Preview

Rational Pharmacotherapy in Cardiology

Advanced search

Monitoring of Aspirin Therapy in Patients with Cerebrovascular Pathology

https://doi.org/10.20996/1819-6446-2021-08-15

Full Text:

Abstract

Aim. Evaluation of various methods for determining the effectiveness of aspirin therapy and aspirin resistance in patients with cerebrovascular disease (CVD) depending on the presence of type 2 diabetes mellitus (T2DM).

Materials and methods. The prospective study included 78 patients with various manifestations of CVD. All patients received acetylsalicylic acid (ASA) 75 mg daily. Along with a comprehensive clinical examination, a laboratory assessment of platelet function with the usage of Born method with aggregometer, a detailed biochemical blood test (including the determination of the small subunit of low density lipoprotein [s-LDL]), as well as therapeutic drug monitoring of salicylates were performed on a gas chromatograph-mass spectrometer.

Results. In 53% of cases, the absence or insufficiency of the effect of ASA on platelet aggregation was noted. Two subgroups were separately identified: with T2DM; (n=40) and without T2DM (n=38). Insufficient effect of the drug on platelet aggregation characteristics were observed in 65% of patients with T2DM and in 38% without T2DM. The differences were revealed between the groups in triglycerides, s-LDL, glycemic and glycated hemoglobin (p <0.05). In the group of patients with T2DM, the median ASA concentration was 0.01 [0; 0.32] μg/ml, and salicylic acid (SA)

– 0.20 [0; 0.39] μg/ml, while in patients without T2DM higher values were noted: ASA 0.29 [0.15; 0.55] μg/ml, SA – 0.33 [0.05; 0.73] μg/ml. A decrease in the concentration of ASA was associated with an increase in the level of ADP-induced platelet aggregation. There was an increase in the levels of ADPand adrenaline-induced platelet aggregation with a decrease in the concentration of ASA (p=0.004) and SA (p=0.006). Therapeutic drug monitoring revealed a more significant decrease in ASA level in T2DM than in the comparison group (p=0.025).

Conclusion. It is advisable to monitor aspirin therapy both with the assessment of platelet aggregation and with therapeutic drug monitoring. The relationship between the level of ASA and SA in the blood plasma and the functional activity of platelets was confirmed. The presence of T2DM is associated with a decrease in the concentration of ASA and aspirin resistance detected in therapeutic drug monitoring.

About the Authors

M. M. Tanashyan
Research Center of Neurology
Russian Federation

Marine M. Tanashyan

Moscow



A. A. Raskurazhev
Research Center of Neurology
Russian Federation

Anton A. Raskurazhev

Moscow



A. A. Kornilova
Research Center of Neurology
Russian Federation

Anastasia A. Kornilova

Moscow



A. A. Shabalina
Research Center of Neurology
Russian Federation

Alla A. Shabalina

Moscow



D. A. Abaimov
Research Center of Neurology
Russian Federation

Denis A. Abaimov

Moscow



A. V. Naminov
Research Center of Neurology
Russian Federation

Aleksandr V. Naminov

Moscow



References

1. World health statistics 2020: monitoring health for the SDGs, sustainable development goals. Geneva: World Health Organization; 2020.

2. de Havenon A, Meyer C, McNally JS, et al. Subclinical Cerebrovascular Disease: Epidemiology and Treatment. Curr Atheroscler Rep. 2019;21(10):39. DOI:10.1007/s11883-019-0799-1.

3. Godin O, Tzourio C, Maillard P, et al. Antihypertensive treatment and change in blood pressure are associated with the progression of white matter lesion volumes: the Three-City (3C)-Dijon Magnetic Resonance Imaging Study. Circulation. 2011;123(3):266-73. DOI:10.1161/CIRCULATIONAHA.110.961052.

4. de Havenon A, Majersik JJ, Tirschwell DL, McNally JS et al. Blood pressure, glycemic control, and white matter hyperintensity progression in type 2 diabetics. Neurology. 2019;92(11):e1168-75. DOI:10.1212/WNL.0000000000007093.

5. Suslina, ZA, Tanashyan, MM, Domashenko MA. Individual antiaggregant treatment of patients with cerebrovascular disorders. Clinical Pharmacology and Therapy. 2011;20(5):70-4 (In Russ.)

6. Zhao B, Wu Q, Wang L, et al. Pros and Cons of Aspirin for the Primary Prevention of Cardiovascular Events: A Secondary Study of Trial Sequential Analysis. Front Pharmacol. 2021;11:592116. DOI:10.3389/fphar.2020.592116.

7. Bowman L, Mafham M, Stevens W, et al.; ASCEND Study Collaborative Group. ASCEND: A Study of Cardiovascular Events in Diabetes: Characteristics of a randomized trial of aspirin and of omega-3 fatty acid supplementation in 15,480 people with diabetes. Am Heart J. 2018;198:135-44. DOI:10.1016/j.ahj.2017.12.006.

8. Tanashyan MM, Domashenko MA, Raskurazhev AA. Aspirin Resistance: Clinical and Molecular Genetic Evaluation Techniques. Human Physiology. 2017;43:904-9. DOI:10.1134/S0362119717080126.

9. Hankey GJ, Eikelboom JW. Aspirin resistance. Lancet. 2006;367(9510):606-17. DOI:10.1016/S01406736(06)68040-9.

10. Ionova VG, Suslina ZA, Demina EG. A method for studying the antiaggregatory action of drugs by determining platelet aggregation in vitro. Patent No. 2188419

11. Raskurazhev A.A., Khamidova Z.M., Shabalina A.A et al. Genetic markers of aspirin-sensitivity in patients with cerebrovascular disease. European Stroke Conference. 23rd Conference, Nice, France, May 6-9, 2014: Abstract e-Book. Verebrovasc Dis. 2014;37(Suppl. 1):1-2. DOI:10.1159/000362854.

12. Method for quantitative determination of salicylates in blood plasma. RF patent No. RU2622 996 dated 06.21.2017 [cited on 03.20.2021]. Available at: https://i.moscow/patents/RU2622996C1_20170621 (In Russ.).

13. Dedov II, Tkachuk VA, Gusev NB, et al. Type 2 diabetes and metabolic syndrome: identification of the molecular mechanisms, key signaling pathways and transcription factors aimed to reveal new therapeutical targets. Diabetes Mellitus. 2018;21(5):364-75 DOI:10.14341/DM9730.

14. Dugani S, Ames JM, Manson JE, et al. Weighing the Anti-Ischemic Benefits and Bleeding Risks from Aspirin Therapy: A Rational Approach. Curr Atheroscler Rep. 2018;20(3):15. DOI:10.1007/s11883018-0717-y.

15. Neergaard-Petersen S, Hvas AM, Grove EL, et al. The Influence of Haemoglobin A1c Levels on Platelet Aggregation and Platelet Turnover in Patients with Coronary Artery Disease Treated with Aspirin. PLoS One. 2015;10(7):e0132629. DOI:10.1371/journal.pone.0132629.

16. Miroshnichenko II. Rational dosing and monitoring of drugs. Moscow: Medical Information Agency; 2011 (In Russ.) .

17. Orme R, Judge HM, Storey RF. Monitoring Antiplatelet Therapy. Semin Thromb Hemost. 2017;43(3):311-9. DOI:10.1055/s-0036-1597298.

18. Born GV. Aggregation of blood platelets by adenosine diphosphate and its reversal. Nature. 1962;194:927-9. DOI:10.1038/194927b0.

19. Method for resistance to antiplatelet drugs determination in patients with progressive cerebral atherosclerosis. RF patent No. RU 2478965 C1, 10.04.2013. from 24.02.2012 [cited by Mar 20, 2021]. Available from: http://www.freepatent.ru/patents/2478965 (In Russ.).

20. Paven E, Dillinger JG, Bal DitSollier C, et al. Determinants of aspirin resistance in patients with type 2 diabetes. Diabetes Metab. 2020;46(5):370-6. DOI:10.1016/j.diabet.2019.11.002.

21. Winocour PD, Kinlough-Rathbone RL, Mustard JF. Platelet survival in rats with spontaneous diabetes mellitus. J Lab Clin Med. 1987;109(4):464-8. PMID: 3819581.

22. Antovic JP, Skeppholm M, Eintrei J, et al. Evaluation of coagulation assays versus LC-MS/MS for determinations of dabigatran concentrations in plasma. Eur J Clin Pharmacol. 2013;69(11):187581. DOI:10.1007/s00228-013-1550-4.


For citation:


Tanashyan M.M., Raskurazhev A.A., Kornilova A.A., Shabalina A.A., Abaimov D.A., Naminov A.V. Monitoring of Aspirin Therapy in Patients with Cerebrovascular Pathology. Rational Pharmacotherapy in Cardiology. 2021;17(4):537-543. (In Russ.) https://doi.org/10.20996/1819-6446-2021-08-15

Views: 278


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


ISSN 1819-6446 (Print)
ISSN 2225-3653 (Online)