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This editorial refers to ‘Liver function abnormalities, clinical profile, and outcome in acute decompensated heart failure’†, by M. Nikolaou et al., on page 742

The liver in heart failure

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

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