From Joints to Arteries: How Rheumatoid Arthritis Therapies Influence Atherosclerotic Cardiovascular Disease Risk

Patients with rheumatoid arthritis face a markedly increased likelihood of developing atherosclerotic cardiovascular disease, driven by conventional cardiovascular risk factors as well as persistent systemic inflammation. Proinflammatory cytokines and immune dysregulation accelerate endothelial dysfunction and promote plaque formation, positioning rheumatoid arthritis as a model of inflammation-driven vascular disease. Although current therapeutics to manage rheumatoid arthritis are designed to control joint inflammation and improve overall morbidity and mortality, their effects on vascular health are complex and variable, requiring a more personalized approach to therapy. Some treatments, such as NSAIDs and glucocorticoids, may aggravate atherogenesis, whereas others-including traditional, biologic and synthetic disease-modifying antirheumatic drugs-can reduce atherosclerotic risk by modulating inflammatory pathways but may also alter lipid profiles, thrombosis, or metabolic risk, counteracting their anti-inflammatory benefits. This review explores the clinical and mechanistic evidence linking rheumatoid arthritis therapies to atherosclerosis progression or mitigation, emphasizing the importance of individualized treatment strategies that consider both articular and vascular outcomes and the patient's cardiovascular profile. A deeper understanding of how these drugs shape vascular health and disease could guide future therapeutic choices and research directions.