title: Etanercept normalises left ventricular mass in patients with rheumatoid arthritis.
abstract: BACKGROUND
  Cardiovascular mortality is increased in patients with rheumatoid arthritis (RA). RA is associated with an increased left ventricular mass index (LVMI), a strong marker of cardiovascular mortality, and vessel abnormalities. Experimental studies have suggested that tumour necrosis factor α (TNFα) may induce LV hypertrophy.
  
  
  OBJECTIVE
  To study the effect of medium-term (3- and 6-months) treatment with the TNFα inhibitor etanercept (ETN) and synthetic disease-modifying antirheumatic drugs (sDMARDs) on LV morphological features and arterial stiffness in patients with RA.
  
  
  METHODS
  Consecutive female patients with active RA requiring treatment with ETN (n=28) or sDMARDs (n=20) were included. Clinical and biological monitoring, echocardiography and pulse wave velocity (PWV) assessment were performed at inclusion and at 3 and 6 months after the start of treatment. Paired t tests and multivariate linear regression analysis were used.
  
  
  RESULTS
  Mean LVMI tended to be higher at baseline in the ETN group than in the sDMARD group (96.5±19.8 vs 84.3±26.8 g/m2; p=0.11 for the ETN and sDMARD groups, respectively). In patients with ETN treatment, mean LVMI was significantly decreased at 3 and 6 months (-6.3±7.6 and -14.2±9.3 g/m2; p<0.001), with no change from baseline for patients with sDMARD treatment (-2.2±10.9 and -2.7±10.2 g/m2, respectively). Blood pressure (BP) and aortic PWV were not changed by either treatment.
  
  
  CONCLUSIONS
  ETN induced a significant decrease in LVMI with medium-term treatment with no change in BP or PWV. TNFα may be an important factor of LV hypertrophy, which may explain the benefit of TNF inhibitors on cardiovascular morbidity and mortality in RA. These results need to be confirmed by larger studies and with other TNF inhibitors.
authors.affiliation: Department of Rheumatology, University Montpellier I, Lapeyronie Hospital, Montpellier, France.
authors.forename: Claire Immediato
authors.initials: CI
authors.lastname: Daïen
authors.forename: Pierre
authors.initials: P
authors.lastname: Fesler
authors.forename: Guilhem
authors.initials: G
authors.lastname: du Cailar
authors.forename: Vincent
authors.initials: V
authors.lastname: Daïen
authors.forename: Thibault
authors.initials: T
authors.lastname: Mura
authors.forename: Anne-Marie
authors.initials: AM
authors.lastname: Dupuy
authors.forename: Jean-Paul
authors.initials: JP
authors.lastname: Cristol
authors.forename: Jean
authors.initials: J
authors.lastname: Ribstein
authors.forename: Bernard
authors.initials: B
authors.lastname: Combe
authors.forename: Jacques
authors.initials: J
authors.lastname: Morel
mesh_terms: D000328:Adult; D000368:Aged; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D015331:Cohort Studies; D004452:Echocardiography; D000068800:Etanercept; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000209:etiology; D007074:Immunoglobulin G / Q000627:therapeutic use*; D007555:Isoxazoles / Q000627:therapeutic use; D000077339:Leflunomide; D008727:Methotrexate / Q000627:therapeutic use; D008875:Middle Aged; D063177:Pulse Wave Analysis; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D012460:Sulfasalazine / Q000627:therapeutic use; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*; D059289:Vascular Stiffness / Q000187:drug effects
chemical_list: D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D007555:Isoxazoles; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D012460:Sulfasalazine; D000077339:Leflunomide; D000068800:Etanercept; D008727:Methotrexate