Features of platelet hemostasis changes and antiplatlet treatment sensitivity in patients with stable forms of ischemic heart disease

Authors

DOI:

https://doi.org/10.15587/2519-4798.2017.116580

Keywords:

ischemic heart disease, angina, platelets aggregation, antiplatelet treatment, resistance to antiplatelet drugs

Abstract

Aim: To study and to estimate the aggregation activity of platelets in patients with stable forms of IHD, taking into account their sensitivity to the antiplatelet treatment and influence of ITGA2 polymorphism.

Materials and methods: there were examined 45 patients, who were on treatment in the Clinic “PheopHanya” (city Kyiv) and in Kyiv clinical hospital of railway transport № 2: 22 women and 23 men (mean age – 66,8±9,5 years). The study included patients with stable forms of IHD (stable effort angina of ІІ-ІІІ FC). All patients received the antiplatelet treatment with acetylsalicylic acid (48,9%), clopidrogel (37,8%) or their combination (13,3%).

The functional activity of platelets was studied on the laser aggregometer Biola Aggregation Analyser. The reaction to the antiplatelet treatment was confirmed using Aggredyne-test. C807T polymorphism of ITGA2 was determined by the method of polymerase chain reaction (PCR).

Based on the results of aggregation activity, sensitivity to the antiplatelet treatment, patients were distributed in two groups: І group – persons with the different degree of resistance to antiplatelet drugs (21 patients), ІІ group – sensitive to the treatment (24 persons). Polymorphism of ITGA2 and features of platelets functional activity depending on genotype were analyzed in each group.

Results: Among all inductors of aggregation, only the reaction to arachidonic acid (AA) was less than control values (by 12,7%, р<0,05). The degree of the spontaneous and adenosine dyphosphate (ADP)-induced aggregation didn’t differ from the norm, collagen-induced one was 1,21 times higher than the control. The quantity of patients, insufficiently sensitive to the treatment was 46,7 % (21persons), according to the data of Aggredyne-test, 24 persons had an adequate response to the treatment. At the analysis of ITGA2 polymorphism Т/Т genotype prevailed in patients “non-respondents”, in ‘respondents” - С/С genotype. Т-allele presence among respondents was 90,5% persons, so the probability of its influence on sensitivity to the antiplatelet treatment was rather high.

Conclusions: The decrease of sensitivity to antiplatelet drugs, connected with ITGA 2 polymorphism was observed in 46,7% of patients with stable IHD: resistance to the antiplatelet therapy is associated with Т/Т genotype of ITGA 2, presence of Т-allele in the genotype of patients-“non-respondents” was observed in 90,5% of persons, С/С genotype prevails at a positive response to the treatment

Author Biography

Ada Liakhotska, Bogomolets National Medical University T. Schevchenka blvd., 13, Kyiv, Ukraine, 01601

Postgraduate student

Department of propedeutic of internal medicine No. 1

References

  1. Mathers, C. D., Loncar, D. (2006). Projections of Global Mortality and Burden of Disease from 2002 to 2030. PLoS Medicine, 3 (11), e442. doi: 10.1371/journal.pmed.0030442
  2. Stable ischemic heart disease. Adapted clinical insight, based on evidence (2016). NICS named after M.M. Amosova NAMS of Ukraine.
  3. ESC guidelines on the management of stable coronary artery disease (2013). European Heart Journal, 34 (38), 2949–3003. doi: 10.1093/eurheartj/eht296
  4. Health indicators of population and use of health care resources in Ukraine 2016. Ministry of Health of Ukraine. SI "Center of medical statistics".
  5. The National Centers for Environmental Prediction (NCEP) recomendations (1994).
  6. Boden, W. E., O’Rourke, R. A., Teo, K. K., Hartigan, P. M., Maron, D. J., Kostuk, W. J. et. al. (2007). Optimal Medical Therapy with or without PCI for Stable Coronary Disease. New England Journal of Medicine, 356 (15), 1503–1516. doi: 10.1056/nejmoa070829
  7. Mischenko, O. Y. Anti-aggregate therapy of ischemic heart disease. Modern pharmacy. Available at: http://modern-pharmacy.com.ua/antiagregantna-terapiya-ishemichnoyi-hvorobi-sertsya
  8. Patrono, C. (2004). Expert Consensus Document on the Use of Antiplatelet Agents The Task Force on the Use of Antiplatelet Agents in Patients with Atherosclerotic Cardiovascular Disease of the European Society of Cardiology. European Heart Journal, 25 (2), 166–181. doi: 10.1016/j.ehj.2003.10.013
  9. Netyazhenko, V. Z. (2005). "Aspirin" as evidence of the effectiveness of the antiplatelet strategy in primary and secondary prevention of cardiovascular diseases. Heart and blood vessels, 3, 19–26.
  10. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE) (1996). The Lancet, 348 (9038), 1329–1339. doi: 10.1016/s0140-6736(96)09457-3
  11. Frére, C., Cuisset, T., Gaborit, B., Alessi, M.-C., Hulot, J.-S. (2009). The CYP2C19*17 allele is associated with better platelet response to clopidogrel in patients admitted for non-ST acute coronary syndrome. Journal of Thrombosis and Haemostasis, 7 (8), 1409–1411. doi: 10.1111/j.1538-7836.2009.03500.x
  12. Buryakina, T. A., Zateyshchikov, D. A. (2012). The use of reversible inhibitors of P2Y12 receptor in acute coronary syndrome. Kardiologiya, 52 (4), 74–79.
  13. Ovsyannikova, A. N., Mashin, V. V., Belova, L. A., Saenko, Y. V., Vasitsky, N. R., Abramova, V. V. (2014). Analysis of gene polymorphism at hemostasis system in the development of acute cerebral ischemia in patients of young and middle age. Modern problems of science and education, 5.
  14. Valgimigli, M., Bueno, H., Byrne, R. A., Collet, J.-P., Costa, F., Jeppsson, A. et. al. (2017). 2017 ESC focused update on dual antiplatelet therapy in coronary artery disease developed in collaboration with EACTS. European Heart Journal. doi: 10.1093/eurheartj/ehx419
  15. Neubauer, H., Kaiser, A. F., Endres, H. G., Krüger, J. C., Engelhardt, A., Lask, S. et. al. (2011). Tailored antiplatelet therapy can overcome clopidogrel and aspirin resistance – The BOchum CLopidogrel and Aspirin Plan (BOCLA-Plan) to improve antiplatelet therapy. BMC Medicine, 9 (1). doi: 10.1186/1741-7015-9-3
  16. Wurtz, M., Lerkevang Grove, E. (2012). Interindividual Variability in the Efficacy of Oral Antiplatelet Drugs: Definitions, Mechanisms and Clinical Importance. Current Pharmaceutical Design, 18 (33), 5344–5361. doi: 10.2174/138161212803251925
  17. Grinstein, J., Cannon, C. P. (2012). Aspirin Resistance: Current Status and Role of Tailored Therapy. Clinical Cardiology, 35 (11), 673–680. doi: 10.1002/clc.22031
  18. Watson, S. P., Auger, J. M., McCarty, O. J. T., Pearce, A. C. (2005). GPVI and integrin alphaIIbbeta3 signaling in platelets. Journal of Thrombosis and Haemostasis, 3 (8), 1752–1762. doi: 10.1111/j.1538-7836.2005.01429.x
  19. Stanton, A. (1999). Glantz Primer of biostatistics. Moscow: Praktika, 459.
  20. Karpenko, О. О. (2016). Pharmacogenetic testing for CYP2C19 gene polymorphism for optimization of using antiplatelet therapy in patients with ischemic heart disease. ScienceRise: Medical Science, 8 (4), 15–20. doi: 10.15587/2519-4798.2016.76377

Downloads

Published

2017-11-30

How to Cite

Liakhotska, A. (2017). Features of platelet hemostasis changes and antiplatlet treatment sensitivity in patients with stable forms of ischemic heart disease. ScienceRise: Medical Science, (11 (19), 31–36. https://doi.org/10.15587/2519-4798.2017.116580

Issue

No. 11 (19) (2017)

Section

Medical Science

License

Copyright (c) 2017 Ada Liakhotska

Creative Commons License

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

Our journal abides by the Creative Commons CC BY copyright rights and permissions for open access journals.

Authors, who are published in this journal, agree to the following conditions:

1. The authors reserve the right to authorship of the work and pass the first publication right of this work to the journal under the terms of a Creative Commons CC BY, which allows others to freely distribute the published research with the obligatory reference to the authors of the original work and the first publication of the work in this journal.

 2. The authors have the right to conclude separate supplement agreements that relate to non-exclusive work distribution in the form in which it has been published by the journal (for example, to upload the work to the online storage of the journal or publish it as part of a monograph), provided that the reference to the first publication of the work in this journal is included.