Interplay of inflammation, oxidative stress and cardiovascular disease in rheumatoid arthritis

Rheumatoid arthritis (RA) is a chronic autoimmune/autoinflammatory disorder characterised by a symmetric erosive polyarthritis, with an additive and progressive evolution leading to joint deformities and bone anchyloses. The prevalence is about 1% of the general population, and its presence is associated to a marked increased risk of cardiovascular death, particularly due to coronary artery disease (CAD) and heart failure (HF).1 RA occurs in postmenopausal women and middle-age men who often have the traditional cardiovascular risk factors; however, such risk factors cannot fully account for the increased risk observed in these patients. A combined interaction of cytokine spillover, oxidative stress, abnormal innate and specific immune adaptation and coagulation abnormalities have been considered as potential mechanisms of increased cardiovascular risk.2Systemic cytokines (especially interleukin-1β (IL-1β), interleukin-6 (IL-6), tumour necrosis factor alpha (TNF-α)) and inflammatory biomarkers (such as C reactive proteins) are directly associated with the severity of CAD and the risk of atherothrombotic events.2 Patients with RA also have an increased risk of develop non-ischaemic HF.3 The underlying pathophysiological mechanisms are far from being completely …