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Myocardial infarction in rheumatic diseases
Yuliya Fedorchenko1, Darkhan Suigenbayev2, Zhaxybek Sagtaganov3
1Department of Pathophysiology, Ivano-Frankivsk National Medical University, Halytska Str. 2, Ivano-Frankivsk, 76018, Ukraine. yufedorchenko@ifnmu.edu.ua.
Rheumatology International
|November 10, 2025
Summary
Patients with rheumatic diseases face a significantly higher risk of myocardial infarction (MI) due to chronic inflammation and immune issues. Certain therapies may protect against or increase cardiovascular risk, highlighting the need for integrated care.
Area of Science:
- Rheumatology and Cardiology
- Immunology and Cardiovascular Pathology
Background:
- Rheumatic diseases (e.g., rheumatoid arthritis, lupus) involve chronic inflammation and immune dysregulation.
- These conditions elevate the risk of cardiovascular disease, particularly myocardial infarction (MI), by 1.5- to 3-fold compared to the general population.
- Mechanisms include chronic inflammation, endothelial dysfunction, oxidative stress, and immune-mediated vascular injury, accelerating atherothrombosis.
Purpose of the Study:
- To elucidate the complex relationship between rheumatic diseases and myocardial infarction.
- To understand the impact of immune activation, vascular injury, and therapeutic interventions on cardiovascular outcomes in rheumatic disease patients.
- To emphasize the need for improved risk stratification and integrated care strategies.
Main Methods:
- Review of accumulating evidence on the mechanisms linking rheumatic diseases to MI.
- Analysis of the role of specific cytokines (TNF-α, IL-6, IL-1β) and autoantibodies in vascular damage.
- Evaluation of the cardiovascular effects of various anti-inflammatory and immunomodulatory therapies.
Main Results:
- Systemic inflammation, endothelial dysfunction, and immune factors synergistically promote atherothrombosis and plaque instability in rheumatic diseases.
- Disease-specific autoantibodies and cytokines contribute to amplified vascular damage and impaired endothelial function.
- Myocardial infarction in rheumatic diseases often presents atypically, leading to delayed diagnosis, less frequent revascularization, and higher mortality.
- Certain therapies (e.g., TNF-α inhibitors, hydroxychloroquine) show cardioprotective effects, while others (glucocorticoids, JAK inhibitors) may increase adverse cardiovascular outcomes.
Conclusions:
- Myocardial infarction in rheumatic diseases is a complex, underrecognized condition at the intersection of systemic inflammation and cardiovascular pathology.
- Integrated cardio-rheumatologic care, early risk stratification, and precision-based therapeutic strategies are crucial for mitigating cardiovascular burden.
- Further research into the interplay between immune activation, vascular injury, and treatment is essential for improving patient prognosis.
Keywords:
AtherosclerosisAutoimmune diseaseCardiovascular riskEndothelial dysfunctionInflammationMyocardial infarctionPercutaneous coronary interventionRheumatic diseasesRheumatoid arthritisSystemic lupus erythematosusMore Related Videos
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