibrosis, fibrillatory waves were driven by the endocardium, which generated endoepicardial delays. The delays in the connected regions (up to 10 ms, but generally < 5 ms) were prolonged by higher fibrosis density and weaker coupling. Disconnected regions allowed longer delays (> 15 ms) and promoted the occurrence of breakthroughs. These breakthroughs had short lifespan (< 10-20 ms) and were more prevalent with higher fibrosis density and heterogeneous dissociation (larger disconnected regions). Severe remodeling (< 500 connected regions) was needed to produce clinically reported rates (> 0.1 breakthrough/cycle/cm2).

conclusionHeterogeneous endoepicardial dissociation aggravates activation delays and increases the prevalence of epicardial breakthroughs.

Indexed as

Atrial FibrillationComputer SimulationHeart AtriaModels, CardiovascularPericardiumEndocardiumFibrosisHumansPrevalence

Identifiers

PMID39576793
PMCPMC11584087

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