Bile acids (BAs) have traditionally been viewed as mere ‘detergent’ molecules responsible for absorption of dietary fats and lipid-soluble vitamins. However, over the past decade, research in the field of bile acid biology has provided evidence which redefine BAs as potent circulating signalling molecules with the ability to regulate cell biology, metabolism and function of various extrahepatic organs,1 with potential effects on the heart. BAs are secreted in the duodenum and then reabsorbed efficiently from the ileum back to the liver via mesenteric and portal veins. This tightly regulated enterohepatic circulation is disrupted in diseases of the liver such as obstructive jaundice, intrahepatic cholestasis of pregnancy, chronic viral hepatitis and cirrhosis, which leads to spillage of these metabolites into the systemic circulation at pathologically high concentrations (>100–200 µmol/L), resulting in organ dysfunction.2 ,3

It has long been known that high levels of bile acids are toxic to the heart. The cardiotoxicity of bile acids was documented as early as 1863, by Röhrig, who showed that filtered ox bile when injected into the jugular veins of rabbits caused bradycardia, while repeated doses caused cardiac arrest, a phenomenon he described as ‘cardiac paralysis’. At the same time, Landois …