Association of beta-1 and beta-2 Adrenergic Receptor Gene Polymorphisms With Myocardial Infarction


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Yilmaz A., Kaya M. G. , Merdanoglu U., ERGÜN M. A. , Cengel A., Menevse S.

JOURNAL OF CLINICAL LABORATORY ANALYSIS, vol.23, no.4, pp.237-243, 2009 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 23 Issue: 4
  • Publication Date: 2009
  • Doi Number: 10.1002/jcla.20327
  • Title of Journal : JOURNAL OF CLINICAL LABORATORY ANALYSIS
  • Page Numbers: pp.237-243

Abstract

Both beta(1)- and beta(2)-adrenergic receptors (beta(1)- and beta(2)-AR) have important roles in heart function mainly in response to catecholamines. Some specific polymorphisms in the beta(1)- and beta(2)-AR genes, named ADRB1 and ADRB2, respectively, have been implicated in several cardiovascular and noncardiovascular phenotypes. In this study, we aimed to investigate the possible relationship between Ser49Gly and Arg389Gly polymorphisms of the ADRB1 and Arg16Gly and Gln27Glu polymorphisms of the ADRB2 gene with ST elevation myocardial infarction (MI) in a Turkish population. One hundred patients with ST elevation MI and 100 healthy control subjects were genotyped using the PCR-RFLP method. Although the Arg389 allele of the ADRB1 gene was associated with an elevated risk of MI, the Glu27 allele of the ADRB2 gene was associated with a decreased risk of MI. Carriers of the ADRB1 Arg389 allele (heterozygotes + homozygotes) had an approximately 3.5-fold increased risk for MI than Gly389 homozygotes (OR = 3.59, 95% Cl = 0.96-13.47, P = 0.045). For the ADRB2 Gln27GIu polymorphism, subjects having one or two copies of the Glu27 allele showed a decreased risk of MI compared with Gln27 homozygote subjects (OR = 0.48, 95% Cl = 0.24-0.94, P = 0.03). Haplotype analysis of these polymorphisms showed no significant differences between groups. These results suggest that the Arg389Gly and Gln27GIu polymorphisms may be associated with an altered risk of MI in this Turkish population. J. Clin. Lab. Anal. 23:237-243, 2009. (C) 2009 Wiley-Liss, Inc.