Rheumatoid arthritis is sufficient to cause atheromatosis but not arterial stiffness or hypertrophy in the absence of classical cardiovascular risk factors
Abstract
Rheumatoid arthritis (RA) associates with increased cardiovascular disease (CVD) mortality thought to be due to accelerated arterial disease. Different components of arterial disease, namely, atheromatosis, arteriosclerosis, and arterial wall hypertrophy, are differentially affected by classical CVD risk factors, which are highly prevalent in these patients. We hypothesized that RA disease per se may also differentially affect these components. Of 267 consecutive RA patients, we selected specifically those who were free of established CVD and CVD risk factors (18 %); of them, 41 patients (36 women, 49 ± 13 years) could be matched effectively 1:1 for age and gender to healthy controls. Atheromatosis was assessed by the presence of carotid and/or femoral artery plaques, arteriosclerosis by pulse wave velocity and local wall elasticity, and arterial hypertrophy by intima-media thickness and cross-sectional area. More patients had atheromatic plaques than controls (29 vs. 12 %, p = 0.039), and multiarterial atheromatosis was more prevalent in RA (22 vs. 2 %, p = 0.026). Accelerated atheromatosis was not associated with rheumatoid factor, or anti-cyclic citrullinated peptide (CCP) autoantibody status. Plaque burden in patients with ...Continue Reading
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