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LIPID DISORDERS AND ESSENTIAL ARTERIAL HYPERTENSION RISK DEPENDING ON AGTR1 (RS5186) AND VDR (RS2228570) GENES POLYMORPHISM
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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.
Ovid Technologies (Wolters Kluwer Health)
Title: LIPID DISORDERS AND ESSENTIAL ARTERIAL HYPERTENSION RISK DEPENDING ON AGTR1 (RS5186) AND VDR (RS2228570) GENES POLYMORPHISM
Description:
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.
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