title: Hepatic dysfunction after left ventricular mechanical assist in patients with end-stage heart failure: role of inflammatory response and hepatic microcirculation.
abstract: BACKGROUND
  In the condition of preexisting vital organ failure induced by heart failure, hepatic failure often progresses despite establishment of adequate hemodynamic support through a left ventricular assist device (LVAD) and results in a high mortality rate. We hypothesized that inflammatory responses, including those induced by infection and their influence on organ perfusion, may contribute to the pathogenesis of this progressive hepatic failure and subsequent multiple organ failure as reported in the current investigation on multiple organ failure after major surgery or trauma.
  
  
  METHODS
  Hepatic function and its relation to inflammatory response and hepatic microcirculation were evaluated in 16 consecutive patients who received an implantation of LVAD for end-stage cardiomyopathy, between 1992 and 2000. Patients were divided into two groups: 5 patients who died from multiple organ failure after severe hepatic failure (group 1) and 11 patients who did not develop severe hepatic failure (group 2). Serum levels of CRP, interleukin (IL)-6, IL-8, and serum hyaluronan, a known indicator of hepatic sinusoidal function, were measured pre- and postoperatively in both groups.
  
  
  RESULTS
  Serum ALT and AST levels during LVAD support were similar in the two groups. Serum total bilirubin (T-Bil), CRP, IL-6, and IL-8 levels before and during the first 20 days of LVAD support were significantly higher in group 1 than those in group 2 (p < 0.01 to 0.05). Serum hyaluronan levels in both groups were significantly correlated with T-Bil levels (r = 0.60, p < 0.05 in group 1; r = 0.68, p < 0.0001 in group 2). Histopathological examination by transvenous liver biopsy in a group 1 patient showed hepatic sinusoidal damage as well as cholestasis and fibrosis.
  
  
  CONCLUSIONS
  Patients with hyperbilirubinemia and inflammatory reactions before LVAD support showed increased hyperbilirubinemia and inflammatory cytokine and hyarulonan levels despite adequate hemodynamics achieved under LVAD support. These results suggest that inflammatory response contributes to subsequent aggravation of hepatic dysfunction, probably with underlying and continuing derangement in hepatic sinusoidal microcirculation even under systemic circulatory support.
authors.affiliation: Department of Surgery, Osaka University Graduate School of Medicine, Suita, Japan.
authors.forename: Takafumi
authors.initials: T
authors.lastname: Masai
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Sawa
authors.forename: Shigeaki
authors.initials: S
authors.lastname: Ohtake
authors.forename: Toshirou
authors.initials: T
authors.lastname: Nishida
authors.forename: Motonobu
authors.initials: M
authors.lastname: Nishimura
authors.forename: Norihide
authors.initials: N
authors.lastname: Fukushima
authors.forename: Takashi
authors.initials: T
authors.lastname: Yamaguchi
authors.forename: Hikaru
authors.initials: H
authors.lastname: Matsuda
mesh_terms: D000328:Adult; D005260:Female; D006333:Heart Failure / Q000503:physiopathology / Q000628:therapy*; D006353:Heart-Assist Devices; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006932:Hyperbilirubinemia / Q000503:physiopathology; D018836:Inflammation Mediators / Q000502:physiology*; D008102:Liver Circulation / Q000502:physiology*; D017093:Liver Failure / Q000503:physiopathology*; D008111:Liver Function Tests; D008297:Male; D008833:Microcirculation / Q000503:physiopathology; D008875:Middle Aged; D012307:Risk Factors
chemical_list: D018836:Inflammation Mediators