Evidence map›Paper›PMID 40434291›Full record

ReviewThe Journal of physiology2026

Atrial fibrosis in atrial fibrillation: Mechanisms, mapping techniques and clinical applications.

Caterina Vidal Horrach, Laura Bevis, Cynthia Nwanna, Alexander M Zolotarev, Mahmoud Ehnesh, Semhar Biniam Misghina, Sayed Al-Aidarous, Shohreh Honarbakhsh, Caroline H Roney

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The Journal of physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–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

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Role of interatrial connection ablation in re-entry dynamics: an in silico evaluation.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 · 2026
    Article
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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

9 authors.

Caterina Vidal HorrachSchool of Engineering and Materials Science, Queen Mary University of London, London, UK.
Laura BevisSchool of Engineering and Materials Science, Queen Mary University of London, London, UK.
Cynthia NwannaSchool of Engineering and Materials Science, Queen Mary University of London, London, UK.
Alexander M ZolotarevSchool of Engineering and Materials Science, Queen Mary University of London, London, UK.
Mahmoud EhneshSchool of Engineering and Materials Science, Queen Mary University of London, London, UK.
Semhar Biniam MisghinaSchool of Engineering and Materials Science, Queen Mary University of London, London, UK.
Sayed Al-AidarousElectrophysiology Department, Barts Heart Centre, Barts Health NHS Trust, London, UK.
Shohreh HonarbakhshElectrophysiology Department, Barts Heart Centre, Barts Health NHS Trust, London, UK.
Caroline H RoneySchool of Engineering and Materials Science, Queen Mary University of London, London, UK.

Funding

British Heart Foundation (BHF) FS/ICRF/22/26034UKRI | Medical Research Council (MRC) MR/W004720/1
6 · The paper itself

Abstract

Atrial fibrosis plays a pivotal role in the initiation and progression of atrial fibrillation (AF), creating a substrate for AF through structural, electrical and functional remodelling. Atrial remodelling results from various factors, including inflammation, obesity, hypertension and ischaemia, which collectively disrupt cellular coupling and ion channel function. The heterogeneity formed by the distribution of atrial fibrosis creates a substrate for abnormal electrical propagation and arrhythmias through alterations in ionic currents and conduction slowing. The extent of atrial fibrosis may be investigated through multiple modalities, including imaging and electroanatomic mapping. The pathological processes underlying atrial fibrosis are exacerbated in the transition from paroxysmal to persistent AF, highlighting the need for advanced diagnostic and therapeutic strategies. In this review, we cover the role of atrial fibrosis in AF, evaluate the modalities used to quantify and characterize atrial fibrosis, giving an overview of their clinical applications in stratifying patients and guiding treatment strategies, and discuss the integration of fibrosis information in computational AF models. We explore how the combination of experimental and computational techniques can enhance our understanding of the arrhythmogenic effects of fibrosis and the challenges inherent in translating mechanistic insights into effective therapies.

Indexed as

Atrial FibrillationHeart AtriaAnimalsAtrial RemodelingFibrosisHumansatrial fibrillationatrial fibrosisdigital twinselectroanatomic mappingfibrosis‐targeted ablationmagnetic resonance imaging

Identifiers

PMID40434291
PMCPMC13327766

What Socratic 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 Socratic graph.