Rheumatoid arthritis is characterized by early and accelerated atherosclerosis leading to increased cardiovascular morbidity and mortality. Beyond traditional cardiovascular risk factors, several pathogenetic mechanisms have been proposed, including emerging inflammatory and autoimmune mechanisms. Inflammatory stimuli are now believed to cause vascular damage, which can be estimated by well-established noninvasive techniques. Carotid intima-media thickness, pulse-wave velocity and flow-mediated dilatation, markers of subclinical atherosclerosis, arterial stiffness, and endothelial function, respectively, have been recently used to detect vascular dysfunction in the wide spectrum of autoimmune diseases. The role of anti-tumor necrosis factor α and novel biologic agents remains unclear, although early control of the inflammatory process seems crucial for reducing cardiovascular risk. Considering the importance of cardiovascular risk management, further well-designed studies are warranted to clarify the potential benefits and harms of anti-inflammatory treatment.