Full Papers
Determinants of subclinical cardiovascular remodelling measured by carotid intima-media thickness in early rheumatoid arthritis: a longitudinal analysis
H. Kocaayan1, S. Genc Kocaayan2, A. Ozkan3, O. Yogurtcu4, K. Gonderen5, M. Ozmen6, D. Solmaz7, S. Akar8
- Division of Rheumatology, Department of Internal Medicine, Izmir Katip Celebi University School of Medicine, Izmir, Turkey. hasankocaayan@gmail.com
- Izmir Kavram Vocational School, Izmir, Turkey.
- Division of Rheumatology, Department of Internal Medicine, Izmir Katip Celebi University School of Medicine, Izmir, Turkey.
- Division of Rheumatology, Department of Internal Medicine, Izmir Katip Celebi University School of Medicine, Izmir, Turkey.
- Department of Internal Medicine Izmir Katip Celebi University School of Medicine, Izmir, Turkey.
- Division of Rheumatology, Department of Internal Medicine, Izmir Katip Celebi University School of Medicine, Izmir, Turkey.
- Division of Rheumatology, Department of Internal Medicine, Izmir Katip Celebi University School of Medicine, Izmir, Turkey.
- Division of Rheumatology, Department of Internal Medicine, Izmir Katip Celebi University School of Medicine, Izmir, Turkey.
CER19684
Full Papers
PMID: 42024551 [PubMed]
Received: 12/01/2026
Accepted : 09/03/2026
In Press: 15/04/2026
Abstract
OBJECTIVES:
Rheumatoid arthritis (RA) increases cardiovascular disease (CVD) risk beyond traditional factors. Carotid intima-media thickness (CIMT) reflects subclinical vascular damage. We investigated short-term changes in CIMT and their determinants in early RA.
METHODS:
Thirty-four patients with early RA (mean symptom duration 7 ± 5 months) and 33 matched controls were studied prospectively. Assessments were performed at baseline, 3, and 6 months in RA and once in controls. Body composition (bioimpedance), laboratory tests, and disease activity (DAS28-CRP, EULAR response) were recorded. CIMT was measured by B-mode ultrasound at baseline and 6 months (mean of the right and left common carotid arteries). Generalised estimating equations (GEE) were used to model determinants of CIMT. Model 1 included age, education, steroid use, Framingham risk score (FRS), CRP, and fat mass (%); Model 2 replaced CRP with EULAR response.
RESULTS:
Mean CIMT increased significantly over 6 months (0.70 ± 0.13 to 0.74 ± 0.12 mm; GEE estimate +0.043 mm, 95% CI 0.017–0.068, p=0.001). In multivariable GEE models, Framingham risk score (β=0.005–0.006 mm per 1% risk, p≤0.008) and fat mass percentage (β=0.003–0.004 mm per 1%, p≤0.044) were independently associated with greater CIMT. CRP also remained significant in Model 1 (p=0.046), whereas the EULAR response was not significant in Model 2 (p=0.976).
CONCLUSIONS:
In early RA, CIMT thickened within six months despite marked improvement in disease activity scores, with residual inflammatory burden (CRP) continuing to independently contribute to vascular remodelling.
