title: Liver function abnormalities, clinical profile, and outcome in acute decompensated heart failure.
abstract: OBJECTIVE
  The aim of this study was to assess the prevalence of abnormal liver function tests (LFTs) and the associated clinical profile and outcome(s) in acute decompensated heart failure (ADHF) patients. Alteration in LFTs is a recognized feature of ADHF, but prevalence and outcomes data from a broad contemporary cohort of ADHF are scarce and the mechanism(s) of ADHF-induced cholestasis is unknown.
  
  
  RESULTS
  We conducted a post hoc analysis of SURVIVE, a large clinical trial including ADHF patients treated with levosimendan or dobutamine. All LFTs were available in 1134 patients at baseline. Abnormal LFTs were seen in 46% of ADHF patients: isolated abnormal alkaline phosphatase (AP) was noted in 11%, isolated abnormal transaminases in 26%, and a combination of abnormal AP and transaminases in 9%. Abnormal AP was associated with marked signs of systemic congestion and elevated right-sided filling pressure. Abnormal AP had no relationship with 31-day mortality but was associated with worse 180-day mortality (23.5 vs. 34.9%, P = 0.001 vs. patients with normal AP). Abnormal transaminases were associated with clinical signs of hypoperfusion and with greater 31-day and 180-day mortality compared with normal transaminase profiles (17.6 vs. 8.4% and 31.6 vs. 22.4%, respectively; both P < 0.001). There was no additive value of abnormal AP plus abnormal transaminase on a long-term outcome.
  
  
  CONCLUSIONS
  Abnormal LFTs were present in about a half of patients presenting with ADHF treated with inotropes. Abnormal AP and abnormal transaminases were associated with specific clinical, biological, and prognostic features, including a short-term overmortality with increased transaminases but not with biological signs of cholestasis, in ADHF patients.
authors.affiliation: UMRS 942 Inserm, F-75010 Paris, France.
authors.forename: Maria
authors.initials: M
authors.lastname: Nikolaou
authors.forename: John
authors.initials: J
authors.lastname: Parissis
authors.forename: M Birhan
authors.initials: MB
authors.lastname: Yilmaz
authors.forename: Marie-France
authors.initials: MF
authors.lastname: Seronde
authors.forename: Matti
authors.initials: M
authors.lastname: Kivikko
authors.forename: Said
authors.initials: S
authors.lastname: Laribi
authors.forename: Catherine
authors.initials: C
authors.lastname: Paugam-Burtz
authors.forename: Danlin
authors.initials: D
authors.lastname: Cai
authors.forename: Pasi
authors.initials: P
authors.lastname: Pohjanjousi
authors.forename: Pierre-François
authors.initials: PF
authors.lastname: Laterre
authors.forename: Nicolas
authors.initials: N
authors.lastname: Deye
authors.forename: Pentti
authors.initials: P
authors.lastname: Poder
authors.forename: Alain
authors.initials: A
authors.lastname: Cohen-Solal
authors.forename: Alexandre
authors.initials: A
authors.lastname: Mebazaa
mesh_terms: D000208:Acute Disease; D000368:Aged; D000469:Alkaline Phosphatase / Q000378:metabolism*; D002316:Cardiotonic Agents / Q000627:therapeutic use; D002779:Cholestasis / Q000201:enzymology / Q000209:etiology / Q000401:mortality; D004280:Dobutamine / Q000627:therapeutic use; D005260:Female; D006333:Heart Failure / Q000150:complications* / Q000201:enzymology / Q000401:mortality; D006801:Humans; D006835:Hydrazones / Q000627:therapeutic use; D008107:Liver Diseases / Q000201:enzymology* / Q000209:etiology / Q000401:mortality; D008111:Liver Function Tests; D008297:Male; D011379:Prognosis; D011446:Prospective Studies; D011724:Pyridazines / Q000627:therapeutic use; D016032:Randomized Controlled Trials as Topic; D000077464:Simendan; D000637:Transaminases / Q000378:metabolism*
chemical_list: D002316:Cardiotonic Agents; D006835:Hydrazones; D011724:Pyridazines; D000077464:Simendan; D004280:Dobutamine; D000637:Transaminases; D000469:Alkaline Phosphatase