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Revision as of 12:49, 1 July 2020

For COVID-19 frequently asked inpatient questions, click here
For COVID-19 frequently asked outpatient questions, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mounika Reddy Vadiyala, M.B.B.S.[2]

Synonyms and keywords: Novel coronavirus, COVID-19, Wuhan Coronavirus, Coronavirus Disease-19, Coronavirus Disease 2019, SARS-CoV-2, COVID-19, COVID-19, 2019-nCoV, 2019 novel coronavirus, Cardiovascular finding in COVID-19, Myocardial injury in COVID-19, Myocarditis, Myocarditis in COVID-19, COVID-19-associated Myocarditis, SARS-CoV2-associated Myocarditis, Myocardial injury in COVID-19, COVID-19 myocarditis

Overview

COVID-19 is caused by the novel coronavirus, also known as SARS-CoV-2. It mainly affects the lungs, causing severe acute respiratory syndrome. It invades through the Angiotensin-converting enzyme 2 (ACE2) receptors present abundantly not only in the lungs but also in the heart, kidneys, intestine, brain, skin thus causing multiorgan dysfunction. Studies have demonstrated that COVID-19 interacts with the cardiovascular system, thereby causing myocardial injury and dysfunction as well as increasing morbidity among patients with underlying cardiovascular conditions.

Historical Perspective

The novel coronavirus, SARS-CoV-2, is identified as the cause of an outbreak of respiratory illness first detected in Wuhan, China in late December 2019. SARS-CoV-2 has rapidly spread across China and in other countries, raising major global concerns. This novel coronavirus, SARS-CoV-2, was named the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) for it similarity severe acute respiratory syndrome related coronaviruses such as SARS-CoV, which caused acute respiratory distress syndrome (ARDS) in 2002–2003.^[1]^[2]^[3]^[4]^[5]
On January 30, 2020,the World Health Organization(WHO) declared the outbreak as a Public Health Emergency of International Concern.^[6]
On March 12, 2020, the World Health Organization declared the COVID-19 outbreak a pandemic.^[7]

Classification

There is no established system for the classification of the myocarditis seen in COVID-19.
For more information regarding general classification, see the myocarditis classification.

Pathophysiology

Myocarditis is an inflammatory disease of the heart characterized by inflammatory infiltrates and myocardial injury without an ischemic cause.^[8]
The major cause of myocarditis in the United States and other developed countries is viral.^[9] ^[10]
The exact mechanisms of COVID-19 induced myocarditis are not yet well known, although several have been proposed based on the limited data outside of case reports.

Proposed pathophysiologies of SARS-CoV-2 myocarditis

Direct invasion of the virus into cardiomyocytes:
- SARS-CoV-2 infection is caused by receptor-mediated endocytosis via binding of the viral surface spike protein (primed by TMPRSS2 - Transmembrane Protease Serine 2) to the human angiotensin-converting enzyme 2 (ACE2) receptor.^[11]^[12]

- ACE2 is expressed in the lung, principally type II alveolar cells which appears to be the principal portal of entry.^[13]
- ACE2 is highly expressed in the heart as well.^[14]
- Although, there are limited reports showing pathological evidence that COVID-19 directly invades the heart.^[15]

Hyperinflammation and Cytokine storm
- Naive T lymphocytes can be primed for viral antigens via antigen-presenting cells.^[16]
- The primed CD8+ T lymphocytes migrate to the cardiomyocytes and through cell-mediated cytotoxicity, cause myocardial inflammation.
- In the cytokine storm syndrome, proinflammatory cytokines such as Interleukin-6 (IL-6) are released into the circulation, which further augments T-lymphocyte activation and causes the release of more cytokines.^[17]
- Cytokine storms result in increased vascular wall permeability and myocardial edema.^[18]^[19]
- A positive feedback loop of immune activation and myocardial damage is established.^[20]^[8]
- Thus cytokine storm activated by T helper cells (Th1 and Th2) and a systemic hyperinflammatory response is triggered.^[21]^[22]

Hypoxic injury
- Respiratory dysfunction and hypoxemia due to COVID-19 can result in damage to myocardial cells.^[23]

Pathological changes in the myocardium

They could be due to viral replication in the myocardium or immune responses caused by the infection or due to systemic responses to respiratory failure.
Interstitial mononuclear inflammatory infiltration has been observed in the heart tissue in COVID-19 autopsy studies.^[24]
In one of the studies of myocarditis in COVID-19, the viral particles were observed in interstitial cytopathic macrophages. Cardiac myocytes showed non‐specific features consisting of focal myofibrillar lysis, and lipid droplets but viral particles in myocytes and endothelia.^[15]

Causes

Myocarditis in COVID-19 is caused by:

Direct invasion of endothelial cells by SARS-CoV-2
Pro-inflammatory cytokine storm
Hypoxic injury

Differentiating COVID-19 associated myocarditis from other Diseases

Myocarditis in COVID-19 must be differentiated from other diseases that cause chest pain, dyspnea, elevated cardiac biomarkers, ventricular dysfunction, such as:

Acute Coronary Syndrome
Stress-induced cardiomyopathy (Takotsubo cardiomyopathy)
Heart failure

Epidemiology and Demographics

The prevalence of cardiovascular disease among patients with COVID-19 is high, and >7% of patients experience myocardial injury from the infection.^[25]
The overall incidence of acute cardiac injury caused by COVID-19 ranges from 7 to 28% among hospitalized patients.^[26]^[27]^[28]
The prevalence of myocarditis among COVID-19 patients has not yet been reported. Though many anecdotal reports of myocarditis have been noted, there are only a few case reports of myocarditis related to COVID-19 .^[27]^[19]^[29]^[18]^[30]^[31]^[15]^[32]^[33]
Myocarditis has also been reported as the cause of death in some COVID-19 patients.^[34]

Age

COVID-19-associated myocarditis is more commonly observed among elderly patients.^[27]^[28]

Gender

There is no data on gender predilection to myocarditis in COVID-19.

Race

There is no data on racial predilection to myocarditis in COVID-19.

Risk Factors

There are no established risk factors for myocarditis.
But the prevelance of COVID-19-associated myocarditis has been more in elderly patients [age>50] and patients with pre-existing cardiovascular diseases.^[28]^[27]

Screening

There is insufficient evidence to recommend routine screening for myocarditis in COVID-19 patients.

Natural History, Complications and Prognosis

Natural history

If left untreated, myocarditis of patients with COVID-19 may progress to develop cardiogenic shock, heart failure, and succumb to death.^[32]

Complications

Common complications of [myocarditis] include:

Prognosis

Prognosis is generally poor.
A retrospective analysis of the cause of death in Chinese patients infected with COVID-19 revealed that 40% of patients died at least in part because of myocardial injury and circulatory collapse.^[34]
In another study, patients hospitalized for COVID-19 infection developed cardiac injury in roughly 20% of cases; thus leading to greater than 50% mortality.^[27]

Diagnosis

Diagnostic Criteria

The diagnosis of myocarditis cannot be made with a single test or examination. When indicated, the diagnosis requires a combination of:

Signs and Symptoms

Clinical presentations have varied in the reported COVID-19 cases with myocarditis in the literature with a potential overlap in symptomatology in patients with primary COVID-19 infection and COVID-19 patients with clinically suspected myocarditis. Clinical presentation of SARS-CoV-2 myocarditis varies among cases from mild to severe to fulminant.

Mild - fatigue and dyspnea,^[29]^[18], chest pain or chest tightness on exertion.^[19]^[30]
Severe - Many patients deteriorate and show symptoms of tachycardia and acute-onset heart failure with cardiogenic shock.^[19]^[29]^[18] They may also present with signs of right-sided heart failure, including raised jugular venous pressure, right upper quadrant pain, and peripheral edema.^[10]
Fulminant - Fulminant myocarditis is defined as ventricular dysfunction and heart failure within 2–3 weeks of infection.^[8]^[35]^[31]^[36] The early signs resemble those of sepsis: fever, low pulse pressure, cold extremities, and sinus tachycardia.^[10]^[19]

According to a study, ventricular arrhythmias are also seen in the patients of myocarditis.^[37]

Physical Examination

Physical examination of patients with severe myocarditis may be remarkable for:

Physical examination of patients with fulminant myocarditis may be remarkable for:

Laboratory Findings

Inflammatory biomarkers

Elevated levels of inflammatory markers including erythrocyte sedimentation rate, C reactive protein, and procalcitonin are usually seen in myocarditis but they are non-specific and do not confirm the diagnosis. Increases levels of Interleukin-6 (IL-6), d-dimer, serum ferritin, prothrombin time were seen in COVID-19 patients.^[27]^[17]

Cardiac biomarkers

Levels of cardiac enzymes such as cardiac troponins (cardiac troponin I(cTnI), cardiac troponin T (cTnT)) and natriuretic peptides (N-terminal pro-B-type natriuretic peptide (NT-proBNP), and Brain natriuretic peptide (BNP)) usually are elevated in myocarditis due to acute myocardial injury and possible ventricular dilation.
Elevations of both troponin and NT-proBNP levels were observed in the COVID-19–related myocarditis cases.^[19]^[29]^[18]^[30]^[35]^[38]
Elevated NT-pro-BNP level has been associated with worse clinical outcomes in severe COVID-19 patients.^[39]^[40]
Cardiac troponins and brain natriuretic peptides are sensitive but non-specific in the diagnosis of myocarditis. It requires other supplementary findings and investigations.^[41]^[42]^[43]
Although a negative troponin result cannot exclude myocarditis, negative serial high-sensitivity cardiac troponin (hs-cTn) still is helpful in the acute phase and makes the diagnosis of acute myocarditis significantly less likely.^[44]

Electrocardiogram

ECG is usually abnormal in myocarditis but it is neither sensitive nor specific in the diagnosis.^[45]^[9]
ECG abnormalities ST-elevation and PR depression may be observed in myocarditis in COVID-19 patients.^[29]^[9]^[35]
However, these abnormalities are not sensitive in detecting myocarditis in COVID-19. For example, one COVID-19–related myocarditis case showed neither ST-elevation nor PR depression.^[19]
Other ECG abnormalities, including new-onset bundle branch block, premature ventricular complexes, QT prolongation, and bradyarrhythmia with advanced atrioventricular nodal block, can be observed in myocarditis.^[18]

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.^[10] 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.^[46]

Echocardiography

The prominent signs of myocarditis on an echocardiogram are increased wall thickness, chamber dilation, diffuse hypokinesia/dyskinesia, and pericardial effusion in the background of ventricular systolic dysfunction.^[47]^[48]^[9]
These findings were noted in COVID-19 related myocarditis cases.^[18]^[29]^[19]

Cardiac Magnetic Resonance

Cardiac Magnetic resonance (CMR) has major imaging advantages with highest diagnostic accuracy over echocardiography^[49], but it has limitations of availability, the requirement for some breath-holding, the requirement for deep cleaning after use given the high contagious risk of COVID-19 and slower throughput.
If CMR is performed, revised Lake Louise consensus criteria are used to interpret the results.^[50] 1) edema 2) irreversible cell injury 3) hyperemia or capillary leak.
In all of the SARS-CoV-2–related myocarditis cases for which CMR results were reported, myocardial edema and/or scarring were observed.^[29]^[18]^[30]

Cardiac Computed Tomography

Cardiac Computed Tomography scan (CT scan) with contrast enhancement and ECG gating is an effective alternative to CMR in terms of rapid testing and minimal requirement of breath-holding, especially when the patient has to undergo a high-resolution CT scan (HRCT) of the chest for assessment of acute respiratory distress syndrome.
Myocardial hypertrophy due to edema was observed in COVID -19 related myocarditis.^[18]

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).^[51] 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.^[52] 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.^[9]^[10]^[49]
EMB samples if obtained should be tested for inflammatory infiltrates and for the presence of viral genomes by DNA/RNA extraction.^[9]
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.^[30]

Treatment

Medical Therapy

There is no definitive treatment for COVID-19-related-myocarditis; the mainstay of therapy is supportive care.
As per AHA recommendations, in the patients of fulminant myocarditis, initial management includes the protocol of cardiogenic shock which is the administration of inotropes and/vasopressors and mechanical ventilation^[29]^[31]; and use of extracorporeal membrane oxygenation(ECMO), ventricular assistive devices (VAD) in severe cases.^[19]^[53]^[35] This protocol has been the mainstay of treatment in COVID-19-related-myocarditis cases as well and proved beneficial in mitigating ventricular systolic dysfunction.
Though the ESC did not approve the use of intravenous immunoglobulins (IVIG) and corticosteroids in active-infection myocarditis, COVID-19 related myocarditis cases have been reported in which use of immunoglobulins and corticosteroids have been successful.^[31]^[19]^[29]^[38]
Tocilizumab, an anti–IL-6 receptor monoclonal antibody, is being tested in a randomized controlled trial of COVID-19 patients with raised IL-6 levels.^[54] This might be beneficial in the setting of cytokine storm syndrome and help reduce myocardial inflammation.^[44]

Prevention

There are no primary preventive measures available for COVID-19-associated myocarditis.
For effective measures for the primary prevention of [COVID-19], refer to COVID-19 primary prevention.

References

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↑ Luetkens, Julian Alexander; Isaak, Alexander; Zimmer, Sebastian; Nattermann, Jacob; Sprinkart, Alois Martin; Boesecke, Christoph; Rieke, Gereon Jonas; Zachoval, Christian; Heine, Annkristin; Velten, Markus; Duerr, Georg Daniel (2020). "Diffuse Myocardial Inflammation in COVID-19 Associated Myocarditis Detected by Multiparametric Cardiac Magnetic Resonance Imaging". Circulation: Cardiovascular Imaging. 13 (5). doi:10.1161/CIRCIMAGING.120.010897. ISSN 1941-9651.
↑ ^34.0 ^34.1 Ruan, Qiurong; Yang, Kun; Wang, Wenxia; Jiang, Lingyu; Song, Jianxin (2020). "Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China". Intensive Care Medicine. 46 (5): 846–848. doi:10.1007/s00134-020-05991-x. ISSN 0342-4642.
↑ ^35.0 ^35.1 ^35.2 ^35.3 Irabien-Ortiz, Ángela; Carreras-Mora, José; Sionis, Alessandro; Pàmies, Julia; Montiel, José; Tauron, Manel (2020). "Fulminant myocarditis due to COVID-19". Revista Española de Cardiología (English Edition). 73 (6): 503–504. doi:10.1016/j.rec.2020.04.005. ISSN 1885-5857.
↑ Wang, Daowen; Li, Sheng; Jiang, Jiangang; Yan, Jiangtao; Zhao, Chunxia; Wang, Yan; Ma, Yexin; Zeng, Hesong; Guo, Xiaomei; Wang, Hong; Tang, Jiarong; Zuo, Houjuan; Lin, Li; Cui, Guanglin (2018). "Chinese society of cardiology expert consensus statement on the diagnosis and treatment of adult fulminant myocarditis". Science China Life Sciences. 62 (2): 187–202. doi:10.1007/s11427-018-9385-3. ISSN 1674-7305.
↑ Peretto, Giovanni; Sala, Simone; Rizzo, Stefania; Palmisano, Anna; Esposito, Antonio; De Cobelli, Francesco; Campochiaro, Corrado; De Luca, Giacomo; Foppoli, Luca; Dagna, Lorenzo; Thiene, Gaetano; Basso, Cristina; Della Bella, Paolo (2020). "Ventricular Arrhythmias in Myocarditis". Journal of the American College of Cardiology. 75 (9): 1046–1057. doi:10.1016/j.jacc.2020.01.036. ISSN 0735-1097.
↑ ^38.0 ^38.1 Doyen, Denis; Moceri, Pamela; Ducreux, Dorothée; Dellamonica, Jean (2020). "Myocarditis in a patient with COVID-19: a cause of raised troponin and ECG changes". The Lancet. 395 (10235): 1516. doi:10.1016/S0140-6736(20)30912-0. ISSN 0140-6736.
↑ Gao, Lei; Jiang, Dan; Wen, Xue-song; Cheng, Xiao-cheng; Sun, Min; He, Bin; You, Lin-na; Lei, Peng; Tan, Xiao-wei; Qin, Shu; Cai, Guo-qiang; Zhang, Dong-ying (2020). "Prognostic value of NT-proBNP in patients with severe COVID-19". Respiratory Research. 21 (1). doi:10.1186/s12931-020-01352-w. ISSN 1465-993X.
↑ Han, Huan; Xie, Linlin; Liu, Rui; Yang, Jie; Liu, Fang; Wu, Kailang; Chen, Lang; Hou, Wei; Feng, Yong; Zhu, Chengliang (2020). "Analysis of heart injury laboratory parameters in 273 COVID‐19 patients in one hospital in Wuhan, China". Journal of Medical Virology. 92 (7): 819–823. doi:10.1002/jmv.25809. ISSN 0146-6615.
↑ Lauer, Bernward; Niederau, Christoph; Kühl, Uwe; Schannwell, Mira; Pauschinger, Matthias; Strauer, Bodo-Eckhard; Schultheiss, Heinz-Peter (1997). "Cardiac Troponin T in Patients With Clinically Suspected Myocarditis". Journal of the American College of Cardiology. 30 (5): 1354–1359. doi:10.1016/S0735-1097(97)00317-3. ISSN 0735-1097.
↑ Heymans, S. (2007). "Myocarditis and heart failure: need for better diagnostic, predictive, and therapeutic tools". European Heart Journal. 28 (11): 1279–1280. doi:10.1093/eurheartj/ehm111. ISSN 0195-668X.
↑ Jensen, Juliana; Ma, Li-Ping; Fu, Michael L. X.; Svaninger, David; Lundberg, Per-Arne; Hammarsten, Ola (2010). "Inflammation increases NT-proBNP and the NT-proBNP/BNP ratio". Clinical Research in Cardiology. 99 (7): 445–452. doi:10.1007/s00392-010-0140-z. ISSN 1861-0684.
↑ ^44.0 ^44.1 Siripanthong, Bhurint; Nazarian, Saman; Muser, Daniele; Deo, Rajat; Santangeli, Pasquale; Khanji, Mohammed Y.; Cooper, Leslie T.; Chahal, C. Anwar A. (2020). "Recognizing COVID-19–related myocarditis: The possible pathophysiology and proposed guideline for diagnosis and management". Heart Rhythm. doi:10.1016/j.hrthm.2020.05.001. ISSN 1547-5271.
↑ Ukena, Christian; Mahfoud, Felix; Kindermann, Ingrid; Kandolf, Reinhard; Kindermann, Michael; Böhm, Michael (2011). "Prognostic electrocardiographic parameters in patients with suspected myocarditis". European Journal of Heart Failure. 13 (4): 398–405. doi:10.1093/eurjhf/hfq229. ISSN 1388-9842.
↑ Hendren, Nicholas S.; Drazner, Mark H.; Bozkurt, Biykem; Cooper, Leslie T. (2020). "Description and Proposed Management of the Acute COVID-19 Cardiovascular Syndrome". Circulation. 141 (23): 1903–1914. doi:10.1161/CIRCULATIONAHA.120.047349. ISSN 0009-7322.
↑ Pinamonti, Bruno; Alberti, Ezip; Cigalotto, Alessandro; Dreas, Lorella; Salvi, Alessandro; Silvestri, Furio; Camerini, Fulvio (1988). "Echocardiographic findings in myocarditis". The American Journal of Cardiology. 62 (4): 285–291. doi:10.1016/0002-9149(88)90226-3. ISSN 0002-9149.
↑ Felker, G.Michael; Boehmer, John P; Hruban, Ralph H; Hutchins, Grover M; Kasper, Edward K; Baughman, Kenneth L; Hare, Joshua M (2000). "Echocardiographic findings in fulminant and acute myocarditis". Journal of the American College of Cardiology. 36 (1): 227–232. doi:10.1016/S0735-1097(00)00690-2. ISSN 0735-1097.
↑ ^49.0 ^49.1 Friedrich, Matthias G.; Strohm, Oliver; Schulz-Menger, Jeanette; Marciniak, Heinz; Luft, Friedrich C.; Dietz, Rainer (1998). "Contrast Media–Enhanced Magnetic Resonance Imaging Visualizes Myocardial Changes in the Course of Viral Myocarditis". Circulation. 97 (18): 1802–1809. doi:10.1161/01.CIR.97.18.1802. ISSN 0009-7322.
↑ Friedrich, Matthias G.; Sechtem, Udo; Schulz-Menger, Jeanette; Holmvang, Godtfred; Alakija, Pauline; Cooper, Leslie T.; White, James A.; Abdel-Aty, Hassan; Gutberlet, Matthias; Prasad, Sanjay; Aletras, Anthony; Laissy, Jean-Pierre; Paterson, Ian; Filipchuk, Neil G.; Kumar, Andreas; Pauschinger, Matthias; Liu, Peter (2009). "Cardiovascular Magnetic Resonance in Myocarditis: A JACC White Paper". Journal of the American College of Cardiology. 53 (17): 1475–1487. doi:10.1016/j.jacc.2009.02.007. ISSN 0735-1097.
↑ Dennert, R.; Crijns, H. J.; Heymans, S. (2008). "Acute viral myocarditis". European Heart Journal. 29 (17): 2073–2082. doi:10.1093/eurheartj/ehn296. ISSN 0195-668X.
↑ Cooper, Leslie T.; Baughman, Kenneth L.; Feldman, Arthur M.; Frustaci, Andrea; Jessup, Mariell; Kuhl, Uwe; Levine, Glenn N.; Narula, Jagat; Starling, Randall C.; Towbin, Jeffrey; Virmani, Renu (2007). "The Role of Endomyocardial Biopsy in the Management of Cardiovascular Disease". Circulation. 116 (19): 2216–2233. doi:10.1161/CIRCULATIONAHA.107.186093. ISSN 0009-7322.
↑ Rao, Sangeetha; Sasser, William; Diaz, Franco; Sharma, Nirmal; Alten, Jeffrey (2014). "Coronavirus Associated Fulminant Myocarditis Successfully Treated With Intravenous Immunoglobulin and Extracorporeal Membrane Oxygenation". Chest. 146 (4): 336A. doi:10.1378/chest.1992018. ISSN 0012-3692.
↑ "Favipiravir Combined With Tocilizumab in the Treatment of Corona Virus Disease 2019 - Full Text View - ClinicalTrials.gov".

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@@ Line 10: / Line 10: @@
 ==Overview==
-Studies have demonstrated that [[COVID-19]] interacts with the [[cardiovascular system]], thereby causing [[myocardial injury]] and dysfunction as well as increasing [[morbidity]] among patients with underlying cardiovascular conditions.
+[[COVID-19]] is caused by the [[novel coronavirus]], also known as [[SARS-CoV-2]]. It mainly affects the lungs, causing [[severe acute respiratory syndrome]]. It invades through the [[Angiotensin-converting enzyme 2]] (ACE2) receptors present abundantly not only in the [[lungs]] but also in the [[heart]], [[kidneys]], [[intestine]], [[brain]], [[skin]] thus causing [[multiorgan dysfunction]]. Studies have demonstrated that [[COVID-19]] interacts with the [[cardiovascular system]], thereby causing [[myocardial injury]] and dysfunction as well as increasing [[morbidity]] among patients with underlying cardiovascular conditions.
 ==Historical Perspective==
@@ Line 138: / Line 138: @@
 *Elevations of both [[troponin]] and [[NT-proBNP]] levels were observed in the [[COVID-19–related myocarditis]] cases.<ref name="ZengLiu2020">{{cite journal|last1=Zeng|first1=Jia-Hui|last2=Liu|first2=Ying-Xia|last3=Yuan|first3=Jing|last4=Wang|first4=Fu-Xiang|last5=Wu|first5=Wei-Bo|last6=Li|first6=Jin-Xiu|last7=Wang|first7=Li-Fei|last8=Gao|first8=Hong|last9=Wang|first9=Yao|last10=Dong|first10=Chang-Feng|last11=Li|first11=Yi-Jun|last12=Xie|first12=Xiao-Juan|last13=Feng|first13=Cheng|last14=Liu|first14=Lei|title=First case of COVID-19 complicated with fulminant myocarditis: a case report and insights|journal=Infection|year=2020|issn=0300-8126|doi=10.1007/s15010-020-01424-5}}</ref><ref name="InciardiLupi2020">{{cite journal|last1=Inciardi|first1=Riccardo M.|last2=Lupi|first2=Laura|last3=Zaccone|first3=Gregorio|last4=Italia|first4=Leonardo|last5=Raffo|first5=Michela|last6=Tomasoni|first6=Daniela|last7=Cani|first7=Dario S.|last8=Cerini|first8=Manuel|last9=Farina|first9=Davide|last10=Gavazzi|first10=Emanuele|last11=Maroldi|first11=Roberto|last12=Adamo|first12=Marianna|last13=Ammirati|first13=Enrico|last14=Sinagra|first14=Gianfranco|last15=Lombardi|first15=Carlo M.|last16=Metra|first16=Marco|title=Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19)|journal=JAMA Cardiology|year=2020|issn=2380-6583|doi=10.1001/jamacardio.2020.1096}}</ref><ref name="HanKim2020">{{cite journal|last1=Han|first1=Seongwook|last2=Kim|first2=Hyun Ah|last3=Kim|first3=Jin Young|last4=Kim|first4=In-Cheol|title=COVID-19-related myocarditis in a 21-year-old female patient|journal=European Heart Journal|volume=41|issue=19|year=2020|pages=1859–1859|issn=0195-668X|doi=10.1093/eurheartj/ehaa288}}</ref><ref name="EspositoGodino2020">{{cite journal|last1=Esposito|first1=Antonio|last2=Godino|first2=Cosmo|last3=Basso|first3=Cristina|last4=Cappelletti|first4=Alberto Maria|last5=Tresoldi|first5=Moreno|last6=De Cobelli|first6=Francesco|last7=Vignale|first7=Davide|last8=Villatore|first8=Andrea|last9=Palmisano|first9=Anna|last10=Gramegna|first10=Mario|last11=Peretto|first11=Giovanni|last12=Sala|first12=Simone|title=Acute myocarditis presenting as a reverse Tako-Tsubo syndrome in a patient with SARS-CoV-2 respiratory infection|journal=European Heart Journal|volume=41|issue=19|year=2020|pages=1861–1862|issn=0195-668X|doi=10.1093/eurheartj/ehaa286}}</ref><ref name="Irabien-OrtizCarreras-Mora2020">{{cite journal|last1=Irabien-Ortiz|first1=Ángela|last2=Carreras-Mora|first2=José|last3=Sionis|first3=Alessandro|last4=Pàmies|first4=Julia|last5=Montiel|first5=José|last6=Tauron|first6=Manel|title=Fulminant myocarditis due to COVID-19|journal=Revista Española de Cardiología (English Edition)|volume=73|issue=6|year=2020|pages=503–504|issn=18855857|doi=10.1016/j.rec.2020.04.005}}</ref><ref name="DoyenMoceri2020">{{cite journal|last1=Doyen|first1=Denis|last2=Moceri|first2=Pamela|last3=Ducreux|first3=Dorothée|last4=Dellamonica|first4=Jean|title=Myocarditis in a patient with COVID-19: a cause of raised troponin and ECG changes|journal=The Lancet|volume=395|issue=10235|year=2020|pages=1516|issn=01406736|doi=10.1016/S0140-6736(20)30912-0}}</ref>
 *Elevated NT-pro-BNP level has been associated with worse clinical outcomes in severe [[COVID-19]] patients.<ref name="GaoJiang2020">{{cite journal|last1=Gao|first1=Lei|last2=Jiang|first2=Dan|last3=Wen|first3=Xue-song|last4=Cheng|first4=Xiao-cheng|last5=Sun|first5=Min|last6=He|first6=Bin|last7=You|first7=Lin-na|last8=Lei|first8=Peng|last9=Tan|first9=Xiao-wei|last10=Qin|first10=Shu|last11=Cai|first11=Guo-qiang|last12=Zhang|first12=Dong-ying|title=Prognostic value of NT-proBNP in patients with severe COVID-19|journal=Respiratory Research|volume=21|issue=1|year=2020|issn=1465-993X|doi=10.1186/s12931-020-01352-w}}</ref><ref name="HanXie2020">{{cite journal|last1=Han|first1=Huan|last2=Xie|first2=Linlin|last3=Liu|first3=Rui|last4=Yang|first4=Jie|last5=Liu|first5=Fang|last6=Wu|first6=Kailang|last7=Chen|first7=Lang|last8=Hou|first8=Wei|last9=Feng|first9=Yong|last10=Zhu|first10=Chengliang|title=Analysis of heart injury laboratory parameters in 273 COVID‐19 patients in one hospital in Wuhan, China|journal=Journal of Medical Virology|volume=92|issue=7|year=2020|pages=819–823|issn=0146-6615|doi=10.1002/jmv.25809}}</ref>
-*Cardiac troponins and brain natriuretic peptides are sensitive but non-specific in the diagnosis of myocarditis.<ref name="LauerNiederau1997">{{cite journal|last1=Lauer|first1=Bernward|last2=Niederau|first2=Christoph|last3=Kühl|first3=Uwe|last4=Schannwell|first4=Mira|last5=Pauschinger|first5=Matthias|last6=Strauer|first6=Bodo-Eckhard|last7=Schultheiss|first7=Heinz-Peter|title=Cardiac Troponin T in Patients With Clinically Suspected Myocarditis|journal=Journal of the American College of Cardiology|volume=30|issue=5|year=1997|pages=1354–1359|issn=07351097|doi=10.1016/S0735-1097(97)00317-3}}</ref><ref name="Heymans2007">{{cite journal|last1=Heymans|first1=S.|title=Myocarditis and heart failure: need for better diagnostic, predictive, and therapeutic tools|journal=European Heart Journal|volume=28|issue=11|year=2007|pages=1279–1280|issn=0195-668X|doi=10.1093/eurheartj/ehm111}}</ref><ref name="JensenMa2010">{{cite journal|last1=Jensen|first1=Juliana|last2=Ma|first2=Li-Ping|last3=Fu|first3=Michael L. X.|last4=Svaninger|first4=David|last5=Lundberg|first5=Per-Arne|last6=Hammarsten|first6=Ola|title=Inflammation increases NT-proBNP and the NT-proBNP/BNP ratio|journal=Clinical Research in Cardiology|volume=99|issue=7|year=2010|pages=445–452|issn=1861-0684|doi=10.1007/s00392-010-0140-z}}</ref>
+*Cardiac troponins and brain natriuretic peptides are sensitive but non-specific in the diagnosis of myocarditis. It requires other supplementary findings and investigations.<ref name="LauerNiederau1997">{{cite journal|last1=Lauer|first1=Bernward|last2=Niederau|first2=Christoph|last3=Kühl|first3=Uwe|last4=Schannwell|first4=Mira|last5=Pauschinger|first5=Matthias|last6=Strauer|first6=Bodo-Eckhard|last7=Schultheiss|first7=Heinz-Peter|title=Cardiac Troponin T in Patients With Clinically Suspected Myocarditis|journal=Journal of the American College of Cardiology|volume=30|issue=5|year=1997|pages=1354–1359|issn=07351097|doi=10.1016/S0735-1097(97)00317-3}}</ref><ref name="Heymans2007">{{cite journal|last1=Heymans|first1=S.|title=Myocarditis and heart failure: need for better diagnostic, predictive, and therapeutic tools|journal=European Heart Journal|volume=28|issue=11|year=2007|pages=1279–1280|issn=0195-668X|doi=10.1093/eurheartj/ehm111}}</ref><ref name="JensenMa2010">{{cite journal|last1=Jensen|first1=Juliana|last2=Ma|first2=Li-Ping|last3=Fu|first3=Michael L. X.|last4=Svaninger|first4=David|last5=Lundberg|first5=Per-Arne|last6=Hammarsten|first6=Ola|title=Inflammation increases NT-proBNP and the NT-proBNP/BNP ratio|journal=Clinical Research in Cardiology|volume=99|issue=7|year=2010|pages=445–452|issn=1861-0684|doi=10.1007/s00392-010-0140-z}}</ref>
 *Although a negative troponin result cannot exclude myocarditis, negative serial [[high-sensitivity cardiac troponin]] (hs-cTn) still is helpful in the acute phase and makes the diagnosis of acute myocarditis significantly less likely.<ref name="SiripanthongNazarian2020">{{cite journal|last1=Siripanthong|first1=Bhurint|last2=Nazarian|first2=Saman|last3=Muser|first3=Daniele|last4=Deo|first4=Rajat|last5=Santangeli|first5=Pasquale|last6=Khanji|first6=Mohammed Y.|last7=Cooper|first7=Leslie T.|last8=Chahal|first8=C. Anwar A.|title=Recognizing COVID-19–related myocarditis: The possible pathophysiology and proposed guideline for diagnosis and management|journal=Heart Rhythm|year=2020|issn=15475271|doi=10.1016/j.hrthm.2020.05.001}}</ref>