COVID-19 Cardiovascular Complications: Difference between revisions

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=====Prevention=====
=====Prevention=====
*[[Identification]] and [[treatment]] of [[acute]] [[reversible]] causes of [[sudden cardiac death]].
*[[Identification]] and [[treatment]] of [[acute]] [[reversible]] causes of [[sudden cardiac death]].<ref name="pmidPMID: 19252119">{{cite journal| author=Koplan BA, Stevenson WG| title=Ventricular tachycardia and sudden cardiac death. | journal=Mayo Clin Proc | year= 2009 | volume= 84 | issue= 3 | pages= 289-97 | pmid=PMID: 19252119 | doi=10.1016/S0025-6196(11)61149-X | pmc=2664600 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19252119  }} </ref>
*Evaluation and management of [[structural]] [[heart disease]] and [[arrhythmia]].
*Evaluation and management of [[structural]] [[heart disease]] and [[arrhythmia]].


Revision as of 01:46, 25 June 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mitra Chitsazan, M.D.[2]Mandana Chitsazan, M.D. [3]Tayyaba Ali, M.D.[4]Ayesha Javid, MBBS[5]Mounika Reddy Vadiyala, M.B.B.S.[6]Sara Haddadi, M.D.[7]

Overview

Cardiovascular Complications

Acute Myocardial Injury

Coronavirus disease 2019 (COVID-19) is a rapidly expanding global pandemic which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), resulting in significant morbidity and mortality. Some hospitalized patients can develop an acute COVID-19 myocardial injury, which can manifest with a variety of clinical presentations but often presents as an acute cardiac injury with cardiomyopathy, ventricular arrhythmias, and hemodynamic instability, acute coronary syndrome, cardiogenic shock. patents with preexisting cardiovascular disease have higher morbidity and mortality.

Myocardial injury

  • COVID-19 patients with cardiovascular comorbidities have higher mortality.
  • Hospitalized patients with COVID-19 and Cardiovascular disease seem to be more prevalent in both the USA and China. [1]
  • In a case series with 187 patients who had confirmed COVID-19, 27.8% of patients had a myocardial injury, which caused cardiac dysfunction and arrhythmias. The result was significantly higher mortality among patients with myocardial injury.
  • It seems to be advisable to triage patients with COVID-19 based on their underlying CVD for a more aggressive treatment plan.
  • The mortality during hospitalization was shown to be 7.62% for patients without underlying CVD and normal TnT levels, 13.33% for those with underlying CVD and normal TnT levels, 37.50% for those without underlying CVD but elevated TnT levels, and 69.44% for those with underlying CVD and elevated TnTs.[2]

Acute Coronary Syndromes

Pathophysiology

The mechanism of COVID-19 cardiovascular injury has not been fully understood and is likely multifactorial.

  • SARS-CoV-2 virus attaches to ACE 2 protein for ligand binding before entering the cell via receptor-mediated endocytosis.
    • Based on single-cell RNA sequencing more than 7.5% of myocardial cells have positive ACE2 expression. This protein can mediate the entry of SARS-CoV-2 and result in direct cardiotoxicity.
  • The cytokine release caused by the virus may lead to vascular inflammation, plaque instability, myocardial inflammation, a hypercoagulable state, or direct myocardial suppression.

Pathological changes:

  • In the level of cardiac tissue: minimal change to interstitial inflammatory infiltration and myocyte necrosis
  • In the level of vasculature: micro-thrombosis and vascular inflammation[1]

Signs and Symptoms

The signs and symptoms of acute coronary syndrome include:[3]

Treatment

In patients with ACS, and COVID-19, treatment should follow the guidelines of the updated Society for Cardiovascular Angiography and Interventions.[1] [4]

ST-Elevation Myocardial Infarction (STEMI)

A US model from 9 major centers showed a 38% drop in total STEMI activations during the COVID-19 pandemic. There is a 40% reduction noted in Spain as well. there was also a delay between the first presentation to a medical encounter up to 318 min. This is important since COVID-19 can potentially be a cause of STEMI through microthrombi, cytokine storm, coronary spasm, or direct endothelial injury.[5]

  • Potential etiologies for the reduction in STEMI PPCI activations:
    • avoidance of medical care due to social distancing or concerns of contracting COVID-19 in the hospital
    • STEMI misdiagnosis
    • increased use of pharmacological reperfusion due to COVID-19

It is very important to realize if patients' anxiety is the reason behind decreasing the presentation of STEMI to U.S. hospitals.[6]

  • Treatment of STEMI & COVID-19: The specific protocols for the treatment have been evolving. Early recommendations showed intravenous thrombolysis as first-line therapy for STEMI patients with confirmed COVID-19 since most hospitals do not have protected cardiac catheterization labs.[5]

Heart Failure

Pathophysiology

  • Patients with chronic heart failure (HF) may be at higher risk of developing severe COVID-19 infection due to the advanced age and the presence of multiple comorbidities.
  • Both de novo acute heart failure and acute decompensation of chronic heart failure can occur in patients with COVID-19.
  • Presumed pathophysiologic mechanisms for the development of new or worsening heart failure in patients with COVID-19 include:[7] [8] [9] [10] [11]
    • Acute exacerbation of chronic heart failure
    • Acute myocardial injury (which in turn can be caused by several mechanisms)
    • Stress cardiomyopathy (i.e., Takotsubo cardiomyopathy)
    • Impaired myocardial relaxation resulting in diastolic dysfunction [i.e., Heart failure with preserved ejection fraction (HFpEF)]
    • Right-sided heart failure, secondary to pulmonary hypertension caused by hypoxia and acute respiratory distress syndrome (ARDS)

Symptoms and signs

  • Dyspnea: may overlap with dyspnea due to concomitant respiratory involvement and ARDS due to COVID-19 infection
  • Lower limb edema
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Confusion and altered mentation
  • Cool extremities
  • Cyanosis
  • Syncope
  • Fatigue
  • Hemoptysis
  • Palpitations
  • Weakness
  • Wheezing or cardiac asthma
  • Distended jugular veins
  • Crackles on auscultation

Electrocardiography (ECG)

  • There is no specific electrocardiographic sign for acute heart failure in COVID-19 patients.
  • The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors such as ischemia, myocarditis, and arrhythmias.
  • These ECG findings may include:
    • Low QRS Voltage
    • Left ventricular hypertrophy
    • Left atrial enlargement
    • Left bundle branch block
    • Poor R progression
    • ST-T changes

Chest x-ray (CXR)

  • The Chest x-ray may show evidence of:
    • Cardiomegaly
    • Pulmonary congestion
    • Increased pulmonary vascular markings.
  • Signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19.

Echocardiography

  • A complete standard transthoracic (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.[12]
  • To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
  • In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
    • Cardiac point-of-care ultrasound (POCUS)
    • Focused cardiac ultrasound study (FoCUS)
    • Critical care echocardiography
  • Cardiac ultrasound can help in assessing the following parameters:
    • Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
    • Left ventricular diastolic function
    • Left ventricular structural abnormalities, including LV size and LV wall thickness
    • Left atrial size
    • Right ventricular size and function
    • Detection and quantification of valvular abnormalities
    • Measurement of systolic pulmonary artery pressure
    • Detection and quantification of pericardial effusion
    • Detection of regional wall motion abnormalities/reduced strain that would suggest an underlying ischemia

Cardiac biomarkers

  • Cardiac Troponins:
    • Elevated cardiac troponin levels suggest the presence of myocardial cell injury or death.
    • Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.[13]
  • Natriuretic Peptides:
    • Natriuretic peptides (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.[14]
    • Elevated BNP and NT-proBNP are of both diagnostic and prognostic significance in patients with heart failure.
    • Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
    • Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.[15] [16]
    • However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.[17] [18] [19] [20] [21]
    • Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.

Treatment

  • Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including beta-blockers, ACEI or ARB, and mineralocorticoid receptor antagonists. [22]
  • Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
    • Fluid restriction
    • Diuretic therapy
    • Vasopressors and/or inotropes
    • Ventricular assisted devices and extracorporeal membrane oxygenation (ECMO)
  • Beta-blockers should not be initiated during the acute stage due to their negative inotropic effects.[23]
  • Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.[24]

Cardiogenic Shock

Myocarditis

Pathophysiology

Signs and symptoms

Clinical presentation of SARS-CoV-2 myocarditis varies among cases from mild to severe to fulminant.

According to a study, ventricular arrhythmias are also seen in the patients of myocarditis.[44]

Diagnostic testing

The American Heart Association (AHA) recommends further testing with 1 or more cardiac imaging methods such as an echocardiogram or cardiovascular magnetic resonance (CMR) for patients having signs consistent with myocarditis.[28] However, echocardiogram or cardiac imaging can be avoided or delayed until recovery from COVID-19 in the patients with COVID-19 and myocardial injury who are hemodynamically and electrophysiologically stable with mild to moderate elevations of troponin unless the patient clinically deteriorates and develops hemodynamic instability, shock, ventricular arrhythmias, or a severely elevated or rapidly rising troponins.[54]

  • Cardiac Computed Tomography
  • Endomyocardial biopsy:
    • Endomyocardial biopsy (EMB) has been recommended as the definitive diagnostic tool for myocarditis by the American Heart Association (AHA) and European Society of Cardiology (ESC).[59] In non–COVID-19 cases, endomyocardial biopsy has traditionally been recommended in fulminant presentations to exclude the rare presentation of eosinophilic, hypersensitive,and giant-cell myocarditis.[60] However, in COVID-19, it may not be feasible because of the instability of the patient, requirement of expertise, false-negative rate and risk of contagiousness, especially if the biopsy results would not change clinical management.[27][28][57]
    • EMB samples if obtained should be tested for inflammatory infiltrates and for the presence of viral genomes by DNA/RNA extraction.[27]
    • In a COVID-19 case reported, EMB showed diffuse T-lymphocytic inflammatory infiltrates with huge interstitial edema and no replacement fibrosis, suggesting an acute inflammatory process. SARS-CoV-2 genome was absent within the myocardium in molecular analysis.[32]

Treatment

Pericarditis

Pericarditis is a rare manifestation of COVID-19. There are very few case reports of pericarditis in COVID-19 patients.[63][30][64][65]

Pathophysiology

  • Viral infections are a common cause of pericarditis. It is hypothesized that viruses cause pericardial inflammation via direct cytotoxic effects or via immune-mediated mechanisms.[66]
  • COVID-19 has been reported to trigger an exaggerated inflammatory response in patients which might be leading to pericarditis and subsequent pericardial effusion in certain patients; however, the exact mechanism is unclear.

Signs and Symptoms

Diagnostic testing

Treatment

Arrhythmias

Pathophysiology:

Signs and Symptoms:

Arrhythmia or conduction system disease is the nonspecific clinical presentation of COVID-19. Patients may be tachycardic (with or without palpitations) in the setting of other COVID-19-related symptoms (eg, fever, shortness of breath, pain, etc).

  • Palpitations: According to a study done in Hubei province,palpitations were reported as a presenting symptom by 7.3 percent of patients.[69][70]
  • Prolong QT Interval: According to a multicenter study done in New York that involved 4250 COVID-19 patients, 260 patients (6.1 percent) had corrected QT interval (QTc) >500 milliseconds at the time of admittance. However, in another study that involved 84 patients who got hydroxychloroquine and azithromycin, the baseline QTc interval was 435 milliseconds before receiving these medications.[71][72]
  • Atrial Arrhythmia: According to a study, among 393 patients with COVID-19, atrial arrhythmias were more common among patients requiring invasive mechanical ventilation than noninvasive mechanical ventilation (17.7 versus 1.9 percent).[73]
  • Ventricular Arrhythmia: According to a study done in Wuhan, China. among 187 hospitalized patients with COVID-19, 11 patients (5.9 percent) developed ventricular tachyarrhythmias.[2]
  • Cardiac Arrest: According to a Lombardia Cardiac Arrest Registry (Lombardia CARe) of the region Lombardia in Italy. Out of 9806 cases of COVID-19, 362 cases of out-of-hospital cardiac arrest were reported during the study time frame in 2020. During a similar period in 2019, 229 cases of out-of-hospital cardiac arrest were reported, which means an increment of 58% was observed in 2020 among COVID-19 patients. According to the records from a tertiary care hospital in Wuhan. Out of 761 patients with severe COVID-19, 151 patients developed in-hospital cardiac arrest. 136 patients received resuscitation. Out of 136 patients, 119 patients had a respiratory cause. 10 patients had a cardiac cause. 7 patients had other causes. Ventricular fibrillation or pulseless ventricular tachycardia was observed in 8 patients (5.9%), Pulseless electrical activity in 6 patients (4.4%), and asystole in 122 COVID-19 patients (89.7%).[74][75]

Diagnostic Testing:

  • ECG: Most patients with the severe COVID-19, and especially patients who receive QT-prolonging medications, should have a baseline electrocardiogram (ECG) performed at the time of admission to the hospital.The best technique to get the QT interval is with a 12-lead electrocardiogram (ECG). However, to scale back exposure to hospital workers, this could not perpetually be possible. A single-lead ECG might underestimate the QT interval, and there ought to be an effort to use a multiple-lead telemetry system to observe the QT interval.[76][77]
  • Transthoracic echocardiography: Transthoracic echocardiography is recommended for an inpatient with heart failure, arrhythmia, ECG changes, or newly diagnosed cardiomegaly on chest x-ray or CT-chest.[30]

Treatment:

  • Polymorphic Ventricular Tachycardia (torsades de pointes): All patients with torsades de pointes (TdP) should be determined if they are hemodynamically stable or unstable through immediate evaluation of the symptoms, vital signs, and level of consciousness.[78]
    • Unstable patients: Patients with COVID-19 with sustained torsades de pointes (TdP) usually become hemodynamically unstable, severely symptomatic because of perfusion failure, or pulseless and should be treated according to standard resuscitation algorithms, including cardioversion/defibrillation. Initial treatment with antiarrhythmic medications is not indicated for hemodynamically unstable or pulseless patients except intravenous (IV) magnesium.
    • Stable patients: In a patient with a single episode of TdP, treatment with IV magnesium along with correction of metabolic/electrolyte disturbances or removal of any inciting medications may be sufficient. The patient should be kept under observation until the electrolytes, and the QT interval nearly normalizes. An IV bolus of 2-gram magnesium sulfate is the standard therapy for an adult. This is equivalent to a dose of 8.12 mmol of magnesium. The clinical situation of a patient determines the rate of magnesium infusion. Infusion occurs over one to two minutes in patients with pulseless cardiac arrest. The infusion should occur over 15 minutes in patients without cardiac arrest as a rapid IV bolus of magnesium can result in hypotension and asystole. Some patients are given a continuous bolus of IV magnesium at a rate of 3 to 20 mg/min until the QT interval is below 0.50 seconds.[79][80]
  • Other Cardiac arrhythmia: The treatment for other arrhythmias in COVID-19 patients is the same as in patients with arrhythmias without COVID-19 infection.

Out-of-hospital cardiac arrest and Sudden Cardiac Death

Pathophysiology
  • Drug induced:

Since the COVID-19 pandemic, several pharmacological therapies have been proposed, one of them is of two anti-malarial and antirheumatic drugs called Chloroquine or Hydroxychloroquine. Due to their cost-effectiveness and easy availability, there is a surge in the use of Chloroquine and Hydroxychloroquine, with or without Azithromycin. The clinical trials in order to estimate their efficacy are still in the preliminary stage, however, a notable concern is of their cardiac adverse effects. This includes QT prolongation and Torsade de pointes (TdP) leading to sudden cardiac death. The risk is there when these drugs are prescribed separately, however it increases several folds when these drugs are administered together, especially in patients with underlying hepatic disease or renal failure.

  • Genetic susceptibility:

Epidemiological studies have shown that African Americans have higher COVID-19 associated morbidity and mortality as compared to people from other ethnic groups. Recent studies show that this ethnic predilection is due to the genetics factors which contribute to a common ion channel variant p.Ser1103Tyr-SCN5A which confer an increased risk of drug-induced long QT syndrome (DI-LQTS) and drug-induced sudden cardiac death (DI-SCD). p.Ser1103Tyr-SCN5A generates late or persistent sodium current which is further aggravated by hypoxia or respiratory acidosis secondary to lungs involvement in COVID-19. This has and has been linked to an increased risk of ventricular arrhythmia (VA) such as torsade de pointes and sudden cardiac death (SCD) in African Americans.

Out of hospital Sudden cardiac arrest and death

Epidemiology

  • Incidence

There is a two-times rise in the incidence of Out of hospital Sudden cardiac arrest (OHCA) during the COVID-19 pandemic as compared to the non-pandemic time period.[81]

  • Mortality

There is a significant increase in the mortality rate of the OHCA patients.[81]

  • Age

Mean age 69·7 years is observed among patients who experienced Out of hospital Sudden cardiac arrest (OHCA) .[81] .

  • Gender

Studies show that males have a slightly higher incidence of Out of hospital Sudden cardiac arrest (OHCA) as compared to the females.[81]

  • Race

A higher incidence is seen among Blacks as compared to whites.[82]

Diagnosis

Treatment

  • Cardiopulmonary resuscitation
  • Implantable Cardioverter Defibrillator (ICD)
  • Pharmacologic therapy in survivors of sudden cardiac arrest
Prevention

Spontaneous Coronary Artery Dissection

Pathophysiology

  • In patients with an inflammatory overload, a localized inflammation of the coronary adventitia and periadventitial fat can occur. This could lead to the development of sudden coronary artery dissection in a susceptible patient.

Signs and symptoms

Treatment

References

  1. ↑ 1.0 1.1 1.2 Kang Y, Chen T, Mui D, Ferrari V, Jagasia D, Scherrer-Crosbie M; et al. (2020). "Cardiovascular manifestations and treatment considerations in covid-19". Heart. doi:10.1136/heartjnl-2020-317056. PMC 7211105 Check |pmc= value (help). PMID 32354800 Check |pmid= value (help).
  2. ↑ 2.0 2.1 Guo T, Fan Y, Chen M, Wu X, Zhang L, He T; et al. (2020). "Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19)". JAMA Cardiol. doi:10.1001/jamacardio.2020.1017. PMC 7101506 Check |pmc= value (help). PMID 32219356 Check |pmid= value (help).
  3. ↑ Abidov A, Rozanski A, Hachamovitch R, Hayes SW, Aboul-Enein F, Cohen I; et al. (2005). "Prognostic significance of dyspnea in patients referred for cardiac stress testing". N Engl J Med. 353 (18): 1889–98. doi:10.1056/NEJMoa042741. PMID 16267320. Review in: Evid Based Med. 2006 Jun;11(3):91
  4. ↑ Szerlip M, Anwaruddin S, Aronow HD, Cohen MG, Daniels MJ, Dehghani P; et al. (2020). "Considerations for cardiac catheterization laboratory procedures during the COVID-19 pandemic perspectives from the Society for Cardiovascular Angiography and Interventions Emerging Leader Mentorship (SCAI ELM) Members and Graduates". Catheter Cardiovasc Interv. doi:10.1002/ccd.28887. PMID 32212409 Check |pmid= value (help).
  5. ↑ 5.0 5.1 Ullah W, Sattar Y, Saeed R, Ahmad A, Boigon MI, Haas DC; et al. (2020). "As the COVID-19 pandemic drags on, where have all the STEMIs gone?". Int J Cardiol Heart Vasc. 29: 100550. doi:10.1016/j.ijcha.2020.100550. PMC 7261452 Check |pmc= value (help). PMID 32550258 Check |pmid= value (help).
  6. ↑ Garcia S, Albaghdadi MS, Meraj PM, Schmidt C, Garberich R, Jaffer FA; et al. (2020). "Reduction in ST-Segment Elevation Cardiac Catheterization Laboratory Activations in the United States During COVID-19 Pandemic". J Am Coll Cardiol. 75 (22): 2871–2872. doi:10.1016/j.jacc.2020.04.011. PMC 7151384 Check |pmc= value (help). PMID 32283124 Check |pmid= value (help).
  7. ↑ PMID 32219357 (PMID 32219357)
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  8. ↑ PMID 32360242 (PMID 32360242)
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  9. ↑ PMID 32186331 (PMID 32186331)
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  10. ↑ PMID 30625066 (PMID 30625066)
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  11. ↑ PMID 32140732 (PMID 32140732)
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  12. ↑ PMID 32391912 (PMID 32391912)
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  13. ↑ PMID 20863950 (PMID 20863950)
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  14. ↑ PMID 28062628 (PMID 28062628)
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  15. ↑ PMID 32293449 (PMID 32293449)
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  16. ↑ PMID 32232979 (PMID 32232979)
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  17. ↑ PMID 18298480 (PMID 18298480)
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  18. ↑ PMID 16442916 (PMID 16442916)
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  19. ↑ PMID 28322314 (PMID 28322314)
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  20. ↑ PMID 23837838 (PMID 23837838)
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  21. ↑ PMID 21478812 (PMID 21478812)
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  22. ↑ PMID 31129923 (PMID 31129923)
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  23. ↑ PMID 24251454 (PMID 24251454)
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  24. ↑ PMID 12656651 (PMID 12656651)
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  25. ↑ 25.0 25.1 Clerkin, Kevin J.; Fried, Justin A.; Raikhelkar, Jayant; Sayer, Gabriel; Griffin, Jan M.; Masoumi, Amirali; Jain, Sneha S.; Burkhoff, Daniel; Kumaraiah, Deepa; Rabbani, LeRoy; Schwartz, Allan; Uriel, Nir (2020). "COVID-19 and Cardiovascular Disease". Circulation. 141 (20): 1648–1655. doi:10.1161/CIRCULATIONAHA.120.046941. ISSN 0009-7322.
  26. ↑ 26.0 26.1 26.2 Esfandiarei, Mitra; McManus, Bruce M. (2008). "Molecular Biology and Pathogenesis of Viral Myocarditis". Annual Review of Pathology: Mechanisms of Disease. 3 (1): 127–155. doi:10.1146/annurev.pathmechdis.3.121806.151534. ISSN 1553-4006.
  27. ↑ 27.0 27.1 27.2 27.3 27.4 27.5 Caforio, A. L. P.; Pankuweit, S.; Arbustini, E.; Basso, C.; Gimeno-Blanes, J.; Felix, S. B.; Fu, M.; Helio, T.; Heymans, S.; Jahns, R.; Klingel, K.; Linhart, A.; Maisch, B.; McKenna, W.; Mogensen, J.; Pinto, Y. M.; Ristic, A.; Schultheiss, H.-P.; Seggewiss, H.; Tavazzi, L.; Thiene, G.; Yilmaz, A.; Charron, P.; Elliott, P. M. (2013). "Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: A position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases". European Heart Journal. 34 (33): 2636–2648. doi:10.1093/eurheartj/eht210. ISSN 0195-668X.
  28. ↑ 28.0 28.1 28.2 28.3 28.4 Kociol, Robb D.; Cooper, Leslie T.; Fang, James C.; Moslehi, Javid J.; Pang, Peter S.; Sabe, Marwa A.; Shah, Ravi V.; Sims, Daniel B.; Thiene, Gaetano; Vardeny, Orly (2020). "Recognition and Initial Management of Fulminant Myocarditis". Circulation. 141 (6). doi:10.1161/CIR.0000000000000745. ISSN 0009-7322.
  29. ↑ 29.0 29.1 29.2 29.3 29.4 29.5 29.6 29.7 29.8 29.9 Zeng, Jia-Hui; Liu, Ying-Xia; Yuan, Jing; Wang, Fu-Xiang; Wu, Wei-Bo; Li, Jin-Xiu; Wang, Li-Fei; Gao, Hong; Wang, Yao; Dong, Chang-Feng; Li, Yi-Jun; Xie, Xiao-Juan; Feng, Cheng; Liu, Lei (2020). "First case of COVID-19 complicated with fulminant myocarditis: a case report and insights". Infection. doi:10.1007/s15010-020-01424-5. ISSN 0300-8126.
  30. ↑ 30.00 30.01 30.02 30.03 30.04 30.05 30.06 30.07 30.08 30.09 30.10 30.11 Inciardi, Riccardo M.; Lupi, Laura; Zaccone, Gregorio; Italia, Leonardo; Raffo, Michela; Tomasoni, Daniela; Cani, Dario S.; Cerini, Manuel; Farina, Davide; Gavazzi, Emanuele; Maroldi, Roberto; Adamo, Marianna; Ammirati, Enrico; Sinagra, Gianfranco; Lombardi, Carlo M.; Metra, Marco (2020). "Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)". JAMA Cardiology. doi:10.1001/jamacardio.2020.1096. ISSN 2380-6583.
  31. ↑ 31.0 31.1 31.2 31.3 31.4 31.5 31.6 31.7 31.8 Han, Seongwook; Kim, Hyun Ah; Kim, Jin Young; Kim, In-Cheol (2020). "COVID-19-related myocarditis in a 21-year-old female patient". European Heart Journal. 41 (19): 1859–1859. doi:10.1093/eurheartj/ehaa288. ISSN 0195-668X.
  32. ↑ 32.0 32.1 32.2 32.3 32.4 Esposito, Antonio; Godino, Cosmo; Basso, Cristina; Cappelletti, Alberto Maria; Tresoldi, Moreno; De Cobelli, Francesco; Vignale, Davide; Villatore, Andrea; Palmisano, Anna; Gramegna, Mario; Peretto, Giovanni; Sala, Simone (2020). "Acute myocarditis presenting as a reverse Tako-Tsubo syndrome in a patient with SARS-CoV-2 respiratory infection". European Heart Journal. 41 (19): 1861–1862. doi:10.1093/eurheartj/ehaa286. ISSN 0195-668X.
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  42. ↑ 42.0 42.1 42.2 Fang, Yuan; Wei, Xin; Ma, Fenglian; Hu, Hongde (2020). "Coronavirus fulminant myocarditis treated with glucocorticoid and human immunoglobulin". European Heart Journal. doi:10.1093/eurheartj/ehaa190. ISSN 0195-668X.
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