Rheumatoid Arthritis (RA) is a chronic, systemic inflammatory disease characterized by a relatively high risk of atherosclerotic cardiovascular (CV) events. Notably, such risk has been reported to be similar to that of diabetes mellitus (DM) [1]. Large epidemiological studies suggest that a total of 70% of CV events are attributable to both traditional CV risk factors, mainly hypertension and smoking, combined with disease features [2]. In this setting, besides a genetic component, chronic inflammation may explain at least in part this CV burden by playing a dual role: a direct effect - by promoting endothelial and vessel damage and atherosclerosis progression; and an indirect effect - by modifying traditional CV risk factors such as lipid metabolism [3–5].
