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Inflammation predicts accelerated brachial arterial wall changes in patients with recent-onset rheumatoid arthritis

Suad Hannawi1 email, Thomas H Marwick2* email and Ranjeny Thomas1* email

Diamantina Institute, University of Queensland, Princess Alexandra Hospital, Ipswich Road, Woolloongabba, Queensland 4102, Australia

Department of Medicine, University of Queensland, Princess Alexandra Hospital, Ipswich Road, Woolloongabba, Queensland 4102, Australia

author email corresponding author email* Contributed equally

Arthritis Research & Therapy 2009, 11:R51doi:10.1186/ar2668

Published: 6 April 2009

Abstract

Introduction

Patients with recent-onset rheumatoid arthritis (RA) have impaired brachial artery endothelial function compared with controls matched for age, sex and cardiovascular risk factors. The present study examined endothelium-dependent (flow-mediated dilatation (FMD)) and independent (glyceryl trinitrate (GTN)-mediated dilatation (GMD)) structural responses in early RA patients, and determined progress over one year.

Methods

Brachial artery FMD and GMD and carotid intima media thickness (cIMT) were studied using ultrasound in 20 patients diagnosed with early RA in whom symptoms had been present for less than 12 months, and in 20 control subjects matched for age, sex and established cardiovascular risk factors. FMD and GMD were re-assessed after 12 months in RA patients and the change in each parameter was calculated. Data were analysed by univariate regression.

Results

Mean FMD and GMD were significantly lower in early RA patients at baseline than in controls, but each parameter significantly improved in one year. FMD and GMD responses were positively associated with each other. Patients' age, C-reactive protein (CRP) level and cIMT at baseline and CRP level at one year, were negatively associated with change in brachial responses in one year.

Conclusions

Patients with recent-onset RA have altered brachial artery responses signifying both functional and structural abnormalities. However, early control of inflammation may reduce arterial dysfunction and thus the tendency for atherosclerotic progression.


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