Evidence map›Paper›PMID 25291380›Full record

ArticlePloS one2014

Structural heterogeneity modulates effective refractory period: a mechanism of focal arrhythmia initiation.

Martin J Bishop, Adam Connolly, Gernot Plank

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Impact of effective refractory period personalization on arrhythmia vulnerability in patient-specific atrial computer models.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2024
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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

3 authors at 2 institutions in 2 countries.

Martin J BishopDepartment of Biomedical Engineering, Division of Imaging Sciences & Biomedical Engineering, King's College London, London, United Kingdom.
Adam ConnollyDepartment of Biomedical Engineering, Division of Imaging Sciences & Biomedical Engineering, King's College London, London, United Kingdom.
Gernot PlankInstitute of Biophysics, Medical University of Graz, Graz, Austria; Oxford eResearch Centre, University of Oxford, Oxford, United Kingdom.
King's College London · GBUniversity of Oxford · GB

Funding

NHLBI NIH HHS R01-HL-10119601Wellcome TrustWellcome Trust WT 088641/Z/09/Z
6 · The paper itself

Abstract

Reductions in electrotonic loading around regions of structural and electrophysiological heterogeneity may facilitate capture of focal triggered activity, initiating reentrant arrhythmias. How electrotonic loading, refractoriness and capture of focal ectopics depend upon the intricate nature of physiological structural anatomy, as well as pathological tissue remodelling, however, is not well understood. In this study, we performed computational bidomain simulations with anatomically-detailed models representing the rabbit left ventricle. We used these models to quantify the relationship between local structural anatomy and spatial heterogeneity in action potential (AP) characteristics, electrotonic currents and effective refractory periods (ERPs) under pacing and restitution protocols. Regions surrounding vessel cavities, in addition to tissue surfaces, had significantly lower peak downstream electrotonic currents than well coupled myocardium (72.6 vs 220.4 μA/cm2), with faster maximum AP upstroke velocities (257.3 vs 147.3 mV/ms), although noticeably very similar APDs (167.7 vs 168.4 ms) and AP restitution properties. Despite similarities in APDs, ERPs in regions of low electrotonic load in the vicinity of surfaces, intramural vessel cavities and endocardial structures were up to 40 ms shorter compared to neighbouring well-coupled tissue, leading to regions of sharp ERP gradients. Consequently, focal extra-stimuli timed within this window of ERP heterogeneity between neighbouring regions readily induced uni-directional block, inducing reentry. Most effective induction sites were within channels of low ERPs between large vessels and epicardium. Significant differences in ERP driven by reductions in electrotonic loading due to fine-scale physiological structural heterogeneity provides an important mechanism of capture of focal activity and reentry induction. Application to pathological ventricles, particularly myocardial infarction, will have important implications in anti-arrhythmia therapy.

Indexed as

Models, AnatomicAction PotentialsAlgorithmsAnimalsArrhythmias, CardiacCardiac Pacing, ArtificialComputer SimulationHeart Conduction SystemHeart VentriclesHumansMyocardiumPericardiumRabbits

Identifiers

PMID25291380
PMCPMC4188572
OpenAlexW1985126323

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.