Evidence map›Paper›PMID 25880508›Full record

ReviewComprehensive Physiology2015

Atrial fibrillation: mechanisms, therapeutics, and future directions.

Jason Pellman, Farah Sheikh

Open access · greenAbstract readReview
In one paragraph

Review in Comprehensive Physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing 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

76 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.

  1. The association of coagulation and atrial fibrillation: a systematic review and meta-analysis.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 · 2023
    Pooled it
  2. Sphingomyelin as a key negative mediator in atrial fibrillation via lipid profiling analysis and functional identification.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
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  17. Linking homocysteine and ferroptosis in cardiovascular disease: insights and implications.Apoptosis : an international journal on programmed cell death · 2024
    Review
  18. Ablation-induced left atrial mechanical dysfunction recovers in weeks after ablation.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2024
    Article
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16 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

2 authors at 1 institution in 1 country.

Jason PellmanDepartment of Medicine, University of California, San Diego, La Jolla, California, USA.
Farah Sheikh
University of California, San Diego · US

Funding

The molecular mechanisms underlying arrhythmogenic right ventricular dysplasia/cardiomyopathyR01HL095780 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SHEIKH, FARAH · 2009 to 2018
$3.9M
The Role of SNAP29, a Novel Desmoplakin Interactor, in Cardiac PathophysiologyF31HL120611 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PELLMAN, JASON R · 2013 to 2015
$72k
NHLBI NIH HHS 1F31HL120611-01NHLBI NIH HHS 1R01HL095780-01NHLBI NIH HHS F31 HL120611NHLBI NIH HHS R01 HL095780
6 · The paper itself

Abstract

Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia, affecting 1% to 2% of the general population. It is characterized by rapid and disorganized atrial activation leading to impaired atrial function, which can be diagnosed on an EKG by lack of a P-wave and irregular QRS complexes. AF is associated with increased morbidity and mortality and is a risk factor for embolic stroke and worsening heart failure. Current research on AF support and explore the hypothesis that initiation and maintenance of AF require pathophysiological remodeling of the atria, either specifically as in lone AF or secondary to other heart disease as in heart failure-associated AF. Remodeling in AF can be grouped into three categories that include: (i) electrical remodeling, which includes modulation of L-type Ca(2+) current, various K(+) currents and gap junction function; (ii) structural remodeling, which includes changes in tissues properties, size, and ultrastructure; and (iii) autonomic remodeling, including altered sympathovagal activity and hyperinnervation. Electrical, structural, and autonomic remodeling all contribute to creating an AF-prone substrate which is able to produce AF-associated electrical phenomena including a rapidly firing focus, complex multiple reentrant circuit or rotors. Although various remodeling events occur in AF, current AF therapies focus on ventricular rate and rhythm control strategies using pharmacotherapy and surgical interventions. Recent progress in the field has started to focus on the underlying substrate that drives and maintains AF (termed upstream therapies); however, much work is needed in this area. Here, we review current knowledge of AF mechanisms, therapies, and new areas of investigation.

Indexed as

Models, CardiovascularAnimalsAnti-Arrhythmia AgentsAtrial FibrillationForecastingHeart AtriaHeart Conduction SystemHumansAnti-Arrhythmia Agents

Identifiers

PMID25880508
PMCPMC5240842
OpenAlexW1575382996

What OpenQuestion holds

Textmetadata
LicenceTDM
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.