title: Ventricular assist device in severe heart failure: effects on cytokines, complement and body weight.
abstract: OBJECTIVE
  Inflammatory and immune activation and body wasting are important features of end-stage chronic heart failure. It is not known whether restoration of cardiac output by assist device implantation can improve these abnormalities.
  
  
  METHODS
  We studied 48 patients (39 males; age 45+/-2 years) with NYHA class IV heart failure. All patients underwent ventricular assist device implantation for end-stage heart failure as a bridge to cardiac transplantation. Plasma levels of tumour necrosis factor alpha, and its receptors, interleukin-6, elastase, activated complement, and soluble CD14 receptors were measured at the time of operation and in survivors at 1 week (n=46), 40 days (n=35) and 90 days (n=26). Follow-up was for a minimum of 1 year.
  
  
  RESULTS
  One-year survival was 35% (95% CI: 22-49%). Body mass index was the only predictor of survival (body mass index >25 (n=16); survival 63 (39-86) %; body mass index <25 (n=32); survival 22 (7.5-36) %: P=0.003). Tumour necrosis factor alpha fell from 9.66+/-1.33 pg x ml(-1) to 4.2+/-1.0 at 1 week (P=0.008), but returned to pre-operative levels at 90 days. Interleukin-6, activated complement and elastase fell progressively to 40 days, but were rising at 90 days. There was no change in tumour necrosis factor receptor. There was a gradual rise in CD14 (3.99+/-0.15 microg x ml(-1) at baseline, 5.02+/-0.39 at 90 days, P=0.006). After surgery, body weight fell from 80+/-2 to 73+/-2 kg by 1 month (P<0.001) and to 72+/-2 kg at 90 days.
  
  
  CONCLUSIONS
  Ventricular assist device implantation results in a short-term fall in tumour necrosis factor alpha and interleukin-6, but no change in CD14 or tumour necrosis factor receptor, suggesting that the pathophysiological process resulting in inflammation was not altered by left ventricular assist device implantation. Low body mass index is related to poor outcome after assist device implantation, and no weight gain.
authors.affiliation: Department of Academic Cardiology, Castle Hill Hospital, Cottingham, Hull, UK.
authors.forename: A L
authors.initials: AL
authors.lastname: Clark
authors.forename: M
authors.initials: M
authors.lastname: Loebe
authors.forename: E V
authors.initials: EV
authors.lastname: Potapov
authors.forename: K
authors.initials: K
authors.lastname: Egerer
authors.forename: C
authors.initials: C
authors.lastname: Knosalla
authors.forename: R
authors.initials: R
authors.lastname: Hetzer
authors.forename: S D
authors.initials: SD
authors.lastname: Anker
mesh_terms: D001835:Body Weight; D003165:Complement System Proteins / Q000378:metabolism; D016207:Cytokines / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005858:Germany; D006333:Heart Failure / Q000276:immunology / Q000401:mortality* / Q000473:pathology / Q000628:therapy*; D006353:Heart-Assist Devices; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D018950:Lipopolysaccharide Receptors / Q000097:blood; D008297:Male; D008875:Middle Aged; D010196:Pancreatic Elastase / Q000097:blood; D011184:Postoperative Period; D019919:Prosthesis Implantation; D011669:Pulmonary Wedge Pressure; D012720:Severity of Illness Index; D016019:Survival Analysis; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016207:Cytokines; D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors; D014409:Tumor Necrosis Factor-alpha; D003165:Complement System Proteins; D010196:Pancreatic Elastase