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Noninvasive Assessment of Cardiac Abnormalities in Experimental Autoimmune Myocarditis by Magnetic Resonance Microscopy Imaging in the Mouse
Published on: June 20, 2014
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.
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.
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