Evidence map›Paper›PMID 39060548›Full record

SynthesisWiener klinische Wochenschrift2025

Genetic relationship between rheumatoid arthritis and cardiovascular diseases : A systematic review of Mendelian randomization studies.

Mathias Ausserwinkler, Sophie Gensluckner, Andreas Voelkerer, Jens Thiel, Hans-Jörg Neumann, Maria Flamm, Christian Datz, Elmar Aigner, Bernhard Wernly

Abstract readMeta-AnalysisSystematic Review
In one paragraph

Synthesis in Wiener klinische Wochenschrift, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. 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

9 authors.

Mathias AusserwinklerDepartment of Internal Medicine, Elisabethinen Hospital Klagenfurt, Klagenfurt, Austria.ORCID http://orcid.org/0009-0000-3353-8702
Sophie GenslucknerFirst Department of Medicine, University Clinic Salzburg, Paracelsus Medical University, Salzburg, Austria.
Andreas VoelkererDepartment of Internal Medicine, General Hospital Oberndorf, Teaching Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.
Jens ThielDivision of Rheumatology and Clinical Immunology, Department of Internal Medicine, Medical University Graz, Graz, Austria.
Hans-Jörg NeumannDepartment of Internal Medicine, Elisabethinen Hospital Klagenfurt, Klagenfurt, Austria.
Maria FlammInstitute of General Practice, Family Medicine and Preventive Medicine, Paracelsus Medical University, Strubergasse 21, 5020, Salzburg, Austria.
Christian DatzDepartment of Internal Medicine, General Hospital Oberndorf, Teaching Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.
Elmar AignerFirst Department of Medicine, University Clinic Salzburg, Paracelsus Medical University, Salzburg, Austria.
Bernhard WernlyDepartment of Internal Medicine, General Hospital Oberndorf, Teaching Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria. bernhard@wernly.net.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveRheumatoid arthritis (RA) is recognized as a chronic autoimmune disorder with systemic inflammation and joint damage. Its potential role as a risk factor for cardiovascular diseases (CVD) is increasingly noted. This review delves into the causal relationship between RA and CVD, with Mendelian randomization (MR) offering a genetic perspective.

methodsAn extensive search was conducted in PubMed, Cochrane and Web of Science to identify MR studies addressing the RA-CVD link. Out of 530 studies, 9 met the inclusion criteria, which were rigorously assessed using a critical appraisal checklist. These were further stratified by a sensitivity analysis into categories reflecting the strength of their evidence, from not evaluable to robust.

resultsFrom the nine included studies, eight supported a causal association between RA and an increased risk of CVD, specifically coronary artery disease (CAD) and one did not support a link between RA and heart failure. The results suggest that genetic factors associated with RA may contribute to an elevated risk for CVD. Chronic inflammation, prevalent in RA, emerges as a key mediator in this connection.

conclusionThe systematic review corroborates a genetic causal link between RA and CVD, as evidenced by eight of the nine MR studies reviewed. This suggests a need for integrated cardiovascular risk management in the treatment of RA patients. The findings advocate considering anti-inflammatory treatment that can reduce cardiovascular risk. The overarching evidence signifies a potential direction for new therapeutic strategies aimed at enhancing cardiovascular health in RA patients.

Indexed as

Arthritis, RheumatoidCardiovascular DiseasesGenetic Predisposition to DiseaseMendelian Randomization AnalysisCausalityComorbidityHumansPolymorphism, Single NucleotideRisk FactorsCardiovascular diseasesChronic inflammationGenetic causalityInflammatory joint diseaseMendelian randomizationRheumatoid arthritis

Identifiers

PMID39060548
PMCPMC12081514

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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.