Heart failure is detected in 2% of the population. The leading causes of heart failure are coronary heart disease, arterial hypertension, and valvular heart disease. The number of patients with chronic heart failure continues to increase despite the new methods of diagnosis and treatment. A special contribution is made by damage to target organs in the development of cardiovascular pathology. Impaired liver function or congestive liver is common in heart failure and increases the risk of death and requires further study. The mechanism of liver damage in chronic heart failure is complex and multicomponent. The sensitivity and specificity of standard clinical, laboratory and instrumental methods for the diagnosis of congestive liver are insufficient. With the increase, severity and duration of venous congestion, structural changes in the architectonics occur, leading to the formation of liver fibrosis. The development of cardiac liver fibrosis leads to a complication of the course of chronic heart failure and an increase in mortality. Among the new diagnostic methods, the most important are serological markers of liver fibrosis, which have high diagnostic accuracy, as well as histological determination of fibrosis, as well as ultrasound examination of the liver in B-mode and determination of liver stiffness by elastography. Direct and indirect serological markers have a higher diagnostic value when using their combination in the composition of panels in the development of hepatopathy of different origins. An increase in the concentration of markers of fibrosis and liver stiffness during elastography correlates with the severity of heart failure and a long-term prognosis for mortality, including from extrahepatic diseases. Performing liver elastography in dynamics allows to monitor the course and treatment of heart failure. The optimal diagnostic method is a combination of direct and indirect markers of fibrosis, ultrasound diagnostics and elastography, in addition to clinical assessment of signs and direct assessment of hemodynamic parameters.