Evidence mapPaperPMID 40698654Full record

ReviewPhysiological research2025

Myocardial fibrosis, the silent instigator of diastolic dysfunction in patients with rheumatoid arthritis.

M Jalali, J Števlík, Y Jalali, A Gažová, J Kyselovič, Z Killinger, J Payer

Abstract readReview
In one paragraph

Review in Physiological research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Myocardial infarction in rheumatic diseases.Rheumatology international · 2025
    Review
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.

M JalaliFaculty of Medicine, Comenius University in Bratislava, and Fifth Department of Internal Medicine, University Hospital Bratislava, Ružinov, Bratislava, Slovak Republic. Yashar.jalali@fmed.uniba.sk.
J Števlík
Y Jalali
A Gažová
J Kyselovič
Z Killinger
J Payer

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease associated with increased cardiovascular morbidity and mortality. Myocardial fibrosis, a key pathological consequence of prolonged inflammation, contributes to diastolic dysfunction and the development of heart failure with preserved ejection fraction (HFpEF) in RA patients. Understanding its pathophysiology, early detection, and potential therapeutic strategies is crucial for improving patient outcomes. In this study we explore the underlying mechanisms of myocardial fibrosis in RA, focusing on immune-mediated pathways, oxidative stress, and extracellular matrix dysregulation, with concise look at the impact of immunosuppressive therapy on cardiac remodeling and role of speckle-tracking echocardiography (STE) in detecting subclinical myocardial fibrosis, emphasizing global longitudinal strain (GLS) as a promising surrogate marker. Key words Rheumatoid arthritis " Myocardial fibrosis " Diastolic dysfunction " Cardiovascular disease surveillance " Strain echocardiography.

Indexed as

Arthritis, RheumatoidCardiomyopathiesMyocardiumDiastoleFibrosisHumans

Identifiers

PMID40698654
PMCPMC12462715

What Socratic holds

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LicenceCC BY
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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 Socratic graph.