Relationship of the liver fibrous formation processes and cardiosclerosis in patients with stable coronary heart disease combined with non-alcoholic fatty liver disease.

Abstract

Aim of the study was to determine the features of myocardial remodeling in patients with postinfarction cardiosclerosis combined with non-alcoholic fatty liver disease (NAFLD) and identify the dependence of the liver fibrogenesis processes and cardiosclerosis depending on the liver fibrosis stage. Material and methods. The study included 300 patients with postinfarction cardiosclerosis with and without NAFLD. Patients with NAFLD were divided depending on the liver fibrosis stage. Among them patients with non-alcoholic steatosis and non-alcoholic steatohepatitis (NASH) were observed. General clinical examination, electrocardiography, coronary angiography, echocardiography, elastography, assessment of the liver functional state, serum type IV collagen were conducted. Results. Formation of pathological myocardial remodeling types dependent on the fibrosis liver stage and grew along with the progression of NAFLD (р<0.05). Analysis of the elastography results showed a significant increase of the liver stiffness in all patients (р<0.05). The greatest value of shear wave velocity was observed in patients with severe fibrosis of the liver parenchyma of F4 stage (р<0.05). The level of type IV collagen increased according to the stages of liver fibrosis progression and was the highest in patients with NASH of IVB and VB groups (p<0.05). The direct correlation relationships between stage of fibrosis, level of type IV collagen and myocardial left ventricle mass index in patients with coronary heart disease and NAFLD were revealed. Conclusions. Intensity of fibrotic changes in the liver and myocardium depends on the NAFLD progression and fibrosis stage, and the presence of direct correlative relationship between the liver parenchyma stiffness, level of type IV collagen and myocardial left ventricle mass index indicates mutual aggravating influence of the coronary heart disease and NAFLD on the course of one another, which generally promotes activation of fibrogenesis in liver and myocardium.