Журнал «Здоровье ребенка» 3 (54) 2014

Summary.  Progression of arterial hypertension (AH) and the development of complications, including atherosclerosis and thromboembolic (myocardial infarction, stroke), occurs under the influence of various aggressive factors that impact both directly and indirectly through the formation of endothelial dysfunction.

Objective – To set up the frequency and nature of the distribution of risk factors leading to complications in adolescents with arterial hypertension depending on body weight.

Materials and Methods. We examined 120 adolescents aged 13-18 with hypertension who were assigned to groups according to body mass index ( BMI). The first group included 43 teenagers with hypertension and normal weight ( BMI not greater than 85 ‰), the second - 25 young men with hypertension and overweight (BMI ranged from 85 to 97 ‰), and the third group - 52 teenagers with hypertension and obesity (BMI greater than 97 ‰). All adolescents studied have received blood pressure monitoring ( ABPM ) , cardiac ultrasound , Doppler-Echo test with endothelium-dependent vasodilatation and endothelium-independent vasodilatation. Determined levels of endothelin -I, inflammatory markers have been used (C-reactive protein , interleukin -6, TNF-α) and uric acid in the blood serum.

Results and Discussion. We found that the highest density of hypertension is present in adolescents with normal body weight. With increasing body weight of adolescents with hypertension, there is a rearrangement of myocardial involvement in the process of both left and right ventricles of the heart, the left atrium, with the development of myocardial hypertrophy . In reactive hyperemia in 40,9 % of adolescents with hypertension and normal weight, the gain of artery diameter was below 10% , in patients with hypertension and overweight – 48,6 %, and in groups with hypertension and obesity – 70, 0 %. In the trial-stimulated endothelium-independent vasodilatation for 47,7 % of adolescents with hypertension and normal body weight and 62,0 % of young men with hypertension in overweight and obesity, the increase of the diameter of the brachial artery did not reach the level of 20,0%. We found that the average of endothelin -I was significantly higher in young men with hypertension and obesity ( p <0,001), and in adolescents with normal and overweight, it has a tendency to increase ( p < 0,1), compared with the control group .Values ​​of Interleukina-6 and TNF-α in adolescents with hypertension in the presence of overweight and obesity were higher as compared with the control group, but did not reach the level of reliability and showed no significant difference depending on the body weight. C-reactive protein indicators in adolescents with hypertension increased significantly from the group with normal body weight from the group with excess weight and obesity (p <0,01, p < 0,001) , but the level of microalbuminuria was significantly higher in adolescents with hypertension and normal body weight . Asymptomatic hyperuricemia was found in 56.2 % of adolescents with hypertension in the group as a whole, with some prevailing in adolescents with hypertension and obesity (p < 0,1). Consequently, in adolescents with hypertension and overweight , but especially in those with hypertension and obesity, we found an increase in the level of the most powerful factor vasoconstriction of endothelin-1 , as well as systemic factors of subclinical inflammation ( C-reactive protein , TNF-α), and that determines the destabilization of endothelial function in this category of adolescents, promoting stabilization and progression of the disease.

Conclusions. In the group of adolescents with hypertension, with the growth of body mass index, there is the formation of endothelial dysfunction, maladaptive myocardial remodeling of the left and right ventricles of the heart, the left atrium, the development of hypertrophy (eccentric, concentric remodeling). These phenomena are accompanied by increased levels of endothelin-1, and factors of subclinical inflammation (C-reactive protein, iterleukina-6, TNF-α).