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Lowering interleukin-1 activity with anakinra improves myocardial deformation in rheumatoid arthritis


Objective: Inhibition of Interleukin-1 activity improves nitrooxidative stress, endothelial and coronary function. We investigated a) the association of nitrooxidative stress and endothelial function with myocardial deformation b) the effects of anakinra, an interleukin-1a receptor antagonist on myocardial deformation in patients with rheumatoid arthritis (RA).

Methods: We compared 46 RA patients to 23 normal controls. Twenty-three patients received anakinra (150mg s.c. o.d) and 23 patients a 5mg increase of prednisolone dose for 30 days. At baseline and post-treatment we assessed a) the LV longitudinal, circumferential and radial strain and strain rate, using speckle tracking echocardiography b) the coronary flow reserve (CFR) c) the flow-mediated endothelial-dependent dilation of the brachial artery (FMD) and d) nitrotyrosine (NT) and malondialdehyde blood levels.

Results: Patients had impaired baseline myocardial deformation indices compared to controls (p<0.05). CFR and NT levels were related with longitudinal strain, systolic and diastolic strain rate, circumferential strain and systolic strain rate (p<0.05). FMD was related with longitudinal and circumferential diastolic strain rate (p<0.01). Compared to baseline, anakinra-treated patients increased the longitudinal strain (-17.8 (3.7) vs. -22.1 (3.5) %), systolic (-1.02 (0.23) vs. -1.25 (0.23) l/s) and diastolic (0.96 (0.37) vs. 1.20 (0.39) l/s) longitudinal strain rate, circumferential strain and strain rate (p<0.05 for all comparisons). No significant changes were observed among prednisolone-treated patients.

Conclusions: Myocardial deformation is impaired in RA patients and is related with nitrooxidative stress and endothelial dysfunction. Chronic inhibition of IL-1 improves LV deformation in parallel with endothelial function and nitrooxidative stress.

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