Objective:Hypertension and dyslipidemia represent two of the most relevant modifiable cardiovascular risk factors and they often coexist. The aim of the research was to study lipid disorders and essential arterial hypertension (EAH) risk depending on AGTR1 (rs5186) and VDR (rs2228570) genes polymorphism.Design and method:100 subjects with EAH and target-organ damaging (2nd stage), moderate, high or very high cardiovascular risk were involved in the case-control study. Among them, 70,83% females and 29,17% males, mean age 57,86 ± 7,81y.o. Control group consisted of 60 practically healthy individuals of relevant age. The lipid panel parameters, such as: TC (Total cholesterol), TG (Triglycerides), LDL-C (Low-density lipoprotein cholesterol), HDL-C (High-density lipoprotein cholesterol) were investigated in blood plasma, using diagnostic kits “Accent 200” (Poland). The atherogenic index (IA) was calculated by the formula: (TC – HDL-C)/ HDL-C. Gene polymorphism of AGTR1 (rs5186) and VDR (rs2228570), was detected by polymerase chain reaction (PCR).Results:Decreased HDL-C is associated with 2nd and 3d degrees of EAH (p = 0,048). The risk of EAH increases in C-allele carriers of AGTR1 (rs5186) gene with hypercholesterolemia (TC> 5,0mmol/l) 1,5 times (OR–2,50;p = 0,048), with an increase in LDL-C and IA – 1,58 and 2,12 times (OR–10,80;p = 0,019), respectively. Homozygous carriers of the minor A-allele had extremely higher concentrations of TC, atherogenic LDL-C and IA, than GG-carriers – by 9,29%, 11,11% and 12,80% (pAA<0,05), respectively. Risk of EAH increases with hypertriglycerolemia 1,89 times (OR–2,93;p = 0,03) and with the increase in LDL-C – 1,26 times (OR–3,60;p = 0,038) in AA-genotype carriers of VDR (rs2228570) gene. Risk of EAH synergistically escalates almost twice in A-allele carriers of VDR (rs2228570) gene with a decrease of HDL-C (OR–2,88;p = 0,046) and the increase of IA (OR–2,70;p = 0,039), significantly only in AG-carriers though. ANOVA analysis confirmed the association of VDR (rs2228570) gene with the increase in IA (F = 3,80;p = 0,05).Conclusions: The EAH risk escalates with hypercholesterolemia, elevated both LDL-C and IA in C-allele carriers of AGTR1 (rs5186) gene, as well as with decreased HDL-C and increased IA in A-allele carriers VDR (rs2228570) in the observed.

Objective: The aim of this study was to establish the role of clinical complains and symptoms as risk factors for severe essential arterial hypertension (EAH) in patients with vitamin D deficiency. Design and method: 100 EAH patients with target-organ damage, moderate, high-very high cardiovascular risk were involved in the case-control study. 79.0% females and 21.0% males, mean age 59.87 ± 8.02. They were tested for total serum 25-hydroxyvitamin D concentration (immune luminescent test “MAGLUMI”, “SNIB”, China). All recruited patients were taken history, underwent complex examination and divided into groups depending on level of vitamin D and BP. Control group included 60 practically healthy persons of relevant age. Results: Hypertensive patients with vitamin D deficiency complained on heart pain 14.23% (⇙2 = 2.17; p>0.05), arrythmias – 20.86% (2 = 3.86; p = 0.049), headache – by 27.89% (⇙2 = 7.34; p = 0.007), sleep disturbance – by 29.77% (⇙2 = 7.97; p = 0.005), weakness and fatigue – by 20,59% (⇙2 = 3.88; p = 0.049) more frequent, than patients with normal 25-hydroxyvitamin D concentration. The frequency of patients with fatal cardiovascular risk SCORE >5.0 with vitamin D deficiency prevailed the ones with a normal level of vitamin D – by 20.94% (⇙2 = 3.98; p = 0.046). The risk for arrhythmias, weakness and fatigue increases 1.5 times [OR–2.36; 95% CI OR:1.0–5.61; p0.049 and OR–2.40; 95% CI OR:1.0-5.79; p = 0.049], sleep disturbance, headache and overweight increases 1.7-2.35 times [OR–3.43; 95% CI OR: 1.43-8.22; p = 0.005 and [OR–3.63; 95% CI OR:1.39-9.49; p = 0.007] and [OR–11.50; 95%CI OR:1.33-99.33; p = 0.038], respectively) in patients with 2nd-3d degree of BP elevation and vitamin D deficiency. The fatal cardiovascular risk SCORE >5.0 increases 1.5 times [OR–2.34; 95% CI OR:1.01-5.45; p = 0.046] in hypertensive patients with vitamin D deficiency. Conclusions: Vitamin D deficiency in patients with EAH is associated with severe clinical symptoms: the risk for arrhythmias increases 1.5 times [OR–2.36; p = 0.049], weakness risk increases 1.7 times [OR–2.40; p = 0.049], sleep disturbance risk elevates almost twice [OR–3.43; p = 0.005], risk for headache escalates 2.35 times [OR–3.63; p = 0.007], fatal cardiovascular risk SCORE >5.0 is 1.5 times high [OR–2.34; p = 0.046], respectively.

Objective: The aim of the study was to analyze metabolic and hormonal parameters changes in patients with essential arterial hypertension (EAH) depending on the vitamin D receptor gene (VDR, rs2228570) polymorphism. Design and method: The study involved 100 patients suffering from EAH with target-organ damaging, moderate, high or very high cardiovascular risk. Among them were 79.0% (79) women and 21.0% (21) men, an average age was 59.87±8.02 yo. The control group involved 60 practically healthy persons, matched by age and gender distribution. All enrolled/screened patients signed the Informed Consent to participate in the research. The VDR gene (rs2228570) polymorphism was studied by a real-time polymerase chain reaction (RT-PCR) method. The intact parathyroid hormone (intact PTH) and vitamin 25 (OH) D levels in blood serum were determined by chemiluminescence immunoassay (MAGLUMI). Results: The decreased level of vitamin 25 (OH) D (<30 ng/ml) was found more often in the A-allele carriers of the VDR gene (rs2228570), than in GG-genotype carriers: in the control group - by 36.84% (x2 = 10.32; p = 0.001), in study group - by 42.42% (x2 = 39.27; p<0.001). Hypocalcemia according to the level of ionized blood calcium (Ca2+ <1.12 mmol/l) was registered only in G-allele carriers, both among practically healthy and hypertensive patients. In the control group, GG-genotype carriers had a lower ionized Ca2+ blood level with a compensatory higher concentration of the intact PTH in comparison with A-allele carriers - by 3.42%, 25.19% and 16.03% (p<0.05), respectively. Secondary hyperparathyroidism due to a compensatory increasing of the intact PTH (>65 pg/ml) was found more often in the G-allele carriers of the VDR gene (rs2228570) than in AA-genotype carriers: in control group - by 55.55% (x2 = 11.11; p<0.001), and in the group of patients with EAH - by 62.5% (x2 = 12.5; p<0.001). Conclusions: The GG-genotype of the VDR gene (rs2228570) increases the risk of hypocalcemia by more than 6 times [OR = 6.25; 95% CI: 1.05-37.37; p = 0.046], with the lowest probability in carriers of the A-allele [OR = 0.16; 95% CI: 0.03-0.96].

Objective: To evaluate the role of the polymorphism of AGT genes (rs4762) and GNB3 genes (rs5443) in the development of the essential arterial hypertension separately and by combining their polymorphic variants. Design and method: The case-control study involved 100 patients with EAH stage II, 1-3 degrees of blood pressure (BP), high and very high cardiovascular risk. Among the patients there were 21% (21) men, 79% (79) women. The mean age of patients was 59.86±6.22y.o. The control group consisted of 60 almost healthy individuals, relevant in age (49.13±6.28y.o.) and gender distribution (63% - women, 37% - men). To study of polymorphism of AGT (rs4762) and GNB3 (rs5443) genes was performed a qualitative polymerase chain reaction (PCR) in real time. Results: The mutated T-allele of the AGT gene (rs4762) occurs in 15.97% of hypertensive residents of Northern Bukovyna, that is more frequent than in healthy individuals by 9.72% (p = 0.023); homozygous mutations of the AGT gene were not found in the control group at all. Whereas, the relative frequency of polymorphic variants of the GNB3 gene (rs5443, 825C>T) did not differ significantly between groups. The wild C-allele statistically significantly prevails over the mutated T-allele in both groups according to the AGT (rs4762) and GNB3 (rs5443) genes (p<0.001). Binary logistic regression confirmed an increase in the risk of hypertension inheritance according to dominant and additive models in minor T-allele carriers of the AGT gene (rs4762) almost 3 times higher than in C-allele homozygotes (p = 0.04 and p = 0.03). Inheritance of EAH is not associated with polymorphic variants of the GNB3 gene (rs5443). Conclusions: The T-allele of the AGT gene (rs4762) increases the risk of hypertension almost 3 times, whereas, polymorphic variants of the GNB3 gene (rs5443) are not predictors of EAH in the observed.

Objective: The aim of our study was to evaluate the role of AGT (rs4762) and GNB3 (rs5443) gene polymorphisms as risk factors for severe hypertension. Design and method: The case-control study involved 100 patients with EAH stage II, 1-3 degrees of blood pressure (BP), high and very high cardiovascular risk. Among the patients there were 21% (21) men, 79% (79) women. The mean age of patients was 59.86±6.22 y.o. The control group consisted of 60 almost healthy individuals with relevant age (49.13±6.28y.o.) and gender distribution (63% - women, 37% - men). The AGT (rs4762) gene polymorphism was studied by a qualitative polymerase chain reaction (PCR) in real time. Results: Severity of EAH does not depend on polymorphic variants of AGT (rs4762) and GNB3 (rs5443) genes. The distribution showed no statistically significant differences in the aforementioned distribution. Individuals with the first degree of hypertension met more often with the CC genotype of the GNB3 gene (rs5443) by 22.23% than among patients with the T allele (x2 = 3,66; p = 0,055) in patients with EAH. Conclusions: Epidemiological analysis did not confirm the polymorphic variants of the AGT (rs4762) and GNB3 (rs5443) genes as predictors of the severe course of EAH according to the degrees of BP elevation.