RESEARCH ARTICLE
Carotid Artery Atherosclerosis in Patients with Active Rheumatoid Arthritis: Predictors of Plaque Occurrence and Progression Over 24 Weeks
Janet E. Pope1, *, Tatiana Nevskaya1, Lillian Barra1, Grace Parraga2
Article Information
Identifiers and Pagination:
Year: 2016Volume: 10
First Page: 49
Last Page: 59
Publisher ID: TORJ-10-49
DOI: 10.2174/1874312901610010049
Article History:
Received Date: 11/02/2016Revision Received Date: 30/08/2016
Acceptance Date: 04/09/2016
Electronic publication date: 30/09/2016
Collection year: 2016
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
Abstract
Introduction:
This study evaluated the prevalence and progression of subclinical carotid artery atherosclerosis in active rheumatoid arthritis (RA).
Methods:
Carotid arteries of RA patients were scanned using 3D ultrasound at baseline and 24 weeks for total plaque area, vessel wall volume, and intima-media thickness (IMT), as well as arterial stiffness measured using pulse wave velocity. Variables related to inflammation, lipids and cardiovascular (CV) risk were assessed for associations with plaque progression. Of 195 screened patients, 31 met inclusion criteria (66 Swollen joint count (SJC) plus 68 Tender joint count (TJC)≥8 OR SJC plus TJC≥4 with elevated acute phase reactants) and were enrolled (27 female; mean age 59.3±9.8years). Patients using lipid lowering drugs and uncontrolled comorbidities were excluded.
Results:
Atherosclerotic plaque occurred in 35% and arterial wall hypertrophy (IMT≥0.6mm) in 86% of patients. Most (68%) had an abnormal lipid profile characterized by reduced HDL and/or increased total cholesterol/HDL index, which was adversely affected by disease activity. Stepwise binary logistic regression analysis showed that Framingham risk score (OR=1.155, 95%CI:1.002-1.332, p=0.046) and ESR (OR=1.148, 95%CI:1.015-1.299, p=0.028) predicted plaque burden most strongly. Plaque progression was significantly associated with baseline higher hsCRP, ESR, and heavy smoking, but only hsCRP predicted plaque growth in multivariate regression analysis (p=0.004); and hsCRP was related to higher disease activity (r=0.443, p=0.016), LDL (r=0.544, p=0.007), and smoking (r=0.384, p=0.04).
Conclusion:
RA-related inflammation contributed to augmented CV burden in RA and might mediate its effect on atherosclerosis through hsCRP and modulation of the traditional CV risk factors, such as dyslipidemia.
Keymessages:
- Active rheumatoid arthritis (RA) with long disease duration had a high prevalence of an abnormal lipid bloodprofile, atherosclerotic plaque and carotid artery wall thickness.
- Both traditional CV risk factors and inflammatory disease activity were associated with atherosclerotic burden at baseline and their effects might be interrelated: disease activity had a negative impact on lipid blood profile.
- High-sensitivity CRP serum level was the only significant risk marker for growing atherosclerotic plaque, as measured by 3D ultrasound for total plaque area over 6 months, after adjustment for other covariates.
- The combined effect of traditional cardiovascular risk factors in RA assessed by Framingham risk score failed to predict the high atherosclerotic burden in a quarter of patients; 1.5 multiplication factor recommended for RA patients did not improve risk estimation.
