Coronavirus Disease-2019 (COVID-19) and Cardiovascular Complications
2020; Elsevier BV; Volume: 35; Issue: 6 Linguagem: Inglês
10.1053/j.jvca.2020.04.041
ISSN1532-8422
AutoresLulu Ma, Kaicheng Song, Yuguang Huang,
Tópico(s)Long-Term Effects of COVID-19
Resumo•Cardiac complications are associated with poor outcome in COVID-19 patients.•The possible mechanisms of cardiac injury include direct virus invasion, inflammatory storm, hypoxia and instability of coronary plaque.•Special attention should be paid to medicine used in COVID-19 patients, especially those with cardiac side effects. The coronavirus disease-2019 (COVID-19) has become a global pandemic. It has spread to more than 100 countries, and more than 1 million cases have been confirmed. Although coronavirus causes severe respiratory infections in humans, accumulating data have demonstrated cardiac complications and poor outcome in patients with COVID-19. A large percent of patients have underlying cardiovascular disease, and they are at a high risk of developing cardiac complications. The basics of the virus, the clinical manifestations, and the possible mechanisms of cardiac complications in patients with COVID-19 are reviewed. Before an effective vaccine or medicine is available, supportive therapy and identifying patients who are at high risk of cardiac complications are important. The coronavirus disease-2019 (COVID-19) has become a global pandemic. It has spread to more than 100 countries, and more than 1 million cases have been confirmed. Although coronavirus causes severe respiratory infections in humans, accumulating data have demonstrated cardiac complications and poor outcome in patients with COVID-19. A large percent of patients have underlying cardiovascular disease, and they are at a high risk of developing cardiac complications. The basics of the virus, the clinical manifestations, and the possible mechanisms of cardiac complications in patients with COVID-19 are reviewed. Before an effective vaccine or medicine is available, supportive therapy and identifying patients who are at high risk of cardiac complications are important. SINCE the first case of the novel coronavirus (COVID-19) was first reported on December 31, 2019, in Wuhan, China, the rapid spread of the virus has led to a global pandemic. On March 11, the World Health Organization declared that the spread of COVID-19 had become a pandemic. On April 8, the cumulative numbers of diagnosed patients internationally were 1,514,866 with 88,444 cases of mortality.1Johns Hopkins University and Medicine. COVID-19 dashboard by the Center for Systems Science and Engineering (CSSE) at Johns Hopkins. Available at: https://coronavirus.jhu.edu/map.html. Accessed April 15.Google Scholar With accumulating data of COVID-19, cardiac complications have become a big concern. Myocardial injury also has been detected in COVID-19 patients and is confirmed to be associated with poor outcome.2Guo T. Fan Y. Chen M. et al.Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19).JAMA Cardiol. 2020 Mar 27; ([E-pub ahead of print])Crossref PubMed Scopus (2837) Google Scholar The mortality rate among patients with underlying cardiovascular disease has been reported as 10.5%, which is much higher than that in the general population.3Wu Z. McGoogan J.M. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: Summary of a report of 72314 cases from the Chinese Center for Disease Control and Prevention.JAMA. 2020 Feb 24; ([E-pub ahead of print])Crossref Scopus (12462) Google Scholar In addition, underlying cardiovascular diseases have been demonstrated as one of the risk factors for severe cases. Therefore, a systemic understanding of cardiac complications in COVID-19 patients is important. The aim of this review is to provide essential knowledge of COVID-19 infection, its clinical manifestations, and possible mechanisms of cardiac complications. The outbreak of COVID-19 started in early December 2019 when a series of pneumonia cases of unknown cause were detected in Wuhan, China.4Zhu N. Zhang D. Wang W. et al.A novel coronavirus from patients with pneumonia in China, 2019.N Engl J Med. 2020; 382: 727-733Crossref PubMed Scopus (18380) Google Scholar On January 7, the pathogen was identified as a novel coronavirus by the Chinese Center for Disease Control and Prevention, and it was named 2019-nCoV by the World Health Organization on January 12, 2020, or SARS-CoV-2 by the International Committee on Taxonomy of Viruses. 2019-nCoV is made of a single-strand ribonucleic acid, and its genome has been confirmed to be closely related with the coronavirus SARS-CoV, that which causes severe acute respiratory syndrome (SARS).5Lu R. Zhao X. Li J. et al.Genomic characterisation and epidemiology of 2019 novel coronavirus: Implications for virus origins and receptor binding.Lancet. 2020; 395: 565-574Abstract Full Text Full Text PDF PubMed Scopus (8118) Google Scholar Structural analysis has shown that 2019-nCoV has the ability to bind to the angiotensin-converting enzyme 2 receptors (ACE2) in humans. The presence of ACE2 protein in the lower respiratory tract and on the enterocytes in the small intestine suggests the possible entry of the virus,6Hamming I. Timens W. Bulthuis M.L.C. et al.Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis.J Pathol. 2004; 203: 631-637Crossref PubMed Scopus (4144) Google Scholar and it has been confirmed that 2019-nCoV uses ACE2 to enter the host cell.7Hoffmann 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 (271–80.e8)Abstract Full Text Full Text PDF Scopus (13250) Google Scholar Pneumonia and cardiac disease often present in the same patient. The association between pneumonia and cardiac complications has been confirmed previously.8Cilli A. Cakin O. Aksoy E. et al.Acute cardiac events in severe community-acquired pneumonia: A multicenter study.Clin Respir J. 2018; 12: 2212-2219Crossref PubMed Scopus (23) Google Scholar, 9Corrales-Medina V.F. Musher D.M. Wells G.A. et al.Cardiac complications in patients with community-acquired pneumonia: Incidence, timing, risk factors, and association with short-term mortality.Circulation. 2012; 125: 773-781Crossref PubMed Scopus (315) Google Scholar, 10Corrales-medina V.F. Suh K.N. 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Falcone M. et al.Relation of cardiac complications in the early phase of community-acquired pneumonia to long-term mortality and cardiovascular events.Am J Cardiol. 2015; 116: 647-651Abstract Full Text Full Text PDF PubMed Scopus (100) Google Scholar Cardiac complications also have been reported in patients with coronavirus infections.15Yu C.M. Wong R.S. Wu E.B. et al.Cardiovascular complications of severe acute respiratory syndrome.Postgrad Med J. 2006; 82: 140-144Crossref PubMed Scopus (265) Google Scholar, 16Li S.S. Cheng C.W. Fu C.L. et al.Left ventricular performance in patients with severe acute respiratory syndrome: A 30-day echocardiographic follow-up study.Circulation. 2003; 108: 1798-1803Crossref PubMed Scopus (164) Google Scholar, 17Alhogbani T. Acute myocarditis associated with novel Middle East respiratory syndrome coronavirus.Ann Saudi Med. 2016; 36: 78-80Crossref PubMed Scopus (266) Google Scholar In SARS patients, hypotension and tachycardia are common but usually are self-limiting. Arrhythmia and cardiomegaly are rare in patients diagnosed with SARS.15Yu C.M. Wong R.S. Wu E.B. et al.Cardiovascular complications of severe acute respiratory syndrome.Postgrad Med J. 2006; 82: 140-144Crossref PubMed Scopus (265) Google Scholar Reversible subclinical diastolic dysfunction without systolic involvement also has been observed in SARS patients.16Li S.S. Cheng C.W. Fu C.L. et al.Left ventricular performance in patients with severe acute respiratory syndrome: A 30-day echocardiographic follow-up study.Circulation. 2003; 108: 1798-1803Crossref PubMed Scopus (164) Google Scholar Acute myocarditis developed after infection of the Middle East respiratory syndrome coronavirus (MERS-CoV), and myocardial edema was confirmed with magnetic resonance imaging. Furthermore, severe left ventricular dysfunction was persistent on 3-month follow-up.17Alhogbani T. Acute myocarditis associated with novel Middle East respiratory syndrome coronavirus.Ann Saudi Med. 2016; 36: 78-80Crossref PubMed Scopus (266) Google Scholar The effects of COVID-19 on the cardiovascular system are both similar to and different from those of SARS and MERS. Among COVID-19 patients, cardiovascular disease is the most common comorbidity, and cardiac complications are the most common complications.18Wang D. Hu B. Hu C. et al.Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China.JAMA. 2020; 323: 1601-1609Crossref Scopus (16041) Google Scholar,19Huang C. Wang Y. Li X. et al.Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China.Lancet. 2020; 395: 497-506Abstract Full Text Full Text PDF PubMed Scopus (32462) Google Scholar The prevalence of hypertension and other cardiovascular disease has been reported as 15% to 32.6% and 2.5% to 15%, respectively.2Guo T. Fan Y. Chen M. et al.Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19).JAMA Cardiol. 2020 Mar 27; ([E-pub ahead of print])Crossref PubMed Scopus (2837) Google Scholar,18Wang D. Hu B. Hu C. et al.Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China.JAMA. 2020; 323: 1601-1609Crossref Scopus (16041) Google Scholar, 19Huang C. Wang Y. 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Shen B. et al.Association of cardiac injury with mortality in hospitalized patients with COVID-19 in Wuhan, China.JAMA Cardiol. 2020 Mar 25; ([E-pub ahead of print])Crossref PubMed Scopus (2976) Google Scholar be severely ill,18Wang D. Hu B. Hu C. et al.Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China.JAMA. 2020; 323: 1601-1609Crossref Scopus (16041) Google Scholar or require intensive care.22Shi 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 Mar 25; ([E-pub ahead of print])Crossref PubMed Scopus (2976) Google Scholar Cardiac injury, which is indicated by elevated cardiac troponin I (cTnI), also has been confirmed in COVID-19 patients. The incidence of cardiac injury has ranged from 7.2% to 27.8%,2Guo T. Fan Y. 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Monitoring cTnI longitudinally during hospitalization may help predict the progression of the disease.25Lippi 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 Mar 10; ([E-pub ahead of print])Crossref Scopus (503) Google Scholar Left ventricular dysfunction, persistent hypotension, acute myopericarditis, myocarditis, arrhythmia, and heart failure also have been reported in COVID-19 patients.18Wang D. Hu B. Hu C. et al.Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China.JAMA. 2020; 323: 1601-1609Crossref Scopus (16041) Google Scholar,26Inciardi R.M. Lupi L. Zaccone G. et al.Cardiac involvement in a patient with coronavirus disease 2019 (COVID-19).JAMA Cardiol. 2020 Mar 27; ([E-pub ahead of print])Crossref PubMed Scopus (1284) Google Scholar, 27Hu H. Ma F. 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Patient characteristics, the severity of infection, and host reaction all participate in the development of cardiac complications.10Corrales-medina V.F. Suh K.N. Rose G. et al.Cardiac complications in patients with community- acquired pneumonia : A systematic review and meta- analysis of observational studies.PLoS Med. 2011; 8e1001048Crossref PubMed Scopus (190) Google Scholar Direct damage by the virus, systemic inflammatory responses, instability of coronary plaque, and hypoxia have been proposed as possible mechanisms (Fig 1).2Guo T. Fan Y. Chen M. et al.Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19).JAMA Cardiol. 2020 Mar 27; ([E-pub ahead of print])Crossref PubMed Scopus (2837) Google Scholar Direct pathogen invasion in severe pneumonia patients has been confirmed. 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Ferraretti A. et al.Serum interleukin 6 and 10 levels in Takotsubo cardiomyopathy: Increased admission levels may predict adverse events at follow-up.Atherosclerosis. 2016; 254: 28-34Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar The virus triggers a series of immune responses and the production of cytokines storm may contribute to systemic presentation and multiple organ dysfunctions in COVID-19 patients.Table 1Proinflammatory Cytokines and Their Role in Heart DiseaseCytokinesRole in Heart DiseaseSelected Registered Trials for COVID-19TNF-α•Increased in patients with heart failure•Positive correlation between TNF-α expression and the severity of heart failure, left ventricular dilation/hypertrophy, and dysfunctionIL-1β•Elevated in patients with acute myocarditis•NCT04330638IL-6•Increased in patients with acute myocardial infarction and heart failure•Predict the outcome of acute coronary syndrome and chronic heart failure•NCT04321993•NCT04317092•NCT04330638•NCT04329650IL-8•Increased in patients with acute myocardial infarction•Associated with mortality in acute coronary syndromeIL-10•Elevated in patients with acute myocarditis•Poor outcome in Takotsubo cardiomyopathyAbbreviations: COVID-19, coronavirus 2019; IL, interleukin; TNF-α, tumor necrosis factor-alpha. 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Shen B. et al.Association of cardiac injury with mortality in hospitalized patients with COVID-19 in Wuhan, China.JAMA Cardiol. 2020 Mar 25; ([E-pub ahead of print])Crossref PubMed Scopus (2976) Google Scholar SARS-CoV-2 shares the same host receptor (ACE2) with SARS-CoV, and its affinity to ACE2 is 10- to 20-fold greater than that of SARS-CoV.52Wrapp D. Wang N. Corbett K.S. et al.Cryo-EM structure of the 2019-nCoV spike in the prefusion conformation.Science. 2020; 367: 1260-1263Crossref PubMed Scopus (95) Google Scholar The use of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (ACEIs/ARBs) leads to increased expression of ACE2, and concerns about whether the use of ACEIs/ARBs will increase the risk of SARS-CoV-2 infection have been raised. However, in a mice model, SARS-CoV mediated myocardial injury through ACE2 with a remarkable decreased expression of ACE2,31Oudit G.Y. Kassiri Z. Jiang C. et al.SARS-coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS.Eur J Clin Invest. 2009; 39: 618-625Crossref PubMed Scopus (658) Google Scholar and blocking the renin-angiotensin pathway can attenuate the severity of lung injury.53Kuba K. Imai Y. Rao S. et al.A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury.Nat Med. 2005; 11: 875-879Crossref PubMed Scopus (2626) Google Scholar This result suggested the possible protective effect of ACEIs/ARBs in COVID-19 patients. Abrupt discontinuation of ACEIs/ARBs and switching to other antihypertensive drugs may result in adverse cardiac outcome. At present, clinical trials are recruiting patients to evaluate the safety and efficacy ACEIs/ARBs in COVID-19 patients. Guo et al.2Guo T. Fan Y. Chen M. et al.Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19).JAMA Cardiol. 2020 Mar 27; ([E-pub ahead of print])Crossref PubMed Scopus (2837) Google Scholar demonstrated that there was no difference in mortality among patients with or without the use of ACEIs/ARBs. Before more data are available, the authors believe that it is unwise to discontinue ACEIs/ARBs in patients with COVID-19.54Vaduganathan M. Vardeny O. Michel T. et al.Renin – angiotensin – aldosterone aystem inhibitors in patients with Covid-19.N Engl J Med. 2020; 382: 1653-1659Crossref PubMed Scopus (1563) Google Scholar At present, there is no effective vaccination or drug for COVID-19; only sympathetic therapy and empirical/supportive treatment are available. COVID-19 patients have died due to their original comorbidities instead of pneumonia,55Wang T. Du Z. Zhu F. et al.Comorbidities and multi-organ injuries in the treatment of COVID-19.Lancet. 2020; 395: e52Abstract Full Text Full Text PDF PubMed Scopus (433) Google Scholar which suggested the necessity of special attention to their original comorbidities while treating pneumonia. Whether the medications patients used for cardiovascular disease will interfere with the treatment or the outcome of COVID-19 is still unknown. The possible effects of these drugs on pneumonia were taken from studies on patients with CAP/other virus pneumonia. As previously mentioned, at present there is no evidence for stopping the administration of ACEIs/ARBs in COVID-19 patients. In addition, previous reports about the effects of ACEIs/ARBs on outcome of patients with CAP have been conflicting.56Akram A.R. Singanayagam A. Choudhury G. et al.Incidence and prognostic implications of acute kidney injury on admission in patients with community-acquired pneumonia.Chest. 2010; 138: 825-832Abstract Full Text Full Text PDF PubMed Scopus (63) Google Scholar, 57Mortensen E.M. Restrepo M.I. Copeland L.A. et al.Impact of previous statin and angiotensin II receptor blocker use on mortality in patients hospitalized with sepsis.Pharmacotherapy. 2007; 27: 1619-1626Crossref PubMed Scopus (67) Google Scholar, 58Myles P.R. Hubbard R.B. Gibson J.E. et al.The impact of statins, ACE inhibitors and gastric acid suppressants on pneumonia mortality in a UK general practice population cohort.Pharmacoepidemiol Drug Saf. 2009; 18: 697-703Crossref PubMed Scopus (51) Google Scholar Statins can reduce systemic inflammation59Chalmers J.D. Singanayagam A. Murray M.P. et al.Prior statin use is associated with improved outcomes in community-acquired pneumonia.Am J Med. 2008; 121 (1002–7.e1)Abstract Full Text Full Text PDF Scopus (155) Google Scholar and improve outcome in CAP patients58Myles P.R. Hubbard R.B. Gibson J.E. et al.The impact of statins, ACE inhibitors and gastric acid suppressants on pneumonia mortality in a UK general practice population cohort.Pharmacoepidemiol Drug Saf. 2009; 18: 697-703Crossref PubMed Scopus (51) Google Scholar,59Chalmers J.D. Singanayagam A. Murray M.P. et al.Prior statin use is associated with improved outcomes in community-acquired pneumonia.Am J Med. 2008; 121 (1002–7.e1)Abstract Full Text Full Text PDF Scopus (155) Google Scholar; however, beta-blockers were associated with increased 30-day mortality and the need for mechanical ventilation in patients with CAP.59Chalmers J.D. Singanayagam A. Murray M.P. et al.Prior statin use is associated with improved outcomes in community-acquired pneumonia.Am J Med. 2008; 121 (1002–7.e1)Abstract Full Text Full Text PDF Scopus (155) Google Scholar Calcium channel blockers, beta-blockers, and thiazide were associated with a greater risk of 90-day hospitalization with pneumonia.60Shah S. McArthur E. Farag A. et al.Risk of hospitalization for community acquired pneumonia with renin-angiotensin blockade in elderly patients: A population-based study.PLoS One. 2014; 9e110165Crossref PubMed Scopus (20) Google Scholar No studies have demonstrated the effect of statins, beta-blockers, calcium channel blockers, and diuretics on decreasing cardiac complications in patients with pneumonia. Furthermore, specific attention should be paid to medications with cardiovascular side effects for COVID-19, especially in patients with underlying cardiovascular disease. Common antibiotics, which are used for secondary bacterial infections, exert effects on the cardiovascular system. Macrolides (eg, azithromycin)61Falagas M.E. Rafailidis P.I. Rosmarakis E.S. Arrhythmias associated with fluoroquinolone therapy.Int J Antimicrob Agents. 2007; 29: 374-379Crossref PubMed Scopus (86) Google Scholar and fluoroquinolone61Falagas M.E. Rafailidis P.I. Rosmarakis E.S. Arrhythmias associated with fluoroquinolone therapy.Int J Antimicrob Agents. 2007; 29: 374-379Crossref PubMed Scopus (86) Google Scholar have proarrhythmic effects, which include QT- interval prolongation and polymorphic ventricular tachyarrhythmia. Vancomycin can induce the release of histamine, leading to peripheral vasodilation and severe hypotension.61Falagas M.E. Rafailidis P.I. Rosmarakis E.S. Arrhythmias associated with fluoroquinolone therapy.Int J Antimicrob Agents. 2007; 29: 374-379Crossref PubMed Scopus (86) Google Scholar Some formulations of intravenous antibiotics contain a substantial amount of sodium, and attention should be paid to the daily sodium loads, especially in patients with heart failure.48Corrales-Medina V.F. Musher D.M. Shachkina S. et al.Acute pneumonia and the cardiovascular system.Lancet. 2013; 381: 496-505Abstract Full Text Full Text PDF PubMed Scopus (291) Google Scholar Chloroquine/hydroxychloroquine, which is an old drug for malaria, has been confirmed to be effective in patients with COVID-19.62Gao J. Tian Z. Yang X. Breakthrough: Chloroquine phosphate has shown apparent efficacy in treatment of COVID-19 associated pneumonia in clinical studies.Biosci Trends. 2020; 14: 72-73Crossref PubMed Google Scholar,63Gautret P. Lagier J.C. Parola P. et al.Hydroxychloroquine and azithromycin as a treatment of COVID-19: Results of an open-label non-randomized clinical trial.Int J Antimicrob Agents. 2020 Mar 20; ([E-pub ahead of print])Crossref PubMed Scopus (3697) Google Scholar However, their cardiotoxicity, which includes arrhythmia, heart failure, and myocardial disorder, may be severe and irreversible.64Chatre C. Roubille F. Vernhet H. et al.Cardiac complications attributed to chloroquine and hydroxychloroquine: A systematic review of the literature.Drug Saf. 2018; 41: 919-931Crossref PubMed Scopus (273) Google Scholar Anti-inflammatory therapies also have been used in patients with COVID-19. Clinical trials about the effects of tocilizumab, a recombinant IL-6 monoclonal antibody, and baricitinib, an orally administrated selective inhibitor of JAK1 and JAK2, on COVID-19, are recruiting patients. However, both drugs have been proven to be associated with elevated cholesterol levels.65Gabay C. Emery P. van Vollenhoven R. et al.Tocilizumab monotherapy versus adalimumab monotherapy for treatment of rheumatoid arthritis (ADACTA): A randomised, double-blind, controlled phase 4 trial.Lancet. 2013; 381: 1540Abstract Full Text Full Text PDF PubMed Scopus (535) Google Scholar,66Qiu C. Zhao X. She L. et al.Baricitinib induces LDL-C and HDL-C increases in rheumatoid arthritis: A meta-analysis of randomized controlled trials.Lipids Health Dis. 2019; 18: 54Crossref PubMed Scopus (21) Google Scholar Although the association between altered lipid levels and cardiovascular risks is not identified, this side effect cannot be dismissed. Anti-PD-1 antibody, as a checkpoint inhibitor, also has been applied in the treatment of COVID-19 (NCT04268537 and NCT04333914). However, its pulmonary, cardiac, and neurologic toxicity, which is usually fatal, should not be underestimated. Glucocorticoids, which can suppress inflammation, have been used as empirical treatment in severely ill COVID-19 patients,19Huang C. Wang Y. Li X. et al.Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China.Lancet. 2020; 395: 497-506Abstract Full Text Full Text PDF PubMed Scopus (32462) Google Scholar and several clinical trials are recruiting patients to evaluate their effectiveness and safety. However, corticosteroid use in patients with SARS,67Stockman L.J. Bellamy R. Garner P. SARS: Systematic review of treatment effects.PLoS Med. 2006; 3: e343Crossref PubMed Scopus (979) Google Scholar MERS,68Arabi Y.M. Mandourah Y. Al-Hameed F. et al.Corticosteroid therapy for critically ill patients with Middle East respiratory syndrome.Am J Respir Crit Care Med. 2018; 197: 757-767Crossref PubMed Scopus (829) Google Scholar and influenza69Ni Y.N. Chen G. Sun J. et al.The effect of corticosteroids on mortality of patients with influenza pneumonia: A systematic review and meta-analysis.Crit Care. 2019; 23: 99Crossref PubMed Scopus (273) Google Scholar did not improve patient outcome. In addition, their use was not recommended as treatment for COVID-19 outside of clinical trials.70Russell C.D. Millar J.E. Baillie J.K. Clinical evidence does not support corticosteroid treatment for 2019-nCoV lung injury.Lancet. 2020; 395: 473-475Abstract Full Text Full Text PDF PubMed Scopus (1521) Google Scholar COVID-19 is rapidly spreading globally. At present, very little is known about this virus. Before vaccination is available, there is no effective therapy at present. As new clinical evidence emerges, the diagnosis and treatment may change. Clinical trials are necessary to determine the risk factors of cardiac complications, the mechanisms of cardiac injury, and possible treatments to improve the outcome of patients with COVID-19.
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