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Lowering interleukin-1 activity with anakinra improves myocardial deformation in rheumatoid arthritis
  1. Ignatios Ikonomidis (ignoik{at}otenet.gr)
  1. 2nd Cardiology Dep., Attikon Hospital, University of Athens, Greece
    1. Stavros Tzortzis
    1. 2nd Cardiology Dep., Attikon Hospital, University of Athens, Greece
      1. John Lekakis
      1. 2nd Cardiology Dep., Attikon Hospital, University of Athens, Greece
        1. Ioannis Paraskevaidis
        1. 2nd Cardiology Dep., Attikon Hospital, University of Athens, Greece
          1. Ioanna Andreadou
          1. Department of Pharmaceutical Chemistry, University of Athens School of Pharmacy, Athens, Greece
            1. Maria Nikolaou
            1. 2nd Cardiology Dep., Attikon Hospital, University of Athens, Greece
              1. Theofania Kaplanoglou
              1. 1st Department of Orthopaedics, Attikon Hospital, University of Athens, Greece
                1. Pelagia Katsimbri
                1. 1st Department of Orthopaedics, Attikon Hospital, University of Athens, Greece
                  1. Grigorios Skarantavos
                  1. 1st Department of Orthopaedics, Attikon Hospital, University of Athens, Greece
                    1. Panayotis Soucacos
                    1. 1st Department of Orthopaedics, Attikon Hospital, University of Athens, Greece
                      1. Dimitrios T H Kremastinos
                      1. 2nd Cardiology Dep., Attikon Hospital, University of Athens, Greece

                        Abstract

                        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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