By Sally Robertson, medwireNews Reporter
Patients with rheumatoid arthritis (RA) exhibit a sub-clinical vasculitis that may underlie their increased risk for cardiovascular disease (CVD), shows research.
This risk may be reduced with the use of anti-tumour necrosis factor alpha (anti-TNF-α) therapy, which decreases aortic inflammation and stiffness in RA patients, say Zahi A Fayad (Mount Sinai School of Medicine, New York, USA) and colleagues.
"We have demonstrated that patients with RA have increased inflammation along the entire length of the aorta in comparison to age-matched CVD patients and that anti-TNF-α therapy leads to a reduction of inflammation in the whole aorta as well as in the most diseased segment [MDS]," they write in an editorial in Circulation.
The team says the findings highlight the importance of CV risk management in RA, which is currently inadequately dealt with.
Using F-fluorodeoxyglucose positron emission tomography and computer tomography (F-FDG PET/CT) imaging, the researchers found that the mean arterial maximum target-to-background ratio (TBRmax), a measure of vascular inflammation, was significantly higher at baseline in 17 RA patients compared with 34 individuals with stable CVD who acted as positive controls, at 2.02 versus 1.74.
The mean TBRmax in the whole aorta was significantly higher in RA patients compared with CV patients, at 2.02 versus 1.74, while the mean TBRmax in the MDS was not significantly different between the groups, at 2.51 versus 2.31, respectively.
The RA patients also had a significantly higher proportion of inflamed aortic slices (defined as a TBRmax of more than 2.0) within the aorta than CVD patients, at 49.5% versus 22.9%, respectively.
However, following treatment of the RA patients with 8 weeks of TNF-α antagonist therapy, there was a significant reduction in mean TBRmax, from 2.02 to 1.90 and the proportion of inflamed aortic slices was reduced from 49.5% to 33.3%.
The mean TBRmax in the MDS also fell, from 2.51 to 2.05, which was significantly lower than in the CVD patients at baseline.
Furthermore, aortic pulse wave velocity, a measure of arterial stiffness, was also reduced after the anti-TNF-α therapy, from 9.09 to 8.63, and this reduction in stiffness correlated with the reduction in aortic inflammation.
"This suggests that vascular inflammation could be the mechanism by which inflammation leads to aortic stiffening," says the team.
"Our data suggest that vascular inflammation could underpin the mechanism of increased CVD in RA, and also demonstrates that PET/CT scanning could be a useful tool for CVD risk stratification and for monitoring risk reduction of anti-inflammatory therapies in patients with chronic inflammatory diseases."
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