title: Increased serum bilirubin levels coincident with heart failure decompensation indicate the need for intravenous inotropic agents.
abstract: We have reported that chronic heart failure (HF) patients with increased serum bilirubin coincident with acute decompensation have a poor prognosis, indicating severe congestion and low tissue perfusion. The aim of this study was to analyze the possibility of increased bilirubin coincident with acute decompensation as a parameter which indicates the need for intravenous inotropic agents. We stratified 131 decompensated chronic HF patients with a LVEF <or= 40% and systolic blood pressure between 90 and 120 mmHg, based on total bilirubin levels on admission. In patients with high bilirubin (T-Bil >or= 1.2 mg/dL), intravenous inotropics contributed to significantly more abundant diuresis, body weight reduction, and decreases in bilirubin and serum creatinine in the first 5 in-hospital days compared to those without (group A: inotropics +; n = 24 versus group B: -; n = 38: 1726 +/- 418 versus 1458 +/- 424 mL/day: P < 0.05, -3.1 +/- 1.6 versus -2.1 +/- 2.2 kg: P < 0.05, -0.74 +/- 0.51 versus -0.04 +/- 0.60 mg/dL: P < 0.01, -0.29 +/- 0.89 versus -0.01 +/- 0.24 mg/dL: P < 0.01), in spite of no significant difference in the doses of diuretics between the 2 groups. On the contrary, patients with low bilirubin (T-Bil < 1.2 mg/dL) recovered from decompensation equally irrespective of inotropic administration (group C: inotropics +; n = 15 versus group D: -; n = 54: 1557 +/- 329 versus 1507 +/- 406 mL/day, -2.9 +/- 1.7 versus -2.8 +/- 1.5 kg, -0.01 +/- 0.25 versus -0.08 +/- 0.23 mg/dL, 0.02 +/- 0.24 versus 0.47 +/- 0.19 mg/dL; NS, respectively). Inotropics were administered after all because of unimproved hemodynamics in 26% of group B patients, compared to 4% of group D patients (P < 0.01). Increased bilirubin coincident with HF decompensation can be a useful marker indicating the need for intravenous inotropic agent administration.
authors.affiliation: Department of Cardio-angiology, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.
authors.forename: Hisahito
authors.initials: H
authors.lastname: Shinagawa
authors.forename: Takayuki
authors.initials: T
authors.lastname: Inomata
authors.forename: Toshimi
authors.initials: T
authors.lastname: Koitabashi
authors.forename: Hironari
authors.initials: H
authors.lastname: Nakano
authors.forename: Ichiro
authors.initials: I
authors.lastname: Takeuchi
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Osaka
authors.forename: Mototsugu
authors.initials: M
authors.lastname: Nishii
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Takehana
authors.forename: Tohru
authors.initials: T
authors.lastname: Izumi
mesh_terms: D000368:Aged; D001663:Bilirubin / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D002316:Cardiotonic Agents / Q000008:administration & dosage*; D015331:Cohort Studies; D004232:Diuretics / Q000008:administration & dosage; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000188:drug therapy*; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D020380:Needs Assessment; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D002316:Cardiotonic Agents; D004232:Diuretics; D001663:Bilirubin