Cardiohepatic Interactions in Heart Failure Management

Summary

Heart failure induces hepatic congestion and hypoperfusion, leading to a spectrum of liver abnormalities collectively termed congestive hepatopathy. Elevated central venous pressure impairs sinusoidal blood flow, while reduced cardiac output compromises hepatic perfusion. These derangements trigger inflammation, oxidative stress and fibrotic remodelling in the liver, which in turn release metabolic mediators that may exacerbate cardiac dysfunction. Emerging evidence highlights the role of hepatokines in modulating systemic metabolism and organ cross-talk. Quantitative assessment of liver function using biochemical scores and imaging biomarkers has become integral to risk stratification in heart failure. Therapeutic approaches that relieve venous congestion, optimise forward flow and target inter-organ signalling pathways hold promise for improving outcomes. Given the global burden of heart failure and its associated hepatic complications, a multidisciplinary strategy is required to integrate hepatological assessment into routine cardiac care.

Research from Nature Portfolio

Recent studies have demonstrated that serum γ-glutamyltransferase independently predicts adverse events in heart failure with preserved ejection fraction. Higher γ-glutamyltransferase levels correlate with both left- and right-sided haemodynamic alterations and are linked to increased hospitalisation and mortality. Echocardiographic measures of atrial pressure and chamber dimensions show a graded association with this enzyme, suggesting that simple liver function tests can enhance risk stratification when advanced diagnostic modalities are not available.

Cardiohepatic Interactions in Heart Failure Management publication trend

The graph below shows the total number of articles in cardiohepatic interactions in heart failure management across all publications each year (not limited to Nature Index journals).

Technical terms

Congestive hepatopathy: Hepatic injury resulting from elevated venous pressure and reduced perfusion in heart failure.

Hepatokines: Bioactive proteins secreted by hepatocytes that regulate systemic metabolism and inter-organ signalling.

MELD-XI score: A prognostic index of liver dysfunction calculated from serum bilirubin and creatinine, excluding coagulation parameters.

Albumin–bilirubin (ALBI) score: A quantitative assessment of hepatic reserve based on albumin and bilirubin concentrations.

Cholestasis: Impairment of bile formation or flow, reflected by elevations in alkaline phosphatase and bilirubin.

References

  1. Cardiac Hepatopathy: New Perspectives on Old Problems through a Prism of Endogenous Metabolic Regulations by Hepatokines. Antioxidants (2023).
  2. Liver tests and outcomes in heart failure with reduced ejection fraction: findings from DAPA‐HF. European Journal of Heart Failure (2022).
  3. Serum levels of gamma-glutamyltransferase predict outcome in heart failure with preserved ejection fraction. Scientific Reports (2019).

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