Myocardial infarction in rheumatic diseases
Fedorchenko Y. Suigenbayev D. Sagtaganov Z. Imanbayeva N. Mahmudzoda K.
December 2025Springer Science and Business Media Deutschland GmbH
Rheumatology International
2025#45Issue 12
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.
Atherosclerosis , Autoimmune disease , Cardiovascular risk , Endothelial dysfunction , Inflammation , Myocardial infarction , Percutaneous coronary intervention , Rheumatic diseases , Rheumatoid arthritis , Systemic lupus erythematosus
Text of the article Перейти на текст статьи
Department of Pathophysiology, Ivano-Frankivsk National Medical University, Halytska Str. 2, Ivano-Frankivsk, 76018, Ukraine
Heart Center Shymkent, Shymkent, Kazakhstan
Department of Science, Education and Strategy, Heart Center Shymkent, Shymkent, Kazakhstan
Department of Internal Medicine N4, Astana Medical University, Astana, Kazakhstan
Department of Propaedeutics of Internal Diseases, Avicenna Tajik State Medical University, Dushanbe, Tajikistan
Department of Pathophysiology
Heart Center Shymkent
Department of Science
Department of Internal Medicine N4
Department of Propaedeutics of Internal Diseases
10 лет помогаем публиковать статьи Международный издатель
Книга Публикация научной статьи Волощук 2026 Book Publication of a scientific article 2026