Heart failure affects liver morphology and function. What are the clinical implications?

Liver dysfunction in heart failure is common and usually clinically significant, especially in patients with advanced or severe acute heart failure. Lesions are caused by an impaired hepatic circulation due to congestion and hypoperfusion. Congestive lesions are more common and typically manifested by painful hepatomegaly and increased direct bilirubin and alkaline phosphatase. The inferior vena cava and hepatic veins are usually dilated. Congestive lesions are characterized by dilatation of the central vein with fibrotic changes in the surrounding areas on histological examination. Isolated ischaemic lesions are rare and occur due to severe and prolonged ineffective perfusion, often accompanied by hypoxemia. Ineffective perfusion is reflected by an increase in total bilirubin and significantly increased transaminase levels. The prognosis of ischaemic lesions without an adequate treatment of the cause of hypoperfusion is poor. Increased levels of bilirubin and liver function tests, as well as signs of impaired liver proteosynthetic function, are associated with a poor prognosis. Knowledge of the phenotypes of hepatic lesions in heart failure is important to select the appropriate treatment for an acute decompensation. Changes in biochemical markers, hepatic perfusion or stiffness of the liver can be used to evaluate the effectiveness of diuretic treatment and achieve euvolemic status in the patients with heart failure (Tab. 1, Fig. 3, Ref. 28).