Abstract 16526: Arterial Wall Inflammation in Patients with Rheumatoid Arthritis is Equivalent to Coronary Artery Disease Patients without Autoimmune Disease

Abstract

Background: Rheumatoid arthritis (RA) is associated with premature atherosclerosis and increased prevalence of cardiovascular disease. 18-fluoro-deoxyglucose positron emission tomography (18-FDG-PET) is an imaging technique that has been used previously to evaluate vascular inflammation. Individuals with coronary artery disease (CAD) have been shown to have increased 18-FDG-PET uptake. In this study we compare vascular inflammation in individuals with RA with patients with established CAD.

Hypothesis: Vascular inflammation measured by 18-FDG-PET is high in individuals with RA and is comparable or exceeds inflammation in high risk individuals with established CAD without autoimmune disease. Increased vascular inflammation may be a mechanism for increased risk for atherosclerosis in RA patients.

Methods: 26 RA patients (aged 35-64) and 70 CAD patients (aged 41-76) without autoimmune disease were recruited as two separate cohorts and underwent PET scans after injection of 10mCi of FDG to measure vascular inflammation. Metrics of PET uptake; the mean, maximum and most diseased segment (MDS) target to background ratios (TBR) were computed for aorta and carotid arteries and compared across the two groups. Multivariate regression models were run to adjust for differences in age, gender and BMI between groups. p values < 0.05 were considered significant.

Results: None of the RA patients had a history of CAD, MI or stroke and none of the CAD patients had any history of autoimmune diseases. Table 1 shows median +/- standard deviations of mean, maximum and MDS 18-FDG-PET uptake in the two groups both without and with adjustments for age gender and BMI.

Conclusions: Our data indicates that RA patients without known CAD have heightened aortic wall inflammation and similar levels of carotid wall inflammation when compared to CAD patients without autoimmune disease. Increased aortic inflammation might be a mechanism for increased risk for atherosclerosis in RA patients.