|
rs118204057
|
|
|
0.020 |
GeneticVariation |
BEFREE |
In the present study, the association of the heterozygous forms of low-density lipoprotein receptor gene mutations causing FH as well as of LPL gene mutations causing (P207L and G188E) or not causing (D9N and N291S) complete loss of LPL activity with angiographically assessed CAD was estimated in a cohort of 412 French Canadian men aged <60 years who consecutively underwent coronary angiography for the investigation of retrosternal pain.
|
9708657 |
1998 |
|
rs118204057
|
|
|
0.020 |
GeneticVariation |
BEFREE |
The LPL(Gly188-->Glu) and LPL(Asn291-->Ser) mutations may confer genetic susceptibility to premature CAD in a small number (approximately 2.4%) of patients; overall these four LPL alleles do not appear to contribute significantly to CAD risk in French Canadians.
|
9627528 |
1998 |
|
rs118204060
|
|
|
0.020 |
GeneticVariation |
BEFREE |
In the present study, the association of the heterozygous forms of low-density lipoprotein receptor gene mutations causing FH as well as of LPL gene mutations causing (P207L and G188E) or not causing (D9N and N291S) complete loss of LPL activity with angiographically assessed CAD was estimated in a cohort of 412 French Canadian men aged <60 years who consecutively underwent coronary angiography for the investigation of retrosternal pain.
|
9708657 |
1998 |
|
rs118204060
|
|
|
0.020 |
GeneticVariation |
BEFREE |
No CAD or control subjects were identified with the LPL(Pro207-->Leu) or LPL(Asp250-->Asn) alleles.
|
9627528 |
1998 |
|
rs118204068
|
|
|
0.010 |
GeneticVariation |
BEFREE |
No CAD or control subjects were identified with the LPL(Pro207-->Leu) or LPL(Asp250-->Asn) alleles.
|
9627528 |
1998 |
|
rs141383962
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Studies have been conducted to evaluate the possible "protective" role of PON, and especially the influence of the Arg-->Gln 192 polymorphism, in coronary artery disease.
|
9746266 |
1998 |
|
rs200353509
|
|
|
0.010 |
GeneticVariation |
BEFREE |
In the present study, the association of the heterozygous forms of low-density lipoprotein receptor gene mutations causing FH as well as of LPL gene mutations causing (P207L and G188E) or not causing (D9N and N291S) complete loss of LPL activity with angiographically assessed CAD was estimated in a cohort of 412 French Canadian men aged <60 years who consecutively underwent coronary angiography for the investigation of retrosternal pain.
|
9708657 |
1998 |
|
rs753248521
|
|
|
0.010 |
GeneticVariation |
BEFREE |
In the present study, the association of the heterozygous forms of low-density lipoprotein receptor gene mutations causing FH as well as of LPL gene mutations causing (P207L and G188E) or not causing (D9N and N291S) complete loss of LPL activity with angiographically assessed CAD was estimated in a cohort of 412 French Canadian men aged <60 years who consecutively underwent coronary angiography for the investigation of retrosternal pain.
|
9708657 |
1998 |
|
rs879254642
|
|
|
0.010 |
GeneticVariation |
BEFREE |
In the present study, the association of the heterozygous forms of low-density lipoprotein receptor gene mutations causing FH as well as of LPL gene mutations causing (P207L and G188E) or not causing (D9N and N291S) complete loss of LPL activity with angiographically assessed CAD was estimated in a cohort of 412 French Canadian men aged <60 years who consecutively underwent coronary angiography for the investigation of retrosternal pain.
|
9708657 |
1998 |
|
rs879254851
|
|
|
0.010 |
GeneticVariation |
BEFREE |
In the present study, the association of the heterozygous forms of low-density lipoprotein receptor gene mutations causing FH as well as of LPL gene mutations causing (P207L and G188E) or not causing (D9N and N291S) complete loss of LPL activity with angiographically assessed CAD was estimated in a cohort of 412 French Canadian men aged <60 years who consecutively underwent coronary angiography for the investigation of retrosternal pain.
|
9708657 |
1998 |
|
rs699
|
|
|
0.800 |
GeneticVariation |
BEFREE |
The significant relations observed between the AGT M235T variant, its protein product, and the cardiovascular disease phenotypes provide evidence for a possible role of elevated circulating AGT in the pathogenesis of coronary artery disease.
|
10097233 |
1999 |
|
rs699
|
|
|
0.800 |
GeneticVariation |
BEFREE |
These associations did not disappear when the analyses were corrected for multiple comparisons for other gene polymorphisms (ACE I/D gene variation, angiotensinogen T174M and M235T gene polymorphisms, AT1 receptor gene variation, phox C242T gene polymorphism, paraoxonase PON54 and PON191 gene variations) (2p = 0.01 in MLR for the presence of CAD; 2p = 0.039 in multiple regression for the extent of CAD).
|
10488959 |
1999 |
|
rs1217691063
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Homozygosity for the 677C-->T mutation of MTHFR is common and is associated with an increased risk of premature CAD in this population.
|
10595952 |
1999 |
|
rs1217691063
|
|
|
0.100 |
GeneticVariation |
BEFREE |
The homozygous C677T genotype has previously been associated with coronary heart disease in Ireland.
|
9974399 |
1999 |
|
rs1217691063
|
|
|
0.100 |
GeneticVariation |
BEFREE |
The present study extends previous observations by the finding that carriers of the N5,N10-methylenetetrahydrofolate reductase C677T TT genotype with various coronary high risk profiles had clearly higher coronary heart disease scores than individuals with at least one C677T C allele.
|
10337543 |
1999 |
|
rs1799983
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Homozygosity for a common NOS 3 polymorphism (894 G-->T) which encodes a Glu298-->Asp amino acid substitution in eNOS is a risk factor for angiographic CAD and recent MI in this population.
|
10510054 |
1999 |
|
rs1799983
|
|
|
0.100 |
GeneticVariation |
BEFREE |
A missense mutation of the nitric oxide synthase (eNOS) gene (Glu298Asp) in five patients with coronary artery disease--case reports.
|
10451235 |
1999 |
|
rs1799983
|
|
|
0.100 |
GeneticVariation |
BEFREE |
In conclusion, the eNOS Glu-298-->Asp mutation is common, occurring with an allele frequency of 32.5%, but is not associated with either the occurrence or severity of CAD in the Australian population or with other established coronary risk factors assessed in our study.
|
10475066 |
1999 |
|
rs268
|
|
|
0.090 |
GeneticVariation |
BEFREE |
This study, in a large cohort of CAD patients, has shown that PH-LPL activity is decreased (22%; P = 0.001) when compared to controls; that the D9N and N291S, and S447X LPL variants are genetic determinants, respectively, in CAD patients of low and high LPL PH-LPL activities; and that PH-LPL activity is strongly associated with changes in lipids and lipoproteins.
|
10191298 |
1999 |
|
rs268
|
|
|
0.090 |
GeneticVariation |
BEFREE |
Neither the Ser447Ter nor the Asn291Ser mutation had a major impact on susceptibility to CAD, progression or regression of CAD, clinical events rate or response to fluvastatin therapy in LCAS population.
|
10407505 |
1999 |
|
rs1805087
|
|
|
0.080 |
GeneticVariation |
BEFREE |
Methyltetrahydrofolate reductase (MTHFR) 677C-->T, cystathionine beta synthase (CBS) 68-bp insertion at exon 8, and methionine synthase (MS) 2756A-->G were typed in 685 Australian caucasian patients aged < or =65 years with and without angiographically documented coronary artery disease (CAD).
|
10487496 |
1999 |
|
rs1267969615
|
|
|
0.060 |
GeneticVariation |
BEFREE |
These associations did not disappear when the analyses were corrected for multiple comparisons for other gene polymorphisms (ACE I/D gene variation, angiotensinogen T174M and M235T gene polymorphisms, AT1 receptor gene variation, phox C242T gene polymorphism, paraoxonase PON54 and PON191 gene variations) (2p = 0.01 in MLR for the presence of CAD; 2p = 0.039 in multiple regression for the extent of CAD).
|
10488959 |
1999 |
|
rs4762
|
|
|
0.050 |
GeneticVariation |
BEFREE |
These associations did not disappear when the analyses were corrected for multiple comparisons for other gene polymorphisms (ACE I/D gene variation, angiotensinogen T174M and M235T gene polymorphisms, AT1 receptor gene variation, phox C242T gene polymorphism, paraoxonase PON54 and PON191 gene variations) (2p = 0.01 in MLR for the presence of CAD; 2p = 0.039 in multiple regression for the extent of CAD).
|
10488959 |
1999 |
|
rs142677199
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Our observations allow the assumption that the p22 phox A640G gene polymorphism is independently associated with the presence and extent of coronary artery disease.
|
10488959 |
1999 |
|
rs150629733
|
|
|
0.010 |
GeneticVariation |
BEFREE |
These associations did not disappear when the analyses were corrected for multiple comparisons for other gene polymorphisms (ACE I/D gene variation, angiotensinogen T174M and M235T gene polymorphisms, AT1 receptor gene variation, phox C242T gene polymorphism, paraoxonase PON54 and PON191 gene variations) (2p = 0.01 in MLR for the presence of CAD; 2p = 0.039 in multiple regression for the extent of CAD).
|
10488959 |
1999 |