Abstract

The development and progression of heart failure accelerate obesity, disorders of carbohydrate and lipid metabolism. These states are united by the term The hepatic manifestation of the metabolic syndrome is a non-alcoholic fatty liver disease (NAFLD). The combination of NAFLD and cardiovascular disease leads to increased risk of cardiovascular complications and has a significant impact on the prognosis and outcome of CHF. A key factor in the pathogenesis and progression of CHF is myocardial remodeling. The metabolic products of collagen (N-terminal pro-peptide of type III collagen) are considered as promising candidates for markers of myocardial remodeling and development of heart failure. In a number of papers increased level of PIIINP is a predictor of cardiac mortality or rehospitalization due to decompensation of heart failure associated with an increased risk of death. Materials and Methods: The study group included 39 patients with CHF and MS. The control group included 38 patients with chronic heart failure, without the metabolic syndrome. In all patients the diagnosis of heart failure was confirmed by quality measuring the NT-proBNP. The severity of the clinical manifestations of heart failure, functional status of the patient were assessed. All patients underwent biochemical blood tests. The size of the heart chambers, wall thickness of the myocardium and epicardial fat were estimated by echocardiography. All the patients underwent the calculation of Fatty Liver Index, NAFLD Fibrosis Score. Results: The level of the main group PIIINP is 3,3 ± 1,5 g / l; in the control group - 2,3 ± 1,3 g / l (p = 0,00046). Statistical analysis revealed significant correlation (p<0.05) between laboratory data and PIIINP: the level of uric acid, glucose level, GFR, value FLI, NFS; between the data of echocardiography and PIIINP: thickness of epicardial fat, IVS thickness, LV myocardial mass, RA dimensions, LA, ESD LV, ratio E / A, ratio E / e. Conclusions: The use of PIIINP in clinical practice will identify patients with CHF and MS with structural and functional changes in the myocardium in the early stages of the disease. Also the determination of the level of PIIINP in patients with CHF and MS will allow identifying patients with liver disease and selecting the ones for further assessment and selection of therapy taking into consideration attendant pathology.

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