The relation between serum visfatin levels and cardiovascular involvement in rheumatoid arthritis
Objectives: To investigate the effect of visfatin on the cardiovascular system in rheumatoid arthritis (RA) patients.
Methods: Twenty patients diagnosed with RA were recruited, as well as 15 age and sex-matched healthy controls. The RA patients underwent thorough clinical examination including body mass index (BMI) and waist/hip ratio measurement. The disease activity score (DAS 28) was calculated. Echocardiography and coronary artery calcium scoring (CACS) were performed, as well as measurement of serum visfatin levels, total cholesterol, high density lipoproteins (HDL), low density lipoproteins (LDL), and serum triglycerides. The healthy control group had serum visfatin levels measured. Another group for risk stratification (RS) included 30 non-RA female patients who were referred for calcium scoring to exclude coronary artery disease and for lipid profile assessment.
Results: RA patients’ ages ranged from27 to 61 years (mean: 43.9±11.6). They all had normal echocardiographic findings. Serum visfatin levels were significantly higher in the RA group (58.8±6.6 ng/ml) versus the controls (13.8±8.11 ng/ml).ElevenRApatients (55%) had evidence of coronary atherosclerotic changes with a mean CACS of 86.4±360. There was a significant correlation between serum triglycerides andCACS (P=0.014); however, therewas no significant correlation of theCACSwith the
visfatin level, disease duration and DAS. Serum visfatin levels did not correlate with BMI or waist/hip ratio. Compared to the RS group, the RA group was significantly younger (43.9±11.6 versus 56.8±11.6 years, P<0.0001). However, there was no statistically significant difference in the frequency of coronary artery calcification between the RA group (55%) and the RS group (32%) (P=0.65) and no significant difference between the two groups in the CACS.
Conclusion: Coronary atherosclerosis occurs at least 10 years earlier in female patients withRA. Serum visfatin levels are elevated in RA patients; however, it does not explain early subclinical atherosclerosis.