title: Effect of Long-Term TNF-α Inhibition with Infliximab on Left Ventricular Torsion in Patients with Rheumatoid Arthritis.
abstract: BACKGROUND
  We evaluated the impact of tumor necrosis factor alpha (TNF-α) inhibition on left ventricular torsion (LVtor) in patients with rheumatoid arthritis (RA) using speckle-tracking echocardiography (STE).
  
  
  METHODS
  Thirty-eight RA patients without cardiovascular disease and 30 healthy subjects were enrolled in the study. Twenty patients received infliximab, a monoclonal antibody against TNF-α, and 18 patients received increasing doses of prednisolone for 180 days. Global systolic longitudinal strain (G-LS), global systolic radial strain (G-RS) and global systolic circumferential strain (G-CS) were determined by STE. LV basal and apical rotations from the base and apex were obtained and used for calculation of LVtor. Pre-treatment LVtor levels were compared with LVtor levels after therapy in both treatment groups.
  
  
  RESULTS
  RA patients had lower G-LS (-16.5 ± 2.9; p<0.01), G-RS (37.6 ± 1.5; p<0.01) and higher GCS (-23.6 ± 3.5; p=0.04) compared with control subjects (-20.0 ± 2.8, 40.7 ± 4.8, -22.4 ± 2.5, respectively; p<0.01). LVtor levels were significantly higher in RA patients compared to controls (16.4 ± 2.7 vs. 15.1 ± 2.5; p=0.04), which might be attributed to higher values of apical rotation (9.7 ± 2.4 vs. 8.8 ± 2.3; p=0.01). Patients treated with infliximab experienced a significant decrease in LVtor (p=0.04), and a significant increase in G-LS (p<0.01) and G-RS (p<0.01). No significant changes were observed among patients treated with prednisolone. Percentage changes in LVtor were correlated with percent changes in C-reactive protein CRP (r=0.58; p<0.01), disease activity score (r=0.78; p<0.01), and G-LS (r=-0.40; p=0.04) in patients treated with infliximab.
  
  
  CONCLUSIONS
  RA is characterized by increased LVtor. Long term TNF-α inhibition improves LV longitudinal and radial systolic deformation and decreases LVtor.
authors.affiliation: Department of Internal Medicine, Diskapi Education and Training Hospital, Ankara, Turkey.
authors.forename: Yasemin Ozden
authors.initials: YO
authors.lastname: Ayyildiz
authors.forename: Mustafa Gokhan
authors.initials: MG
authors.lastname: Vural
authors.forename: Tolga Han
authors.initials: TH
authors.lastname: Efe
authors.forename: Ahmet Goktug
authors.initials: AG
authors.lastname: Ertem
authors.forename: Cemal
authors.initials: C
authors.lastname: Koseoglu
authors.forename: Mehmet
authors.initials: M
authors.lastname: Ayturk
authors.forename: Ekrem
authors.initials: E
authors.lastname: Yeter
authors.forename: Göksal
authors.initials: G
authors.lastname: Keskin
authors.forename: Ramazan
authors.initials: R
authors.lastname: Akdemir
mesh_terms: D000328:Adult; D000368:Aged; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D002097:C-Reactive Protein / Q000378:metabolism; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D000069285:Infliximab / Q000627:therapeutic use*; D008875:Middle Aged; D011239:Prednisolone / Q000627:therapeutic use; D014102:Torsion Abnormality / Q000000981:diagnostic imaging; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D014463:Ultrasonography
chemical_list: D000893:Anti-Inflammatory Agents; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D011239:Prednisolone; D000069285:Infliximab