title: Infliximab, an anti-TNF-alpha agent, improves left atrial abnormalities in patients with rheumatoid arthritis: preliminary results.
abstract: BACKGROUND
  Rheumatoid arthritis (RA) is associated with increased cardiovascular morbidity and mortality. In the current prospective study, we addressed the impact of RA on left atrial (LA) function and electrical remodelling. Further, we tried to demonstrate the effects of infliximab, an anti-TNF-alpha agent, on echocardiographical LA abnormality in RA patients with preserved left ventricular (LV) ejection fraction.
  
  
  METHODS
  We compared 38 female RA patients without clinical evidence of heart disease and 30 female controls without RA and clinical evidence of heart disease. Further, we compared RA patients receiving infliximab and increasing doses of prednisolone over a three-month period. At baseline and post treatment, this study assessed (1) LA and LV parameters using conventional and speckle tracking echocardiography (STE), and (2) electrocardiographic P-wave changes.
  
  
  RESULTS
  The values of C-reactive protein (CRP), isovolumic relaxation time (IVRT), A wave, and deceleration time (DT) were significantly higher in RA patients compared to the control group (p < 0.05), whereas E/E' and E/A values were found to be lower (p < 0.05) in RA patients. E/E' values were lower in prednisolone- compared to infliximab-treated patients (p < 0.05). After three months of infliximab and prednisolone treatment, CRP and disease activity score (DAS 28) values decreased in both groups (p < 0.05), and Duke activity status index (DASI) increased (p < 0.05). Maximal left atrial volume index (LAVImax), pre-contraction left atrial volume index (LAVIpreA) and maximum P wave (Pmax) of the RA patients were higher compared to the control group (p < 0.05), whereas LA global strain was found to be lower (p < 0.05). There was no difference in Pmax values between groups before and after the treatment period. E/E', LAVImax and LAVIpreA values of infliximab-treated patients decreased and LA global strain increased after three months of therapy compared to baseline (p < 0.05). At baseline in both treatment groups, E/E' and LA global late diastolic strain rate were lower in prednisolone-compared to infliximab-treated patients (p < 0.05).
  
  
  CONCLUSIONS
  There was echocardiographic LA abnormality in these RA patients. In this patient group there was also a meaningful increase in maximum P wave assessed by electrocardiography. Infliximab therapy for a period of three months improved LA abnormality.
authors.forename: Süha
authors.initials: S
authors.lastname: Çetin
authors.affiliation: Department of Cardiology, 29 Mayis Hospital, Ankara, Turkey. ceramos3@gmail.com.
authors.forename: Çetin
authors.initials: Ç
authors.lastname: Süha
authors.forename: Gökhan
authors.initials: G
authors.lastname: Mustafa
authors.affiliation: Department of Cardiology, Dişkapi Research and Education Hospital, Ankara, Turkey.
authors.forename: Vural Mustafa
authors.initials: VM
authors.lastname: Gökhan
authors.forename: Göksal
authors.initials: G
authors.lastname: Keskin
authors.affiliation: Department of Internal Medicine, Dişkapi Research and Education Hospital, Ankara, Turkey.
authors.forename: Keskin
authors.initials: K
authors.lastname: Göksal
authors.forename: Ekrem
authors.initials: E
authors.lastname: Yeter
authors.affiliation: Department of Cardiology, Dişkapi Research and Education Hospital, Ankara, Turkey.
authors.forename: Yeter
authors.initials: Y
authors.lastname: Ekrem
authors.forename: Mehmet
authors.initials: M
authors.lastname: Doğan
authors.affiliation: Department of Cardiology, Dişkapi Research and Education Hospital, Ankara, Turkey.
authors.forename: Doğan
authors.initials: D
authors.lastname: Mehmet
authors.affiliation: Department of Rheumatology, School of Medicine, Gazi University, Ankara, Turkey.
authors.forename: Mehmet Akif
authors.initials: MA
authors.lastname: Öztürk
authors.forename: Öztürk Mehmet
authors.initials: ÖM
authors.lastname: Akif
mesh_terms: D000911:Antibodies, Monoclonal / Q000008:administration & dosage*; D018501:Antirheumatic Agents / Q000008:administration & dosage; D001172:Arthritis, Rheumatoid / Q000150:complications* / Q000188:drug therapy; D015150:Echocardiography, Doppler; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006325:Heart Atria / Q000000981:diagnostic imaging / Q000187:drug effects / Q000503:physiopathology*; D006801:Humans; D000069285:Infliximab; D008875:Middle Aged; D020127:Recovery of Function / Q000187:drug effects*; D012189:Retrospective Studies; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors; D018497:Ventricular Dysfunction, Right / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D016278:Ventricular Function, Right / Q000187:drug effects*
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab