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
1 Schulich School of Medicine & Dentistry, Western University, Rheumatology, St. Joseph's Hospital 268 Grosvenor Street London, Ontario, N6A 4V2, Canada
2 Schulich School of Medicine & Dentistry, Western University, Robarts Research Institute,1151 Richmond St. N., London, Ontario, N6A 5B7, Canada


Article Metrics

CrossRef Citations:
4
Total Statistics:

Full-Text HTML Views: 503
Abstract HTML Views: 329
PDF Downloads: 85
ePub Downloads: 51
Total Views/Downloads: 968
Unique Statistics:

Full-Text HTML Views: 284
Abstract HTML Views: 179
PDF Downloads: 70
ePub Downloads: 46
Total Views/Downloads: 579



© Pope et al.; Licensee Bentham Open

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.

* Address correspondence to this author at the Schulich School of Medicine & Dentistry, Western University, Rheumatology, St. Joseph's Hospital 268 Grosvenor Street London, Ontario, N6A 4V2, Canada; Tel: +519-646-6332; Fax: +519-646-6334; E-mail: janet.pope@sjhc.london.on.ca


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.

Keywords: Atherosclerosis, Cardiovascular disease, Carotid plaque progression, Rheumatoid arthritis.
Keymessages:
  1. Active rheumatoid arthritis (RA) with long disease duration had a high prevalence of an abnormal lipid bloodprofile, atherosclerotic plaque and carotid artery wall thickness.
  2. 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.
  3. 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.
  4. 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.
.