Evidence map›Paper›PMID 40517266›Full record

ArticleAdvances in rheumatology (London, England)2025

Determinants of myocardial fibrosis in patients with immune-mediated inflammatory diseases.

Nicholas Black, Joshua Bradley, Fardad Soltani, John P Farrant, Josephine H Naish, Matthias Schmitt, Maya H Buch, Christopher A Miller

Abstract read
In one paragraph

Article in Advances in rheumatology (London, England), 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. 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

8 authors.

Nicholas BlackDivision of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Oxford Road, Manchester, M13 9PL, UK.ORCID 0000-0002-0089-6180
Joshua BradleyDivision of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Oxford Road, Manchester, M13 9PL, UK.ORCID 0000-0002-0958-7392
Fardad SoltaniDivision of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Oxford Road, Manchester, M13 9PL, UK.ORCID 0000-0003-2030-9761
John P FarrantDivision of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Oxford Road, Manchester, M13 9PL, UK.ORCID 0000-0002-9241-2410
Josephine H NaishManchester University NHS Foundation Trust, Southmoor Road, Wythenshawe, Manchester, M23 9LT, UK.ORCID 0000-0002-8980-8924
Matthias SchmittDivision of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Oxford Road, Manchester, M13 9PL, UK.ORCID 0000-0001-8514-0261
Maya H BuchManchester University NHS Foundation Trust, Southmoor Road, Wythenshawe, Manchester, M23 9LT, UK.ORCID 0000-0002-8962-5642
Christopher A MillerDivision of Cardiovascular Sciences, School of Medical Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Oxford Road, Manchester, M13 9PL, UK. Christopher.Miller@manchester.ac.uk.ORCID 0000-0002-5957-7088

Funding

British Heart Foundation AA/18/4/34221EPA EP-C-15-003Manchester Biomedical Research Centre NIHR 203308National Institute for Health and Care Research CS-2015-15-003
6 · The paper itself

Abstract

backgroundMyocardial fibrosis is an important adverse prognostic marker, however; determinants of myocardial fibrosis in immune-mediated inflammatory diseases (IMIDs) remain poorly defined. We aimed to identify determinants of myocardial fibrosis in patients with IMIDs, as measured by cardiovascular magnetic resonance (CMR) extracellular volume (ECV).

methodsCross-sectional study of 116 patients with IMIDs undergoing clinical CMR at Manchester University NHS Foundation Trust. IMIDs included rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis (SSc), ankylosing spondylitis, psoriatic arthritis and vasculitis. CMR included pre- and post-contrast T1 mapping to measure myocardial ECV, with same day blood sampling. Determinants of ECV were investigated with univariable and multivariable linear regression.

resultsECV varied significantly according to IMID diagnosis (ANOVA F statistic 2.80, P = 0.015); ECV was higher in patients with SSc compared to other IMIDs. Major determinants of ECV as a continuous variable were SSc, smoking and body mass index (BMI); regression coefficients 3.33 (95% confidence interval 0.82-5.84), 3.08 (0.73-5.43), and - 0.19 (-0.29 - -0.09) respectively, P < 0.01 (SSc, smoking and lower BMI were associated with increased ECV). Approximately a quarter of the variability in ECV could be explained by these predictors (optimism adjusted R

conclusionSSc is associated with a higher burden of myocardial fibrosis compared to other IMIDs. In patients with IMIDs, independent determinants of myocardial fibrosis were presence of SSc, smoking and BMI. Importantly, participants underwent CMR for clinical indications and may not be representative of IMID populations in the community.

Indexed as

CardiomyopathiesMyocardiumAdultAgedBody Mass IndexCross-Sectional StudiesFemaleFibrosisHumansInflammationMagnetic Resonance ImagingMaleMiddle AgedScleroderma, SystemicSmokingExtracellular volumeImmune-mediated inflammatory diseaseMyocardial fibrosis

Identifiers

PMID40517266
PMCPMC12167332

What Socratic 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 Socratic graph.