- Poster presentation
- Open Access
Does the burden of inflammation determined prospectively in patients with early inflammatory arthritis determine the progression of atherosclerosis?
© BioMed Central Ltd 2005
- Received: 11 January 2005
- Published: 17 February 2005
- Rheumatoid Arthritis
- Erythrocyte Sedimentation Rate
- Psoriatic Arthritis
- Intimal Medial Thickness
- Carotid Intimal Medial Thickness
Accelerated atherosclerosis accounts for the increased mortality seen in patients with established rheumatoid arthritis (RA). Recent research has shown that RA is associated with an increase in the carotid intimal medial thickness (IMT). To date, there is no prospective study in RA that examines this question and none that includes an inflammatory disease control.
To evaluate prospectively the burden of inflammation in a cohort of patients with early inflammatory arthritis, including RA and psoriatic arthritis (PsA). To correlate inflammatory burden with IMT in this cohort and to compare with normal age-matched control subjects.
RA and PsA patients with disease duration of more than 5 years were selected from the early arthritis clinic database for further study. Controls without inflammatory conditions were recruited from the general clinic. Men older than 40 years and women older than 50 years were excluded. Patients with known predisposing risks for ischaemic heart disease were also excluded. At the time of clinical assessment blood samples were collected for erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) together with fasting lipid samples, and carotid artery ultrasound was performed at the same time. The mean IMT was then calculated by averaging the values at three points, 1 cm above, at, and 1 cm below the area of maximal IMT for each carotid artery.
To date, 61 patients (29 RA, 26 PsA and six control subjects) have been reviewed. Twenty-one (72%) of the RA patients compared with 11 (42%) of the PsA patients had an increased IMT (normal IMT < 0.5 cm). Mean ± standard deviation IMT values in the RA cohort (0.6 ± 0.14) and in the PsA cohort (0.5 ± 0.15) were significantly greater than controls (P = 0.003, P = 0.03, respectively). IMT values in the RA cohort were greater than in PsA (P = 0.017). There was a significant correlation between IMT and age in the RA cohort. However, mean age in the three groups was not different and no correlation between IMT and age was seen in either the PsA or the control group. The area under the curve (AUC) ESR correlated with the AUC CRP in the group as a whole and in both RA and PsA separately. No correlation was found between the AUC for ESR or CRP and IMT in the different subgroups or in patients with an increased IMT.
Patients with inflammatory arthritis (RA > PsA) are at a greater risk of developing atherosclerosis compared with control subjects. No correlation has been found to date between IMT values and the burden of inflammation as measured by ESR and CRP over time. Some additional mechanism of accelerated atherosclerosis in inflammation, yet to be determined, may well apply. The results are preliminary and recruitment with additional analysis is ongoing.