The study aim was to analyse the frequency of polymorphic variants of angiotensinogen gene polymorphism (AGT 704T>C, rs699) in essential arterial hypertension (EAH) patients. METHODS: Seventy-two individuals with EAH and hypertension-mediated organ damage (stage 2), moderate, high or very high cardiovascular risks were involved in the case-control study. Among them, 70.84 % (51) were females and 29.16 % (21) were males; mean age was 59.87±7.98 y. The control group consisted of fi fty practically healthy individuals at relevant age (49.13±6.28 y) and with relevant sex distribution (62 % were females, 38 % were males). AGT (704T>C) gene polymorphism was examined by RT-PCR. RESULTS: The distribution of genotypes in the study group was as follows: TT -14 %, TC -60 %, CC -26 %, which corresponded to the distribution in the control group -16 %, 54 % and 30 %, respectively, and did not deviate from the Hardy-Weinberg equilibrium. Smoking, type 2 diabetes mellitus (DM2) and obesity increased the relative risk of EAH in the examined population 2.5 times [OR=2.81; p=0.049], 3.75 times [OR=4.68; p=0.005] and almost twofold [OR=2.90; p=0.004], respectively. The probability of EAH increases fourfold with the angiotensin II elevation in the serum. Genotypes and alleles of the AGT (704T>C) gene were not signifi cant risk factors for EAH and DM2 in the studied population. However, the TC-genotype (lesser T-allele) increases the risk of obesity in EAH patients more than 1.5 times [OR=2.93; p=0.03]. In addition, the T-allele increases the risk for blood pressure (BP) to elevate up to grade 2-3 [OR=3.64; p < 0.001]. CONCLUSIONS: One-way ANOVA analysis confi rmed the AGT (704T>C) gene polymorphism to be associated with systolic and diastolic BP elevation (F=7.80; p < 0.001 and F=4.90; p=0.01, respectively), especially in TT-genotype carriers (p < 0.05), and with body mass index increase, albeit only in women (F=13.94; p < 0.001) (Tab. 4, Fig. 3, Ref. 26).
BACKGROUND: Cardiovascular (CV) diseases are the most spread cause of mortality in the world. Essential arterial hypertension (EAH), as a major risk factor for the development of CV diseases, is a multifactorial disease involving environmental and genetic factors together with risk-conferring behaviors. AIM: The purpose of this study was to analyze lipid metabolism changes in patients with EAH depending on the Vitamin D receptor (VDR rs2228570 (aka rs10735810)) and angiotensinogen (AGT rs699) genes polymorphism. MATERIALS AND METHODS: The single-stage study involved 100 patients suffering from Stage 2 EAH, 1–3 degrees of blood pressure increase, high and very high CV risks, 21% (21) men, and 79% (79) women. The average age of patients was 59.86 ± 6.22 years old. The control group included 60 practically healthy individuals of an appropriate age and sex distribution. To examine the VDR gene (rs10735810, rs2228570) and AGT gene (rs699) polymorphism, a qualitative real-time polymerase chain reaction was made. The lipid metabolism was studied by determining the blood plasma content of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TGs). RESULTS: Т allele of AGT gene is associated with reduced HDL-C level in men and increased TGs level in women. The EAH risk increases 4.5 times as much among the ТС-genotype carriers and lowered HDL-C level (odds ratio [OR] = 6.43; p = 0.01). The EAH risk increases as far as the HDL-C level reduction, irrespective of the VDR gene alleles condition 1.83 times (OR = 2.37; OR 95% confidence interval [CI]: 1.02–5.51; p = 0.04) and 1.9 times (OR=2.43; OR 95% CI: 0.99–5.97; p = 0.04). HDL-C reduction and LDL-C elevation in women increase the EAH risk 2.4 times (OR = 3.27; p = 0.01) and 1.24 times (OR = 3.67; p = 0.01), respectively. CONCLUSIONS: The EAH risk increases with a reduced HDL-C level in the TC genotype carriers of the AGT gene and irrespective of VDR gene polymorphic variants.
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 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.
Objective: Metabolic changes and obesity play important roles in arterial hypertension pathogenesis and progression. Whereas hepatic steatosis (HS) and AH have multiple common mechanisms of development involving metabolic and immune changes, the aim of study was to investigate the influence of Pro12Ala polymorphism of PPAR-↖2 gene and I/D polymorphism of ACE gene on metabolic profile and cytokines in obese patients with HS and AH. Design and method: Study involved 154 AH patients with HS (87 males, 67 females, age 50.06±7.34). Duration of HS 1-5 years, AH 3-21 years. Metabolic disorders were defined with body mass index (BMI), glycaemia, immunoreactive insulin (IRI), total cholesterol (TC), low and high density cholesterol (LDL-C, HDL-C), triglycerides (TG), C-peptide (CP) levels and HOMA-IR index. TNF- ↑ and leptin plasma levels were assessed by ELISA. Genes’ polymorphism of PPAR-↖2 (Pro12Ala), and ACE (I/D) alone or in combination was studied with PCR. Results: Differences of BMI, plasma glucose, IRI, HOMA-IR, CP and leptin are independent from ACE gene genotypes (p>.05). Pro-allele carriers of PPAR-↖2 gene have higher BMI than AlaAla carriers (32.7±2.1 and 27.9±1.1 kg/m2 vs 25.6±0.8 kg/m2, accordingly (p<.05), leptin level – 14.3±0.41 and 8.6±0.25 ng/ml vs 3.7±0.22 ng/ml, (p<.001), glucose level – to 10.2% and 10.9% accordingly (p<.05); CP level was higher in ProPro-genotype than in Ala-allele carriers to 15.7% (p<.05). Risk group of dyslipidemia are ProPro-genotype carriers of PPAR-↖2 gene with higher level of TC, TG and LDL-C to 16.4%, 17.3% and 27.9% (p<.05) and lower level of HDL-C in women to 25.6% (p = .038). Lipids levels are independent on ACE I/D polymorphism. Baseline TNF-↑ plasma levels did not significantly deviate between genotypes of PPAR-↖2 gene, but D-allele carriers (I/D+DD) of ACE gene had higher baseline TNF-↑ plasma levels (91.61 and 109.11 pg/ml, accordingly p<.01). Conclusions: In HS hypertensive patients metabolic disorders are clearly associated with PPAR-↖2 Pro-allele (carbohydrates) and ProPro-genotype (lipids). Presence of D-allele of ACE gene is associated with reliably higher level of TNF-↑ plasma levels.
Objective:Renin-angiotensin aldosterone system plays a major role in blood pressure regulation. Aldosterone, synthesized in the adrenal cortex by aldosterone synthase is encoded by the cytochrome 11B2 aldosterone synthase gene (CYP11B2). The aim of the study was to analyze the association of aldosterone synthase gene (CYP11B2) biallelic polymorphism (-344C/T) with Chronic Kidney Disease (CKD) in patients with essential arterial hypertension (EAH) in West-Ukrainian population.Design and method:One-hundred 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 79.0% (79) females and 21.0% (21) males, mean age 59.87 ± 8.02 yo; disease duration from 6 to 25 years. CKD was determined by the National Kidney Foundation recommendations (Kidney Disease: Improving Global Outcomes (KDIGO), 2012) after glomerular filtration rate (GFR) decline < 60 ml/min/1.73sq.m for over 3 months (by Cockroft-Gault formula and CKD-EPI for Cystatin-C and Creatinine serum levels depending on gender). CKD was diagnosed in 29 persons. All enrolled / screened patients signed the Informed Consent to participate in the research. Control group included 48 practically healthy persons of relevant age. Gene polymorphism of aldosterone synthase gene CYP11B2 (-344C/T) was examined by polymerase chain reaction (PCR).Results:The probability of EAH in observed population increased 1.49 times in T-allele carriers of CYP11B2 gene, but only in females [OR = 1.90; 95%CI:1.02–3.54; p = 0.029], with contrary decreasing in C-allele women (p = 0.041). No relevant dependences were observed in hypertensive males. Also T-allele increased probability of CKD (GFR< 60 ml/min/1,73m2) in hypertensive population 1.48 times [OR = 1.86; 95%CI:1.01–3.58; p = 0.049], especially in T-allele females 1.53 times [OR = 6.51; 95%CI:1.39–30.60; p = 0.007] with low CKD risk in T-allele males [OR = 0.15; 95%CI:0.03–0.72; p = 0.009], respectively. Some predictors like DM2, the 2nd and 3rd grades of Obesity, and the 3rd grade level of Blood Pressure elevation escalated the risk of CKD 2.4, 2.08–2.32 and 2.91 times, accordingly (p< 0.05).Conclusions:Aldosterone synthase gene CYP11B2 (-344C/T) is associated with EAH. T-allele increased risk of CKD in hypertensive population, especially in females.
Objective:The crucial function of endothelium’s regulatory mechanisms is to maintain the balance between Monoxide Nitrogen (NO) release and endothelium-derived contracting factors production. Therefore, it is prognostically important to clarify the endothelial function (EF) deterioration pathway through the early biomarkers of EF and carotid intima media thickness (IMT) changes depending on GNB3 (rs5443) and NOS3 (rs2070744) genes’ polymorphism in essential arterial hypertension (EAH).Design and method:One-hundred EAH patients with hypertensive-mediated organ damage (moderate-very high cardiovascular risks, aged 45–65 years) and 48 practically healthy (control) participated in the cohort case-control study. Soluble Vascular Cell Adhesion Molecule (sVCAM-1), total NO metabolites (NO2-/NO3-), transcriptional activity of NOS3 gene, Endothelium-Dependent Flow-Mediated Dilation of the Brachial Artery (FMD BA) and carotid IMT were studied. GNB3 (rs5443) and NOS3 (rs2070744) genotyping performed by TaqMan probes (CFx96ÔReal-Time PCR).Results:The connections of NOS3 (rs2070744) with decreased total NO metabolites (F = 71.11; p < 0.001), reduced NOS3 gene’s transcription activity (F = 8.71; p < 0.001) and sVCAM-1 increase (F = 6.96; p = 0.002) were found, especially in the C-allele carriers (particularly in CC-genotype patients with lower total NO metabolites value – by 16.46% and 40.88% (p < 0.001), lower transcription activity of NOS3 gene – 46.03% and 7 times (p < 0.001), higher sVCAM-1 – 35.48% and 89.48% (p < 0.001), respectively). ANOVA analysis didn’t confirm association of GNB3 (rs5443) gene with EF and carotid IMT. Severe EAH is associated with increased carotid IMT – 50.0% (p < 0.001) and 57.14% (p < 0.007), dilated carotid arteries – 17.36% (p = 0.012) and 21.79% (p = 0.004), decreased NOS3 gene’s transcription activity – 34.54% (p = 0.003). Severe structural carotid IMT changes in EAH patients (IMT > 0.9 mm) is followed by higher blood pressure values (p < 0.001), deterioration of EF: FMD BA decrease – 11.80% with compensatory increase of carotid arteries diameters – 17.38% and 21.99% (p < 0.001) and serum sVCAM-1 concentration – by 20.49% (p = 0.005).Conclusions:NOS3 (rs2070744), but not GNB3 (rs5443) gene associate with endothelial function impairment and carotid IMT in EAH patients.
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