2007 Volume 48 Issue 2 Pages 195-204
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 ≤ 40% and systolic blood pressure between 90 and 120 mmHg, based on total bilirubin levels on admission. In patients with high bilirubin (T-Bil ≥ 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.