Contributions
Abstract: PB2508
Type: Publication Only
Background
Normal vascular system function is of highest importance in pregnancy. Endothelial dysfunction (ED) is an early nonspecific vascular trouble mark, leading eventually to various pathologies including thrombotic disorders. At present, technology of noninvasive quantitative ED evaluation by means of EndoPAT device is developed, that gives the value of Reactive Hyperemia Index (RHI).
Allelic polymorphisms of genes participating in vascular tone, lipid metabolism and thromboresistance regulation might influence ED development, predisposing progression of states involved in ED pathogenesis, e.g. arterial hypertension and dyslipidemia.
Aims
To evaluate genetic polymorphisms impact in ED development in pregnant women.
Methods
The study included 18 pregnant women with confirmed diagnosis of arterial hypertension, gestational or type II diabetes mellitus, and/or obesity. ED evaluation was performed with use of EndoPAT 2000 device, RHI value of ≤1,67 was considered as ED mark. Control group consisted of 200 healthy persons.
Molecular genetic typing was performed by PCR for following genetic polymorphisms: angiotensinogen (AGT) T704C, angiotensin-converting enzyme (ACE) Ins/Del, angiotensin II receptor type 1 (ATGR1) A1166C, G-protein β3 subunit (GNB3) C825T, apolipoprotein E (ApoE) E2/E3/E4 and endothelial NO-sinthase (eNOS) T786C.
STATISTICA 6.0 was used. Median (Me) and 95% confidence interval (CI) for RHI were calculated. Fisher exact test was used to assess the differencies in genotype frequencies. Odds ratios (OR) and their 95% CI were calculated.
Results
The patients had the following RHI values: Me 1,4, 95% CI 1,1-1,8, that confirms ED presence. Genotype frequencies in pregnant women with ED are represented in Table 1.
Table 1. Genotype frequencies in pregnant women with ED.
| Pregnants with ED,% (n=18) | Controls,% (n=200) | OR; 95%CI |
| Pregnants with ED,% (n=18) | Controls,% (n=200) | OR; 95%CI |
AGT 704 C/C | 38,9
| 25,5 | 1,9; 0,7-5,1 | Apo E3/E4 | 38,9* | 17,0 | 3,1; 1,1-8,6 |
AGT 704 T/C | 33,3 | 46,0 | 0,6; 0,2-1,6 | Apo E2/E4 | 5,6
| 1,0 | 5,8; 0,5-67,6 |
AGT 704 T/T | 27,8 | 28,5 | 1,0; 0,3-2,8 | Apo E3/E3 | 50,0 | 61,0 | 0,6; 0,2-1,7 |
ACE Del/Del | 50,0* | 26,5 | 2,8; 1,0-7,4 | Apo E2/E3 | 5,6 | 18,5 | 0,3; 0,03-2,0 |
ACE Ins/Del | 27,8 | 48,5 | 0,4; 0,1-1,2 | Apo E2/E2 | 0 | 0,5 | 0 |
ACE Ins/Ins | 22,2 | 25,0 | 0,9; 0,3-2,7 | Apo E4/E4 | 0 | 2,0 | 0 |
ATGR1 1166 C/C | 5,6 | 7,0 | 0,8; 0,1-6,3 | eNOS 786 C/C | 11,1 | 13,0 | 0,8; 0,2-3,9 |
ATGR1 1166 A/C | 38,9 | 37,0 | 1,1; 0,4-2,9 | eNOS 786 T/C | 27,8 | 47,0 | 0,4; 0,1-1,3 |
ATGR1 1166 A/A | 55,6 | 56,0 | 1,0; 0,4-2,6 | eNOS 786 T/T | 61,1 | 40.0 | 2,4; 0,9-6,3 |
GNB3 825 T/T | 11,1 | 11,0 | 1,0; 0,2-4,7 |
* significant difference, p<0,05. | |||
GNB3 825 C/T | 66,7 | 44,5 | 2,5; 0,9-6,9 | ||||
GNB3 825 C/C | 22,2 | 44,5 | 0,4; 0,1-1,1 | ||||
Conclusion
Pregnant women with ED had significantly higher ACE Del/Del and Apo E3/E4 genotypes frequencies, OR values indicate the direct correlation of these genotypes with ED development in pregnants. Unexpectedly homozygous and heterozygous eNOS 786 C allelle carriers as a tendency were found less frequently among pregnant women with ED, whereas eNOS 786 T/T genotype frequency had a tendency to be higher in pregnants with ED, showing invert correlation (not statistically significant) of eNOS 786 C allelle carriage with ED development in pregnancy.
Session topic: 35. Thrombosis and vascular biology & translational Research
Keyword(s): Endothelial dysfunction, Genetic polymorphism
Abstract: PB2508
Type: Publication Only
Background
Normal vascular system function is of highest importance in pregnancy. Endothelial dysfunction (ED) is an early nonspecific vascular trouble mark, leading eventually to various pathologies including thrombotic disorders. At present, technology of noninvasive quantitative ED evaluation by means of EndoPAT device is developed, that gives the value of Reactive Hyperemia Index (RHI).
Allelic polymorphisms of genes participating in vascular tone, lipid metabolism and thromboresistance regulation might influence ED development, predisposing progression of states involved in ED pathogenesis, e.g. arterial hypertension and dyslipidemia.
Aims
To evaluate genetic polymorphisms impact in ED development in pregnant women.
Methods
The study included 18 pregnant women with confirmed diagnosis of arterial hypertension, gestational or type II diabetes mellitus, and/or obesity. ED evaluation was performed with use of EndoPAT 2000 device, RHI value of ≤1,67 was considered as ED mark. Control group consisted of 200 healthy persons.
Molecular genetic typing was performed by PCR for following genetic polymorphisms: angiotensinogen (AGT) T704C, angiotensin-converting enzyme (ACE) Ins/Del, angiotensin II receptor type 1 (ATGR1) A1166C, G-protein β3 subunit (GNB3) C825T, apolipoprotein E (ApoE) E2/E3/E4 and endothelial NO-sinthase (eNOS) T786C.
STATISTICA 6.0 was used. Median (Me) and 95% confidence interval (CI) for RHI were calculated. Fisher exact test was used to assess the differencies in genotype frequencies. Odds ratios (OR) and their 95% CI were calculated.
Results
The patients had the following RHI values: Me 1,4, 95% CI 1,1-1,8, that confirms ED presence. Genotype frequencies in pregnant women with ED are represented in Table 1.
Table 1. Genotype frequencies in pregnant women with ED.
| Pregnants with ED,% (n=18) | Controls,% (n=200) | OR; 95%CI |
| Pregnants with ED,% (n=18) | Controls,% (n=200) | OR; 95%CI |
AGT 704 C/C | 38,9
| 25,5 | 1,9; 0,7-5,1 | Apo E3/E4 | 38,9* | 17,0 | 3,1; 1,1-8,6 |
AGT 704 T/C | 33,3 | 46,0 | 0,6; 0,2-1,6 | Apo E2/E4 | 5,6
| 1,0 | 5,8; 0,5-67,6 |
AGT 704 T/T | 27,8 | 28,5 | 1,0; 0,3-2,8 | Apo E3/E3 | 50,0 | 61,0 | 0,6; 0,2-1,7 |
ACE Del/Del | 50,0* | 26,5 | 2,8; 1,0-7,4 | Apo E2/E3 | 5,6 | 18,5 | 0,3; 0,03-2,0 |
ACE Ins/Del | 27,8 | 48,5 | 0,4; 0,1-1,2 | Apo E2/E2 | 0 | 0,5 | 0 |
ACE Ins/Ins | 22,2 | 25,0 | 0,9; 0,3-2,7 | Apo E4/E4 | 0 | 2,0 | 0 |
ATGR1 1166 C/C | 5,6 | 7,0 | 0,8; 0,1-6,3 | eNOS 786 C/C | 11,1 | 13,0 | 0,8; 0,2-3,9 |
ATGR1 1166 A/C | 38,9 | 37,0 | 1,1; 0,4-2,9 | eNOS 786 T/C | 27,8 | 47,0 | 0,4; 0,1-1,3 |
ATGR1 1166 A/A | 55,6 | 56,0 | 1,0; 0,4-2,6 | eNOS 786 T/T | 61,1 | 40.0 | 2,4; 0,9-6,3 |
GNB3 825 T/T | 11,1 | 11,0 | 1,0; 0,2-4,7 |
* significant difference, p<0,05. | |||
GNB3 825 C/T | 66,7 | 44,5 | 2,5; 0,9-6,9 | ||||
GNB3 825 C/C | 22,2 | 44,5 | 0,4; 0,1-1,1 | ||||
Conclusion
Pregnant women with ED had significantly higher ACE Del/Del and Apo E3/E4 genotypes frequencies, OR values indicate the direct correlation of these genotypes with ED development in pregnants. Unexpectedly homozygous and heterozygous eNOS 786 C allelle carriers as a tendency were found less frequently among pregnant women with ED, whereas eNOS 786 T/T genotype frequency had a tendency to be higher in pregnants with ED, showing invert correlation (not statistically significant) of eNOS 786 C allelle carriage with ED development in pregnancy.
Session topic: 35. Thrombosis and vascular biology & translational Research
Keyword(s): Endothelial dysfunction, Genetic polymorphism