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Carotid intima-media thickness and endothelial function: useful surrogate markers for establishing cardiovascular risk in patients with inflammatory rheumatic disease

DOI: 10.1186/ar2409

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We recently reported [2] that carotid artery IMT had good ability to predict development of cardiovascular events over a 5-year period of follow up in 47 patients with RA without clinically evident cardiovascular disease at the time of evaluation by carotid ultrasonography. In our study carotid IMT, categorized in quartiles, was strongly associated with cardiovascular events; specifically, none of the RA patients with carotid IMT less than 0.77 mm suffered cardiovascular events. However, six of the 10 patients with carotid IMT greater than 0.91 mm experienced cardiovascular events. When logistic regression models were performed, carotid IMT at the time of ultrasonographic study had high power to predict development of cardiovascular events over the 5-year period of follow up. Although the area under the receiver operating characteristic curve was 0.86 when using age at the onset of the study, it was greater in models that included carotid IMT. In this regard, the area under the receiver operating characteristic curve was 0.93 for a model that included only carotid IMT. Based on these findings, we propose that ultrasonographic assessment of the carotid artery should be performed in all patients with RA in order to identify the subgroup of patients at high risk for cardiovascular complications.In the same editorial, Veldhuijzen van Zanten and Kitas [1] emphasize that endothelial function is highly dependent on current levels of inflammation. We agree entirely with the authors on this point; we observed endothelial dysfunction in patients with biopsy-proven giant cell arteritis (GCA) – an inflammatory disease that involves large and middle-sized blood vessels. However, steroid therapy was able to improve endothelial function. This effect was observed when laboratory markers of inflammation returned to normal levels [3]. Whether normalization of endothelial function might lead to 'protection' against development of accelerated atherosclerosis in chronic inflammatory dis


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