Affiliation:
1. Republican Specialized Center of Cardiology
Abstract
Aim. To study influence of coronary heart disease (CHD) in family history on distribution of polymorphism apolipoprotein A1, В and E genes of the lipidtransport systems and major adverse cardiac events (MACE) in patients of Uzbek nationality with unstable angina (UA). Material and methods. There were examined 125 patients of Uzbek nationality with UA. I group (n=63) consisted of patients with burdened family history and II group (n=62) without family history. The control group consisted of 58 healthy persons. The G-A polymorphism of apolipoprotein A1 (APO A1) gene, -516C/T polymorphism of apolipoprotein В (APO B) gene and є2/є3/є4 polymorphism of apolipoprotein E (APO E) gene was determined using reagents Diatom TM DNA Prep 200 (production of LLC « IsoGen Laboratory») Results. In studying the distribution of «damaging» alleles of studied genes among the patients with UA in comparison with healthy persons, has been found a more prevalence of A allele carriers of the APO А1 (HR 3,63, 95% CI 1,638,04, P=0,002). The distribution of «damaging» alleles in comparative analysis of the II group with healthy persons did not differ significantly, whereas in I group had significantly greater accumulation of alleles: «А» G-А polymorphism of APO А1 gene (HR 5,99, 95% CI 2,52-14,24,P=0,001), «є4» polymorphism of APO E gene (HR 2,91, 95%, CI 1,12-7,62 P=0,044). At the same time there was no difference in the frequency of carriage «T» allele of -516C / T polymorphism of APO B gene. In patients with carriage of «damaging» alleles it was observed high frequency surgical revascularisations (HR 3,43, 95 %, CI 1,26-9,31, P=0,02) within one year. Conclusion. Presence of CHD in family history among patients of Uzbek nationality with UA is associated with the accumulation of «damaging» alleles: «А» (M1-) G-A polymorphism of APO A1, «є4» of APO E gene, and «D» I/D polymorphism of ACE gene. In patients with carriage of «damaging» alleles it was observed high frequency surgical revascularisations within one year.
Reference14 articles.
1. Van't Hooft, F. M., S. Jormsjo, B. Lundahl, P. Tornvall, P Eriksson, and A. Hamsten. A functional polymorphism in the apolipoprotein B promoter that influences the level of plasma low density lipoprotein. J. Lipid Res 1999; 40:1686-1694.
2. Zou Yangchun, Hu Dayi, Yang Xinchun et al. Relationships among apolipoprotein A1 gene polymorphisms, lipid levels and coronary atherosclerosis disease. Chinese Medical Journal 2003; 116:5:665-668.
3. Gerdes L.U., Jeune B., Ranberg K.A. et al. Estimation of apolipoprotein Egenotype specific relative mortality from the distribution of genotypes in centenarians and middle-aged men: Apolipoprotein E gene is a «frailty gene», not a «longevity gene» Genetic Epidemiol 2000;19:202-210.
4. Jeenah M., Kessling A, Miller N., Humphries SE. G to A substitution in the promoter region of the apolipoprotein AI gene is associated with elevated serum apolipoprotein AI and high density lipoprotein cholesterol concentrations. Mol Biol Med 1990;7:233-241.
5. Pagani F., Sidoli A., Giudici G.A. et al. Human apolipoprotein A-I gene promoter polymorphism: association with hyperalphalipoproteinemia. J Lipid Res 1990;31:1371-1377.