Rheumatoid arthritis (RA) patients have an increased prevalence of preclinical atherosclerosis independent of traditional risk factors, according to a new study¹ that augments a growing body of evidence suggesting that chronic inflammation may be atherogenic. The matched cross-sectional study appears in the February 21 issue of the Annals of Internal Medicine.

In the study, which compared 98 RA patients to 98 control subjects matched by age, sex, and ethnicity, RA patients had a 3-fold increase in carotid atherosclerotic plaque compared with RA-free controls. Specifically, 44% of RA patients had atherosclerotic plaque, compared with 15% of control patients (P <.001). These findings held even though RA patients tended to have more favorable risk factor profiles then their RA-free counterparts. Moreover, the relationship between RA and carotid atherosclerotic plaque remained after controlling for age, serum cholesterol levels, smoking history, and hypertensive status. Age and current cigarette use were also significantly associated with carotid atherosclerotic plaque (P <.001 and P <.014, respectively).

The study also showed that among RA patients, atherosclerosis was related to age, hypertension status, and use of tumor necrosis factor-alpha (TNF-a) inhibitors, which may serve as a possible marker of disease severity. All study participants underwent cardiovascular risk factor assessment and carotid ultrasonography. RA patients also were assessed for disease severity, treatment, and inflammatory markers.

"Our study shows us that RA is very clearly associated with premature atherosclerosis independent of traditional risk factors," says lead researcher Mary J. Roman, MD, professor of medicine at Weill Medical College of Cornell University in New York City. "Using a very straightforward, widely accepted definition of atherosclerosis, the results are unequivocal," she tells CIAOMed.

The researchers point out that the exact mechanism by which premature atherosclerosis develops in RA patients is not known, but chronic inflammation may be responsible. The cross-sectional study design, however, does not permit an estimate of lifelong inflammatory burden.

Treat cardiovascular disease risk factors and RA aggressively

"Rheumatologists should have a lower threshold for suspecting coronary artery disease in patients who might have suggestive symptoms and a lower threshold for being aggressive about controlling traditional cardiovascular risk factors," says Dr. Roman.

"I also think that the [RA] itself should be treated more aggressively, and I gather that is happening," Dr. Roman explains. For example, she says, "it used to be that the TNF-a antagonists were used only in patients who failed other therapies. These agents are now first line, [and this] may completely change the natural history of RA, not only in terms of traditional symptoms, but also [in terms of] atherosclerosis," she says.

Reference

1. Roman MJ, Moeller E, Davis AB, et al. Preclinical carotid atherosclerosis in patients with rheumatoid arthritis. Ann Intern Med. 2006;144:249-256.