Open Access Open Badges Research article

Predictors of new atherosclerotic carotid plaque development in patients with rheumatoid arthritis: a longitudinal study

Evangelia Zampeli1, Athanase Protogerou1, Kimon Stamatelopoulos2, Kalliopi Fragiadaki1, Christina G Katsiari1, Katerina Kyrkou1, Christos M Papamichael2, Myron Mavrikakis2, Peter Nightingale3, George D Kitas4 and Petros P Sfikakis1*

Author Affiliations

1 First Department of Propaedeutic and Internal Medicine, Laikon Hospital, Athens University Medical School, Ag Thoma, 17, GR-11527 Athens, Greece

2 Vascular Laboratory, Department of Clinical Therapeutics, Alexandra Hospital, Athens University Medical School, V Sofias and Lourou 1, GR-11528, Athens, Greece

3 Wellcome Trust Clinical Research Facility, University Hospital Birmingham NHS Foundation Trust, Birmingham, Queen Elizabeth Hospital, Queen Elizabeth Medical Centre, Birmingham, B15 2TH, UK

4 The Dudley Group of Hospitals NHS Foundation Trust, Dudley, and Arthritis Research Campaign Epidemiology Unit, University of Manchester, Manchester, West Midlands, DY1 2HQ, UK

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Arthritis Research & Therapy 2012, 14:R44  doi:10.1186/ar3757

Published: 5 March 2012



Rheumatoid arthritis (RA) is associated with increased cardiovascular morbidity and mortality attributed to both classical risk factors and chronic inflammation. We assessed longitudinally the factors associated with new carotid plaques in nondiabetic RA patients and apparently healthy individuals.


In our present prospective observational study, carotid plaques were identified by ultrasonography at baseline and follow-up end, separated by an average of 3.6 ± 0.2 years, in 64 patients (mean age 59.2 ± 12.0 and disease duration at baseline 7.8 ± 6.2 years, 83% women, clinical and laboratory evaluation every 3 to 6 months). In a substudy, 35 of the patients were matched 1:1 for traditional cardiovascular risk factors with 'healthy' controls and were studied in parallel.


New atherosclerotic plaques formed in 30% of patients (first plaque in 9%) who were significantly older than the remaining patients. Tobacco use, blood pressure, body mass index, average cumulative low-density lipoprotein, high-sensitivity C-reactive protein, erythrocyte sedimentation rate level, RA stage, functional class, disease duration and treatment modalities during follow-up did not differ significantly between subgroups after application of the Bonferroni correction. RA was in clinical remission, on average, for approximately 70% of the follow-up time and was not different between subgroups. Multivariate analysis including all the above parameters revealed that age (P = 0.006), smoking (P = 0.009) and duration of low-dose corticosteroid use (P = 0.016) associated independently with new plaque formation. RA patients displayed similar numbers of newly formed carotid plaques to the tightly matched for traditional cardiovascular risk factors 'healthy' controls, although more patients than controls had carotid plaques at baseline.


Formation of new atherosclerotic plaques in this small cohort of patients with well-controlled RA depended mainly on traditional cardiovascular risk factors and corticosteroid use, whereas an adverse effect of residual systemic inflammation was not readily detectable.