What does the liver tell us about the failing heart?

Abstract

This editorial refers to ‘Liver function abnormalities, clinical profile, and outcome in acute decompensated heart failure’, by M. Nikolaou et al. , doi:10.1093/eurheartj/ehs332 The high metabolic activity of the liver results in a high perfusion rate of ∼1 mL/g/min. Under resting conditions, this is about a quarter of the bodýs total blood supply. The oxygen-rich blood of the hepatic artery contributes to about a quarter of the total liver perfusion that may rise substantially under conditions of excessive oxygen demand. The complex blood supply makes the liver extraordinarily vulnerable to acute circulatory disturbances. Both the severity and the pattern of hepatic injury depend on the relative contribution of passive congestion and diminished perfusion.1 Increased central venous pressure results in passive hepatic congestion and causes elevations of alkaline phosphatase (AP), γ-glutamyltransferase (GGT), and direct and indirect serum bilirubin. This ‘congestive hepatic injury’ is known as nutmeg liver on pathology. Decreased cardiac output with impaired organ perfusion is associated with acute centrilobular (zone 3 of the acinus) hepatocellular damage and necrosis. ‘Hepatic ischaemic injury’ results in elevations in serum aminotransferases ( Figure 1 ).2,3 Figure 1 Haemodynamic disturbances in heart failure and mechanisms resulting in different patterns of elevated liver enzymes. Congestive hepatic injury (left panel) and ischaemic hepatic injury (right panel). In contrast to acute perfusion abnormalities, prolonged and chronic haemodynamic disturbances may result in bridging fibrosis, ‘cardiac’ cirrhosis, and impaired hepatic function with decreased synthesis of coagulation factors and albumin. Hepatic congestion occurs without particular symptoms in most cases. Some patients may suffer from jaundice, stretching of the liver capsule with right upper quadrant discomfort, and ascites. Rare cases of congestive heart failure (HF) associated with fulminant hepatic failure have been reported. However, most such cases occur in the setting of superimposed cardiogenic shock and consecutive hepatic ischaemic injury.4 …