Evidence map›Paper›PMID 26705366›Full record

ReviewCardiovascular research2016

The value of basic research insights into atrial fibrillation mechanisms as a guide to therapeutic innovation: a critical analysis.

Jordi Heijman, Vincent Algalarrondo, Niels Voigt, Jonathan Melka, Xander H T Wehrens, Dobromir Dobrev, Stanley Nattel

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 2 pooled it
13.6field-weighted citation impact, top 1% 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

116 citing papers in PubMed, 2 syntheses or guidelines pooled it, 195 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Review
  5. Differential effects of semaglutide and colchicine on atrial remodeling in rats with reduced ejection fraction after myocardial infarction.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
  6. Article
  7. Review
  8. Mechanisms underlying atrial fibrillation in chronic kidney disease.Journal of molecular and cellular cardiology · 2025
    Review
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  11. Article
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  13. Article
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  15. Article
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56 more citing papers are in PubMed but not listed here.

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

7 authors at 6 institutions in 4 countries.

Jordi HeijmanDepartment of Cardiology, Cardiovascular Research Institute Maastricht, Faculty of Health, Medicine, and Life Sciences, Maastricht University, Maastricht, The Netherlands.
Vincent AlgalarrondoDepartment of Medicine, Montreal Heart Institute and Université de Montréal, 5000 Belanger St. E., Montreal, Canada H1T 1C8 Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada.
Niels VoigtInstitute of Pharmacology, West German Heart and Vascular Center, Faculty of Medicine, University Duisburg-Essen, Hufelandstr. 55, D-45122 Essen, Germany.
Jonathan MelkaDepartment of Medicine, Montreal Heart Institute and Université de Montréal, 5000 Belanger St. E., Montreal, Canada H1T 1C8 Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada.
Xander H T WehrensCardiovascular Research Institute, Baylor College of Medicine, Houston, TX, USA Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX, USA Department of Medicine (Cardiology), Baylor College of Medicine, Houston, TX, USA Pediatrics, Baylor College of Medicine, Houston, TX, USA.
Dobromir DobrevInstitute of Pharmacology, West German Heart and Vascular Center, Faculty of Medicine, University Duisburg-Essen, Hufelandstr. 55, D-45122 Essen, Germany dobromir.dobrev@uk-essen.de stanley.nattel@icm-mhi.org.
Stanley NattelDepartment of Medicine, Montreal Heart Institute and Université de Montréal, 5000 Belanger St. E., Montreal, Canada H1T 1C8 Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada Institute of Pharmacology, West German Heart and Vascular Center, Faculty of Medicine, University Duisburg-Essen, Hufelandstr. 55, D-45122 Essen, Germany dobromir.dobrev@uk-essen.de stanley.nattel@icm-mhi.org.
West German Heart and Vascular Center Essen · DEBaylor College of Medicine · USMaastricht University · NLMcGill University · CAMontreal Heart Institute · CAUniversité de Montréal · CA

Funding

Ryanodine receptor regulation in post-operative atrial fibrillationR01HL089598 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WEHRENS, XANDER H.T. · 2007 to 2022
$6.5M
Regulation of Sarcoplasmic Reticulum Calcium Release in Heart FailureR01HL091947 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WEHRENS, XANDER H.T. · 2009 to 2019
$3.2M
Determining the Role of Junctophilin-2 in Cardiac DiseaseR01HL117641 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WEHRENS, XANDER H.T. · 2014 to 2017
$2.3M
Development of novel compounds for the treatment of atrial fibrillationR41HL129570 · NHLBI · ELEX BIOTECH, LLC · PI WEHRENS, XANDER H.T. · 2015 to 2015
$428k
Canadian Institutes of Health Research 44365Canadian Institutes of Health Research 6957NHLBI NIH HHS HL089598NHLBI NIH HHS HL091947NHLBI NIH HHS HL117641NHLBI NIH HHS HL129570NHLBI NIH HHS R01 HL089598NHLBI NIH HHS R01 HL091947NHLBI NIH HHS R01 HL117641NHLBI NIH HHS R41 HL129570
6 · The paper itself

Abstract

Atrial fibrillation (AF) is an extremely common clinical problem associated with increased morbidity and mortality. Current antiarrhythmic options include pharmacological, ablation, and surgical therapies, and have significantly improved clinical outcomes. However, their efficacy remains suboptimal, and their use is limited by a variety of potentially serious adverse effects. There is a clear need for improved therapeutic options. Several decades of research have substantially expanded our understanding of the basic mechanisms of AF. Ectopic firing and re-entrant activity have been identified as the predominant mechanisms for arrhythmia initiation and maintenance. However, it has become clear that the clinical factors predisposing to AF and the cellular and molecular mechanisms involved are extremely complex. Moreover, all AF-promoting and maintaining mechanisms are dynamically regulated and subject to remodelling caused by both AF and cardiovascular disease. Accordingly, the initial presentation and clinical progression of AF patients are enormously heterogeneous. An understanding of arrhythmia mechanisms is widely assumed to be the basis of therapeutic innovation, but while this assumption seems self-evident, we are not aware of any papers that have critically examined the practical contributions of basic research into AF mechanisms to arrhythmia management. Here, we review recent insights into the basic mechanisms of AF, critically analyse the role of basic research insights in the development of presently used anti-AF therapeutic options and assess the potential value of contemporary experimental discoveries for future therapeutic innovation. Finally, we highlight some of the important challenges to the translation of basic science findings to clinical application.

Indexed as

ResearchAnimalsAnti-Arrhythmia AgentsAtrial FibrillationDisease ProgressionElectrophysiologyHeart Conduction SystemHumansAnti-Arrhythmia AgentsAblationAntiarrhythmic drugsAtrial fibrillationCellular electrophysiologyEctopic activityImagingRe-entry

Identifiers

PMID26705366
PMCPMC4777910
OpenAlexW2278492526

What OpenQuestion holds

Textmetadata
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.