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The insertion/deletion variation in the alpha2B-adrenoceptor does not seem to modify the risk for acute myocardial infarction, but may modify the risk for hypertension in sib-pairs from families with type 2 diabetes

Snapir, Amir ; Scheinin, Mika ; Groop, Leif LU and Orho-Melander, Marju LU (2003) In Cardiovascular Diabetology 2.
Abstract
BACKGROUND: An insertion/deletion polymorphism in the alpha2B-adrenoceptor (AR) has been associated with the risk for acute myocardial infarction (AMI) and sudden cardiac death. In this study we tested whether this polymorphism is associated with the risk for AMI among members of families with type 2 diabetes. METHODS: 154 subjects with a history of AMI were matched for age and sex with one of their siblings who did not have a history of AMI. The prevalence of the genotypes of the alpha2B-AR insertion/deletion polymorphism was compared between the siblings using McNemar's test. We also explored the data to see whether this genetic variation affects the risk for hypertension by using logistic regression models in the two subpopulations of... (More)
BACKGROUND: An insertion/deletion polymorphism in the alpha2B-adrenoceptor (AR) has been associated with the risk for acute myocardial infarction (AMI) and sudden cardiac death. In this study we tested whether this polymorphism is associated with the risk for AMI among members of families with type 2 diabetes. METHODS: 154 subjects with a history of AMI were matched for age and sex with one of their siblings who did not have a history of AMI. The prevalence of the genotypes of the alpha2B-AR insertion/deletion polymorphism was compared between the siblings using McNemar's test. We also explored the data to see whether this genetic variation affects the risk for hypertension by using logistic regression models in the two subpopulations of subjects, with and without a history of AMI. RESULTS: Among all study subjects, 73 (24%) carried the alpha2B-AR deletion/deletion genotype, 103 (33%) carried the insertion/insertion genotype, and 132 (43%) were heterozygous. The distribution of genotypes of the alpha2B-AR insertion/deletion variation in the group of subjects with a history of AMI and their phenotype-discordant siblings did not statistically significantly differ from that expected by random distribution (p = 0.52): the deletion/deletion genotype was carried by 34 subjects with AMI (22%), and by 39 subjects without AMI (25%). Neither did we observe any significant difference in deletion allele frequencies of the alpha2B-AR insertion/deletion polymorphism between patients with a history of AMI (0.44) and their sib-pair controls (0.46, p = 0.65). In an exploratory analysis, the alpha2B-AR deletion/deletion genotype was associated with increased odds for hypertension compared with subjects carrying any of the other genotypes. CONCLUSIONS: The deletion/deletion genotype of the alpha2B-AR does not emerge in this study as a risk factor for AMI among members of families with type 2 diabetes; however, it might be involved in the development of hypertension. (Less)
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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Cardiovascular Diabetology
volume
2
article number
15
publisher
BioMed Central (BMC)
external identifiers
  • pmid:14633283
  • scopus:2942546503
ISSN
1475-2840
DOI
10.1186/1475-2840-2-15
language
English
LU publication?
yes
id
7ff64f52-1240-4dee-b995-05621b4d90f7 (old id 1127611)
date added to LUP
2016-04-01 16:33:58
date last changed
2024-01-11 10:28:48
@article{7ff64f52-1240-4dee-b995-05621b4d90f7,
  abstract     = {{BACKGROUND: An insertion/deletion polymorphism in the alpha2B-adrenoceptor (AR) has been associated with the risk for acute myocardial infarction (AMI) and sudden cardiac death. In this study we tested whether this polymorphism is associated with the risk for AMI among members of families with type 2 diabetes. METHODS: 154 subjects with a history of AMI were matched for age and sex with one of their siblings who did not have a history of AMI. The prevalence of the genotypes of the alpha2B-AR insertion/deletion polymorphism was compared between the siblings using McNemar's test. We also explored the data to see whether this genetic variation affects the risk for hypertension by using logistic regression models in the two subpopulations of subjects, with and without a history of AMI. RESULTS: Among all study subjects, 73 (24%) carried the alpha2B-AR deletion/deletion genotype, 103 (33%) carried the insertion/insertion genotype, and 132 (43%) were heterozygous. The distribution of genotypes of the alpha2B-AR insertion/deletion variation in the group of subjects with a history of AMI and their phenotype-discordant siblings did not statistically significantly differ from that expected by random distribution (p = 0.52): the deletion/deletion genotype was carried by 34 subjects with AMI (22%), and by 39 subjects without AMI (25%). Neither did we observe any significant difference in deletion allele frequencies of the alpha2B-AR insertion/deletion polymorphism between patients with a history of AMI (0.44) and their sib-pair controls (0.46, p = 0.65). In an exploratory analysis, the alpha2B-AR deletion/deletion genotype was associated with increased odds for hypertension compared with subjects carrying any of the other genotypes. CONCLUSIONS: The deletion/deletion genotype of the alpha2B-AR does not emerge in this study as a risk factor for AMI among members of families with type 2 diabetes; however, it might be involved in the development of hypertension.}},
  author       = {{Snapir, Amir and Scheinin, Mika and Groop, Leif and Orho-Melander, Marju}},
  issn         = {{1475-2840}},
  language     = {{eng}},
  publisher    = {{BioMed Central (BMC)}},
  series       = {{Cardiovascular Diabetology}},
  title        = {{The insertion/deletion variation in the alpha2B-adrenoceptor does not seem to modify the risk for acute myocardial infarction, but may modify the risk for hypertension in sib-pairs from families with type 2 diabetes}},
  url          = {{http://dx.doi.org/10.1186/1475-2840-2-15}},
  doi          = {{10.1186/1475-2840-2-15}},
  volume       = {{2}},
  year         = {{2003}},
}