Nowadays, coronary heart disease and non-alchoholic fatty liver disease are significant problems in Ukraine and world. Functional liver disorders potentiate the development and progression of CHD. The initiation process of atherosclerosis is a chronic systemic inflammation of low intensity. This view on atherosclerosis development has been forming during the past two decades. The aim of the research was to study the features/characteristics of systemic inflammation of low intensity in patients with coronary heart disease in combination with non-alcoholic fatty liver disease. The research involved 135 people with CHD: stable angina, I-II functional class, 0-I heart failure in combination with non-alcoholic fatty liver disease and 30 healthy individuals. We examined patients in terms of blood levels of cytokines -TNFα and IL-10, the content of the acute phase reactant and the coagulation factor, the marker of endothelial dysfunction is the amount of circulating endothelial microparticles (CEM) CD32+ CD40+ and the expression level of IkBα gene NF-kB in mononuclear peripheral blood. We studied the level of expression of the mRNA gene of IkBα in mononuclear cells, which reflects the level of transcriptional activity of NF-kB in patients with stable coronary artery disease and CHD in combination with NAFLD showed a significant increase in the expression of the mRNA gene of IkBα by 88.5% compared to patients with stable stable coronary heart disease. The analysis of the functional state of the endothelium with help of CEM CD32+ CD40+ has shown the presence of endothelial dysfunction in the groups of patients with CHD and CHD in combination with of NAFLD. Comparison of the indicators of systemic inflammation of low intensity and marker of endothelial dysfunction in patients with CHD in combination with NAFLD revealed a significant increase of TNFα, acute phase reactant and coagulation fibrinogen factor and expression of the mRNA IkBα gene in patients with comorbidity, indicating an increase the level of systemic inflammation of low intensity in patients with CHD in combination with NAFLD as compared with the group of patients with CHD.
The actual problem of modern medicine is the identification of common pathogenetic mechanisms of IHD and NAFLD in order to develop a complex, personalized approach in treatment and prevention of comorbid pathology. Aim of the study: to determine the clinical course peculiarities of ischemic heart disease under conditions of comorbidity with non-alcoholic fatty liver disease. The study involved 135 patients with ischemic heart disease: stable voltage angina, I-II FC, HF 0-1, combined with non-alcoholic fatty liver disease and 30 healthy individuals. At the first stage of the study an assessment of ischemic heart disease tendencies under circumstances of concomitant NAFLD was conducted taking into consideration the peculiarities of clinical symptoms, and in comparison groups there was no significant difference discovered eventually in cardiovascular systems complaints, which were caused by IHD development. In patients with IHD combined with NAFLD the incidence of myocardial bioelectric activity disorders and the frequency of rhythm disorders prevailed comparing to patients with IHD. A significant increase in total cholesterol and a blood atherogenic index was found in patients with IHD combined with NAFLD compared to the patients with IHD (p <0.05) in the analysis of lipidogram indices. No significant difference among other lipidogram indicators (LDL cholesterol, HDL cholesterol, TG) was observed (p> 0.05). Thus, the detected lipid metabolism disorders were noted in patients with IHD combined with NAFLD at statin therapy. Due to results of echocardiography a diastolic dysfunction and a moderate decrease of systolic function were found in both study groups comparing to the healthy group, regardless of the presence or absence of NAFLD. A higher incidence of LV hypertrophy was observed in patients with comorbid pathology.
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