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ORIGINAL ARTICLE
Year : 2013  |  Volume : 1  |  Issue : 1  |  Page : 25-29

β 2 -adrenergic receptor gene polymorphisms in normal and in patients with myocardial infarction in the eastern province of Saudi Arabia


1 Department of Internal Medicine, King Fahd Hospital of the University, Al-Khobar, Kingdom of Saudi Arabia
2 Department of Pathology, King Fahd Hospital of the University, Al-Khobar, Kingdom of Saudi Arabia
3 College of Medicine, University of Dammam, Dammam, Kingdom of Saudi Arabia
4 King Fahd Hospital, Al-Ahssa, Kingdom of Saudi Arabia
5 King Fahd Military Medical Complex, Dammam, King Fahd Hospital of the University, Al-Khobar, Kingdom of Saudi Arabia
6 Utrecht Medical Complex, The Netherlands
7 Prince Mohammed Center for Research and Consultation Studies, University of Dammam, Dammam, Kingdom of Saudi Arabia

Correspondence Address:
Amein Al-Ali
College of Medicine, Prince Mohammed Center for Research and Consultation Studies, University of Dammam, P.O. Box 1982, Dammam 31441
Kingdom of Saudi Arabia
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DOI: 10.4103/1658-631X.112913

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Introduction: Single nucleotide polymorphisms (SNPs) of the β2 -adrenergic receptor (β2 -AR) gene have been implicated in the pathogenesis of cardiovascular diseases. This study evaluated two β2 -AR SNPs in association with myocardial infarction (MI), namely arginine-glycine (G16R) substitution at codon 16 and glutamine-glutamic (Q27E) substitution at condon 27. Objectives: Therefore, our main objective was to determine the association of these two SNPs among patients with MI with and without type 2 diabetes (T2D). Materials and Methods: Blood samples were collected from 201 MI patients with and without diabetes and from 115 controls and the β2 -AR gene polymorphisms at codon 16 and codon 27 were assessed by restriction fragment length polymorphism. The χ2 test was used to compare differences between groups. Results: The SNPs did not deviate significantly from Hardy-Weinberg equilibrium in the control population. The allele and genotype frequencies of the β2 -AR gene polymorphism at codon 16 (G16R) was significantly different between MI cases and controls (χ2 = 10.495, P < 0.05 and χ2 = 8.849, P < 0.05, respectively). No significant difference in genotype and allele frequencies at codon 27 was shown between these two groups (χ2 = 2.661, P ≥ 0.05 and χ2 = 1.587, P ≥ 0.05, respectively). When the MI patients with and without T2D were pooled together, genotype distribution was different between cases and controls at codon 16 (χ2 = 4.631, P = 0.099) and codon 27 (χ2 = 7.247, P = 0.027). However, no significant differences were found in allele frequencies for codon 16 and codon 27 between the two groups (χ2 = 0.628, P = 0.428; χ2 = 0.33, P = 0.565, respectively). Conclusion: Our findings indicate a moderate association of the β2 -AR G16R gene polymorphism with MI suggesting that this gene plays a universal role in the development of MI across ethnicities. However, there was no association of β2 -AR G16R gene polymorphism with diabetic patients with MI.


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