title: Infliximab reduces cardiac output in rheumatoid arthritis patients without heart failure.
abstract: OBJECTIVE
  Human anti-tumor necrosis factor (TNF-α) monoclonal antibody (infliximab) is used to treat autoimmune diseases such as rheumatoid arthritis (RA). Although the risk of worsening heart failure has been described in patients under chronic treatment, the acute cardiovascular effects of this drug are unknown in RA patients without heart failure.
  
  
  METHODS
  14 RA patients with normal echocardiography and no history of heart failure were evaluated during the 2-hour infliximab (3-5 mg/kg) infusion period, using a noninvasive hemodynamic beat-to-beat system (Portapres). Stroke volume (SV); systolic, diastolic and mean blood pressures (SBP, DBP and MBP, respectively); cardiac output (CO); heart rate (HR); and total peripheral vascular resistance (PVR) were recorded. All patients also received saline infusion instead of infliximab as a control. Significant differences in hemodynamic parameters were determined using Tuckey's test. All values were expressed as mean ± standard deviation (SD).
  
  
  RESULTS
  Fourteen RA patients (6M/8F) with mean age of 47.2 ± 8.8 years were evaluated. A significant decrease was found in cardiac output and stroke volume (7.04 ± 2.3 to 6.12 ± 2.1 l/min and 91 ± 29.0 to 83 ± 28.8 mL/beat, respectively) after infliximab infusion. Although not statistically significant, a progressive increase was detected in SBP, DBP and total PVR during infusion. Saline infusion did not cause significant hemodynamic changes in the same group of RA patients. No adverse effects were observed during the infusion period.
  
  
  CONCLUSIONS
  Acute infliximab administration decreased cardiac output due to low stroke volume in RA patients without heart disease. The results also demonstrated that, in spite of its negative inotropic effect, infliximab enhanced BP, probably by increasing PVR.
authors.affiliation: Department of Medicine, Faculty of Medical Sciences, Universidade Estadual de Campinas, Campinas, SP, Brazil.
authors.forename: Rodrigo Cardoso
authors.initials: RC
authors.lastname: Santos
authors.forename: Valéria Nasser
authors.initials: VN
authors.lastname: Figueiredo
authors.forename: Luiz Cláudio
authors.initials: LC
authors.lastname: Martins
authors.forename: Carolina de Haro
authors.initials: Cde H
authors.lastname: Moraes
authors.forename: Thiago
authors.initials: T
authors.lastname: Quinaglia
authors.forename: Leandro
authors.initials: L
authors.lastname: Boer-Martins
authors.forename: Sílvia Elaine
authors.initials: SE
authors.lastname: Ferreira-Melo
authors.forename: Michel Alexandre
authors.initials: MA
authors.lastname: Yazbek
authors.forename: Manoel
authors.initials: M
authors.lastname: Bertolo
authors.forename: Heitor
authors.initials: H
authors.lastname: Moreno
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal / Q000008:administration & dosage* / Q000009:adverse effects; D018501:Antirheumatic Agents / Q000008:administration & dosage*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000187:drug effects*; D004452:Echocardiography; D005260:Female; D006333:Heart Failure / Q000175:diagnosis; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D013318:Stroke Volume / Q000502:physiology
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D000069285:Infliximab