Features of coronary artery disease in patients with different genotypes of PAI-1 gene

Cover Page


Cite item

Abstract

Aim. To investigate the relation of different genotypes and alleles of PAI-1 gene with the course of coronary artery disease.

Methods. We observed 80 patients with coronary artery disease (51 males and 29 females) aged 39 to 65 years living in the city of Baku. Genotyping of a polymorphic marker 4G(-675)5G was performed by means of polymerase chain reaction followed by restriction fragment length analysis. Genomic deoxyribonucleic acid (DNA) was extracted from venous blood leukocytes. To determine the frequency distribution of genotypes and alleles of PAI-1 in ischemic heart disease all patients were divided into 6 groups depending on the course of the disease and its outcomes.

Results. In the population of Baku genotype 44 of PAI-1 gene is significantly more common in people with coronary artery disease compared to individuals without coronary artery disease and is a risk factor for this disease. Genotype 55 of PAI-1 gene is more common in people without coronary artery disease and thus is a protective genotype against this disease. Allele 4 of PAI-1 was statistically more frequently recorded in patients with ischemic heart disease, and allele 5 was significantly more frequently observed in patients without this pathology. Therefore, allele 4 is a risk factor for the occurrence of coronary heart disease and allele 5 is protective against this disease. Alleles 5 and 4 are not associated with the course and outcomes of ischemic heart disease.

Conclusion. According to the results of the study on the population of Baku, genotype 44 of PAI-1 gene is a risk factor of ischemic heart disease, genotype 55 of PAI-1 gene is protective against this pathology, allele 4 is characteristic for people with coronary artery disease (a risk factor), allele 5 is characteristic for people without it (protective role) whereas the named genotypes of PAI-1 are not connected to the course and outcomes of this disease.

About the authors

A M Babaev

Scientific-Research Institute of Cardiology named after Dzh. Abdullayev

Email: sonaxanum@mail.ru
Baku, Azerbaijan

Dzh B Zul’fugarova

Scientific-Research Institute of Cardiology named after Dzh. Abdullayev

Author for correspondence.
Email: sonaxanum@mail.ru
Baku, Azerbaijan

References

  1. Баранов B.C., Хавинсон В.Х. Определение генетической предрасположенности к некоторым мультифакториальным заболеваниям. Генетический паспорт. СПб.: Фолиант. 2009; 48 с.
  2. Беленков Ю.Н. ИБС как основная причина сердечной недостаточности. Сердечн. недостат. 2001; 2 (5): 77-78.
  3. Iwai N., Shimoike H., Nakamura Y. et al. The 4G/5G polymorphism of the plasminogen activator inhibitor gene is associated with the time course of progression to acute coronary syndromes. Atherosclerosis. 1998; 136 (1): 109-114. doi: 10.1016/S0021-9150(97)00191-3.
  4. Iacoviello L., Burzotta F., Di Castelnuovo A. et al. The 4G/5G polymorphism of PAI-1 promoter gene as a risk factor for myocardial infarction: a meta-analysis. Tromb. Hemost. 1998; 80: 1029-1030.
  5. Eriksson P., Kallin B., van Hooft F.M. et al. Allele-specific increase in basal transcription of the plasminogenactivator inhibitor 1 gene is associated with myocardial infarction. Proc. Natl. Acad. Sci. USA. 1995; 92 (6): 1851-1855. doi: 10.1073/pnas.92.6.1851.
  6. Abboud N., Ghazouani L., Saidi S. et al. Association of PAI-1 4G/5G and -844G/A gene polymorphisms and changes in PAI-1/tissue plasminogen activator levels in myocardial infarction: a case-control study. Genet. Test Mol. Biomarkers. 2010; 14: 23-27. doi: 10.1089/gtmb.2009.0039.
  7. Ahmed W., Malik M., Saeed I. et al. Role of tissue plasminogen activator and plasminogen activator inhibitor polymorphism in myocardial infarction. Mol. Biol. Rep. 2011; 38: 2541-2548. doi: 10.1007/s11033-010-0392-8.
  8. Ashavaid T.F., Todur S.P., Kondkar A.A. et al. Platelet polymorphisms: frequency distribution and association with coronary artery disease in an Indian population. Platelets. 2011; 22: 85-91. doi: 10.3109/09537104.2010.522275.
  9. Cao X.L., Zhou Y., Yin L. et al. Reactive protein, plasminogen activator inhibitor type-1 (PAI-1) levels, PAI-1 promoter 4G/5G polymorphism and acute myocardial infarction. J. Geriatr. Cardiol. 2010; 7: 147-151.
  10. Isordia-Salas I., Leanos-Miranda A., Sainz I.M. et al. Association of the plasminogen activator inhibitor-1 gene 4G/5G polymorphism with ST elevation acute myocardial infarction in young patients. Rev. Esp. Cardiol. 2009; 62: 365-372. doi: 10.1016/S0300-8932(09)70893-0.
  11. Koch W., Schrempf M., Erl A. et al. 4G/5G polymorphism and haplotypes of SERPINE1 in atherosclerotic diseases of coronary arteries. Thromb. Haemost. 2010; 103: 1170-1180. doi: 10.1160/TH09-10-0702.
  12. Liang Z., Jiang W., Ouyang M., Yang K. PAI-1 4G/5G polymorphism and coronary artery disease risk: a meta-analysis. Int. J. Clin. Exp. Med. 2015; 8 (2): 2097-2107.
  13. Lima L.M., Carvalho M.D., Fonseca Neto C.P. et al. PAI-1 4G/5G polymorphism and plasma levels association in patients with coronary artery disease. Arq. Bras. Cardiol. 2011; 97: 462-389. doi: 10.1590/S0066-782X2011005000110.
  14. Onalan O., Balta G., Oto A. et al. Plasminogen activator inhibitor-1 4G4G genotype is associated with myocardial infarction but not with stable coronary artery disease. J. Thromb. Thrombolysis. 2008; 26: 211-217. doi: 10.1007/s11239-007-0083-z.
  15. Sarecka B., Zak I., Krauze J. Synergistic effects of the polymorphisms in the PAI-1 and IL-6 genes with smoking in determining their associated risk with coronary artery disease. Clin. Biochem. 2008; 41: 467-473. doi: 10.1016/j.clinbiochem.2008.01.028.
  16. Tassies D., Roque M., Monteagudo J. et al. Thrombin-activatable fibrinolysis inhibitor genetic polymorphisms as markers of the type of acute coronary syndrome. Thromb. Res. 2009; 24: 614-618. doi: 10.1016/j.thromres.2009.07.004.
  17. Var A., Utük O., Akçali S. et al. Impact of hemostatic gene single point mutations in patients with non-diabetic coronary artery disease. Mol. Biol. Rep. 2009; 36: 2235-2243. doi: 10.1007/s11033-008-9439-5.

© 2017 Babaev A.M., Zul’fugarova D.B.

Creative Commons License

This work is licensed
under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.





This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies