Evidence map›Paper›PMID 30721963›Full record

ArticleEuropean heart journal2019

Body composition and atrial fibrillation: a Mendelian randomization study.

Emmi Tikkanen, Stefan Gustafsson, Joshua W Knowles, Marco Perez, Stephen Burgess, Erik Ingelsson

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

Article in European heart journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
5.6field-weighted citation impact, top 3% 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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 59 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 3 countries.

Emmi TikkanenDivision of Cardiovascular Medicine, Department of Medicine, Stanford University School of Medicine, 300 Pasteur Dr, Stanford, CA, USA.
Stefan GustafssonDepartment of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, EpiHubben, MTC-huset, Uppsala, Sweden.
Joshua W KnowlesDivision of Cardiovascular Medicine, Department of Medicine, Stanford University School of Medicine, 300 Pasteur Dr, Stanford, CA, USA.
Marco PerezDivision of Cardiovascular Medicine, Department of Medicine, Stanford University School of Medicine, 300 Pasteur Dr, Stanford, CA, USA.
Stephen BurgessMRC Biostatistics Unit, Cambridge Institute of Public Health, University of Cambridge, Forvie Site, Robinson Way, Cambridge Biomedical Campus, Cambridge, UK.
Erik IngelssonDivision of Cardiovascular Medicine, Department of Medicine, Stanford University School of Medicine, 300 Pasteur Dr, Stanford, CA, USA.
Science for Life Laboratory · SEStanford University · USCardiovascular Institute of the South · USUniversity of Cambridge · GB

Funding

Stanford Islet Research CoreP30DK116074 · NIDDK · STANFORD UNIVERSITY · PI Seung K Kim · 2017 to 2026
$19.5M
Beyond GWAS of insulin resistance: An integrated approach to translate genetic association to functionR01DK106236 · NIDDK · STANFORD UNIVERSITY · PI KNOWLES, JOSHUA WILEY · 2016 to 2020
$2.4M
Molecular Mechanisms of Insulin Resistance Associated LociR01DK107437 · NIDDK · STANFORD UNIVERSITY · PI QUERTERMOUS, THOMAS · 2016 to 2019
$2.2M
Causal associations of circulating biomarkers with cardiovascular diseaseR01HL135313 · NHLBI · STANFORD UNIVERSITY · PI INGELSSON, ERIK · 2017 to 2019
$1.6M
British Heart Foundation RG/13/13/30194British Heart Foundation RG/18/13/33946Medical Research Council MC_PC_17228Medical Research Council MC_QA137853Medical Research Council MC_UU_00002/7NHLBI NIH HHS R01 HL135313NIDDK NIH HHS P30 DK116074NIDDK NIH HHS R01 DK106236NIDDK NIH HHS R01 DK107437Wellcome Trust 204623/Z/16/Z
6 · The paper itself

Abstract

aimsIncreases in fat-free mass and fat mass have been associated with higher risk of atrial fibrillation (AF) in observational studies. It is not known whether these associations reflect independent causal processes. Our aim was to evaluate independent causal roles of fat-free mass and fat mass on AF. METHODS AND

resultsWe conducted a large observational study to estimate the associations between fat-free mass and fat mass on incident AF in the UK Biobank (N = 487 404, N events = 10 365). Genome-wide association analysis was performed to obtain genetic instruments for Mendelian randomization (MR). We evaluated the causal effects of fat-free mass and fat mass on AF with two-sample method by using genetic associations from AFGen consortium as outcome. Finally, we evaluated independent causal effects of fat-free mass and fat mass with multivariate MR. Both fat-free mass and fat mass had observational associations with incident AF [hazard ratio (HR) = 1.77, 95% confidence interval (CI) 1.72-1.83; HR = 1.40, 95% CI 1.37-1.43 per standard deviation increase in fat-free and fat mass, respectively]. The causal effects using the inverse-variance weighted method were 1.55 (95% CI 1.38-1.75) for fat-free mass and 1.30 (95% CI 1.17-1.45) for fat mass. Weighted median, Egger regression, and penalized methods showed similar estimates. The multivariate MR analysis suggested that the causal effects of fat-free and fat mass were independent of each other (causal risk ratios: 1.37, 95% CI 1.06-1.75; 1.28, 95% CI 1.03-1.58).

conclusionGenetically programmed increases in fat-free mass and fat mass independently cause an increased risk of AF.

Indexed as

Atrial FibrillationMendelian Randomization AnalysisBiomarkersBody CompositionGenome-Wide Association StudyHumansPolymorphism, Single NucleotideBiomarkersAtrial fibrillationBioimpedanceCausal effectFat-free massFat massGenetics

Identifiers

PMID30721963
PMCPMC6475522
OpenAlexW2911959957

What OpenQuestion holds

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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.