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TNF Inhibitors Protect Against Plaque Buildup in RA Patients


 

FROM THE ANNUAL MEETING OF THE AMERICAN COLLEGE OF RHEUMATOLOGY

ATLANTA – Patients with rheumatoid arthritis showed significant arterial thickening over a 3-year period, but tumor necrosis factor inhibitor use slowed the progression, based on data from 158 patients. The findings were presented at the annual scientific meeting of the American College of Rheumatology.

"We know that many of our patients with autoimmune disease have higher risk for cardiovascular disease," said Dr. Joan M. Bathon, professor of medicine and director of the Johns Hopkins Arthritis Center at the Johns Hopkins University in Baltimore. But few studies have examined what drives the plaque buildup in these patients.

Dr. Bathon and her colleagues examined a subgroup of patients enrolled in a larger study of cardiovascular disease and RA. They used ultrasound to measure the thickness of the walls of the common carotid artery (CCA) and internal carotid artery (ICA) and compared data on each patient at two visits approximately 3 years apart. The average age of the patients was 60 years, 36% were male, and the average duration of RA at baseline was 8.5 years.

Thickening of the CCA occurred in 82% of the patients over 3 years, with a median yearly increase of 16 mcm. Thickening of the ICA occurred in 70% of the patients, with median yearly increase of 25 mcm.

However, patients who used a tumor necrosis factor inhibitor (TNFi) agents at baseline had a 37% lower rate of CCA thickening compared to those who did not use a TNFi agent (14 mcm/year vs. 22 mcm/year), after controlling for demographic variables, cardiovascular risk factors, and baseline arterial thickening.

"We found that progression in the common carotid was much more pronounced in patients with early disease than in later disease," said Dr. Bathon. "There seems to be a particular risk when the disease first starts."

Thickening of the ICA was independently associated with prednisone use, but progression was significantly lower in patients who were taking statins at baseline, Dr. Bathon said.

A total of 68 patients showed at least some plaque development, and 14% of patients developed new plaque during the study period. Patients who developed plaque over time had higher average swollen joint counts and higher average C-reactive protein levels than those who did not show atherosclerosis progression, Dr. Bathon noted.

"The data need to be confirmed in other studies," Dr. Bathon said, "but they suggest that prednisone promotes atherosclerosis in RA, even in the tiny doses that we use." But the findings also support the protective value of statins and TNFi agents against atherosclerosis in RA patients, she said.

The study was supported in part by the American College of Rheumatology Research and Education Foundation. Dr. Bathon said she had no financial conflicts to disclose.

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