The fi rst atherosclerotic stage is characterized by endothelial activation and the subsequent up-regulation of adhesion molecules, including E-selectin, VCAM-1 and ICAM-1, is a crucial step in this process (Libby et al. 2010). Enhanced expression of adhesion molecules and increased levels of their soluble (s) forms have been demonstrated in patients with RA and systemic autoimmune disease. VCAM-1 plasma levels correlated with surrogate marker of subclinical ATS in RA, a part of traditional CV risk factors and other markers of infl ammation (Bartoloni et al. 2010a). Such fi nding may suggest that adhesion molecules, expressed on both endothelial and smooth muscle cells, play a relevant role in the initiation and perpetuation of ATS damage by favouring leukocyte and monocyte infi ltration in subendothelial space with consequent impairment of smooth muscle component of vessel wall media layer.