Evidence map›Paper›PMID 26606047›Full record

ArticlePloS one2015

Effects of Persistent Atrial Fibrillation-Induced Electrical Remodeling on Atrial Electro-Mechanics - Insights from a 3D Model of the Human Atria.

Ismail Adeniran, David H MacIver, Clifford J Garratt, Jianqiao Ye, Jules C Hancox, Henggui Zhang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Article
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  4. Human atrial fibrillation and genetic defects in transient outward currents: mechanistic insights from multi-scale computational models.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
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  8. Analysis of a coupled fluid-structure interaction model of the left atrium and mitral valve.International journal for numerical methods in biomedical engineering · 2019
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  13. Observational
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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

6 authors at 4 institutions in 1 country.

Ismail AdeniranBiological Physics Group, School of Physics and Astronomy, University of Manchester, Manchester, United Kingdom.
David H MacIverBiological Physics Group, School of Physics and Astronomy, University of Manchester, Manchester, United Kingdom.
Clifford J GarrattManchester Heart Centre, Manchester Royal Infirmary, Manchester, United Kingdom.
Jianqiao YeDepartment of Engineering, Lancaster University, Lancaster, United Kingdom.
Jules C HancoxBiological Physics Group, School of Physics and Astronomy, University of Manchester, Manchester, United Kingdom.
Henggui ZhangBiological Physics Group, School of Physics and Astronomy, University of Manchester, Manchester, United Kingdom.
University of Manchester · GBLancaster University · GBManchester Royal Infirmary · GBUniversity of Bristol · GB

Funding

British Heart Foundation FS/14/5/30533
6 · The paper itself

Abstract

aimsAtrial stunning, a loss of atrial mechanical contraction, can occur following a successful cardioversion. It is hypothesized that persistent atrial fibrillation-induced electrical remodeling (AFER) on atrial electrophysiology may be responsible for such impaired atrial mechanics. This simulation study aimed to investigate the effects of AFER on atrial electro-mechanics. METHODS AND

resultsA 3D electromechanical model of the human atria was developed to investigate the effects of AFER on atrial electro-mechanics. Simulations were carried out in 3 conditions for 4 states: (i) the control condition, representing the normal tissue (state 1) and the tissue 2-3 months after cardioversion (state 2) when the atrial tissue recovers its electrophysiological properties after completion of reverse electrophysiological remodelling; (ii) AFER-SR condition for AF-remodeled tissue with normal sinus rhythm (SR) (state 3); and (iii) AFER-AF condition for AF-remodeled tissue with re-entrant excitation waves (state 4). Our results indicate that at the cellular level, AFER (states 3 & 4) abbreviated action potentials and reduced the Ca2+ content in the sarcoplasmic reticulum, resulting in a reduced amplitude of the intracellular Ca2+ transient leading to decreased cell active force and cell shortening as compared to the control condition (states 1 & 2). Consequently at the whole organ level, atrial contraction in AFER-SR condition (state 3) was dramatically reduced. In the AFER-AF condition (state 4) atrial contraction was almost abolished.

conclusionsThis study provides novel insights into understanding atrial electro-mechanics illustrating that AFER impairs atrial contraction due to reduced intracellular Ca2+ transients.

Indexed as

Atrial RemodelingModels, CardiovascularAction PotentialsAtrial FibrillationAtrial FunctionCalciumComputer SimulationHeart AtriaHeart Conduction SystemHumansMyocardial ContractionMyocytes, CardiacSarcoplasmic ReticulumCalcium

Identifiers

PMID26606047
PMCPMC4659575
OpenAlexW2278415057

What OpenQuestion holds

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LicenceCC BY
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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.