Effect of Rheumatoid Factor on Vascular Stiffness in General Population without Joint Symptoms.
- Author:
Ji Hyun LEE
1
;
Hee Sang TAG
;
Geun Tae KIM
;
Min Jeong KIM
;
Seung Geun LEE
;
Eun Kyung PARK
;
Dong Wan KOO
Author Information
- Publication Type:Original Article
- Keywords: Pulse wave analysis; Rheumatoid factor; Vascular stiffness
- MeSH: Joints*; Pulse Wave Analysis; Rheumatoid Factor*; Vascular Stiffness*
- From:Kosin Medical Journal 2017;32(1):25-35
- CountryRepublic of Korea
- Language:English
- Abstract: OBJECTIVES: The role of rheumatoid factor (RF) in vascular stiffness and cardiovascular risk in subjects without joint symptoms remains unclear. We investigated vascular stiffness in subjects without joint symptoms using pulse wave velocity (PWV), calculated Framingham risk scores (FRS), an estimator of cardiovascular risk, and analyzed whether vascular stiffness and FRS were affected by RF. METHODS: Two hundred forty-two subjects were included in this population-based study. RF was quantified with turbid immunometry using a cut-off of RF > 15 IU/ml to denote RF positivity. Information was then obtained on joint symptoms. Brachial-ankle PWV (baPWV) was measured using an automated device. RESULTS: Of the 242 subjects, 15 were RF-positive. RF-positive subjects without joint symptoms had a higher baPWV and FRS than RF-negative subjects without joint symptoms, but the difference did not reach statistical significance. However, when we stratified the subjects into two groups (group A – high RF: RF ≥ 40 IU/ml; group B – low RF: RF < 40 IU/ml), group A showed significantly higher baPWV (1640.7 ± 179.6 ㎝/s vs. 1405.7 ± 225.7 ㎝/s, P = 0.008) and FRS (25.7 ± 4.87 vs. 11.8 ± 9.6, P < 0.001). Multiple regression analysis was used to examine potential confounders, and RF exhibited significant but modest effects on baPWV (adjusted R-squared = 0.038, P = 0.030). CONCLUSIONS: In a sample of the general population without joint symptoms, higher levels of RF were associated with increased vascular stiffness, suggesting a pathophysiologic link between RF and endothelial dysfunction.
