Evidence map›Paper›PMID 35583917›Full record

SynthesisArthritis & rheumatology (Hoboken, N.J.)2022

Genetic Liability to Rheumatoid Arthritis in Relation to Coronary Artery Disease and Stroke Risk.

Shuai Yuan, Paul Carter, Amy M Mason, Fangkun Yang, Stephen Burgess, Susanna C Larsson

Open access · hybridAbstract readMeta-Analysis
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Arthritis & rheumatology (Hoboken, N.J.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 6 pooled it
10.1field-weighted citation impact, top 1% 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

34 citing papers in PubMed, 6 syntheses or guidelines pooled it, 57 citations in OpenAlex.

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  12. Mendelian randomization of autoimmune hepatitis and cardiovascular diseases.American heart journal plus : cardiology research and practice · 2025
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  18. Smoking may increase the usage of antidepressant: evidence from genomic perspective analysis.European archives of psychiatry and clinical neuroscience · 2025
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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.

Shuai YuanKarolinska Institutet, Stockholm, Sweden.ORCID 0000-0001-5055-5627
Paul CarterUniversity of Cambridge, Cambridge, UK.
Amy M MasonUniversity of Cambridge, Cambridge, UK.
Fangkun YangNingbo First Hospital and Zhejiang University, Ningbo, China.
Stephen BurgessUniversity of Cambridge, Cambridge, UK.
Susanna C LarssonKarolinska Institutet, Stockholm, Sweden, and Uppsala University, Uppsala, Sweden.ORCID 0000-0003-0118-0341
University of Cambridge · GBKarolinska Institutet · SENingbo First Hospital · CNUppsala University · SE

Funding

British Heart Foundation RG/13/13/30194British Heart Foundation RG/18/13/33946Department of HealthMedical Research Council MC_PC_17228Medical Research Council MC_QA137853Medical Research Council MC_UU_00002/7Wellcome Trust 204623/Z/16/Z
6 · The paper itself

Abstract

objectiveTo assess the causality of the associations of rheumatoid arthritis (RA) with coronary artery disease (CAD) and stroke using the Mendelian randomization approach.

methodsIndependent single-nucleotide polymorphisms strongly associated with RA (n = 70) were selected as instrumental variables from a genome-wide association meta-analysis including 14,361 RA patients and 43,923 controls of European ancestry. Summary-level data for CAD, all stroke, any ischemic stroke and its subtypes, intracerebral hemorrhage (ICH), and subarachnoid hemorrhage were obtained from meta-analyses of genetic studies, international genetic consortia, the UK Biobank, and the FinnGen consortium. We obtained summary-level data for common cardiovascular risk factors and related inflammatory biomarkers to assess possible mechanisms.

resultsGenetic liability to RA was associated with an increased risk of CAD and ICH. For a 1-unit increase in log odds of RA, the combined odds ratios were 1.02 (95% confidence interval [1.01, 1.03]; P = 0.003) for CAD and 1.05 (95% confidence interval [1.02, 1.08]; P = 0.001) for ICH. Genetic liability to RA was associated with increased levels of tumor necrosis factor and C-reactive protein (CRP). The association with CAD was attenuated after adjustment for genetically predicted CRP levels. There were no associations of genetic liability to RA with the other studied outcomes.

conclusionThis study found that genetic liability to RA was associated with an increased risk of CAD and ICH and that the association with CAD might be mediated by CRP. The heightened cardiovascular risk should be actively monitored and managed in RA patients, and this may include dampening systemic inflammation.

Indexed as

Arthritis, RheumatoidCoronary Artery DiseaseStrokeBiomarkersC-Reactive ProteinGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMendelian Randomization AnalysisPolymorphism, Single NucleotideRisk FactorsTumor Necrosis FactorsBiomarkersC-Reactive ProteinTumor Necrosis Factors

Identifiers

PMID35583917
PMCPMC9804931
OpenAlexW4280548369

What OpenQuestion holds

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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.