Evidence map›Paper›PMID 25054116›Full record

ReviewGlobal cardiology science & practice2014

Improved understanding of the pathophysiology of atrial fibrillation through the lens of discrete pathological pathways.

Muhammad A Balouch, Matthew J Kolek, Dawood Darbar

Open access · diamondAbstract readReview
In one paragraph

Review in Global cardiology science & practice, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  6. Review
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  11. Gene-guided therapy for catheter-ablation of atrial fibrillation: are we there yet?Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2016
    Article
  12. Review
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

3 authors at 1 institution in 1 country.

Muhammad A BalouchDivision of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Matthew J KolekDivision of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Dawood DarbarDivision of Cardiovascular Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Vanderbilt University Medical Center · US

Funding

Pharmacogenomics of Arrhythmia TherapyU19HL065962 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RODEN, DAN M · 2010 to 2014
$17.4M
Training In Cardiovascular ResearchT32HL007411 · NHLBI · VANDERBILT UNIVERSITY · PI BECKMAN, JOSHUA A · 1985 to 2020
$7.2M
Positional Cloning and Candidate Gene Approach to Familial Atrial FibrillationR01HL092217 · NHLBI · VANDERBILT UNIVERSITY · PI DARBAR, DAWOOD · 2009 to 2017
$2.9M
NHLBI NIH HHS R01 HL092217NHLBI NIH HHS T32 HL007411NHLBI NIH HHS U19 HL065962
6 · The paper itself

Abstract

Atrial fibrillation (AF) is a common disorder with a complex and incompletely understood pathophysiology. Genetic approaches to understanding the pathophysiology of AF have led to the identification of several biological pathways important in the pathogenesis of the arrhythmia. These include pathways important for cardiac development, generation and propagation of atrial electrical impulses, and atrial remodeling and fibrosis. While common and rare genetic variants in these pathways are associated with increased susceptibility to AF, they differ substantially among patients with lone versus typical AF. Furthermore, how these pathways converge to a final common clinical phenotype of AF is unclear and might also vary among different patient populations. Here, we review the contemporary knowledge of AF pathogenesis and discuss how derangement in cardiac development, ion channel dysfunction, and promotion of atrial fibrosis may contribute to this common and important clinical disorder.

Indexed as

Atrial fibrillationfibrosisgeneticsinflammationpathophysiology

Identifiers

PMID25054116
PMCPMC4104374
OpenAlexW2065682171

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.