Key aspects of cardiovascular damage in COVID-19

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Abstract

To date, the COVID-19 pandemic remains one of the biggest public health challenges in recent memory. At the moment, more than 600 million people around the world have become its victims. SARS-CoV-2 is characterized by multiple organ damage, but the lungs and heart are most involved in the pathological process. Elevated levels of cardiospecific enzymes are common in patients with COVID-19 infection and indicate myocardial damage. Possible mechanisms of myocardial injury include: 1) renin-angiotensin-aldosterone system dysfunction, 2) direct viral damage to the heart, 3) hyperinflammation and «cytokine storm», 4) endothelial dysfunction, hypercoagulation and development of coronary microvascular thrombosis, 5) hypoxemia and hypoxia, due to both respiratory failure and destabilization of coronary plaques and/or mismatch of supply and demand, leading to ischemia/myocardial infarction. The presence of cardiac pathology in patients with COVID-19 has become one of the most significant predictors of an unfavorable prognosis and made it necessary to single out patients with cardiovascular diseases as a separate risk group. In total, cardiac pathology (heart failure) accounts for approximately 40% of all deaths in patients with COVID-19. In the presence of cardiovascular diseases, lethality was more marked in elderly and senile patients, which is associated with a greater prevalence of cardiac pathology, functional disorders of the immune system, as well as with more frequent cardiotoxicity against the background of reduced metabolism during etiotropic therapy for coronavirus infection.

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About the authors

V. V. Salukhov

S.M. Kirov Military Medical Academy

Author for correspondence.
Email: vlasaluk@yandex.ru
ORCID iD: 0000-0003-1851-0941

Dr. Sci. (Med.), Associate Professor, Head of the 1st Department (Advanced Therapy for Physicians)

Russian Federation, St. Petersburg

B. V. Sagun

S.M. Kirov Military Medical Academy

Email: vlasaluk@yandex.ru
ORCID iD: 0000-0002-7142-5554
Russian Federation, St. Petersburg

References

  1. Su S., Wong G., Shi W., et al. Epidemiology, genetic recom bi-nation, and pathogenesis of coronaviruses. Trends Microbiol. 2016;24(6):490–502. doi: 10.1016/j.tim.2016.03.003.
  2. Falsey A.R., Walsh E.E., Hayden F.G. Rhinovirus and coronavirus infection-associated hospitalizations among older adults. J Infect Dis. 2002;185(9):1338–41. doi: 10.1086/339881.
  3. Министерство здравоохранения Российской Федерации. Временные методические рекомендации: профилактика, диагностика и лечение новой коронавирусной инфекции (COVID-19). Версия 15. (22.02.2022). [Ministry of Health of the Russian Federation. Interim Guidelines: Prevention, Diagnosis, and Treatment of Novel Coronavirus Infection (COVID-19). Version 15. (22.02.2022). (In Russ.)]. URL: https://edu-rosminzdrav.ru.com.
  4. Шляхто Е.В., Конради А.О., Арутюнов Г.П. и др. Руководство по диагностике и лечению болезней системы кровообращения (БСК) в контексте пандемии COVID-19 (краткая версия). 2020. С. 5–30. [Shlyakhto E.V., Konradi A.O., Arutyunov G.P. et al. Guidelines for the Diagnosis and Management of Circulatory System Diseases (CVDs) in the Context of the COVID-19 Pandemic (Short Version). 2020. P. 5–30. (In Russ.)]. doi: 10.15829/1560-4071-2020-3-3801.
  5. Guo T., Fan Y., Chen M., et al. Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19). JAMA Cardiol. 2020;5(7):811–18. doi: 10.1001/jamacardio.2020.1017.
  6. Lu R., et al. Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. Lancet. 2020;395:565–74. doi: 10.1016/S0140-6736(20)30251-8.
  7. Wu F., et al. A new coronavirus associated with human respiratory disease in China. Nature. 2020;579:265–69. doi: 10.1038/s41586-020-2008-3.
  8. Zhou F., et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020;395:1054–62. doi: 10.1016/S0140-6736(20)30566-3.
  9. Andersen K.G., Rambaut A., Lipkin W.I., et al. The proximal origin of SARS-CoV-2. Nat Med. 2020;26:450–52. doi: 10.1038/s41591-020-0820-9.
  10. Cui J., Li F., Shi Z.L. Origin and evolution of pathogenic coronaviruses. Nat. Rev. Microbiol. 2019;17:181–92. doi: 10.1038/s41579-018-0118-9.
  11. Hoffmann M., Kleine-Weber H., Schroeder S., et al. SARS-CoV-2 Cell Entry Depends on AFP-2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor. Cell. 2020;181:271–80. doi: 10.1016/j.cell.2020.02.052.
  12. Walls A.C., et al. Structure, function, and antigenicity of the SARS-CoV-2 spike glycoprotein. Cell. 2020;181:281–92. doi: 10.1016/j.cell.2020.02.058.
  13. Tay M.Z., Poh C.M., Renia L., et al. The trinity of COVID-19: immunity, inflammation and intervention. Nat Rev Immunol. 2020;20:363–74. doi: 10.1038/s41577-020-0311-8.
  14. Фисун А.Я., Черкашин Д.В., Тыренко В.В. и др. Роль ренин-ангиотензин-альдостероновой системы во взаимодействии с коронавирусом SARS-CoV 2 и в развитии стратегий профилактики и лечения новой коронавирусной инфекции (COVID 19). Артериальная гипертензия. 2020;26(3):248–62. [Fisun A.Ya., Cherkashin D.V., Tyrenko V.V. et al. The role of the renin-angiotensin-aldosterone system in interaction with the SARS-CoV 2 coronavirus and in the development of strategies for the prevention and treatment of novel coronavirus infection (COVID 19). Arterial’naya gipertenziya. 2020;26(3):248–62. (In Russ.)]. doi: 10.18705/1607-419X-2020-26-3-248-262.
  15. Clerkin K.J., et al. COVID-19 and cardiovascular disease. Circulation. 2020;141:1648–55. doi: 10.1161/CIRCULATIONAHA.120.046941.
  16. Han Y., et al. CSC expert consensus on principles of clinical management of patients with severe emergent cardiovascular diseases during the COVID-19 epidemic. Circulation. 2020;141:e810–16. doi: 10.1161/CIRCULATIONAHA.120.047011.
  17. Zheng Y.Y., Ma Y.T., Zhang J.Y., Xie X. COVID-19 and the cardiovascular system. Nat Rev Cardiol. 2020;17(5):259–60. doi: 10.1038/s41569-020-0360-5.
  18. Huang C., et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet. 2020;395:497–506. doi: 10.1016/S0140-6736(20)30183-5.
  19. Qin C., Zhou L., et al. Dysregulation of immune response in patients with COVID-19 in Wuhan. China Chuan J Chem Inf Model. 2013;53(9):1689–99. doi: 10.1093/cid/ciaa248.
  20. Ruan Q., Yang K., Wang W., et al. Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China. Intens Care Med. 2020;46:846–48. doi: 10.1007/s00134-020-05991-x.
  21. Kang Y., Chen T., Mui D., et al. Cardiovascular manifestations and treatment considerations in COVID-19. Heart. 2020;106:1132–41. doi: 10.1136/heartjnl-2020-317056.
  22. Nishiga M., Wang D.W., Han Y., et al. COVID-19 and cardiovascular disease: from basic mechanisms to clinical perspectives. Nat Rev Cardiol. 2020;17(9):543–58. doi: 10.1038/s41569-020-0413-9.
  23. Bavishi C., Bonow R.O., Trivedi V., et al. Special Article – Acute myocardial injury in patients hospitalized with COVID-19 infection: A review. Prog Cardiovasc Dis. 2020;63(5):682–89. doi: 10.1016/j.pcad.2020.05.013.
  24. Guo J., Huang Z., Lin L., Lv J. Coronavirus Disease 2019 (COVID-19) and Cardiovascular Disease: A Viewpoint on the Potential Influence of Angiotensin-Converting Enzyme Inhibitors/Angiotensin Receptor Blockers on Onset and Severity of Severe Acute Respiratory Syndrome Coronavirus 2 Infection. J Am Heart Assoc. 2020;9:e016219. doi: 10.1161/JAHA.120.016219.
  25. Vaarala M.H., Porvari K.S., Kellokumpu S., et al. Expression of transmembrane serine protease TMPRSS2 in mouse and human tissues. J Pathol. 2001;193(1):134–40. doi: 10.1002/1096-9896(2000)9999:9999<::AID-PATH743>3.0.CO;2-T.
  26. Мареев В.Ю. COVID-19 и сердечно-сосудистые заболевания. Лекция от 14.04.2020 URL: https://www.youtube.com/watch?v=Fe8MN_P_yCQ&feature=youtu.be
  27. ACC Clinical Bulletin COVID-19. Clinical Guidance For the Cardiovascular Care Team. 2020. URL: https://www.S20028-ACC-Clinical-BulletinCoronavirus.pdf
  28. Moore J.B., June C.H. Cytokine release syndrome in severe COVID-19. Science. 2020;368:473–74. doi: 10.1126/science.abb8925.
  29. Mehta P., Mcauley D.F., Brown M., et al. Correspondence COVID-19: consider cytokine storm syndromes and immunosuppression. Lancet. 2020;6736(20):19–20. doi: 10.1016/S0140-6736(20)30628-0.
  30. Chen G., Wu D., Guo W., et al. Clinical and immunologic features in severe and moderate forms of coronavirus disease 2019. medRxiv. 2020;2020.02.16.20023903. doi: 10.1172/JCI137244.
  31. Alvi R.M., Frigault M.J., Fradley M.G., et al. Cardiovascular events among adults treated with chimeric antigen receptor T-cells (CAR-T). J Am Coll Cardiol. 2019;74(25):3099–108. doi: 10.1016/j.jacc.2019.10.038.
  32. Jarrah A.A., Schwarskopf M., Wang E.R., et al. SDF-1 induces TNF-mediated apoptosis in cardiac myocytes. Apoptosis. 2018;23(1):79–91. doi: 10.1007/s10495-017-1438-3.
  33. Zhu Han, et al. Cardiovascular Complications in Patients with COVID-19: Consequences of Viral Toxicities and Host Immune Response. Curr Cardiol Rep. 2020;22(5):32. doi: 10.1007/s11886-020-01292-3.
  34. Xu Z., Shi L., Wang Y., et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet. Respir Med. 2020;2600(20):19–21. doi: 10.1016/S2213-2600(20)30076-X.
  35. Бубнова М.Г., Аронов Д.М. COVID-19 и сердечно-сосудистые заболевания: от эпидемиологии до реабилитации. Пульмонология. 2020;30(5):688–99. [Bubnova M.G., Aronov D.M. COVID-19 and cardiovascular disease: from epidemiology to rehabilitation. Pulmonologiya. 2020;30(5):688–99. (In Russ.)]. doi: 10.18093/0869-0189-2020-30-5-688-699.
  36. Guzik T., Mohiddin S.A., Dimarco A., et al. COVID-19 and the cardiovascular system: implications for risk assessment, diagnosis, and treatment options. Cardiovasc Res. 2020;116(10):1666–87. doi: 10.1093/cvr/cvaa106.
  37. Kreutz R., Algharably E.A., Azizi M., et al. Hypertension, the renin–angiotensin system, and the risk of lower respiratory tract infections and lung injury: implications for COVID-19. Cardiovasc Res. 2020;116(10):1688–99. doi: 10.1093/cvr/cvaa097.
  38. Akhmerov A., Marban E. COVID-19 and the Heart. Circ Res. 2020;126:1443–55. doi: 10.1161/CIRCRESAHA.120.317055.
  39. Davidson J.A., Warren-Gash C. Cardiovascular complications of acute respiratory infections: current research and future directions. Expert Rev Anti-infect Ther. 2019;17:939–42. doi: 10.1080/14787210.2019.168981.
  40. Zhang Y., Xiao M., Zhang S., et al. Coagulopathy and Antiphospholipid Antibodies in Patients with Covid-19. N Engl J Med. 2020;382:e38. doi: 10.1056/NEJMc2007575.
  41. Liu W., Li H. COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism. URL: https://chemrxiv.org/engage/chemrxiv/article-details/60c74fa50f50db305139743d (Accessed 2020 April 14). doi: 10.26434/chemrxiv.11938173.v8.
  42. Zhyvotovska A., Yusupov D., Foronjy R., et al. Insights into Potential Mechanisms of Injury and Treatment Targets in COVID-19, SARS-Cov-2 Infection. Int J Clin Res Trials. 2020;5(1):147. doi: 10.15344/2456-8007/2020/14.
  43. Nagashima S., Mendes M.C., Camargo Martins A.P., et al. Endothelial dysfunction and thrombosis in patients with COVID-19 brief report. Arterioscler Thromb Vasc Biol. 2020;40(10):2404–407. doi: 10.1161/ATVBAHA.120.314860.
  44. Libby P., Luscher T. COVID-19 is, in the end, an endothelial disease. Eur Heart J. 2020;41(32):3038–44. doi: 10.1093/eurheartj/ehaa623.
  45. Siedlinski M., Jozefczuk E., Xu X., et al. White blood cells and blood pressure: a mendelian randomization study. Circulation. 2020;141(16):1307–17. doi: 10.1161/CIRCULATIONAHA.119.045102.
  46. PPetrey A.C., Qeadan F., Middleton E.A., et al. Cytokine release syndrome in COVID-19: Innate immune, vascular, and platelet pathogenic factors differ in severity of disease and sex. J Leukoc Biol. 2021;109(1):55–66. doi: 10.1002/JLB.3COVA0820-410RRR.
  47. Мартынов М.Ю., Боголепова А.Н., Ясаманова А.Н. Эндотелиальная дисфункция при COVID-19 и когнитивные нарушения. Журнал неврологии и психиатрии им. С.С. Корсакова. 2021;121(6):93–9. [Martynov M.Yu., Bogolepova A.N., Yasamanova A.N. Endothelial dysfunction in COVID-19 and cognitive impairment. Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova. 2021;121(6):93–9. 2021;121(6):93–9. (In Russ.)]. doi: 10.17116/jnevro202112106193.
  48. Helms J., Tacquard C., Severac F., et al. CRICS TRIGGERSEP Group (Clinical Research in Intensive Care and Sepsis Trial Group for Global Evaluation and Research in Sepsis). High risk of thrombosis in patients with severe SARS-CoV-2 infection: a multicenter prospective cohort study. Int Care Med. 2020;46(6):1089–98. doi: 10.1007/s00134-020-06062-x.
  49. Page M.J., Bester J., Pretorius E. The inflammatory effects of TNF-alpha and complement component 3 on coagulation. Sci Rep 2018;8:1812. doi: 10.1038/s41598-018-20220-8.
  50. Uthman I.W., Gharavi A.E. Viral infections and antiphospholipid antibodies. Semin. Arthr. Rheum. 2002;31:256–63. doi: 10.1053/sarh.2002.28303.
  51. Makarova Y.A., Ryabkova V.A., Salukhov V.V., et al. Atherosclerosis, Cardiovascular Disorders and COVID-19: Comorbid Pathogenesis. Diagnostics 2023;13:478. doi: 10.3390/diagnostics13030478.

Supplementary files

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1. JATS XML
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2. Fig. 1. COVID-19-associated cardiovascular pathology (adapted from [35])

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3. Fig. 2. Principal scheme of possible pathophysiologic mechanisms of acute myocardial injury in COVID-19 (adapted from [11])

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4. Fig. 3. Mechanism of hemoglobin destruction in COVID-19 (adapted from [60])

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5. Fig. 4. Reciprocal potentiation of the main pathophysiologic mechanisms implicated by SARS-CoV-2 in SSc injury

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