Evidence map›Paper›PMID 28356539›Full record

ArticleJournal of the Royal Society, Interface2017

Mechanisms of stochastic onset and termination of atrial fibrillation studied with a cellular automaton model.

Yen Ting Lin, Eugene T Y Chang, Julie Eatock, Tobias Galla, Richard H Clayton

Abstract read
In one paragraph

Article in Journal of the Royal Society, Interface, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Autonomic modulation before and after paroxysmal atrial fibrillation events in patients with ischemic heart disease.Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc · 2020
    Article
  2. Usage of a new mapping algorithm to detect possible critical substrate for continuity of atrial fibrillation: fractionation mapping in preliminary experience.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2020
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
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

5 authors.

Yen Ting LinTheoretical Physics Division, School of Physics and Astronomy, University of Manchester, Manchester, UK.ORCID 0000-0001-6893-8423
Eugene T Y ChangDepartment of Computer Science and INSIGNEO Institute for in silico Medicine, University of Sheffield, Sheffield, UK.ORCID 0000-0002-1097-4189
Julie EatockDepartment of Computer Science, Brunel University London, Uxbridge UB8 3PH, UK.ORCID 0000-0002-8963-8312
Tobias GallaTheoretical Physics Division, School of Physics and Astronomy, University of Manchester, Manchester, UK.ORCID 0000-0003-3402-2163
Richard H ClaytonDepartment of Computer Science and INSIGNEO Institute for in silico Medicine, University of Sheffield, Sheffield, UK r.h.clayton@sheffield.ac.uk.ORCID 0000-0002-8438-7518

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mathematical models of cardiac electrical excitation are increasingly complex, with multiscale models seeking to represent and bridge physiological behaviours across temporal and spatial scales. The increasing complexity of these models makes it computationally expensive to both evaluate long term (more than 60 s) behaviour and determine sensitivity of model outputs to inputs. This is particularly relevant in models of atrial fibrillation (AF), where individual episodes last from seconds to days, and interepisode waiting times can be minutes to months. Potential mechanisms of transition between sinus rhythm and AF have been identified but are not well understood, and it is difficult to simulate AF for long periods of time using state-of-the-art models. In this study, we implemented a Moe-type cellular automaton on a novel, topologically equivalent surface geometry of the left atrium. We used the model to simulate stochastic initiation and spontaneous termination of AF, arising from bursts of spontaneous activation near pulmonary veins. The simplified representation of atrial electrical activity reduced computational cost, and so permitted us to investigate AF mechanisms in a probabilistic setting. We computed large numbers (approx. 10

Indexed as

Models, CardiovascularAtrial FibrillationFemaleHumansMaleatrial fibrillationcellular automatamodelre-entrytermination

Identifiers

PMID28356539
PMCPMC5378131

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.