title: Infliximab treatment increases left ventricular ejection fraction in patients with rheumatoid arthritis: assessment of heart function by echocardiography, endothelin 1, interleukin 6, and NT-pro brain natriuretic peptide.
abstract: OBJECTIVE
  To study the influence of anti-tumor necrosis factor-α (TNF-α) treatment on echocardiographic measures and concentrations of endothelin 1 (ET-1), interleukin 6 (IL-6), and amino-terminal fragment of pro-brain natriuretic peptide (NT-proBNP) in a cohort of 23 female patients with rheumatoid arthritis (RA).
  
  
  METHODS
  We recruited 23 patients (mean age 51.3 ± 1.55 yrs) with RA resistant to treatment with disease-modifying antirheumatic drugs and average disease duration of 7.1 ± 1.0 years who had been selected to start treatment with the anti-TNF-α antagonist infliximab. Transthoracic echocardiographic examinations were performed before the first infusion and repeated after 1 year of treatment. Data for age, sex, RA disease activity by Disease Activity Score (DAS28) and echocardiographic data, NT-proBNP, IL-6, ET-1, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and other routine laboratory data were collected before treatment and after 1 year.
  
  
  RESULTS
  Twelve months of treatment with infliximab resulted in reduction of RA activity (i.e., reduction of DAS and acute-phase reactants). There was increased left ventricle ejection fraction, from 58.5% before treatment to 63% after. Treatment with infliximab also resulted in significant reduction of ET-1 (1.26 fmol/ml before treatment vs 0.43 fmol/ml after), IL-6 (58.46 pg/ml vs 3.46 pg/ml), and NT-proBNP (43.06 fmol/ml vs 14.78 fmol/ml). These reductions were observed after just 4 months of treatment and remained significant until the termination of the study.
  
  
  CONCLUSIONS
  In patients with RA, treatment with infliximab contributed significantly to increase in left ventricular ejection fraction. Improvement of cardiac function was shown by conventional echocardiography; there was reduction of biochemical markers of heart failure.
authors.affiliation: Department of Internal Medicine and Rheumatology, Medical University of Silesia, ul. Ziolowa 45/47, 40-635 Katowice, Poland. pkotyla@sum.edu.pl
authors.forename: Przemyslaw J
authors.initials: PJ
authors.lastname: Kotyla
authors.forename: Aleksander
authors.initials: A
authors.lastname: Owczarek
authors.forename: Jaroslaw
authors.initials: J
authors.lastname: Rakoczy
authors.forename: Maciej
authors.initials: M
authors.lastname: Lewicki
authors.forename: Eugene J
authors.initials: EJ
authors.lastname: Kucharz
authors.forename: Paul
authors.initials: P
authors.lastname: Emery
mesh_terms: D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D018501:Antirheumatic Agents / Q000494:pharmacology; D001172:Arthritis, Rheumatoid / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D015331:Cohort Studies; D005260:Female; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D000069285:Infliximab; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000494:pharmacology*; D013318:Stroke Volume / Q000187:drug effects* / Q000276:immunology; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D020097:Natriuretic Peptide, Brain; D000069285:Infliximab