Increased serum bilirubin levels coincident with heart failure decompensation indicate the need for intravenous inotropic agents

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= 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.