Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease associated with increased cardiovascular morbidity and mortality. Myocardial fibrosis, a key pathological consequence of prolonged inflammation, contributes to diastolic dysfunction and the development of heart failure with preserved ejection fraction (HFpEF) in RA patients. Understanding its pathophysiology, early detection, and potential therapeutic strategies is crucial for improving patient outcomes. In this study we explore the underlying mechanisms of myocardial fibrosis in RA, focusing on immune-mediated pathways, oxidative stress, and extracellular matrix dysregulation, with concise look at the impact of immunosuppressive therapy on cardiac remodeling and role of speckle-tracking echocardiography (STE) in detecting subclinical myocardial fibrosis, emphasizing global longitudinal strain (GLS) as a promising surrogate marker.
Jalali et al. (Mon,) studied this question.