Key result
Cardiohepatic injury in ADHF linked to up to ~7-fold higher in-hospital mortality.
Why the study?
Abnormal liver biochemistry is common in ADHF, but most studies evaluate individual markers rather than clinically meaningful patterns of hepatic involvement.
Do cardiohepatic injury phenotypes derived from routine liver tests predict short-term mortality and readmission in adults hospitalized with acute decompensated heart failure?
Cohort (n=8,332)
Do cardiohepatic injury phenotypes derived from routine liver tests predict short-term mortality and readmission in adults hospitalized with acute decompensated heart failure?
p-value: p=<0.001
Classifying acute decompensated heart failure patients by cardiohepatic injury phenotypes using routine liver tests provides independent prognostic value, with hepatocellular involvement identifying those at highest risk for short-term mortality and readmission.
Cardiohepatic phenotypes may stratify short-term ADHF risk; leaves open added value beyond standard models in prospective validation.
Background Abnormal liver biochemistry is common in acute decompensated heart failure (ADHF), yet most studies evaluate individual markers rather than clinically meaningful patterns of hepatic involvement. We examined whether cardiohepatic injury phenotypes derived from routine liver tests identify distinct short-term prognostic profiles in patients hospitalized with ADHF. Methods In this retrospective cohort study, we included consecutive adults hospitalized with ADHF between December 2006 and 2017. Using peak in-hospital values of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and total bilirubin, patients were classified into four phenotypes: no hepatic injury, hepatocellular injury, cholestatic injury, or combined injury. Associations with in-hospital mortality were evaluated using multivariable logistic regression. Post-discharge outcomes (30-day mortality, readmission, and their composite) were analyzed using Cox and Fine–Gray models. Results Among 8332 ADHF admissions, 6792 (81.5%) had sufficient data for phenotype classification: 58.1% had no hepatic injury, 22.1% hepatocellular injury, 13.1% cholestatic injury, and 6.7% combined injury. In-hospital mortality differed markedly across phenotypes (3.5%, 16.3%, 9.0%, and 24.3%, respectively; p < 0.001). After adjustment, all injury phenotypes independently predicted in-hospital death compared with no injury. Among 6128 patients included in adjusted post-discharge analyses, hepatocellular and combined injury were independently associated with higher 30-day mortality and the composite outcome, whereas isolated cholestatic injury was not. Hepatocellular and combined injury independently predicted 30-day readmission. Conclusions Routine liver test patterns identify clinically meaningful cardiohepatic phenotypes in ADHF. While all hepatic injury phenotypes are associated with increased in-hospital mortality, only phenotypes with hepatocellular involvement predict adverse early post-discharge outcomes. Pattern-based interpretation of liver tests may improve early risk stratification in patients hospitalized with ADHF.
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Marcus et al. (2026) conducted a cohort in Acute decompensated heart failure (ADHF) (n=8,332). Hepatic injury phenotypes (hepatocellular, cholestatic, or combined) vs. No hepatic injury was evaluated on In-hospital mortality (p=<0.001). Cardiohepatic injury phenotypes in acute decompensated heart failure were associated with significantly higher in-hospital mortality compared to no hepatic injury (up to 24.3% vs 3.5%; P<0.001).
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