Longitudinal predictors of progression of carotid atherosclerosis in rheumatoid arthritis

To explore predictors of change in measures of carotid atherosclerosis among rheumatoid arthritis (RA) patients without known cardiovascular disease (CVD) at baseline.

RA patients underwent carotid ultrasonography at 2 time points separated by a mean ± SD of 3.2 ± 0.3 years. The associations of baseline and average patient characteristics with the average yearly change in the mean maximal intima-media thickness (IMT) of the common carotid artery (CCA) and the internal carotid artery (ICAs) and with incident or progressive plaque in the ICA/carotid bulb, were explored.

Among the 158 RA patients, the maximal CCA-IMT increased in 82% (median 16 microm/year; P < 0.001) and the maximal ICA-IMT increased in 70% (median 25 microm/year; P < 0.001). Incident plaque was observed in 14% of those without plaque at baseline (incidence rate 4.2 per 100 person-years [95% confidence interval 1.6, 6.8]). Plaque progression was observed in 5% of those with plaque at baseline. Among RA predictors, the adjusted average yearly change in the maximal CCA-IMT was significantly greater in patients with earlier RA than in those with disease of longer duration. Those taking tumor necrosis factor (TNF) inhibitors at baseline had a 37% lower adjusted rate of progression in the maximal CCA-IMT compared with nonusers (14 microm/year versus 22 microm/year; P = 0.026). For the maximal ICA-IMT, cumulative prednisone exposure was associated with progression after adjustment (1.2 microm/year per gm [95% confidence interval 0.1, 2.4]) and was lower in patients who were prescribed statins concomitant with prednisone. Higher swollen joint counts and higher average C-reactive protein levels were both associated with incident or progressive plaque, primarily in patients with elevated CVD risk at baseline based on the Framingham Risk Score.

These prospective data provide evidence that inflammation is a contributor to the progression of subclinical atherosclerosis in RA and that it is potentially modified favorably by TNF inhibitors and detrimentally by glucocorticoids.