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Aim. To study the functional state of endothelium in patients with chronic viral hepatitis and liver cirrhosis and impact of left and right ventricle diastolic malfunction and pulmonary hypertension on endothelial function. Methods. 74 patients with chronic viral hepatitis (group 1), 62 patients with cirrhosis (group 2) and 17 healthy volunteers were examined. Doppler echocardiography and brachial artery ultrasonography with endothelium-dependent vasodilation measurement were performed. Results. Endothelium-dependent vasodilatation was reduced in patients of the 1 stgroup (6.2%), and of the 2 ndgroup (2.2%) compared to the controls (13.8%, р 0.05). Sensitivity coefficient for the brachial artery was measured as 0.31 (0.19; 0.35) in patients with chronic viral hepatitis, 0.25 (0.09; 0.35) in patients with cirrhosis compared to 1.27 (0.72; 1.29) in control group, demonstrating the marked endothelial dysfunction in patients of the 1 stand 2 ndgroups (р 0.05). Moderate pulmonary hypertension was accompanied by a more pronounced endothelium-dependent vasodilation impairment in both groups (р 0.05). In patients with viral hepatitis, endothelial malfunction was less common (62%) compared with patients with liver cirrhosis (85%, p=0.002). Presence of left and right ventricle diastolic malfunction did not influence the endothelial function. Conclusion. In patients with viral hepatitis and cirrhosis, endothelium-dependent vasodilatation is affected depending on the severity of the disease and increased if pulmonary hypertension was present. Presence of left and right ventricle diastolic malfunction did not influence the endothelial function.

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The review outlines the current understanding of the clinical syndrome of heart disease in patients with liver cirrhosis and the development of cirrhotic cardiomyopathy. Patients with cirrhosis of the liver often notice chest pain, palpitations, complaints of arterial hypotension and rapid fatigue. Echocardiography shows that the left ventricular ejection fraction in cirrhosis is preserved at rest and decreases under stress. In some patients with viral liver cirrhosis, there is a decrease in global myocardial deformation (the presence of latent systolic dysfunction). More pronounced impairment of left ventricular diastolic function is recorded in patients with ascites and patients with ChildPugh class B and C. In patients with ascites, unfavorable left ventricular remodeling, left heart cavities enlargement, dilatation of the pulmonary artery and its branches are more common. There is an increase in pulmonary artery pressure, the development of portopulmonary hypertension and hepatopulmonary syndrome in patients with liver cirrhosis. Тhe development of these syndromes leads to a sharp decrease in the quality of life of patients with relatively preserved liver function and a worsening of the prognosis for orthotopic liver transplantation. Аpproximately half of patients with liver cirrhosis have electrophysiological disorders: prolongation of the QT interval, tachycardia, supraventricular and ventricular extrasystoles. To date, there are no clinical guidelines for the management of cirrhotic cardiomyopathy. If a patient with liver cirrhosis develops clinically significant heart failure, then general principles of management of such patients are necessary. It is necessary to limit the use of angiotensin-converting enzyme inhibitors and cardiac glycosides. The combined use of nonselective beta-blockers and nitrates reduce cardiac output and QT interval. The use of potassium canrenoate, lisinopril helps reverse the development of structural and functional changes in left ventricle. The positive effect of antiviral therapy on cardiac hemodynamics in patients with viral cirrhosis was noted. Liver transplantation is known to be an effective treatment for cirrhotic cardiomyopathy, but this treatment may worsen latent heart failure. Thus, in patients with liver cirrhosis, heart damage occurs with the development of cirrhotic cardiomyopathy, while the mechanisms of the development of myocardial dysfunction are not fully understood. Further studies of the development of the syndrome are required for timely diagnosis and clinical intervention to improve the survival of patients.

Aim. To study the influence of pulmonary hypertension, viral load, and presence of ascites on indicators of longitudinal global and segmental systolic and diastolic ventricular functions in patients with liver cirrhosis as an outcome of viral hepatitides. Methods. The study included 75 patients with liver cirrhosis class A, В, C by Child-Pugh as an outcome of viral hepatitides who were distributed into 3 groups depending on the presence of pulmonary hypertension, ascites, and of viral load. All patients underwent Doppler echocardiography and tissue Doppler echocardiography. Results. Decreased global longitudinal systolic and diastolic function of the left and right ventricles was revealed in patients with virus-related liver cirrhosis, which decreased in the presence of pulmonary hypertension, moderate viral load and ascites. While studying an association between the structural and functional heart indices and hepatic and portal blood flow, it was found that average mitral and tricuspid valve peak systolic velocity was associated with left ventricle ejection fraction (r=0.71, p 0.05), liver veins diameter and blood flow speed parameters (r=0.32-0.81, p 0.05), pulmonary artery pressure (r=0.37-0.84, p 0.05), and viral load (r=0.92, p 0.05). Conclusion. Patients with virus-related liver cirrhosis have decreased global longitudinal systolic and diastolic function of the left and right ventricles, deteriorated by pulmonary hypertension, ascites, and moderate viral load.