Evidence map›Paper›PMID 35292824›Full record

ArticleInternational journal of epidemiology2022

A phenome-wide bidirectional Mendelian randomization analysis of atrial fibrillation.

Qin Wang, Tom G Richardson, Eleanor Sanderson, Matthew J Tudball, Mika Ala-Korpela, George Davey Smith, Michael V Holmes

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

Article in International journal of epidemiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 4 pooled it
6.9field-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

24 citing papers in PubMed, 4 syntheses or guidelines pooled it, 39 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

7 authors at 3 institutions in 2 countries.

Qin WangClinical Trial Service Unit & Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.
Tom G RichardsonMedical Research Council Integrative Epidemiology Unit, University of Bristol, Bristol, UK.ORCID 0000-0002-7918-2040
Eleanor SandersonMedical Research Council Integrative Epidemiology Unit, University of Bristol, Bristol, UK.ORCID 0000-0001-5188-5775
Matthew J TudballMedical Research Council Integrative Epidemiology Unit, University of Bristol, Bristol, UK.
Mika Ala-KorpelaComputational Medicine, Faculty of Medicine, University of Oulu and Biocenter Oulu, Oulu, Finland.ORCID 0000-0001-5905-1206
George Davey SmithMedical Research Council Integrative Epidemiology Unit, University of Bristol, Bristol, UK.ORCID 0000-0002-1407-8314
Michael V HolmesClinical Trial Service Unit & Epidemiological Studies Unit, Nuffield Department of Population Health, University of Oxford, Oxford, UK.ORCID 0000-0001-6617-0879
University of Bristol · GBNational Institute for Health Research · GBUniversity of Eastern Finland · FI

Funding

British Heart Foundation FS/18/23/33512Medical Research Council MC_UU_00011/1
6 · The paper itself

Abstract

backgroundThe prevalence of atrial fibrillation (AF) is increasing with an aging worldwide population, yet a comprehensive understanding of its causes and consequences remains limited. We aim to assess the causes and consequences of AF via a bidirectional Mendelian randomization (MR) analysis.

methodsWe used publicly available genome-wide association study (GWAS) summary data, centralized and harmonized by an open GWAS database. We assessed the genetically predicted effects of 5048 exposures on risk of AF, and the genetically predicted effects of genetic liability to AF, on 10 308 outcomes via two-sample MR analysis. Multivariable MR analysis was further conducted to explore the comparative roles of identified risk factors.

resultsMR analysis suggested that 55 out of 5048 exposure traits, including four proteins, play a causal role in AF (P <1e-5 allowing for multiple comparisons). Multivariable analysis suggested that higher body mass index, height and systolic blood pressure as well as genetic liability to coronary artery diseases independently cause AF. Three out of the four proteins (DUSP13, TNFSF12 and IL6R) had a drug prioritizing score for atrial fibrillation of 0.26, 0.38 and 0.88, respectively (values closer to 1 indicating stronger evidence of the protein as a potential drug target). Genetic liability to AF was linked to a higher risk of cardio-embolic ischaemic stroke.

conclusionsOur results suggest body mass index, height, systolic blood pressure and genetic liability to coronary artery disease are independent causal risk factors for AF. Several proteins, including DUSP13, IL-6R and TNFSF12, may have therapeutic potential for AF.

Indexed as

Atrial FibrillationBrain IschemiaStrokeGenome-Wide Association StudyHumansMendelian Randomization AnalysisPolymorphism, Single NucleotideRisk FactorsAtrial fibrillationMendelian randomizationproteinsstroke

Identifiers

PMID35292824
PMCPMC9365635
OpenAlexW4214768777

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.