Cердечно-сосудистые заболевания в сочетании с вирусной инфекцией SARS-CoV-2: течение и прогноз
https://doi.org/10.52727/2078-256X-2021-17-3-97-105
Аннотация
В условиях пандемии особую группу составляют пациенты с сердечно-сосудистой патологией. Сердечно-сосудистые заболевания в значительной степени связаны с ростом смертности и повышенным риском осложнений у лиц, пораженных вирусом SARS-CoV-2. Это определяет важность стратификации риска, выбора оптимальной персонализированной терапии и изучения отдаленного прогноза инфаркта миокарда на фоне инфекции, вызванной SARS-CoV-2. Несмотря на стремительно растущее внимание к данному вопросу, механизмы взаимосвязи между сердечно-сосудистыми заболеваниями и COVID-19 не полностью ясны. Нами выполнен систематический обзор с целью обобщить важные аспекты COVID-19 для кардиологов. Авторами обсуждаются как хорошо изученные факторы инфекционного процесса, приводящие к острому повреждению миокарда и декомпенсации имеющихся хронических кардиологических заболеваний, так и новые, фундаментальные, определяющие прогноз и лечение. Использованы сведения по теме из публикаций на основе баз данных PubMed, Google Scholar и eLibrary.ru. Работа проведена при поддержке компании Пфайзер.
Ключевые слова
инфаркт миокарда,
сердечно-сосудистые заболевания,
новая коронавирусная инфекция,
инфекция SARS-CoV-2
При поддержке: Работа проведена при поддержке компании Пфайзер
Об авторах
О. И. Гущина
ФГБОУ ВО «Новосибирский государственный медицинский университет» Минздрава России
Россия
Россия
Олеся Игоревна Гущина, аспирант кафедры факультетской терапии им. проф. Г.Д. Залесского
м.т. +7923 179 6066, SPIN ID: 7709-0829
630091, Россия, Новосибирск, Красный просп., 52
Н. Г. Ложкина
ФГБОУ ВО «Новосибирский государственный медицинский университет» Минздрава России
Россия
Россия
Наталья Геннадьевна Ложкина, д-р мед. наук, проф. кафедры факультетской терапии им. проф. Г.Д. Залесского; куратор отделения для лечения больных с острым коронарным синдромом РСЦ № 1 ГКБ № 1
SPIN ID: 5320-7554
630091, Россия, Новосибирск, Красный просп., 52
Список литературы
1. World Health Organization. Coronavirus disease 2019 (COVID-19) situation report – 47. https://web.archive.org/web/20200308150245/https://www.who.int/docs/default-source/coronaviruse/situationreports/20200307-sitrep-47-covid-19.pdf (accessed April 21, 2020).
2. Wu Z., McGoogan J.M. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: Summary of a report of 72 314 cases from the Chinese Center for Disease Control and Prevention. JAMA, 2020; 323 (13): 1239–1242. doi: 10.1001/jama.2020.2648
3. Guan W., Ni Z., Hu Y. et al. Clinical characteristics of coronavirus disease 2019 in China. N. Engl. J. Med. doi: 10.1056/NEJMoa2002032
4. Wang D., Hu B., Hu C. et al. Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China. JAMA, 2020. doi: 10.1001/jama.2020.1585
5. Du Y., Tu L., Zhu P. et al. Clinical Features of 85 Fatal Cases of COVID-19 from Wuhan. A Retrospective Observational Study. Am. J. Respir. Crit. Care Med., 2020; 201 (11): 1372–1379. doi: 10.1164/rccm.202003-0543OC
6. Chen T. Wu D., Chen H. et al. Clinical characteristics of 113 deceased patients with coronavirus disease 2019: retrospective study. Br. Med. J., 2020; 1091 (March): m1091. doi: 10.1136/bmj. m1091 Li B
7. Characteristics of COVID-19 patients dying in Italy Report based on available data on March 20th, 2020 https://www.epicentro.iss.it/coronavirus/bollettino/Report-COVID-2019_20_marzo_eng.pdf
8. Akhtar Z., Chowdhury F., Aleem M.A. et al. Undiagnosed SARS-CoV-2 infection and outcome in patients with acute MI and no COVID-19 symptoms. Open Heart, 2021; 8: e001617. doi: 10.1136/openhrt-2021-001617)
9. Carfм A., Bernabei R., Landi F.; Gemelli Against COVID-19 Post-Acute Care Study Group. Persistent symptoms in patients after acute COVID-19. JAMA, 2020; 324 (6): 603–605. doi: 10.1001/jama.2020.12603
10. Helms J., Kremer S., Merdji H. et al. Neurologic features in severe SARS-CoV-2 infection. N. Engl. J. Med., 2020; 382 (23): 2268–2270. doi: 10.1056/NEJMc2008597
11. Leisman D.E., 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): 1233–1244. doi: 10.1016/S2213-2600(20)30404-5
12. Rochwerg B., Parke R., Murthy S. et al. Misinformation during the coronavirus disease 2019 outbreak: how knowledge emerges from noise. Crit. Care. Explor., 2020; 2 (4): e0098. doi: 10.1097/CCE.0000000000000098
13. Dickson R.P., Erb-Downward J.R., Martinez F.J., Huffnagle G.B. The microbiome and the respiratory tract. Annu. Rev. Physiol., 2016; 78: 481–504. doi: 10.1146/annurev-physiol-021115-105238
14. Wang W., Xu Y., Gao R. et al. Detection of SARSCoV-2 in different types of clinical specimens. JAMA, 2020; 323 (18): 1843-1844. doi: 10.1001/jama.2020.3786
15. Wang C., Xie J., Zhao L. et al. Alveolar macrophage dysfunction and cytokine storm in the pathogenesis of two severe COVID-19 patients. EBioMedicine, 2020; 57: 102833. doi: 10.1016/j.ebiom.2020.102833
16. Totura A.L., Whitmore A., Agnihothram S. et al. Toll-like receptor 3 signaling via TRIF contributes to a protective innate immune response to severe acute respiratory syndrome coronavirus infection. mBio, 2015; 6 (3): e00638-15. doi: 10.1128/mBio.00638-15
17. Bastard P., Rosen L.B., Zhang Q. et al. Autoantibodies against type I IFNs in patients with life-threatening COVID-19. Science, 2020; 370 (6515): eabd4585. doi: 10.1126/science.abd4585
18. Hadjadj J., Yatim N., Barnabei L. et al Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients. Science, 2020; 369 (6504): 718–724. doi: 10.1126/science.abc6027
19. Cugno M., Meroni P.L., Gualtierotti R. et al. Complement activation in patients with COVID-19: A novel therapeutic target. J .Allergy Clin. Immunol., 2020; 146 (1): 215–217. doi: 10.1016/j.jaci.2020.05.006
20. Holter J.C., Pischke S.E., de Boer E. et al. Systemic complement activation is associated with respiratory failure in COVID-19 hospitalized patients. Proc. Natl. Acad. Sci. USA, 2020; 117 (40): 25018–25025. doi: 10.1073/pnas.2010540117
21. Bao J., Li C., Zhang K. et al. Comparative analysis of laboratory indexes of severe and non-severe patients infected with COVID-19. Clin. Chim. Acta, 2020; 509: 180–194. doi: 10.1016/j.cca.2020.06.009
22. Taneera J., El-Huneidi W., Hamad M. et al. Expression profile of SARS-CoV-2 host receptors in human pancreatic islets revealed upregulation of ACE2 in diabetic donors. Biology (Basel), 2020; 9 (8): 215. doi: 10.3390/biology9080215
23. Pal R., Banerjee M. COVID-19 and the endocrine system: exploring the unexplored. J. Endocrinol. Invest., 2020; 43 (7): 1027–1031. doi: 10.1007/s40618-020-01276-8
24. Yang L., Han Y., Nilsson-Payant B.E. et al. A human pluripotent stem cell-based platform to study SARSCoV-2 tropism and model virus infection in human cells and organoids. Cell Stem. Cell, 2020; 27 (1): 125–136.e7. doi: 10.1016/j.stem.2020.06.015
25. Fosbшl E.L., Butt J.H., Шstergaard L. et al. Association of angiotensin-converting enzyme inhibitor or angiotensin receptor blocker use with COVID-19 diagnosis and mortality. JAMA, 2020; 324 (2): 168–177. doi: 10.1001/jama.2020.11301
26. Nielsen T.B., Pantapalangkoor P., Yan J. et al. Diabetes exacerbates infection via hyperinflammation by signaling through TLR4 and RAGE. mBio, 2017; 8 (4): e00818-17. doi: 10.1128/mBio.00818-17. PMID: 28830942; PMCID: PMC5565964.
27. Quinti I., Lougaris V., Milito C. et al. A possible role for B cells in COVID-19? Lesson from patients with agammaglobulinemia. J. Allergy Clin. Immunol., 2020; 146 (1): 211-213.e4. doi: 10.1016/j.jaci.2020.04.013
28. Soresina A., Moratto D., Chiarini M. et al. Two X-linked agammaglobulinemia patients develop pneumonia as COVID-19 manifestation but recover. Pediatr. Allergy Immunol., 2020; 31 (5): 565–569. doi: 10.1111/pai.13263
29. Montero-Escribano P., Matнas-Guiu J., Gуmez-Iglesias P. et al. Anti-CD20 and COVID-19 in multiple sclerosis and related disorders: A case series of 60 patients from Madrid, Spain. Mult. Scler. Relat. Disord., 2020; 42: 102185. doi: 10.1016/j.msard.2020.102185
30. Galani I.E., Rovina N., Lampropoulou V. et al. Untuned antiviral immunity in COVID-19 revealed by temporal type I/III interferon patterns and flu comparison. Nat. Immunol., 2021; 22 (1): 32–40. doi: 10.1038/s41590-020-00840-x
31. Sinha P., Calfee C.S., Cherian S. et al. Prevalence of phenotypes of acute respiratory distress syndrome in critically ill patients with COVID-19: a prospective observational study. Lancet Respir. Med., 2020; 8 (12): 1209–1218. doi: 10.1016/S2213-2600(20)30366-0
32. Zhou P., Yang X.L., Wang X.G. et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature, 2020; 579: 270–273. doi: 10.1038/s41586-020-2012-7
33. Hoffmann M., Kleine-Weber H., Schroeder S. et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell, 2020; 181 (2): 271–280. doi: 101016/j.cell.2020.02.052
34. Tikellis C., Thomas M.C. Angiotensin-converting enzyme 2 (ACE2) is a key modulator of the renin angiotensin system in health and disease. Int. J. Pept., 2012; 2012: 256294–256294. doi: 101155/2012/256294
35. Zhang H., Penninger J.M., Li Y. et al. Angiotensinconverting enzyme 2 (ACE2) as a SARS-CoV-2 receptor: molecular mechanisms and potential therapeutic target. Intensive Care Med., 2020; 46 (4): 586–590. doi: 101007/s00134-020-05985-9
36. Jirak P., Larbig R., Shomanova Z. et al. Myocardial injury in severe COVID-19 is similar to pneumonias of other origin: results from a multicentre study. ESC Heart Fail., 2021; 8 (1): 37–46. doi: 10.1002/ehf2.13136
37. Varga Z., Flammer A.J., Steiger P. et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet, 2020; 395 (10234): 1417–1418. doi: 10.1016/S0140-6736(20)30937-5
38. Buja L.M., Wolf D.A., Zhao B. et al. The emerging spectrum of cardiopulmonary pathology of the coronavirus disease 2019 (COVID-19): Report of 3 autopsies from Houston, Texas, and review of autopsy findings from other United States cities. Cardiovasc. Pathol., 2020; 48: 107233. doi: 10.1016/j.carpath.2020.107233
39. Sadegh Beigee F., Pourabdollah Toutkaboni M., Khalili N. et al. Diffuse alveolar damage and thrombotic microangiopathy are the main histopathological findings in lung tissue biopsy samples of COVID-19 patients. Pathol. Res. Pract., 2020; 216 (10): 153228. doi: 10.1016/j.prp.2020.153228
40. Gu J., Korteweg C. Pathology and pathogenesis of severe acute respiratory syndrome. Am. J. Pathol., 2007; 170: 1136–1147
41. Schaefer I.M., Padera R.F., Solomon I.H. et al. In situ detection of SARS-CoV-2 in lungs and airways of patients with COVID-19. Mod. Pathol., 2020; 33 (11): 2104–2114. doi: 10.1038/s41379-020-0595-z
42. Su H., Yang M., Wan C. et al. Renal histopathological analysis of 26 postmortem findings of patients with COVID-19 in China. Kidney Int., 2020; 98 (1): 219–227. doi: 10.1016/j.kint.2020.04.003
43. Li G., Fan Y., Lai Y. et al. Coronavirus infections and immune responses. Med. Virol., 2020; 92 (4): 424–32. doi: 101002/jmv.25685
44. Ackermann M., Verleden S.E., Kuehnel M. et al. Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19. N. Engl. J. Med., 2020; 383 (2): 120–128. doi: 10.1056/NEJMoa2015432
45. Copin M.C., Parmentier E., Duburcq T. et al. Time to consider the histologic pattern of lung injury to treat critically ill patients with COVID-19 infection. Intensive Care Med., 2020; 46 (6): 1124–1126. doi: 10.1007/s00134-020-06057-8
46. Zhang Y., Xiao M., Zhang S. et al. Coagulopathy and antiphospholipid antibodies in patients with COVID-19. N. Engl. J. Med., 2020; 382 (17): e38. doi: 10.1056/NEJMc2007575
47. Sinha P., Calfee C.S., Cherian S. et al. Prevalence of phenotypes of acute respiratory distress syndrome in critically ill patients with COVID-19: a prospective observational study. Lancet Respir. Med., 2020; 8 (12): 1209–1218. doi: 10.1016/S2213-2600(20)30366-0
48. Gill S.E., Dos Santos C.C., O’Gorman D.B. et al. Transcriptional profiling of leukocytes in critically ill COVID19 patients: implications for interferon response and coagulation. Intensive Care Med. Exp., 2020; 8 (1): 75. doi: 10.1186/s40635-020-00361-9
49. Lippi G., Lavie C.J., Sanchis-Gomar F. Cardiac troponin I in patients with coronavirus disease 2019 (COVID-19): Evidence from a meta-analysis. Prog. Cardiovasc. Dis., 2020; 63 (3): 390–391. doi: 10.1016/j.pcad.2020.03.001
50. Deng Q., Hu B., Zhang Y. et al. Suspected myocardial injury in patients with COVID-19: Evidence from front-line clinical observation in Wuhan, China. Int. J. Cardiol., 2020; 311: 116–121. doi: 10.1016/j.ijcard.2020.03.087
51. Kotecha T., Knight D.S., Razvi Y. et al. Patterns of myocardial injury in recovered troponin-positive COVID-19 patients assessed by cardiovascular magnetic resonance. Eur. Heart J., 2021; 42 (19): 1866–1878. doi: 10.1093/eurheartj/ehab075
Рецензия
Для цитирования:
Гущина О.И., Ложкина Н.Г. Cердечно-сосудистые заболевания в сочетании с вирусной инфекцией SARS-CoV-2: течение и прогноз. Атеросклероз. 2021;17(3):97-105. https://doi.org/10.52727/2078-256X-2021-17-3-97-105
For citation:
Gushchina O.I., Lozhkina N.G. Cardiovascular diseases in combination with SARS-CoV-2 viral infection: cours and forecast. Ateroscleroz. 2021;17(3):97-105. (In Russ.) https://doi.org/10.52727/2078-256X-2021-17-3-97-105
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