Evidence map›Paper›PMID 27857207›Full record

ArticleScientific reports2016

Genomic contributors to atrial electroanatomical remodeling and atrial fibrillation progression: Pathway enrichment analysis of GWAS data.

Daniela Husser, Laura Ueberham, Borislav Dinov, Jedrzej Kosiuk, Jelena Kornej, Gerhard Hindricks, M Benjamin Shoemaker, Dan M Roden, Andreas Bollmann, Petra Büttner

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–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

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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

3 citing papers in PubMed.

  1. Review
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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

10 authors.

Daniela HusserDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Germany.
Laura UeberhamDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Germany.
Borislav DinovDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Germany.
Jedrzej KosiukDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Germany.
Jelena KornejDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Germany.
Gerhard HindricksDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Germany.
M Benjamin ShoemakerDepartment of Medicine, Vanderbilt University, Nashville, TN, USA.
Dan M RodenDepartment of Medicine, Vanderbilt University, Nashville, TN, USA.
Andreas BollmannDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Germany.
Petra BüttnerDepartment of Electrophysiology, Heart Center Leipzig, Leipzig University, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In atrial fibrillation (AF), left atrial diameter (LAD) and low voltage area (LVA) are intermediate phenotypes that are associated with AF type and progression. In this study, we tested the hypothesis, that these phenotypes share common, genetically-determined pathways using pathway enrichment analysis of GWAS data. Samples from 660 patients with paroxysmal (n = 370) or persistent AF (n = 290) were genotyped for ~1,000,000 SNPs. SNPs found significantly associated with LAD, LVA or AF type were used for gene-based association tests in a systematic biological Knowledge-based mining system for Genome-wide Genetic studies (KGG). Associated genes were tested for pathway enrichment using two enrichment tools (WebGestalt and GATHER) and the databases provided by Kyoto Encyclopedia of Genes and Genomes. The calcium signaling pathway (hsa04020) was the only pathway that reached statistical significance for LAD and LVA in both enrichment tools and was also significantly associated with AF type. Within this pathway, there were 39 genes (i.e. CACNA1C, RyR2) that were associated with LAD, LVA and AF type. In conclusion, there is a genomic contribution to electroanatomical remodeling (LAD, LVA) and AF type via the calcium signaling pathway. Future and larger studies are necessary to replicate and apply these findings.

Indexed as

Genome-Wide Association StudyAgedAtrial FibrillationCalcium SignalingFemaleHumansMaleMiddle AgedPolymorphism, Single Nucleotide

Identifiers

PMID27857207
PMCPMC5114680

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