Cardiohepatic Interactions in Heart Failure an Overview
Cardiohepatic Interactions in Heart Failure an Overview
Given the heterogeneity in LFT abnormalities, HF patients presenting with abnormal liver function should first be evaluated for potential biliary tract obstruction and/or primary hepatic pathology before attributing irregularities to cardiac disease. The differential diagnosis should include biliary stasis/cholelithiasis; hemochromatosis; primary biliary cirrhosis; primary sclerosing cholangitis; forms of hepatitis, including viral, alcoholic, and autoimmune; and primary malignancies of the biliary system.
Cardiomyopathies including iron overload and amyloidosis may have direct hepatic involvement and should not be mistaken for chronic and/or acute hepatic injury secondary to HF. Amyloidosis is an infiltrative cardiomyopathy that should be considered in all patients presenting with proteinuria and neuropathy, especially if there are signs and symptoms of restrictive cardiomyopathy or right-side heart failure.
Once primary biliary pathology and systemic conditions that may concomitantly affect the heart and liver have been ruled out, elevated LFTs in conjunction with increased intracardiac filling pressures suggest some component of cardiogenic liver injury. When combined with a normal (<5 mm Hg) gradient between hepatic wedge pressure and right atrial pressure, one can rule out significant portal hypertension secondary to chronic liver disease. If ascites is present, then diagnostic paracentesis should be performed; however, a liver biopsy remains the gold standard for diagnosing liver disease. In the acute setting, biopsies should be reserved for patients whose diagnosis is unclear or the staging of fibrosis is imperative in treatment decisions (i.e., candidacy for isolated cardiac transplantation).
Management Strategies of HF Patients With Secondary Liver Injury
Given the heterogeneity in LFT abnormalities, HF patients presenting with abnormal liver function should first be evaluated for potential biliary tract obstruction and/or primary hepatic pathology before attributing irregularities to cardiac disease. The differential diagnosis should include biliary stasis/cholelithiasis; hemochromatosis; primary biliary cirrhosis; primary sclerosing cholangitis; forms of hepatitis, including viral, alcoholic, and autoimmune; and primary malignancies of the biliary system.
Cardiomyopathies including iron overload and amyloidosis may have direct hepatic involvement and should not be mistaken for chronic and/or acute hepatic injury secondary to HF. Amyloidosis is an infiltrative cardiomyopathy that should be considered in all patients presenting with proteinuria and neuropathy, especially if there are signs and symptoms of restrictive cardiomyopathy or right-side heart failure.
Once primary biliary pathology and systemic conditions that may concomitantly affect the heart and liver have been ruled out, elevated LFTs in conjunction with increased intracardiac filling pressures suggest some component of cardiogenic liver injury. When combined with a normal (<5 mm Hg) gradient between hepatic wedge pressure and right atrial pressure, one can rule out significant portal hypertension secondary to chronic liver disease. If ascites is present, then diagnostic paracentesis should be performed; however, a liver biopsy remains the gold standard for diagnosing liver disease. In the acute setting, biopsies should be reserved for patients whose diagnosis is unclear or the staging of fibrosis is imperative in treatment decisions (i.e., candidacy for isolated cardiac transplantation).
