Identification of Independent Predictive Factors for Atherosclerosis in Rheumatoid Arthritis: Based on KARRA Cohort Study.
- Author:
Ji Hun KIM
1
;
Jong Wan KANG
;
Na Ri KIM
;
Gi Bum BAE
;
Soo Kon LEE
;
Churl Hyun IM
;
Eon Jeong NAM
;
Young Mo KANG
Author Information
- Publication Type:Original Article
- Keywords: Rheumatoid arthritis; Atherosclerosis; Cardiovascular disease; Inflammation; Erythrocyte sedimentation rate
- MeSH: Arthritis, Rheumatoid; Atherosclerosis; Blood Sedimentation; C-Reactive Protein; Cardiovascular Diseases; Carotid Arteries; Cohort Studies; Humans; Inflammation; Logistic Models; Male; Risk Factors
- From:Journal of Rheumatic Diseases 2012;19(1):30-38
- CountryRepublic of Korea
- Language:Korean
- Abstract: OBJECTIVE: This study sought to investigate independent predictive factors for subclinical atherosclerosis in Korean patients with rheumatoid arthritis (RA). METHODS: We used high-resolution B-mode ultrasonography to measure the carotid artery intima-media thickness (IMT) and carotid plaque in 367 patients with RA. Detailed information on the demographic characteristics, cardiovascular (CV) risk factors, and RA disease characteristics were collected on all subjects. The relationship of the carotid artery IMT and carotid plaque to relevant clinical and laboratory variables were examined. RESULTS: Old age and male sex had the most significant association with increased IMT and presence of plaque than other factors. Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and mKHAQ (Korean version of modified health assessment questionnaire) were significantly associated with both increased IMT and presence of plaque after univariate analysis adjusting for age and sex. A multivariable logistic regression analysis revealed that ESR and TJC68 were independent factors associated with the presence of plaque (p<0.001 and p=0.019, respectively). There was a significant linear correlation between the number of plaques and ESR (p<0.001 and R2=0.07). CONCLUSION: Our results indicated that markers of systemic inflammation contributed significantly to subclinical atherosclerosis in patients with RA. We emphasize the need for aggressive control of RA disease activity in patients who persistently demonstrate highly elevated ESR levels.
