Affiliations 

  • 1 Department of Women and Children's Health, King's College London, Guy's Campus, Hodgkin Building, SE1 1UL London, United Kingdom
  • 2 National Heart and Lung Institute, Imperial Centre for Translational and Experimental Medicine, Imperial College London, Du Cane Road, W12 0NN London, United Kingdom
  • 3 National Heart and Lung Institute, Imperial Centre for Translational and Experimental Medicine, Imperial College London, Du Cane Road, W12 0NN London, United Kingdom; Faculty of Medicine, MARA University of Technology, 40000 Sungai Buloh, Malaysia
  • 4 Department of Women and Children's Health, King's College London, Guy's Campus, Hodgkin Building, SE1 1UL London, United Kingdom. Electronic address: catherine.williamson@kcl.ac.uk
Biochim Biophys Acta Mol Basis Dis, 2018 04;1864(4 Pt B):1345-1355.
PMID: 29317337 DOI: 10.1016/j.bbadis.2017.12.039

Abstract

Cardiac dysfunction has an increased prevalence in diseases complicated by liver cirrhosis such as primary biliary cholangitis and primary sclerosing cholangitis. This observation has led to research into the association between abnormalities in bile acid metabolism and cardiac pathology. Approximately 50% of liver cirrhosis cases develop cirrhotic cardiomyopathy. Bile acids are directly implicated in this, causing QT interval prolongation, cardiac hypertrophy, cardiomyocyte apoptosis and abnormal haemodynamics of the heart. Elevated maternal serum bile acids in intrahepatic cholestasis of pregnancy, a disorder which causes an impaired feto-maternal bile acid gradient, have been associated with fatal fetal arrhythmias. The hydrophobicity of individual bile acids in the serum bile acid pool is of relevance, with relatively lipophilic bile acids having a more harmful effect on the heart. Ursodeoxycholic acid can reverse or protect against these detrimental cardiac effects of elevated bile acids.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.