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Section 2. Medical science
https://doi.org/10.29013/ESR-21-11.12-9-12
Koval Sergiy Nikolayevich, Professor, MD, PhD, Head of Department of Arterial Hypertension and Prevention of Its Complications, Government Institution L. T. Malaya Therapy National Institute of the National Academy of Medical Sciences of Ukraine,
Kharkiv, Ukraine E-mail: sergekovalmd@gmail.com Mysnychenko Olga Vladislavovna, PhD, research fellow of Departmentof Hypertension and Prevention
of Its Complications, Government Institution L. T. Malaya Therapy National Institute of the National Academy of Medical Sciences of Ukraine, Kharkiv, Ukraine E-mail: olga.mysnichenko@mail.ru. Lytvynov Vadym Sergeevich, graduate student, Vasyl Karazin Khar^v National University,
Khar^v, Ukraine Lytvynova Olga Nikolaevna, MD, PhD, DSci, Professor of the Department of Clinical Laboratory Diagnostics, National University
of Pharmacy Khar^v, Ukraine E-mail: olgalitvinovamd@gmail.com
ASPECTS OF METABOLIC DISORDERS IN PATIENTS WITH ARTERIAL HYPERTENSION ON THE BACKGROUND OF ABDOMINAL OBESITY
Abstract. 107 patients with arterial hypertension aged 52 to 69 years (55 men and 52 women) were examined, among whom 57 patients had the disease and the abdominal obesity, and 50 patients had a normal body weight. It was found that in patients with arterial hypertension and obesity, there were a significant disturbance in lipid and carbohydrate metabolism, leptin synthesis, leptin resistance, insulin resistance was found in a significantly larger number of cases than in the group of patients with arterial hypertension and normal body weight. There was also a high incidence of target organ damage in patients with hypertension and abdominal obesity.
Keywords: arterial hypertension, abdominal obesity, leptin, lipid metabolism.
Introduction. Arterial hypertension (AH) has been one of the most common cardiovascular diseases for many decades [1; 2]. Most often, hypertension occurs against the background of various metabolic diseases and, above all, abdominal obesity (AO) [3; 4]. The prevalence of obesity among adults in Europe is 15-40%, and overweight reaches 60% [5]. Arterial hypertension and abdominal obesity are associated with a significantly increased risk of cardiovascular complications and mortality in patients with these diseases [2; 6; 7]. In case of hypertension with AO there is a marked increase in the frequency of prognostically unfavorable metabolic disorders (hyperlipidemia, insulin resistance, hyperuricemia), activation of subclinical inflammation, progression of endothelial dysfunction, leading to accelerated development of atherosclerosis, type 2 diabetes, and a significantly increased cardiovascular risk [2; 8; 9]. The study of the pathogenesis of AO in recent years has led to attention to the possible participation of leptin in the development of metabolic changes in hypertension [4]. The multifunctionality of leptin and the disturbance of its physiological action in abdominal obesity may be one of the leading factors in the disturbance of lipid metabolism and the development of obesity in such patients [10].
The aim of the study was to investigate some aspects of metabolism in patients with hypertension, which occurs on the background of abdominal obesity. The materials and methods. 107 patients aged 52 to 69 years (55 men and 52 women) were examined, among whom 57 patients had hypertension with AO (1 group), and 50 patients had hypertension without AO (group 2). Examination of patients was performed using clinical, laboratory and instrumental methods in the specialized Department of Hypertension and Kidney Diseases, Government Institution «L. T. Malaya Therapy National Institute of the National Academy of Medical Sciences of Ukraine» and in the therapeutic department
of the Kharkov Municipal Clinical Hospital № 2 named after Prof. A. A. Shalimov. Among the examined patients, grade 2 hypertension was detected in 52 (49%) persons, grade 3 - in 54 (51%) persons; abdominal obesity of the first degree was detected in 72 (67%) persons and II degree - in 35 (33%) persons. In the group of patients who were included in the study, burdened heredity of hypertension was found in 84 patients (78%). The control group consisted of 22 healthy individuals:13 men (59%) and 9 women (41%) aged 18 to 52 years. The study did not include patients with secondary hypertension, acute cardiovascular diseases, with diabetes mellitus, acute or chronic inflammatory processes, chronic kidney disease higher than stage II, clinically expressed liver, endocrine and blood diseases. Diagnosis of the grade and stage of hypertension was performed according to the recommendations of the Ukrainian Association of Cardiologists (2013) and the European Society of Hypertension and the European Society of Cardiology (2018) [9]. Analysis of the state of lipid metabolism was performed using the enzymatic method on the analyzer "Hu-mareazer 2106-1709" (Germany). Studies of carbohydrate metabolism, levels of urea, creatinine, uric acid in the blood were performed by determining their levels by enzymatic methods using the analyzer "Humareazer 2000" (Germany). Blood insulin levels were examined by enzyme-linked immunosorbent assay using standard DRG kits (Germany) on an empty stomach and after standard glucose loading (oral glucose tolerance test) and by calculating the IR index (HOMA index) [8]. Blood leptin levels were determined using DRG (USA) Leptin - ELISA kits, solid - phase enzyme - linked immunosorbent assay on a "Humareazer 2000" (Germany) analyzer.
Ethical declaration. The study was approved by local Ethical Committee (Government Institution "L. T. Malaya Therapy National Institute of the National Academy of Medical Sciences of Ukraine",
18.01.2018). All patients have g iven their voluntary informed consent to participate in the study.
The analysis of the obtained data was performed using statistical processing using the computer program SPSS19 for Windows and methods of descriptive statistics.
Results and Discussion. In the group of patients with hypertension and AO we found the following metabolic disorders: in 50 (88%) patients - dyslipo-proteinemia; in 20 patients (36%) - fasting hyperglycemia, in 50 (89%) - insulin resistance (IR) (HOMA index > 2.77) and in 15 (27%) patients - hyperuricemia. A probable increase in baseline heart rate in patients with hypertension and concomitant AO (86.7 ± 1.07 beats per minute) compared with the group of patients with hypertension without AO and the control group (75.8 ± 1.24 beats per minute, p < 0.05).The frequency of target lesions among the examined patients with hypertension and abdominal obesity was as follows: increase in pulse blood pressure (PBP) (PBP > 60 mm Hg) - in 21 (38%) patients, left ventricular hypertrophy - in 40 (73%)) patients, thickening of the intima-media complex and presence of atherosclerotic plaque in the common carotid arteries - in 20 (55%) patients, decrease in glomerular filtration rate to 45-59 ml/min/ 1.73 m2 (chronic kidney disease (CKD)- Stage III) in 11 (20%) patients.
Patients with hypertension and concomitant AO had higher insulin levels in the blood compared with patients with hypertension without AO - 19.9 ± 1.80 ^g IU / ml and 10.4 ± 1.15 ^m IU / ml, respectively (p < 0, 05).Comparative analysis showed a significantly higher (6.2 ng/ml (44.6%) higher) level of blood leptin in patients with hypertension and suppressed AO (13.9 ± 1.4 ng/ml) than in the control group (2.3 ± 0.6 ng/ml), p < 0.05. In patients with hypertension without AO, we also noted an increase in the level of blood leptin by 5.41 ng/ml (70.2%) compared with practically healthy individuals.
When analyzing leptin levels in the group of patients with hypertension and AO, depending on sex, we found a significant increase in blood leptin levels in
women (3.5 ± 0.7 ng/ml) compared with men (1.5 ± ± 0.2 ng/ml) by 57.1% (p < 0.05). Analysis of the results of a study of blood leptin levels separately in men with hypertension and suppressed AO, patients with hypertension without AO and practically healthy individuals in the control group revealed a statistically significant increase in the level of blood leptin in the group of patients with hypertension and suppressed AO, in comparison with patients with hypertension without AO (p < 0.05), on average, this difference was 7.2 ng / ml or 58.1%, as well as compared with practically healthy individuals in the control group (p < 0.001), on average, this difference was 10.7 ng/ml or 86.8%. In the group of men with AH without AO, the level of blood leptin was statistically significantly higher than that in practically healthy individuals of the control group (p < 0.01), and on average this difference was 3.7 ng /ml or 69.6%. It was also found that insulin resistance among patients with hypertension and AO was found in a statistically significantly greater number of cases (41.3% more often) than in the group of patients with hypertension without AO, p < 0.001. In the control group, the HOMA index did not exceed 3.0. Among the examined patients with hypertension and AO, insulin resistance was observed in 89% of cases. The highest rates of insulin resistance (53%) were found in the group of patients with AH without AO with a long history ofAH (more than 10 years). In patients with hypertension and AO with insulin resistance, the average level of blood leptin exceeded by 67.5% this indicator in patients without insulin resistance.
Conclusions. The data obtained in this work indicate that in patients with hypertension and abdominal obesity in comparison to patients with hypertension without abdominal obesity and almost healthy individuals of the control group a significant probable increase in baseline heart rate, hypercholester-olemia and insulin resistance was found. There was also a high incidence of target organ damage in pa-
tients with hypertension and abdominal obesity. The results obtained indicate significant disturbances of lipid and carbohydrate metabolism, leptin synthesis in patients with hypertension and abdominal obesity. Also, in this category of patients there is a resis-
tance to leptin, which is the reason for its increased level in blood. In patients with hypertension and AO in combination with insulin resistance, the average blood leptin level was significantly higher than this parameter in patients without insulin resistance.
References:
1. Cifkova R. Epidemiology of hypertension // In: Manual of hypertension of the European Society of Hypertension / edited by G. Mancia, G. Grassi and J. Redon. 2014.- P. 1-13.
2. 2018 ESC/ESH Guidelines for the management of arterial hypertension European Heart Journal,- 39, 2018.- P. 3021-3104. Doi:10.1093/eurheartj/ehy339.
3. Manual of hypertension of the European Society of Hypertension / edited by G. Mancia, G. Grassi and J. Redon. 2014.- 617 p.
4. Redon J., Martinez F., Fabia M. J. The metabolic syndrom in hypertension// In: Manual of hypertension of the European Society of Hypertension / edited by G. Mancia, G. Grassi and J. Redon. 2014.-P. 433-442.
5. Wilkinsonl J., Berghmans L., Imbert F. et al. Health indicators in the Europian regions-ISARE II // Eur. J. Public Health. 2008.- V. 18.- No. 2.- P. 178-183.
6. Chrostowska M. et al., Szyndler A., Wolf J., Narkiewicz. Obesity and sleep apnea //// In: Manual of hypertension of the European Society of Hypertension / edited by G. Mancia, G. Grassi and J. Redon. 2014.- P. 47-60.
7. Romero-Corral A., Somers V. K., Sierra-Johnson J. et al. Normal weigth obesity: a risk factor for cardio-metabolic dysregulation and cardiovascular mortality // Eur. Heart J.- V. 31. 2010.- P. 737-746.
8. Koval S., Snegurskaya I., Bozhko V., Myloslavsky D. Intercommunication between purine, carbohydrate metabolisms and processes of inflammation in patients with essential hypertension and metabolic syndrome. Journal of Hypertension. 2014.- 32(e-Suppl.1): 363.
9. Koval S. M. Efficacy of fixed dose triple combination of perindopril-indapamide-amlodipine in obese patients with moderate-to-severe arterial hypertension: open-label 6-month study / Koval S. M., Sni-hurska I. O., Lytvynova O. M. and etc. // Biomedical Research and Therapy.- Vol. 6.- No. 11. 2019.-P. 3501-3512.
10. Eckel R. H., Grundy S. M., Zimmet P. Z. The metabolic syndrome. The Lancet.- 365(9468). 2005.-P. 1415-1428.
