Evidence map›Paper›PMID 24667784›Full record

ArticleEuropean journal of human genetics : EJHG2014

Brugada syndrome risk loci seem protective against atrial fibrillation.

Laura Andreasen, Jonas B Nielsen, Stine Darkner, Ingrid E Christophersen, Javad Jabbari, Lena Refsgaard, Jens J Thiis, Ahmad Sajadieh, Arnljot Tveit, Stig Haunsø and 3 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of human genetics : EJHG, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

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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

13 authors at 4 institutions in 2 countries.

Laura Andreasen1] Danish National Research Foundation Centre for Cardiac Arrhythmia, Copenhagen, Denmark [2] Laboratory for Molecular Cardiology, Department of Cardiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark [3] The Ion Channel Group, Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
Jonas B Nielsen1] Danish National Research Foundation Centre for Cardiac Arrhythmia, Copenhagen, Denmark [2] Laboratory for Molecular Cardiology, Department of Cardiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Stine Darkner1] Danish National Research Foundation Centre for Cardiac Arrhythmia, Copenhagen, Denmark [2] Laboratory for Molecular Cardiology, Department of Cardiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Ingrid E Christophersen1] Danish National Research Foundation Centre for Cardiac Arrhythmia, Copenhagen, Denmark [2] Laboratory for Molecular Cardiology, Department of Cardiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark [3] Department of Medical Research, Bærum Hospital, Vestre Viken Hospital Trust, Rud, Norway.
Javad Jabbari1] Danish National Research Foundation Centre for Cardiac Arrhythmia, Copenhagen, Denmark [2] Laboratory for Molecular Cardiology, Department of Cardiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Lena Refsgaard1] Danish National Research Foundation Centre for Cardiac Arrhythmia, Copenhagen, Denmark [2] Laboratory for Molecular Cardiology, Department of Cardiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Jens J ThiisDepartments of Cardiothoracic Surgery and Cardiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Ahmad SajadiehDepartment of Cardiology, Bispebjerg Hospital, University of Copenhagen, Copenhagen, Denmark.
Arnljot TveitDepartment of Medical Research, Bærum Hospital, Vestre Viken Hospital Trust, Rud, Norway.
Stig Haunsø1] Danish National Research Foundation Centre for Cardiac Arrhythmia, Copenhagen, Denmark [2] Laboratory for Molecular Cardiology, Department of Cardiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark [3] Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.
Jesper H Svendsen1] Danish National Research Foundation Centre for Cardiac Arrhythmia, Copenhagen, Denmark [2] Laboratory for Molecular Cardiology, Department of Cardiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark [3] Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.
Nicole Schmitt1] Danish National Research Foundation Centre for Cardiac Arrhythmia, Copenhagen, Denmark [2] The Ion Channel Group, Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
Morten S Olesen1] Danish National Research Foundation Centre for Cardiac Arrhythmia, Copenhagen, Denmark [2] Laboratory for Molecular Cardiology, Department of Cardiology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
Danish National Research Foundation · DKRigshospitalet · DKUniversity of Copenhagen · DKVestre Viken Hospital Trust · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several studies have shown an overlap between genes involved in the pathophysiological mechanisms of atrial fibrillation (AF) and Brugada Syndrome (BrS). We investigated whether three single-nucleotide polymorphisms (SNPs) (rs11708996; G>C located intronic to SCN5A, rs10428132; T>G located in SCN10A, and rs9388451; T>C located downstream to HEY2) at loci associated with BrS in a recent genome-wide association study (GWAS) also were associated with AF. A total of 657 patients diagnosed with AF and a control group comprising 741 individuals free of AF were included. The three SNPs were genotyped using TaqMan assays. The frequencies of risk alleles in the AF population and the control population were compared in two-by-two models. One variant, rs10428132 at SCN10A, was associated with a statistically significant decreased risk of AF (odds ratio (OR)=0.77, P=0.001). A meta-analysis was performed by enriching the control population with allele frequencies from controls in the recently published BrS GWAS (2230 alleles). In this meta-analysis, both rs10428132 at SCN10A (OR=0.73, P=5.7 × 10(-6)) and rs11708996 at SCN5A (OR=0.80, P=0.02) showed a statistically significant decreased risk of AF. When assessing the additive effect of the three loci, we found that the risk of AF decreased in a dose-responsive manner with increasing numbers of risk alleles (OR=0.50, P=0.001 for individuals carrying ≥4 risk alleles vs ≤1 allele). In conclusion, the prevalence of three risk alleles previously associated with BrS was lower in AF patients than in patients free of AF, suggesting a protective role of these loci in developing AF.

Indexed as

Genetic LociAdolescentAdultAgedAllelesAtrial FibrillationBrugada SyndromeCase-Control StudiesFemaleGene FrequencyGenetic Predisposition to DiseaseGenome-Wide Association StudyGenotyping TechniquesHumansLogistic ModelsMale

Identifiers

PMID24667784
PMCPMC4231412
OpenAlexW2048962581

What OpenQuestion holds

Textmetadata
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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.