Background. Beta2-adrenergic receptor (ADRB2) gene polymorphisms, Arg16Gly and Gln27Glu, have been implicated in the pathogenesis of cardiovascular diseases. The aim of this study was to determine the association of these two polymorphisms with the risk of myocardial infarction (MI) in the Egyptian population. Methods. Blood samples were collected from 68 MI patients and 75 healthy controls. They were assessed for the presence of cardiovascular risk factors and genotyped for the Arg16Gly (rs1042713) and Gln27Glu (rs1042714) polymorphisms using allelic-discrimination polymerase chain reaction. Results. There is no significant difference in genotype and allele frequencies at codon 16 between MI patients and controls (). However, at codon 27, MI risk was higher in Gln27 homozygous participants than in Glu27 carriers (). The haplotype frequency distribution showed significant difference among cases and controls (); homozygotes for Gly16/Gln27 haplotype were more susceptible to MI than Gly16/Glu27 carriers. Patients with Arg16/Gln27 haplotype had higher serum total cholesterol levels () and lower frequency of diabetes in MI patients (). However, both Glu27 genotypes and haplotype showed lower frequency of hypertension (). Conclusions. Our findings suggested that the ADRB2 gene polymorphisms may play an important role in susceptibility of MI among Egyptian population. 1. Introduction Myocardial infarction (MI) is a major cause of morbidity and mortality worldwide, accounting for up to 40% of all deaths [1, 2]. It is caused by myocardial cell death due to prolonged ischemia [3]. MI is a multifactorial, polygenic disorder driven by interactions of an individual’s genetic background and several environmental factors [4–7]. Greater understanding of MI etiology is mandatory to identify individuals at high risk and to improve prevention and therapy of this common and important condition. Cardiovascular risk factors, as smoking, obesity, hypertension, dyslipidemia, and diabetes, have long been known [8]. However these risk factors do not explain why some individuals are more susceptible to these environmental determinants in comparison to others with the same given risk factors. Several genomic association studies, family-based and twin studies, and linkage analysis provide insights into multiple susceptible genes underlying MI disease [9, 10]. The beta 2-adrenergic receptors (-AR), a member of the G-protein-coupled receptor superfamily, have attracted great attention due to their multiple physiological and health effects, particularly those involving cardiovascular
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