Evidence map›Paper›PMID 28381281›Full record

ArticleJournal of translational medicine2017

Association of atrial fibrillation susceptibility genes, atrial fibrillation phenotypes and response to catheter ablation: a gene-based analysis of GWAS data.

Daniela Husser, Petra Büttner, Laura Ueberham, Borislav Dinov, Philipp Sommer, Arash Arya, Gerhard Hindricks, Andreas Bollmann

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Transcriptional factors in calcium mishandling and atrial fibrillation development.Pflugers Archiv : European journal of physiology · 2021
    Review
  5. Article
  6. Article
  7. Review
  8. Genetics of atrial fibrillation: an update.Current opinion in cardiology · 2018
    Review
  9. Article
  10. Article
  11. Article
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

8 authors at 2 institutions in 1 country.

Daniela HusserDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Strümpellstr. 39, 04289, Leipzig, Germany. dani11@gmx.net.
Petra BüttnerDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Strümpellstr. 39, 04289, Leipzig, Germany.
Laura UeberhamDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Strümpellstr. 39, 04289, Leipzig, Germany.
Borislav DinovDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Strümpellstr. 39, 04289, Leipzig, Germany.
Philipp SommerDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Strümpellstr. 39, 04289, Leipzig, Germany.
Arash AryaDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Strümpellstr. 39, 04289, Leipzig, Germany.
Gerhard HindricksDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Strümpellstr. 39, 04289, Leipzig, Germany.
Andreas BollmannDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Strümpellstr. 39, 04289, Leipzig, Germany.
Leipzig Heart Institute · DELeipzig University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrevious studies have suggested PITX2, KCNN3 and ZFHX3 as atrial fibrillation (AF) susceptibility genes. Single common genetic polymorphisms of those genes have been linked with AF phenotypes and rhythm outcome of AF catheter ablation although their mechanisms remain elusive. New gene-based association tests may help clarifying genotype-phenotype correlations. Therefore, we hypothesized that PITX2, KCNN3 and ZFHX3 associate with left atrial enlargement and persistent AF and subsequently with ablation outcome. METHODS AND

resultsSamples from 660 patients with paroxysmal (n = 370) or persistent AF (n = 290) undergoing AF catheter ablation were genotyped for ~1,000,000 SNPs. Gene-based association was investigated using two different gene-based association tests (VEGAS, minSNP). Among the three candidate genes, only ZFHX3 associated with left atrial dilatation and AF recurrence after catheter ablation.

conclusionThis study suggests a contribution of ZFHX3 to AF remodeling and response to therapy. Future and larger studies are necessary to replicate and apply these findings with an emphasis on designing AF pathophysiology-based multi-locus risk scores.

Indexed as

Catheter AblationGenetic Predisposition to DiseaseGenome-Wide Association StudyAtrial FibrillationFemaleHumansMaleMiddle AgedPhenotypePolymorphism, Single NucleotideRecurrenceAtrial fibrillationCatheter ablationGene-based analysisGenome wide association study

Identifiers

PMID28381281
PMCPMC5381139
OpenAlexW2604240742

What OpenQuestion holds

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Registered trials

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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.