Impact of smoking status on particular genetic polymorphisms associations with cardiovascular diseases
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Department of Internal Medicine, Medical University of Lublin, Poland
Grzegorz Dzida   

Department of Internal Medicine, Medical University of Lublin, Staszica 16, 20-081 Lublin, Poland.
J Pre Clin Clin Res. 2012;6(1):31–34
Genes encoding : angiotensin converting enzyme (ACE), platelet glycoprotein IIb/IIIa (GP IIb/IIIa) and endothelial nitric oxide synthase (eNOS) meet the criteria for a candidate gene for cardiovascular disease, including myocardial infarction(MI). Myocardial infarction results from an interplay of both genetic and environmental factors. Certain genetic polymorphisms seem to modify the deletorious impact of environmental factors, such as cigarette smoking, and could modify the inherited risk. The aim of the presented study was to assess the influence of cigarette smoking on the incidence of myocardial infarction in the presence of particular ACE, GPIIb/IIIa and eNOS genes polymorphic variants and genotypes.

Material and Methods:
166 individuals of Polish origin were genotyped, all of whom suffered from MI, or had survived it – 138 smokers and 28 non-smokers, all under 55 years of age. Polymorphisms were detected using PCR-RLFP method.

Genotypes including I allele of ACE gene I/D polymorphism (II and ID) occurred more frequently in smokers with MI compared to non-smokers (p=0.013). Similar findings were observed with T allele of the eNOS G894T polymorphism, and occurred more frequently among smokers when compared to non-smokers (p=0.039). The frequencies of A2 variant of the GPIIb/IIIa PL A1/A2 polymorphism were similar in smoking and non-smoking myocardial interaction patients.

Cigarette smoking seems to have an impact on the associations between myocardial infarction with ACE gene I/D and eNOS gene G894T polymorphisms, but no interaction was observed with GPIIb/IIIa gene PLA1/A2 plymorphism.

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