Two clinical cases of genetically determined restenosis of coronary arteries
S.D. MAYANSKAYA1, A.A. GILMANOV2, A.A. KODIROV2, A.YU. TEREGULOV2, M.M. MANGUSHEVA1, E.I. MUKHITOVA3
1Kazan State Medical University, Kazan
2Republican Clinical Hospital, Kazan
3City Clinical Hospital No. 7, Kazan
Contact details:
Mayanskaya S.D. — MD, Professor of the Department of Hospital Surgery
Address: 49 Butlerov St., Kazan, Russian Federation, 420012, tel.: +7-905-316-99-66, e-mail: Smayanskaya@mail.ru
The article presents two clinical cases with a severe, malignant course of coronary heart disease (CHD). In the first case, a patient had a chronic multivessel lesion of the coronary arteries and constant recurrence of occlusive stenosis both in the area of implanted stents and coronary artery bypass grafts. In the second case, three recurrences of atherothrombosis were observed within 1 month resulting in the development of repeated myocardial infarctions of the same localization. At the same time, both patients took all the necessary basic therapy, dual antiplatelet therapy and high doses of statins. Given this circumstance and the low level of platelet disaggregation, the patients underwent genotyping of thrombophilia factors. Mutations of the SERPINE1 (PAI-1) gene were identified, which controls the plasminogen activator inhibitor, as well as pathological genotypes of the platelet glycoprotein receptor ITGB3(PlA1/PlA2). In addition, the homozygous allele of another platelet glycoprotein ITGA2(Phe224Phe) was found in the 1st patient, and the fibrinogen beta chain FGB-455 was found in the 2nd patient. The article discusses the features of these pathological genotypes and their role in the progression of coronary artery disease.
Key words: coronary arteries, acute myocardial infarction, stent restenoses, pathological genotypes SERPINE1, ITGB3, ITGA2, FGB, thrombophilia.
REFERENCES
- Kukharchuk V.V., Ezhov M.V., Sergienko I.V. et al. Diagnosis and correction of lipid metabolism disorders for the prevention and treatment of atherosclerosis Russian recommendations, VII revision. Ateroskleroz i dislipidemii, 2020, vol. 38, no. 1, pp. 7–42 (in Russ.).
- Mayanskaya S.D., Garaeva L.A., Teplyakov A.T. et al. FGB, TNFα, IL-1β, LPL, ITGB3, and TGFB1 gene polymorphism features in patients with recurrent myocardial infarction. Byulleten’ sibirskoy meditsiny, 2020, vol. 19, no. 4, pp. 130–137 (in Russ.).
- Verdoia M., Cassetti E., Schaffer A. et al. Novara Atherosclerosis Study Group (NAS). Relationship Between Glycoprotein IIIa Platelet Receptor Gene Polymorphism and Coronary Artery Disease. Angiology, 2015, vol. 66 (1), pp. 79–85.
- Urano T., Suzuki Y., Iwaki T. et al. Recognition of plasminogen activator inhibitor type 1 as the primary regulator of fibrinolysis. Curr. Drug Targets, 2019, vol. 20, pp. 1695–1701.
- Divella R., Daniele A., Abbate I. et al. Circulating Levels of PAI-1 and SERPINE1 4G/4G Polymorphism Are Predictive of Poor Prognosis in HCC Patients Undergoing TACE. Translational Oncology, 2015, vol. 8, pp. 273–278.
- Van De Craen B., Declerck P.J., Gils A. The biochemistry, physiology and pathological roles of PAI-1 and the requirements for PAI-1 inhibition in vivo. Thromb Res, 2013, vol. 130 (4), pp. 576–585.
- Hendrix P., Foreman P.M., Harrigan M.R. et al. Association of Plasminogen Activator Inhibitor 1 (SERPINE1) Polymorphisms and Aneurysmal Subarachnoid Hemorrhage. World Neurosurgery, 2017, vol. 105, pp. 672–677.
- Koch W., Schrempf M., Erl A. et al. 4G/5G polymorphism and haplotypes of SERPINE1 in atherosclerotic diseases of coronary arteries. Thromb Haemost, 2010, vol. 103 (6), pp. 1170–1180.
- Kellici T.F., Pilka E.S., Bodkin M.J. Therapeutic Potential of Targeting Plasminogen Activator Inhibitor-1 in COVID-19. Trends in Pharmacological Sciences, 2021, vol. 42 (6), pp. 431–433
- Orfanos S., Husseini I. E.l, Nahass T. et al. Observational study of the use of recombinant tissue-type plasminogen activator in COVID-19 shows a decrease in physiological dead space. ERJ Open Res, 2020, vol. 6, pp. 00455–02020.


