Effects of adalimumab treatment on vascular disease associated with early rheumatoid arthritis.

KeY wOrds: FMD = flow-mediated vasodilation ccIMT = common carotid intima-media thickness PWV = pulse-wave velocity RA = rheumatoid arthritis CRP = C-reactive protein vWF = vonWillebrand factor CVD = cardiovascular disease a ccelerated atherosclerosis, as well as increased cardiovascular morbidity and mortality have been associated with rheumatoid arthritis [1-5]. RA is an independent risk factor for accelerated cardiovascular disease [2-4]. Classical, Framingham, as well as inflammatory factors have been implicated in RA-related CVD [1-8]. Among the traditional risk factors, dyslipidemia, smoking and metabolic syndrome have been implicated in the development of atherosclerosis in RA [2,3,8]. Dyslipidemia in RA may be secondary to chronic inflammation [2,3]. Regarding inflammatory mechanisms, both atherosclerotic plaques and the RA synovium contain inflammatory leukocytes, mainly macrophages and T cells, pro-inflammatory cytokines including tumor necrosis factor-alpha, chemokines, matrix-degrading proteases and other inflammatory mediators [1-3,7-9]. It has been suggested that sustained inflammatory activity may be the predominant risk factor for accelerated atherosclerosis and excessive CVD mortality in RA [1-4,9]. Several ultrasonographic techniques have been developed to assess early vascular changes in RA. Accelerated atherosclerosis indicated by increased common carotid intimal-medial thickness has been described in RA [1-4]. As previously reported by us and others, early endothelial dysfunction indicated by