Статья
Перспективы применения комбинации периндоприла и амлодипина у пациентов с артериальной гипертензией и/или ишемической болезнью сердца и COVID-19: фокус на эндотелий
Вспышка пандемии новой коронавирусной инфекции (COVID-19) представляет собой продолжающуюся чрезвычайную ситуацию в области здравоохранения, вызвавшую беспрецедентную заболеваемость и смертность. COVID-19 — это заболевание, вызываемое SARS-CoV-2, вирусом, поражающим не только легкие, но и сердечно-сосудистую систему. Серьезным теоретическим обоснованием мультисистемного эффекта COVID-19 считается наличие тесной взаимосвязи между ним и эндотелиальной дисфункцией, которая, согласно консенсусу экспертов, признана решающей для патогенеза и тяжести заболевания. Учитывая, что эндотелиальная дисфункция рассматривается в качестве основного патофизиологического процесса при тяжелом и/или длительном течении COVID-19 и, вероятно, является общим знаменателем множества клинических аспектов тяжёлого течения заболевания, в настоящем обзоре представлены научные данные о влиянии периндоприла и амлодипина у пациентов с артериальной гипертензией и/или ишемической болезнью сердца и COVID-19 на функцию эндотелия.
1. Kabanova A, Gavriilaki E, Pelzer BW, et al. Effect of the COVID-19 pandemic on laboratory and clinical research: a testimony and a call to action from researchers. Hemasphere. 2020;4:e499. doi:10.1097/hs9.0000000000000499.
2. Phillips S, Williams MA. Confronting our next national health disaster — long-haul covid. N Engl J Med. 2021;385:577-9. doi:10.1056/nejmp2109285.
3. Gavriilaki E, Asteris PG, Touloumenidou T, et al. Genetic justification of severe COVID-19 using a rigorous algorithm. Clin Immunol. 2021;226:108726. doi:10.1016/j.clim.2021.108726.
4. Evans PC, Rainger GE, Mason JC, et al. Endothelial dysfunction in COVID-19: a position paper of the ESC Working Group for Atherosclerosis and Vascular Biology, and the ESC Council of Basic Cardiovascular Science. Cardiovasc Res. 2020;116(14):2177-84. doi:10.1093/cvr/cvaa230.
5. Prasad A, Prasad M. Single Virus Targeting Multiple Organs: What We Know and Where We Are Heading? Front Med (Lausanne). 2020;7:370. doi:10.3389/fmed.2020.00370.
6. Andrianto, Al-Farabi MJ, Nugraha RA, et al. Biomarkers of endothelial dysfunction and outcomes in coronavirus disease 2019 (COVID-19) patients: A systematic review and meta-analysis. Microvasc Res. 2021;138:104224. doi:10.1016/j.mvr.2021.104224.
7. Perico L, Benigni A, Casiraghi F, et al. Immunity, endothelial injury and complementinduced coagulopathy in COVID-19. Nat Rev Nephrol. 2021;17(1):46-64. doi:10.1038/s41581-020-00357-4.
8. Leisman DE, Ronner L, Pinotti R, et al. Cytokine elevation in severe and critical COVID-19: a rapid systematic review, meta-analysis, and comparison with other inflammatory syndromes. Lancet Respir Med. 2020;8(12):1233-44. doi:10.1016/S2213-2600(20)30404-5.
9. Libby P, Lüscher T. COVID-19 is, in the end, an endothelial disease. Eur Heart J. 2020;41(32):3038-44. doi:10.1093/eurheartj/ehaa623.
10. Huertas A, Montani D, Savale L, et al. Endothelial cell dysfunction: a major player in SARS-CoV-2 infection (COVID-19)? Eur Respir J. 2020;56(1):2001634. doi:10.1183/13993003.01634-2020.
11. Nägele MP, Haubner B, Tanner FC, et al. Endothelial dysfunction in COVID-19: Current findings and therapeutic implications. Atherosclerosis. 2020;314:58-62. doi:10.1016/j.atherosclerosis.2020.10.014.
12. Varga Z, Flammer AJ, Steiger P, et al. Endothelial cell infection and endotheliitis in COVID19. Lancet. 2020;395:1417-8. doi:10.1016/s0140-6736(20)30937-5.
13. Ackermann M, Verleden SE, Kuehnel M, et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N Engl J Med. 2020;383(2):120-8. doi:10.1056/NEJMoa2015432.
14. O’Sullivan JM, Gonagle DM, Ward SE, et al. Endothelial cells orchestrate COVID-19 coagulopathy. Lancet Haematol. 2020;7(8):e553-e555. doi:10.1016/S2352-3026(20)30215-5.
15. Guervilly C, Burtey S, Sabatier F, et al. Circulating Endothelial Cells as a Marker of Endothelial Injury in Severe COVID-19. J Infect Dis. 2020;222(11):1789-93. doi:10.1093/infdis/jiaa528.
16. Chioh FW, Fong SW, Young BE, et al. Convalescent COVID-19 patients are susceptible to endothelial dysfunction due to persistent immune activation. Elife. 2021;10:e64909. doi:10.7554/eLife.64909.
17. Escher R, Breakey N, Lämmle B. Severe COVID-19 infection associated with endothelial activation. Thromb Res. 2020;190:62. doi:10.1016/j.thromres.2020.04.014.
18. Neri T, Nieri D, Celi A. P-selectin blockade in COVID-19-related ARDS. Am J Physiol Lung Cell Mol Physiol. 2020;318(6):L1237-L1238. doi:10.1152/ajplung.00202.2020.
19. Smadja DM, Guerin CL, Chocron R, et al. Angiopoietin-2 as a marker of endothelial activation is a good predictor factor for intensive care unit admission of COVID-19 patients. Angiogenesis. 2020;23(4):611-20. doi:10.1007/s10456-020-09730-0.
20. Spadaro S, Fogagnolo A, Campo G, et al. Markers of endothelial and epithelial pulmonary injury in mechanically ventilated COVID-19 ICU patients. Crit Care. 2021;25(1):74. doi:10.1186/s13054-021-03499-4.
21. Mejia-Renteria H, Travieso A, Sagir A, et al. In vivo evidence of systemic endothelial vascular dysfunction in COVID-19. Int J Cardiol. 2021;345:153-5. doi:10.1016/j.ijcard.2021.10.140.
22. Xu Q, Samanapally H, Nathala P, et al. Outcomes and Risk Factors for Cardiovascular Events in Hospitalized COVID-19 Patients. J Cardiothorac Vasc Anesth. 2021;35(12):3581- 93. doi:10.1053/j.jvca.2021.03.035.
23. Kaye AD, Okeagu CN, Tortorich G, et al. COVID-19 impact on the renal system: Pathophysiology and clinical outcomes. Best Pract Res Clin Anaesthesiol. 2021;35(3):449- 59. doi:10.1016/j.bpa.2021.02.004.
24. Levi M, Thachil J, Iba T, et al. Coagulation abnormalities and thrombosis in patients with COVID. Lancet Haematol. 2020;7(6):e438-e440. doi:10.1016/S2352-3026(20)30145-9.
25. Alexander Y, Osto E, Schmidt-Trucksäss A, et al. Endothelial function in cardiovascular medicine: a consensus paper of the European Society of Cardiology Working Groups on Atherosclerosis and Vascular Biology, Aorta and Peripheral Vascular Diseases, Coronary Pathophysiology and Microcirculation, and Thrombosis. Cardiovasc Res. 2021;117(1):29- 42. doi:10.1093/cvr/cvaa085.
26. Schölkens BA, Landgraf W. ACE inhibition and atherogenesis. Can J Physiol Pharmacol. 2002;80(4):354-9. doi:10.1139/y02-038.
27. Cangiano E, Marchesini J, Campo G, et al. ACE inhibition modulates endothelial apoptosis and renewal via endothelial progenitor cells in patients with acute coronary syndromes. Am J Cardiovasc Drugs. 2011;11(3):189-98. doi:10.2165/11589400-000000000-00000.
28. Ceconi C, Francolini G, Bastianon D, et al. Differences in the effect of angiotensinconverting enzyme inhibitors on the rate of endothelial cell apoptosis: in vitro and in vivo studies. Cardiovasc Drugs Ther. 2007;21(6):423-9. doi:10.1007/s10557-007-6068-5.
29. Trump S, Lukassen S, Anker MS, et al. Hypertension delays viral clearance and exacerbates airway hyperinflammation in patients with COVID-19. Nat Biotechnol. 2021;39(6):705-16. doi:10.1038/s41587-020-00796-1.
30. Buda V, Andor M, Baibata DE, et al. Decreased sEng plasma levels in hypertensive patients with endothelial dysfunction under chronic treatment with Perindopril. Drug Des Devel Ther. 2019;13:1915-25. doi:10.2147/DDDT.S186378.
31. Соколова Т.М., Полосков В.В., Шувалов А.Н. и др. Регуляция активности генов TLR/RLR-рецепторов и синтез цитокинов в процессе дифференцировки ТНР-1 моноцитов в макрофагподобные клетки под действием форбол-миристат-ацетата (РМА). Медицинская иммунология. 2017;19(1):27-34. doi:10.15789/1563-0625-2017-1-27-34.
32. Barhoumi T, Alghanem B, Shaibah H, et al. SARS-CoV-2 Coronavirus Spike ProteinInduced Apoptosis, Inflammatory, and Oxidative Stress Responses in THP-1-LikeMacrophages: Potential Role of Angiotensin-Converting Enzyme Inhibitor (Perindopril). Front Immunol. 2021;12:728896. doi:10.3389/fimmu.2021.728896.
33. Su JB, Hoüel R, Héloire F, et al. Stimulation of bradykinin B(1) receptors induces vasodilation in conductance and resistance coronary vessels in conscious dogs: comparison with B(2) receptor stimulation. Circulation. 2000;101(15):1848-53. doi:10.1161/01.cir.101.15.1848.
34. Taddei S, Bortolotto L. Unraveling the Pivotal Role of Bradykinin in ACE Inhibitor Activity. Am J Cardiovasc Drugs. 2016;16(5):309-21. doi:10.1007/s40256-016-0173-4.
35. Shima E, Katsube M, Kato T, et al. Calcium channel blockers suppress cytokineinduced activation of human neutrophils. Am J Hypertens. 2008;21(1):78-84. doi:10.1038/ajh.2007.13.
36. Mason RP, Jacob RF, Corbalan JJ, et al. Amlodipine increased endothelial nitric oxide and decreased nitroxidative stress disproportionately to blood pressure changes. Am J Hypertens. 2014;27(3):482-8. doi:10.1093/ajh/hpt202.
37. He Y, Si D, Yang C, et al. The effects of amlodipine and S(-)-amlodipine on vascular endothelial function in patients with hypertension. Am J Hypertens. 2014;27(1):27-31. doi:10.1093/ajh/hpt138.
38. Nissen SE, Tuzcu EM, Libby P, et al. Effect of antihypertensive agents on cardiovascular events in patients with coronary disease and normal blood pressure: the CAMELOT study: a randomized controlled trial. JAMA. 2004;292(18):2217-25. doi:10.1001/jama.292.18.2217.
39. Khelashvili G, Plante A, Doktorova M, et al. Ca2+-dependent mechanism of membrane insertion and destabilization by the SARS-CoV-2 fusion peptide. Biophys J. 2021;120(6):1105-19. doi:10.1016/j.bpj.2021.02.023.
40. Lai AL, Freed JH. SARS-CoV-2 Fusion Peptide has a Greater Membrane Perturbating Effect than SARS-CoV with Highly Specific Dependence on Ca2. J Mol Biol. 2021;433(10):166946. doi:10.1016/j.jmb.2021.166946.
41. Crespi B, Alcock J. Conflicts over calcium and the treatment of COVID-19. Evol Med Public Health. 2020;9(1):149-56. doi:10.1093/emph/eoaa046.
42. Zhang LK, Sun Y, Zeng H, et al. Calcium channel blocker amlodipine besylate therapy is associated with reduced case fatality rate of COVID-19 patients with hypertension. Cell Discov. 2020;6(1):96. doi:10.1038/s41421-020-00235-0.
43. Артериальная гипертензия у взрослых. Клинические рекомендации 2020. Российский кардиологический журнал. 2020;25(3):3786. doi:10.15829/1560-4071-2020-3-3786.