Rheumatoid arthritis (RA) patients had a threefold increase in preclinical carotid atherosclerotic plaque, independent of traditional risk factors, according to a matched cross-sectional study.

In a study of 98 consecutive outpatients with RA, 44% had preclinical atherosclerosis compared with 15% of 98 controls matched for age, sex, and ethnicity (P< 0.001), researchers reported in the Feb. 21 issue of the Annals of Internal Medicine.

The relationship remained after adjusting for traditional risk factors such as age, serum cholesterol levels, smoking history, and hypertension. In fact, the controls had a poorer risk-factor profile, according to Mary Roman, M.D., of Weill Cornell Medical College here and colleagues.

Adjusted predicted prevalence of carotid plaque was 38.5% (95% CI, 25.4% to 53.5%) for patients with RA versus 7.4% (95% CI, 3.4% to 15.2%) for the controls. Age (P< 0.001) and current cigarette use (P<0.014) were also associated with carotid plaque formation.

Among the RA patients, atherosclerosis was related to age, hypertension status, and use of tumor necrosis factor-alpha inhibitors, which may have been a marker of disease severity, the researchers said. The RA patients’ ages ranged from 20 to 83, with 35 the mean age at diagnosis. Duration of disease was 12 years.

Carotid intima thickness, determined by ultrasonogram, was a direct measure and proxy for generalized atherosclerosis and a surrogate for coronary atherosclerosis, Dr. Roman and colleagues wrote.

Limitations of this study included its cross-sectional design, the fact that inflammatory markers were determined only once, and the inherent inability to establish the probable cause as opposed to documenting associations, Dr. Roman and colleagues said. Also, the study did not permit an estimate of the life-long inflammatory burden of RA, they added.

Nevertheless, the investigators said, “the lack of an association between inflammatory mediators and atherosclerosis does not exclude the possibility that chronic inflammation is atherogenic.”

In conclusion, they emphasized the need for aggressive control of rheumatoid disease activity because chronic inflammation is “probably a driving force for premature atherosclerosis.”