Evidence map›Paper›PMID 22690879›Full record

SynthesisJournal of internal medicine2012

Genetic polymorphisms for estimating risk of atrial fibrillation: a literature-based meta-analysis.

J G Smith, P Almgren, G Engström, B Hedblad, P G Platonov, C Newton-Cheh, O Melander

Open access · greenAbstract readMeta-AnalysisSystematic Review
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Journal of internal medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 2 pooled it
1.3field-weighted citation impact, top 18% 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

9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 14 citations in OpenAlex.

  1. European Heart Rhythm Association (EHRA)/European Association of Cardiovascular Prevention and Rehabilitation (EACPR) position paper on how to prevent atrial fibrillation endorsed by the Heart Rhythm Society (HRS) and Asia Pacific Heart Rhythm Society (APHRS).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 · 2017
    Guideline
  2. Guideline
  3. Review
  4. Article
  5. Article
  6. Review
  7. Genome-wide association studies of late-onset cardiovascular disease.Journal of molecular and cellular cardiology · 2015
    Review
  8. Article
  9. 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

7 authors at 3 institutions in 2 countries.

J G SmithDepartment of Cardiology, Lund University, Lund, Sweden. gustav.smith@med.lu.se
P Almgren
G Engström
B Hedblad
P G Platonov
C Newton-Cheh
O Melander
Lund University · SECenter for Human Genetics · USMassachusetts Institute of Technology · US

Funding

Genetic determinants of cardiac repolarizationK23HL080025 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NEWTON-CHEH, CHRISTOPHER HOLMES · 2005 to 2009
$797k
European Research Council 282255NHLBI NIH HHS K23 HL080025NHLBI NIH HHS K23-HL-080025
6 · The paper itself

Abstract

backgroundGenetic polymorphisms associated with common aetiologically complex diseases have recently been identified through genome-wide association studies. Direct-to-consumer genetic testing for such polymorphisms, with provision of absolute genetic risk estimates, is marketed by several commercial companies. Polymorphisms associated with atrial fibrillation (AF) have shown relatively large risk estimates, but the robustness of such estimates across populations and study designs has not been investigated.

designA systematic literature review with meta-analysis and assessment of between-study heterogeneity was carried out for single-nucleotide polymorphisms (SNPs) in the six genetic regions associated with AF in genome-wide or candidate gene studies.

resultsData were identified from 18 samples of European ancestry (n=12,100 cases, 115,702 controls) for the single-nucleotide polymorphisms (SNP) on chromosome 4q25 (rs220733), from 16 samples (n=12,694 cases, 132,602 controls) for the SNP on 16q22 (rs2106261) and from four samples (n=5272 cases, 59,725 controls) for the SNP in KCNH2 (rs1805123). Only the publications in which the associations were initially reported were identified for SNPs on 1q21 and in GJA5 and IL6R, why meta-analyses were not performed for those SNPs. In overall random-effects meta-analyses, association with AF was observed for both SNPs on chromosomes 4q25 [odds ratio (OR), 1.67; 95% CI, 1.50-1.86, P=2×10(-21)] and 16q22 (OR, 1.21; 95% CI, 1.13-1.29, P=1×10(-8)) from genome-wide studies, but not the SNP in KCNH2 from candidate gene studies (P=0.15). There was substantial effect heterogeneity across case-control and cross-sectional studies for both polymorphisms (I(2)=0.50-0.78, P<0.05), but not across prospective cohort studies (I(2)=0.39, P=0.15). Both polymorphisms were robustly associated with AF for each study design individually (P<0.05).

conclusionsIn meta-analyses including up to 150,000 individuals, polymorphisms in two genetic regions were robustly associated with AF across all study designs but with substantial context-dependency of risk estimates.

Indexed as

Chromosomes, Human, Pair 4Polymorphism, Single NucleotideAtrial FibrillationChromosome MappingGenetic MarkersGenetic Predisposition to DiseaseGenetic TestingGenome-Wide Association StudyHumansModels, StatisticalRisk AssessmentGenetic Markers

Identifiers

PMID22690879
PMCPMC3763745
OpenAlexW1830800555

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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.