Synergistic effects of angiotensin-converting enzyme and angiotensin-II type 1 receptor gene polymorphisms on risk of myocardial infarction

Détails

ID Serval
serval:BIB_1EBEECCE15AB
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Synergistic effects of angiotensin-converting enzyme and angiotensin-II type 1 receptor gene polymorphisms on risk of myocardial infarction
Périodique
Lancet (london, England)
Auteur⸱e⸱s
Tiret L., Bonnardeaux A., Poirier O., Ricard S., Marques-Vidal P., Evans A., Arveiler D., Luc G., Kee F., Ducimetière P.
Collaborateur⸱rice⸱s
[et al.]
ISSN
0140-6736 (Print)
ISSN-L
0140-6736
Statut éditorial
Publié
Date de publication
1994
Peer-reviewed
Oui
Volume
344
Numéro
8927
Pages
910-913
Langue
anglais
Notes
Publication types: Journal Article ; Multicenter Study ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
We reported from our previous multicentre case-control study that the deletion (D) polymorphism of the gene encoding angiotensin-converting enzyme (ACE) was associated with increased risk of myocardial infarction. The main function of ACE is to convert angiotensin I into angiotensin II, which exerts its known cellular actions through the angiotensin II AT1 receptor subtype (AGT1R). We have now investigated the role of a common polymorphism of the AT1 receptor gene (an A-->C transversion at position 1166 of AGT1R) and looked for an interaction between ACE and AGT1R gene polymorphisms on the risk of myocardial infarction. We analysed DNA from 613 patients with myocardial infarction and 723 age-matched population controls. We found a significant interaction between ACE and AGT1R gene polymorphisms; the odds ratio for myocardial infarction associated with the ACE DD genotype was 1.05 (95% CI 0.75-1.49) for subjects without the AGT1R C allele, 1.52 (1.06-2.18) in AC heterozygotes, and 3.95 (1.26-12.4) in CC homozygotes (test for trend, p < 0.02). Among patients defined as low risk by traditional risk factors (serum apolipoprotein B < 1.25 g/L, body-mass index < 26 kg/m2) the interaction was even stronger (odds ratios 1.64 [0.68-3.92], 7.03 [2.61-19.0], and 13.3 [p = 0.05], respectively). These findings, if confirmed, could have clinical implications for the prevention and treatment of coronary heart disease.
Mots-clé
Myocardial Infarction/genetics, Peptidyl-Dipeptidase A/genetics, Receptors, Angiotensin/genetics
Pubmed
Web of science
Création de la notice
01/12/2016 16:02
Dernière modification de la notice
20/08/2019 13:54
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