title: Lowering interleukin-1 activity with anakinra improves myocardial deformation in rheumatoid arthritis.
abstract: OBJECTIVE
  Inhibition of interleukin-1 activity improves nitro-oxidative stress, endothelial and coronary function. The authors investigated (a) the association of nitro-oxidative 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
  The authors compared 46 RA patients to 23 normal controls. 23 patients received anakinra (150 mg subcutaneously once daily) and 23 patients a 5-mg increase of prednisolone dose for 30 days. At baseline and post-treatment this study assessed (a) the left ventricular (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 to longitudinal strain, systolic and diastolic strain rate, circumferential strain and systolic strain rate (p<0.05). FMD was related to 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) l/s vs -1.25 (0.23) l/s) and diastolic (0.96 (0.37) l/s 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 to nitro-oxidative stress and endothelial dysfunction. Chronic inhibition of IL-1 improves LV deformation in parallel with endothelial function and nitro-oxidative stress.
authors.affiliation: 2nd Cardiology Department, Attikon Hospital, University of Athens, Greece. ignoik@otenet.gr
authors.forename: I
authors.initials: I
authors.lastname: Ikonomidis
authors.forename: S
authors.initials: S
authors.lastname: Tzortzis
authors.forename: J
authors.initials: J
authors.lastname: Lekakis
authors.forename: I
authors.initials: I
authors.lastname: Paraskevaidis
authors.forename: I
authors.initials: I
authors.lastname: Andreadou
authors.forename: M
authors.initials: M
authors.lastname: Nikolaou
authors.forename: T
authors.initials: T
authors.lastname: Kaplanoglou
authors.forename: P
authors.initials: P
authors.lastname: Katsimbri
authors.forename: G
authors.initials: G
authors.lastname: Skarantavos
authors.forename: P
authors.initials: P
authors.lastname: Soucacos
authors.forename: D Th
authors.initials: DT
authors.lastname: Kremastinos
mesh_terms: D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000503:physiopathology; D001783:Blood Flow Velocity / Q000187:drug effects; D001916:Brachial Artery / Q000502:physiology; D003326:Coronary Circulation / Q000187:drug effects; D004452:Echocardiography; D005260:Female; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein / Q000627:therapeutic use*; D007375:Interleukin-1 / Q000037:antagonists & inhibitors*; D008297:Male; D008875:Middle Aged; D009206:Myocardium; D018384:Oxidative Stress / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy*
chemical_list: D018501:Antirheumatic Agents; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1