Evidence mapPaperPMID 41212291Full record

ReviewRheumatology international2025

Myocardial infarction in rheumatic diseases.

Yuliya Fedorchenko, Darkhan Suigenbayev, Zhaxybek Sagtaganov, Nurzhamal Imanbayeva, Khaiyom Mahmudzoda

Abstract readReview
PubMed Publisher
In one paragraph

Review in Rheumatology international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
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 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  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

5 authors.

Yuliya FedorchenkoDepartment of Pathophysiology, Ivano-Frankivsk National Medical University, Halytska Str. 2, Ivano-Frankivsk, 76018, Ukraine. yufedorchenko@ifnmu.edu.ua.ORCID http://orcid.org/0000-0002-5042-1191
Darkhan SuigenbayevHeart Center Shymkent, Shymkent, Kazakhstan.ORCID https://orcid.org/0009-0005-5942-8102
Zhaxybek SagtaganovDepartment of Science, Education and Strategy, Heart Center Shymkent, Shymkent, Kazakhstan.ORCID http://orcid.org/0000-0002-6459-398X
Nurzhamal ImanbayevaDepartment of Internal Medicine N4, Astana Medical University, Astana, Kazakhstan.ORCID https://orcid.org/0000-0002-2698-8956
Khaiyom MahmudzodaDepartment of Propaedeutics of Internal Diseases, Avicenna Tajik State Medical University, Dushanbe, Tajikistan.ORCID http://orcid.org/0000-0002-3583-9442

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatic diseases, including rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, and spondyloarthritides, are chronic systemic disorders marked by persistent inflammation and immune dysregulation. These diseases confer an elevated risk of cardiovascular disease, with myocardial infarction (MI) as a leading cause of increased morbidity and premature mortality. Accumulating evidence suggests that patients with rheumatic diseases experience a 1.5- to 3-fold higher incidence of MI compared with the general population. Chronic systemic inflammation, endothelial dysfunction, oxidative stress, and immune-mediated vascular injury act synergistically to accelerate atherothrombosis and plaque instability. Cytokines, such as TNF-α, IL-6, and IL-1β, impair endothelial nitric oxide signaling and promote lipid oxidation. Disease-specific autoantibodies, including anti-citrullinated protein antibodies, antiphospholipid, and anti-endothelial cell antibodies, further amplify vascular damage. In systemic sclerosis, progressive microvascular dysfunction and myocardial fibrosis contribute to ischemic remodeling. Clinically, MI in rheumatic diseases often presents atypically, complicating diagnosis and intervention, with patients less frequently undergoingrevascularization and experiencing higher post-infarction mortality. Importantly, anti-inflammatory and immunomodulatory therapies exert divergent cardiovascular effects: TNF-α inhibitors, conventional disease-modifying antirheumatic drugs, and particularly hydroxychloroquine appear cardioprotective whereas glucocorticoids and janus kinase inhibitors increase adverse outcomes. Understanding the interplay between immune activation, vascular injury, and therapeutic modulation is crucial for improving prognosis. MI in rheumatic diseases represents a complex, underrecognized intersection of systemic inflammation and cardiovascular pathology, underscoring the need for early risk stratification, integrated cardio-rheumatologic care, and precision-based strategies to mitigate cardiovascular burden.

Indexed as

Myocardial InfarctionRheumatic DiseasesAntirheumatic AgentsHumansRisk FactorsAntirheumatic AgentsAtherosclerosisAutoimmune diseaseCardiovascular riskEndothelial dysfunctionInflammationMyocardial infarctionPercutaneous coronary interventionRheumatic diseasesRheumatoid arthritisSystemic lupus erythematosus

Identifiers

What Socratic holds

Textmetadata
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 Socratic graph.