Effect of glucocorticoids on the arteries in rheumatoid arthritis

Glucocorticoids are suspected to cause atherosclerosis. Because of the possibility that their antiinflammatory effect may be antiatherogenic, this study investigated the effect of glucocorticoids on the arteries of patients with rheumatoid arthritis (RA).

We assessed the arteries of 647 patients with RA. Central atherosclerosis was measured using high-resolution carotid ultrasound for the presence of plaque and for the extent of carotid artery intima-media thickness (CaIMT). Peripheral atherosclerosis was assessed using the systolic pressures of the dorsal pedal, posterior tibial, and brachial arteries to obtain the ankle-brachial index (ABI). Cumulative glucocorticoid dose was determined using pharmacy records, supplemented by self-report. Cardiovascular (CV) risk factors and RA clinical manifestations were ascertained using clinical and laboratory methods.

Among the RA patients studied, 427 (66%) had received glucocorticoids. Of those who had never received glucocorticoids, 100 (47%) of 215 had carotid plaque and 17 (8%) of 219 had > or =1 incompressible lower-limb artery (ABI >1.3). Among patients in the highest tertile of lifetime glucocorticoid exposure (>16.24 gm prednisone), the frequency of carotid plaque increased to 85 (62%) of 138 (P = 0.006) and that of lower-limb arterial incompressibility increased to 24 (17%) of 140 (P = 0.008), with differences remaining significant after adjustment for age at onset, disease duration, sex, CV risk factors, and RA clinical manifestations (tender, swollen, and deformed joint counts, subcutaneous nodules, rheumatoid factor seropositivity, and erythrocyte sedimentation rate). The CaIMT also displayed an increase with higher glucocorticoid exposure, but the differences did not reach significance. Lower-limb artery obstruction (ABI < or =0.9) was not associated with glucocorticoid exposure.

In this RA sample, glucocorticoid exposure was associated with carotid plaque and arterial incompressibility, independent of CV risk factors and RA clinical manifestations. This supports a role for glucocorticoids in the CV complications that occur in RA.