Longitudinal predictors of progression of carotid atherosclerosis in rheumatoid arthritis

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

Methods: 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.

Results: Among the 158 RA patients, the maximal CCA-IMT increased in 82% (median 16 μm/year; P < 0.001) and the maximal ICA-IMT increased in 70% (median 25 μm/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 μm/year versus 22 μm/year; P = 0.026). For the maximal ICA-IMT, cumulative prednisone exposure was associated with progression after adjustment (1.2 μm/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.

Conclusion: 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.