Rheumatoid arthritis (RA) patients have an incidence of cardiovascular (CV) diseases at least two times higher than the general population. Atherosclerosis, the main determinant of CV morbidity and mortality, and carotid intima-media thickness, an early preclinical marker of atherosclerosis, also occur early on in RA. Traditional CV risk factors seem to have the same prevalence in RA and non-RA patients, and thus do not fully explain the increased CV burden, suggesting that RA inflammation and therapies play a role in increasing CV risk in these patients. The metabolic syndrome and fat tissue are likely to be the major players in this complex network. The metabolic syndrome (MetS) represents a cluster of cardiovascular risk factors that have in common insulin resistance and increased visceral adiposity. This entity has received great attention in the last few years due to its contribution to the burden of cardiovascular morbidity and mortality. Moreover, recently the adipose tissue has emerged as a dynamic organ that releases several inflammatory and immune mediators (adipokines). The association of MetS and atherosclerosis is thought to be partly mediated by altered secretion of adipokines by the adipose tissue and, on the other hand, there are evidence that adipokines may play some role in inflammatory arthritides. Obesity is now regarded as a systemic, low-grade inflammatory state, and inflammation as a link between obesity, metabolic syndrome, and cardiovascular diseases. To obtain a full control of the CV risk, data suggest that it is therefore mandatory a "tight control" of both RA and MetS inflammations.
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