Keywords
acute myocardial infarction
marker gene polymorphism
systemic inflammation
How to Cite
Abstract
One of the important problems of modern medicine is the continuous increase of cardiovascular disease. An urgent problem at the present stage is the treatment of patients with acute forms of coronary heart disease, since vascular accidents are the leading causative factors of mortality from cardiovascular disease. Recently, an increasing number of studies have determined the role of genetic markers for predicting the adverse course of various cardiovascular diseases, including acute myocardial infarction. The distribution of genes markers of systemic inflammatory responses was determined in patients with STEMI. There are riteria for inclusion in the study: male and female patients from 46 to 75 years old; for postmenopausal women, more than 1 year; the presence of STEMI in the first 12 hours of the onset of the disease; informed consent of the patient to participate in the study. DNA was isolated from leukocytes from whole blood using the Express DNA Blood Kit (Litech). In the process of DNA extraction, the recommendations given in the kit instructions were followed. SNP polymorphisms of C-reactive protein genes were determined G-3014>A, tumor necrosis factor-α G-308>A, interleukin-10 G-1082>A by real-time polymerase chain reaction using a Rotor-Gene 6000 thermocycler (Corbett Research, Australia). The structure of the primers from the standard SNP-express-PB sets (Litech) was used. It was determined, that in patients with STEMI, an increase in the proportion of homozygotes (GG) and a decrease in heterozygotes (GA) of the genotypes of the G-3014>A polymorphism of the C-reactive protein gene are determined in comparison with the Hardy–Weinberg distribution. Polymorphism G-308>A of the tumor necrosis factor-α gene among patients with STEMI had a significant discrepancy with Hardy–Weinberg equilibrium, with an increase in the proportion of homozygotes (GG) and a decrease in heterozygotes (GA) and homozygotes (AA). The distribution of G-1082>A polymorphism of the interleukin-10 gene was characterized by an increase in the proportion of homozygotes (GG) and a decrease in heterozygotes (GA) in patients with STEMI compared to the Hardy–Weinberg distribution.
References
Alabas O.A., Jernberg T., Pujades-Rodriguez M., Rutherford M.J., West R.M., Hall M. et al. (2020). Statistics on mortality following acute myocardial infarction in 842,897 Europeans. Cardiovascular research, vol. 116 (1), pp. 149–157.
Diachuk D.D., Moroz H.Z., Hidzynska I.M., Lasytsia T.S. (2018). Poshyrenist faktoriv ryzyku sertsevo-sudynnykh zakhvoriuvan v Ukraini: suchasnyi pohliad na problemu [Prevalence of risk factors for cardiovascular diseases in Ukraine: a modern view of the problem]. Український кардіологічний журнал – Ukrainian Journal of Cardiology, № 1, pp. 91–101 [in Ukrainian].
Reed G.W., Rossi J.E., Cannon C.P. (2017). Acute myocardial infarction. The Lancet, vol. 389 (10065), pp. 197–210.
Ibanez B., James S., Agewall S., Antunes M.J., Bucciarelli-Ducci C., Bueno H. et al. (2018). 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). European Heart Journal, vol. 39 (2), pp. 119–177.
Rolla R., Lupi A., Bauce G., Appiani A., Portalupi M.R., Pergolini P. et al. (2018). Cardiovascular risk profile of patients hospitalized for myocardial infarction is undestimated by traditional risk factors and is fetter estimated by a genetic analysis based upon single nucleotide polymorphisms: A retrospective study. Journal of Clinical Cardiology and Diagnostics, vol. 1, issue 1, pp. 1–8.
Wang S., Dai Y.X., Chen L.L., Jiang T., Zheng M.Q., Li C.G. et al. (2015). Effect of IL-1β, IL-8, and IL-10 polymorphisms on the development of myocardial infarction. Genet. Mol. Res., vol. 14 (4), pp. 12016–12021.
Subirana I., Fitó M., Diaz O., Vila J., Francés A., Delpon E. et al. (2018). Prediction of coronary disease incidence by biomarkers of inflammation, oxidation, and metabolism. Scientific reports, vol. 8 (1), pp. 1–7.
Podolskaia A.A., Maikova Ye.V., Sharafetdinova L.M., Kravtsova O.A. (2014). Polimorfizm henov provospalitelnykh tsitokinov v assotsiatsii s riskom razvitiia ostroho infarkta miokarda [Genes polymorphism for proinflammatory cytokines in association with the risk of acute myocardial infarction]. Вестник современной клинической медицины – Bulletin of Modern Clinical Medicine, № 7 (2), pp. 147–150 [in Russian].
Thygesen K., Alpert J.S., Jaffe A.S., Simoons M.L., Chaitman B.R., White H.D. et al. (2012). Third universal definition of myocardial infarction. European Heart Journal, vol. 33 (20), pp. 2551–2567.
Thygesen K., Alpert J.S., Jaffe A.S., Chaitman B.R., Bax J.J., Morrow D.A. et al. (2019). Fourth universal definition of myocardial infarction (2018). European Heart Journal, vol. 40, issue 3, pp. 237–269.
Ianni M., Callegari S., Rizzo A., Pastori P., Moruzzi P., Corradi D. et al. (2012). Pro-inflammatory genetic profile and familiarity of acute myocardial infarction. Immunity & Ageing, vol. 9 (1), article number 14.
Biswas S., Ghoshal P.K., Mandal N. (2014). Synergistic effect of anti- and pro-inflammatory cytokine genes and their promoter polymorphism with ST-elevation of myocardial infarction. Gene, vol. 544 (2), pp. 145–151.
Blahodatskikh K.A., Nikitin A.H., Pushkov A.A., Blahodatskikh Ye.H., Osmolovskaia V.S., Aseicheva O.Yu. et al. (2011). Polimorfnyie markery G2667C, G3014A, C3872T, A5237G hena CRP i heneticheskaia predraspolozhennost k neblahopriiatnomu techeniiu ishemicheskoi bolezni serdtsa u bolnykh, perenesshykh obostreniie ishemicheskoi bolezni serdtsa [Polymorphic markers G2667C, G3014A, C3872T, A5237G of the CRP gene and genetic predisposition to an unfavorable course of coronary heart disease in patients with exacerbation of coronary heart disease]. Meditsinskaia henetika – Medical Henetics, vol. 10 (4), pp. 3–9 [in Russian].
Szabó G.V., Acsády G. (2011). Tumor necrosis-factor-α 308 GA polymorphism in atherosclerotic patients. Pathology & Oncology Research, vol. 17 (4), pp. 853–857.
Antonicelli R., Olivieri F., Cavallone L., Spazzafumo L., Bonafè M., Marchegiani F. et al. (2005). Tumor necrosis factor-alpha gene -308G>A polymorphism is associated with ST-elevation myocardial infarction and with high plasma levels of biochemical ischemia markers. Coronary Artery Disease, vol. 16 (8), pp. 489–493.
Chao L., Lei H., Fei J. (2014). A meta-analysis of interleukin-10-1082 promoter genetic polymorphism associated with atherosclerotic risk. Neurology India, vol. 62 (2), pp. 130–136.
Koch W., Tiroch K., von Beckerath N., Schömig A., Kastrati A. (2003). Tumor necrosis factor-α, lymphotoxin-α, and interleukin-10 gene polymorphisms and restenosis after coronary artery stenting. Cytokine, vol. 24 (4), pp. 161–171.
Monraats P.S., Kurreeman F.A., Pons D., Sewgobind V.D., de Vries F.R., Zwinderman A.H. et al. (2007). Interleukin 10: a new risk marker for the development of restenosis after percutaneous coronary intervention. Genes & Immunity, vol. 8 (1), pp. 44–50.