Features of Сlinical-metabolic Disorders and Structural-functional Changes of Heart in Patients with Essential Hypertension with Abdominal Obesity and Heart Hypertrophy

The purpose of the study was to find the relationship between the nature of structural and functional changes in the heart and metabolic factors in patients with hypertension with obesity and determining their role in the progression of HS in this category of patients. Material and methods. 82 patients took part in our study. We compared the data of 66 patients with essential hypertension (main group), abdominal obesity and hypertrophy of the heart and 16 patients with essential hypertension with obesity without heart hypertrophy (control group). The scope of the examination included: general clinical, anthropometric and echocardioscopic methods, blood glucose (fasting and after glucose loading), lipid levels, uric acid, glomerular filtration rate. Results and discussion. In the course of study, we noticed that patients with essential hypertension, abdominal obesity and heart hypertrophy differed from patients with essential hypertension with abdominal obesity without heart hypertrophy. The differences were in age, longer duration of hypertension, more severe heredity for hypertension, more severe clinical course of hypertension, more frequent disorders of carbohydrate metabolism in the main group. The lipid metabolism disorders included elevated the blood triglycerides levels, higher plasma levels of uric acid, frequent occurrence of hyperuricemia, disorders of the functional state of the kidneys. Conclusions. The most common causes affecting the level of SC are obesity, IR, and hypertension. In the patients whom we examined, the plasma level of SC was significantly higher in the main group than in the control group. This can be explained by disorders of the renal secretion of SC, which is probably due to an increase in tubular reabsorption of sodium, induced by insulin. In turn, hyperuricemia leads to the exhausting production of free radicals, to increase the level of TG and to accelerate the processes of LDL oxidation in the artery wall, which also contributes to the progression of atherosclerosis, fibrosis and HS.