Clinical and genetic predictors of cardiovascular events as the risk of an unfavorable course and outcomes of novel coronavirus infection

封面


如何引用文章

全文:

开放存取 开放存取
受限制的访问 ##reader.subscriptionAccessGranted##
受限制的访问 订阅或者付费存取

详细

Numerous data indicate a high incidence of cardiovascular diseases against the background of a novel coronavirus infection, including initially healthy individuals. The development of complications such as cardiac rhythm disturbances, myocardial injury, acute coronary syndrome aggravates the severity of the disease and the prognosis. Moreover, signs of structural and functional damage of the cardiovascular system are detected after recovery, which makes prevention issues especially relevant. Various non-modifiable risk factors for the severe course of COVID-19, such as gender, age, heredity, race, environment, can determine the development of complications, including heart disease. In this matter, genetic characteristics are also important. The literature review presents possible genetic predictors and the mechanism of their influence on the development of cardiovascular complications and the severe course of novel coronavirus infection. The identification of specific genetic predictors can determine biological mechanisms that are relevant to diagnostic and treatment strategies. Moreover, recognizing people at high or low risk of severe COVID-19 can contribute to understanding the course of infection in different people and the development of cardiovascular complications. In addition, the determination of genetic markers contributes to the early detection of developing cardiovascular complications against the background of the novel coronavirus infection and elaboration of the personalized prevention strategy.

全文:

受限制的访问

作者简介

Ekaterina Bratilova

Military Medical Academy named after S.M. Kirov

Email: guanilatciclaza@mail.ru
ORCID iD: 0000-0003-2153-2121
SPIN 代码: 4647-2564
俄罗斯联邦, Saint Petersburg

Vasilii Kachnov

Military Medical Academy named after S.M. Kirov

编辑信件的主要联系方式.
Email: kvasa@mail.ru
ORCID iD: 0000-0002-6601-5366
SPIN 代码: 2084-0290

MD, Cand. Sci. (Med.)

俄罗斯联邦, 6A, Akademika Lebedeva St., Saint Petersburg, 194044

Vadim Tyrenko

Military Medical Academy named after S.M. Kirov

Email: vadim_tyrenko@mail.ru
ORCID iD: 0000-0002-0470-1109
SPIN 代码: 3022-5038
Scopus 作者 ID: 6508262196

MD, Dr. Sci. (Med.), Professor

俄罗斯联邦, Saint Petersburg

Svetlana Kolyubaeva

Military Medical Academy named after S.M. Kirov

Email: ksnwma@mail.ru
SPIN 代码: 2077-2557

Dr. Sci. (Biol.)

俄罗斯联邦, Saint Petersburg

参考

  1. COVID-19 Map [Internet]. Johns Hopkins Coronavirus Resource Center. Available from: https://coronavirus.jhu.edu/map.html. Accessed: Nov 3, 2021.
  2. Madjid M, Miller CC, Zarubaev VV, et al. Influenza epidemics and acute respiratory disease activity are associated with a surge in autopsy-confirmed coronary heart disease death: results from 8 years of autopsies in 34,892 subjects. Eur Heart J. 2007;28(10):1205–1210. doi: 10.1093/eurheartj/ehm035
  3. Kwong JC, Schwartz KL, Campitelli MA. Acute myocardial infarction after laboratory-confirmed influenza infection. N Engl J Med. 2018;378(26):2540–2541. DOI: 10.1056/ NEJMc1805679
  4. Madjid M, Connolly AT, Nabutovsky Y, et al. Effect of high influenza activity on risk of ventricular arrhythmias requiring therapy in patients with implantable cardiac defibrillators and cardiac resynchronization therapy defibrillators. Am J Cardiol. 2019;124(1):44–50. doi: 10.1016/j.amjcard.2019.04.011
  5. Kytömaa S, Hegde S, Claggett B, et al. Association of influenza-like illness activity with hospitalizations for heart failure: The atherosclerosis risk in Communities Study. JAMA Cardiol. 2019;4(4):363–369. doi: 10.1001/jamacardio.2019.0549
  6. Kryukov EV, Shulenin KS, Cherkashin DV, et al. Patogenez i klinicheskie proyavleniya porazheniya serdechno-sosudistoy sistemy u patsientov s novoy koronavirusnoy infektsiey (COVID-19): uchebnoe posobie. Saint Petersburg: Veda Print; 2021. (In Russ.)
  7. Wang L, He W, Yu X, et al. Coronavirus disease 2019 in elderly patients: Characteristics and prognostic factors based on 4-week follow-up. J Infect. 2020;80(6):639–645. doi: 10.1016/j.jinf.2020.03.019
  8. 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
  9. Chen T, Wu D, Chen H, et al. Clinical characteristics of 113 deceased patients with coronavirus disease 2019: retrospective study. BMJ. 2020;368:m1091. doi: 10.1136/bmj.m1091
  10. Zhao YH, Zhao L, Yang XC, Wang P. Cardiovascular complications of SARS-CoV-2 infection (COVID-19): a systematic review and meta-analysis. Rev Cardiovasc Med. 2021;22(1):159–165. doi: 10.31083/j.rcm.2021.01.238
  11. Shi S, Qin M, Shen B, et al. Association of cardiac injury with mortality in hospitalized patients with COVID-19 in Wuhan, China. JAMA Cardiol. 2020;5(7):802–810. doi: 10.1001/jamacardio.2020.0950
  12. Qiang Z, Wang B, Garrett BC, et al. Coronavirus disease 2019: a comprehensive review and meta-analysis on cardiovascular biomarkers. Curr Opin Cardiol. 2021;36(3):367–373. doi: 10.1097/HCO.0000000000000851
  13. Puntmann VO, Carerj ML, Wieters I, et al. Outcomes of cardiovascular magnetic resonance imaging in patients recently recovered from coronavirus disease 2019 (COVID-19). JAMA Cardiol. 2020;5(11):1265–1273. doi: 10.1001/jamacardio.2020.3557
  14. Myhre PL, Heck SL, Skranes JB, et al. Cardiac pathology 6 months after hospitalization for COVID-19 and association with the acute disease severity. Am Heart J. 2021;242:61–70. doi: 10.1016/j.ahj.2021.08.001
  15. Zheng YY, Ma YT, Zhang JY, Xie X. COVID-19 and the cardiovascular system. Nat Rev Cardiol. 2020;17(5):259–260. doi: 10.1038/s41569-020-0360-5
  16. Driggin E, Madhavan MV, Bikdeli B, et al. Cardiovascular considerations for patients, health care workers, and health systems during the COVID-19 pandemic. J Am Coll Cardiol. 2020;75(18):2352–2371. doi: 10.1016/j.jacc.2020.03.031
  17. Chen L, Li X, Chen M, et al. The ACE2 expression in human heart indicates new potential mechanism of heart injury among patients infected with SARS-CoV-2. Cardiovasc Res. 2020;116(6):1097–1100. doi: 10.1093/cvr/cvaa078
  18. SeyedAlinaghi S, Mehrtak M, MohsseniPour M, et al. Genetic susceptibility of COVID-19: a systematic review of current evidence. Eur J Med Res. 2021;26(1):46. doi: 10.1186/s40001-021-00516-8
  19. Fodor A, Tiperciuc B, Login C, et al. Endothelial dysfunction, inflammation, and oxidative stress in COVID-19-mechanisms and therapeutic targets. Oxid Med Cell Longev. 2021;2021:8671713. doi: 10.1155/2021/8671713
  20. Henry BM, Vikse J, Benoit S, et al. Hyperinflammation and derangement of renin-angiotensin-aldosterone system in COVID-19: A novel hypothesis for clinically suspected hypercoagulopathy and microvascular immunothrombosis. Clin Chim Acta. 2020;507:167–173. doi: 10.1016/j.cca.2020.04.027
  21. Senchenkova EY, Russell J, Esmon CT, Granger DN. Roles of coagulation and fibrinolysis in angiotensin II-enhanced microvascular thrombosis. Microcirculation. 2014;21(5):401–407. doi: 10.1111/micc.12120
  22. Hamadeh A, Aldujeli A, Briedis K, et al. Characteristics and outcomes in patients presenting with COVID-19 and ST-segment elevation myocardial infarction. Am J Cardiol. 2020;131:1–6. doi: 10.1016/j.amjcard.2020.06.063
  23. Vremennye metodicheskie rekomendatsii: profilaktika, diagnostika i lechenie novoy koronavirusnoy infektsii (COVID-19). Versiya 13 (14.10.2021) [Internet]. Ministerstvo zdravookhraneniya Rossiyskoy Federatsii. (In Russ.). Available from: https://static-0.minzdrav.gov.ru/system/attachments/attaches/000/058/211/original/BMP-13.pdf. Accessed: Dec 1, 2021.
  24. Corrales-Medina VF, Madjid M, Musher DM. Role of acute infection in triggering acute coronary syndromes. Lancet Infect Dis. 2010;10(2):83–92. doi: 10.1016/S1473-3099(09)70331-7
  25. Chen N, Zhou M, Dong X, et al. Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study. Lancet. 2020;395(10223):507–513. doi: 10.1016/S0140-6736(20)30211-7
  26. Bansal M. Cardiovascular disease and COVID-19. Diabetes Metab Syndr. 2020;14(3):247–250. doi: 10.1016/j.dsx.2020.03.013
  27. Babapoor-Farrokhran S, Rasekhi RT, Gill D, et al. Arrhythmia in COVID-19. SN Compr Clin Med. 2020;2(9):1430–1435. doi: 10.1007/s42399-020-00454-2
  28. Lazzerini PE, Capecchi PL, Laghi-Pasini F. Systemic inflammation and arrhythmic risk: lessons from rheumatoid arthritis. Eur Heart J. 2017;38(22):1717–1727. doi: 10.1093/eurheartj/ehw208
  29. Kochi AN, Tagliari AP, Forleo GB, et al. Cardiac and arrhythmic complications in patients with COVID-19. J Cardiovasc Electrophysiol. 2020;31(5):1003–1008. doi: 10.1111/jce.14479
  30. Wang Y, Wang Z, Tse G, et al. Cardiac arrhythmias in patients with COVID-19. J Arrhythm. 2020;36(5):827–836. doi: 10.1002/joa3.12405
  31. Gopinathannair R, Merchant FM, Lakkireddy DR, et al. COVID-19 and cardiac arrhythmias: a global perspective on arrhythmia characteristics and management strategies. J Interv Card Electrophysiol. 2020;59(2):329–336. doi: 10.1007/s10840-020-00789-9
  32. Zhou F, Yu T, Du R, 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(10229):1054–1062. doi: 10.1016/S0140-6736(20)30566-3
  33. 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):811–818. doi: 10.1001/jamacardio.2020.1017
  34. Coto E, Avanzas P, Gómez J. The renin-angiotensin-aldosterone system and coronavirus disease 2019. Eur Cardiol. 2021;16:e07. doi: 10.15420/ecr.2020.30
  35. Pinto BGG, Oliveira AER, Singh Y, et al. ACE2 expression is increased in the lungs of patients with comorbidities associated with severe COVID-19. J Infect Dis. 2020;222(4):556–563. doi: 10.1093/infdis/jiaa332
  36. Yamamoto N, Yamamoto R, Ariumi Y, et al. Does genetic predisposition contribute to the exacerbation of COVID-19 symptoms in individuals with comorbidities and explain the huge mortality disparity between the East and the West? Int J Mol Sci. 2021;22(9):5000. doi: 10.3390/ijms22095000
  37. Hatami N, Ahi S, Sadeghinikoo A, et al. Worldwide ACE (I/D) polymorphism may affect COVID-19 recovery rate: an ecological meta-regression. Endocrine. 2020;68(3):479–484. doi: 10.1007/s12020-020-02381-7
  38. Petrie JR, Guzik TJ, Touyz RM. Diabetes, hypertension, and cardiovascular disease: clinical insights and vascular mechanisms. Can J Cardiol. 2018;34(5):575–584. doi: 10.1016/j.cjca.2017.12.005
  39. Margaglione M, Grandone E, Vecchione G, et al. Plasminogen activator inhibitor-1 (PAI-1) antigen plasma levels in subjects attending a metabolic ward: relation to polymorphisms of PAI-1 and angiontensin converting enzyme (ACE) genes. Arterioscler Thromb Vasc Biol. 1997;17(10):2082–2087. doi: 10.1161/01.atv.17.10.2082
  40. De Loyola MB, Dos Reis TTA, de Oliveira GXLM, et al. Alpha-1-antitrypsin: A possible host protective factor against Covid-19. Rev Med Virol. 2021;31(2):e2157. doi: 10.1002/rmv.2157
  41. 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.e8. doi: 10.1016/j.cell.2020.02.052
  42. Janciauskiene S, Welte T. Well-known and less well-known functions of Alpha-1 antitrypsin. Its role in chronic obstructive pulmonary disease and other disease developments. Ann Am Thorac Soc. 2016;13 Suppl 4:S280–S288. doi: 10.1513/AnnalsATS.201507-468KV
  43. Pott GB, Chan ED, Dinarello CA, Shapiro L. Alpha-1-antitrypsin is an endogenous inhibitor of proinflammatory cytokine production in whole blood. J Leukoc Biol. 2009;85(5):886–895. doi: 10.1189/jlb.0208145
  44. 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(7):e016219. doi: 10.1161/JAHA.120.016219
  45. Hendren NS, Drazner MH, Bozkurt B, Cooper LTJr. Description and proposed management of the acute COVID-19 cardiovascular syndrome. Circulation. 2020;141(23):1903–1914. doi: 10.1161/CIRCULATIONAHA.120.047349
  46. Biscetti F, Rando MM, Nardella E, et al. Cardiovascular disease and SARS-CoV-2: the role of host immune response versus direct viral injury. Int J Mol Sci. 2020;21(21):8141. doi: 10.3390/ijms21218141
  47. Zhu H, Rhee JW, Cheng P, 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
  48. Chen G, Wu D, Guo W, et al. Clinical and immunological features of severe and moderate coronavirus disease 2019. J Clin Invest. 2020;130(5):2620–2629. doi: 10.1172/JCI137244
  49. Hammoudeh SM, Hammoudeh AM, Bhamidimarri PM, et al. Systems immunology analysis reveals the contribution of pulmonary and extrapulmonary tissues to the immunopathogenesis of severe COVID-19 patients. Front Immunol. 2021;12:595150. doi: 10.3389/fimmu.2021.595150
  50. Troshina EA, Yukina MYu, Nuralieva NF, Mokrysheva NG. The role of HLA genes: from autoimmune diseases to COVID-19. Problems of Endocrinology. 2020;66(4):9–15. (In Russ.). doi: 10.14341/probl12470
  51. Zhu F, Sun Y, Wang M, et al. Correlation between HLA-DRB1, HLA-DQB1 polymorphism and autoantibodies against angiotensin AT(1) receptors in Chinese patients with essential hypertension. Clin Cardiol. 2011;34(5):302–308. doi: 10.1002/clc.20852
  52. Davies RW, Wells GA, Stewart AF, et al. A genome-wide association study for coronary artery disease identifies a novel susceptibility locus in the major histocompatibility complex. Circ Cardiovasc Genet. 2012;5(2):217–225. doi: 10.1161/CIRCGENETICS.111.961243
  53. Wu Z, McGoogan JM. 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
  54. COVID-19 Host Genetics Initiative. Mapping the human genetic architecture of COVID-19. Nature. 2021;600(7889):472–477. doi: 10.1038/s41586-021-03767-x
  55. Smith JD. Apolipoprotein E4: an allele associated with many diseases. Ann Med. 2000;32(2):118–127. DOI: 10.3109/ 07853890009011761
  56. Wang H, Yuan Z, Pavel MA, et al. The role of high cholesterol in age-related COVID19 lethality. bioRxiv. 2021. doi: 10.1101/2020.05.09.086249
  57. Kuo CL, Pilling LC, Atkins JL, et al. APOE e4 genotype predicts severe COVID-19 in the UK Biobank Community Cohort. J Gerontol A Biol Sci Med Sci. 2020;75(11):2231–2232. doi: 10.1093/gerona/glaa131
  58. Zong Y, Li X. Identification of causal genes of COVID-19 using the SMR method. Front Genet. 2021;12:690349. doi: 10.3389/fgene.2021.690349
  59. Taus F, Salvagno G, Canè S, et al. Platelets promote thromboinflammation in SARS-CoV-2 pneumonia. Arterioscler Thromb Vasc Biol. 2020;40(12):2975–2989. doi: 10.1161/ATVBAHA.120.315175
  60. Kang S, Tanaka T, Inoue H, et al. IL-6 trans-signaling induces plasminogen activator inhibitor-1 from vascular endothelial cells in cytokine release syndrome. Proc Natl Acad Sci USA. 2020;117(36):22351–22356. doi: 10.1073/pnas.2010229117
  61. Zhang F, Mears JR, Shakib L, et al. IFN-γ and TNF-α drive a CXCL10+ CCL2+ macrophage phenotype expanded in severe COVID-19 lungs and inflammatory diseases with tissue inflammation. Genome Med. 2021;13(1):64. doi: 10.1186/s13073-021-00881-3
  62. Lee JS, Park S, Jeong HW, et al. Immunophenotyping of COVID-19 and influenza highlights the role of type I interferons in development of severe COVID-19. Sci Immunol. 2020;5(49):eabd1554. doi: 10.1126/sciimmunol.abd1554
  63. Korakas E, Ikonomidis I, Kousathana F, et al. Obesity and COVID-19: immune and metabolic derangement as a possible link to adverse clinical outcomes. Am J Physiol Endocrinol Metab. 2020;319(1):E105–E109. doi: 10.1152/ajpendo.00198.2020
  64. Dimopoulos G, de Mast Q, Markou N, et al. Favorable anakinra responses in severe Covid-19 patients with secondary hemophagocytic lymphohistiocytosis. Cell Host Microbe. 2020;28(1):117–123.e1. doi: 10.1016/j.chom.2020.05.007
  65. Ikonomidis I, Pavlidis G, Katsimbri P, et al. Differential effects of inhibition of interleukin 1 and 6 on myocardial, coronary and vascular function. Clin Res Cardiol. 2019;108(10):1093–1101. doi: 10.1007/s00392-019-01443-9
  66. Frangogiannis NG, Entman ML. Chemokines in myocardial ischemia. Trends Cardiovasc Med. 2005;15(5):163–169. doi: 10.1016/j.tcm.2005.06.005
  67. Buoncervello M, Maccari S, Ascione B, et al. Inflammatory cytokines associated with cancer growth induce mitochondria and cytoskeleton alterations in cardiomyocytes. J Cell Physiol. 2019;234(11):20453–20468. doi: 10.1002/jcp.28647

补充文件

附件文件
动作
1. JATS XML
下载

版权所有 © Bratilova E., Kachnov V., Tyrenko V., Kolyubaeva S., 2022

Creative Commons License
此作品已接受知识共享署名 4.0国际许可协议的许可
СМИ зарегистрировано Федеральной службой по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор).
Регистрационный номер и дата принятия решения о регистрации СМИ: серия ПИ № ФС 77 - 71733 от 08.12.2017.


##common.cookie##