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Myocarditis and COVID-19

The FLARE Four

  • Prior reports from outbreaks of SARS and MERS suggest that coronaviruses may have tropism for cardiac tissue
  • SARS-CoV-2 has been reported to cause a variety of cardiac manifestations in the current pandemic. Some have posited that myocarditis, an inflammatory disease with a variety of etiologies, may be a culprit
  • Reports of COVID-19-related myocarditis are extremely limited, and do not abide by the clearly defined criteria for diagnosis of myocarditis
  • Though patients with COVID-19 may suffer from cardiac compromise, the underlying mechanism is currently not understood. Providers should seek clear evidence of a diagnosis and exercise caution prior to initiating empiric therapy for myocarditis

Many people are saying...that COVID-19 patients can develop acute myocarditis.

Acute Cardiac Failure in COVID-19

Heterogeneous cardiac manifestations have been reported with COVID-19, including biomarker evidence of cardiac necrosis and myocardial distention, type I and type II myocardial infarction, cardiomyopathy and ventricular dysfunction, pericardial effusion, and dysrhythmia. These effects are, in turn, attributed to a variety of mechanisms including increased sympathetic tone, dysregulated coagulation, possible microvascular obstruction, hypoxemia, and the action pro-inflammatory cytokines (Madjid et al. 2020).

In addition, there are a few published reports and anecdotes of COVID-19 associated myocarditis. The term myocarditis, however, implies a certain etiopathogenesis, and treatment strategy.

What is Myocarditis?

Myocarditis is defined as an inflammatory disease of cardiac muscle, generally assessed by histopathologic, immunologic, and immunohistochemical criteria. There are multiple etiologies of myocarditis, including viral, giant cell, myocarditis in association with autoimmune illness, toxins and hypersensitivity. Myocarditis may clinically manifest as electrocardiographic abnormalities (ST-T changes including ST depressions, and also ST segment elevations, which may mimic acute coronary syndrome), cardiac troponin elevation, and echocardiographic evidence of subclinical diastolic impairment and regional or global systolic dysfunction (in absence of obstructive coronary disease). Endomyocardial biopsy is considered the gold-standard for establishment of the diagnosis of myocarditis (histopathologic criterion). In contemporary practice, this is not commonly performed (in part due to risk of native heart biopsy); instead, in the pre-COVID-19 era, cardiac MRI has been used in the evaluation of suspected myocarditis (it is worth noting that in the midst of the COVID-19 epidemic, cardiac MRI is not likely to be a feasible modality due to infection control and viral transmission concerns).

Are Coronaviruses a Known Cause of Viral Myocarditis?

SARS-CoV viral RNA was detected in 7 of 20 autopsied human hearts during the Toronto 2003 SARS outbreak, and these hearts had evidence of myocardial damage, increased macrophage infiltration, and reduction in ACE2 protein. However, while mice infected with the human strain of SARS-CoV demonstrated an ACE2-dependent myocardial tropism and reduction in ACE2 levels associated with the viral infection, no evidence of murine myocarditis was reported (Oudit et al. 2009). Furthermore, the significance of an apparent SARS-CoV-mediated reduction of ACE2 levels is unknown.

single publication on MERS coronavirus reported an acute myocarditis manifesting as late gadolinium enhancement in the inferior and lateral left ventricle subepicardium, a pattern suggestive of myocarditis, along with T2 signal intensity suggesting myocardial edema and an acute pattern of injury (Alhogbani 2016).
While these cases, in aggregate, may suggest some tropism for cardiac tissue in prior major coronaviruses, there is not robust published proof that SARS-CoV or MERS cause myocarditis.

Does COVID-19 Cause Myocarditis?

Isolated case reports only have commented on the possibility of a COVID-19 viral-mediated myocarditis. These include:

  • A report of an autopsy of a 50 year old male from China, who had severe hypoxemia due to COVID-19-related respiratory failure complicated by sudden arrest. At autopsy, the heart showed a few interstitial mononuclear inflammatory cells, without “obvious histological changes” (Xu et al. 2020)
  • A report of a 37-year-old Chinese male with coronavirus infection who presented with chest pain, dyspnea, and hypotension. He had regional electrocardiographic ST segment elevation, very high Troponin T (>10,000 ng/L), and left ventricular ejection fraction of 27%; there was no obstructive coronary disease by computed tomography. He was treated with inotropic and vasopressor support, diuretics, and immune suppression including methylprednisolone and intravenous immunoglobulin with resolution of elevated cardiac biomarkers by 3 weeks (Hu et al. 2020)
  • Finally, there is a report of a 53 year old female with no prior medical history presented in Italy in March 2020 with fever, cough, and hypotension and COVID-19 confirmed by PCR. EKG showed inferolateral ST segment elevation and high sensitivity troponin T level up to 590 ng/L. Echocardiography showed increased LV wall thickness, moderate circumferential pericardial effusion, and mild LV dysfunction; obstructive coronary disease was excluded angiographically. Cardiac MRI showed biventricular interstitial edema and reported diffuse late gadolinium enhancement, but the validity and specificity of the late gadolinium finding has been questioned. The patient was treated with dobutamine, lopinavir/ritonavir, methylprednisone, and chloroquine. Over the following week, LV wall thickness was reported decreased by repeat echocardiography, which was interpreted as a reduction in myocardial edema (Inciardi et al. 2020)

In all, these are case reports without histopathological analysis of the myocardium. Whether there is an alternative explanation for the cMR findings for the third patient remains unknown.

Some larger COVID-19 case series report a substantial incidence of LV systolic dysfunction and cardiac compromise. For example, in a Seattle nursing home cohort, 7 of 21 patients were reported to have “cardiomyopathy,” defined as LV systolic dysfunction, and at least one of: cardiogenic shock, low CvO2, or elevated cardiac biomarkers. The findings of this report must be interpreted in light of the age and comorbidity profile of the studies patients. A retrospective review of 68 COVID-19 related fatalities from Wuhan concluded that 5 of 68 (7%) had myocardial damage and died of circulatory failure, with another 22 who died of combined circulatory and respiratory failure (33%). Cardiac troponin was reported for patients who died versus who were discharged, and on average for the decedents the troponin level was 30 ng/L (with highest ~250 ng/L). Authors concluded “[b]ased on the analysis of the clinical data, we confirmed that some patients died of fulminant myocarditis.” No electrocardiographic, cardiac imaging, or histopathologic findings, were reported for any patient in this series (Ruan et al. 2020).

The mechanism for all such acute cardiac deteriorations is not established, and myocarditis - via direct viral injury and/or an inflammatory response such myocardial macrophage activation - has not yet been proven, according to consensus criteria.

Alternate Mechanisms of Acute Cardiac Failure in Patients with COVID-19

A possible hypothesis is that a cytokine-mediated process is an alternate mechanism for the acute cardiac deteriorations. Many COVID-19 reports feature elevations in other systemic inflammatory markers (ferritin, lactate dehydrogenase, interleukin-6), suggesting, but not proving, an acute inflammatory reaction. The reported troponin elevations observed are believed by some experts to be lower than would be expected for acute viral myocarditis.

There are certainly other possibilities for acute cardiac failure in a critically ill COVID-19 patientsacute cor pulmonale (e.g. from hypoxemia), pulmonary embolism (macrovascular or microvascular obstructions) causing acute cor pulmonale, pericardial tamponade, stress cardiomyopathy, sepsis-induced cardiomyopathy, cardiac microvascular dysfunction akin to catastrophic antiphospholipid antibody syndrome, or even coronary vasospasm have been mentioned.

Management and Treatment Considerations

Clinicians caring for inpatients and ICU patients with COVID-19 must maintain a high index of suspicion for incipient cardiac deterioration; combinations of increased troponin, new arrhythmias, and a heart failure syndrome could be the manifestations of myocarditis. There should be surveillance for markers of malperfusion on exam (capillary refill, impaired pulse pressure, cool and dusky extremities, etc.) and laboratory studies (lactate, CvO2), with cardiac testing (biomarkers like troponin and natriuretic peptides, electrocardiogram, and echocardiography or POCUS) if there is suspicion of cardiac deterioration. Telemetric monitoring is recommended as new malignant tachyarrhythmias, coupled with elevated troponin, could signal underlying cardiomyopathy and possible myocarditis (Driggin et al. 2020).

In the absence of diagnostic and mechanistic certainty, treatment decisions are not data-guided and practice can vary by institution. Standard management of cardiac failure and methods for restoration of perfusion are indicated, including inotrope administration (weighing benefits versus risk, eg of tachyarrhythmia), and careful attention to need for a mechanical circulatory support strategy (like VA-ECMO). Multiple institutions are employing their own local protocols for supplemental immunomodulatory treatments, including experimental anti-inflammatory therapies (i.e. tocilizumab) for possible inflammatory/cytokine-related cardiomyopathy. Other institutions are using corticosteroids (noting that current WHO and CDC recommendations are to avoid corticosteroids in viral pneumonia due to COVID-19 unless there is an alternative indication) and intravenous immunoglobulin. Potential therapies will be the subject of a future FLARE episode, and as data on etiopathogenesis is generated we will revisit that topic as well.


  1. Alhogbani, T. (2016). Acute myocarditis associated with novel Middle east respiratory syndrome coronavirus. Ann. Saudi Med. 36, 78–80.
  2. Arentz, M., Yim, E., Klaff, L., Lokhandwala, S., Riedo, F.X., Chong, M., and Lee, M. (2020). Characteristics and Outcomes of 21 Critically Ill Patients With COVID-19 in Washington State. JAMA.
  3. Driggin, E., Madhavan, M.V., Bikdeli, B., Chuich, T., Laracy, J., Bondi-Zoccai, G., Brown, T.S., Nigoghossian, C.D., Zidar, D.A., Haythe, J., et al. (2020). Cardiovascular Considerations for Patients, Health Care Workers, and Health Systems During the Coronavirus Disease 2019 (COVID-19) Pandemic. J. Am. Coll. Cardiol.
  4. Hu, H., Ma, F., Wei, X., and Fang, Y. (2020). Coronavirus fulminant myocarditis saved with glucocorticoid and human immunoglobulin. Eur. Heart J.
  5. Inciardi, R.M., Lupi, L., Zaccone, G., Italia, L., Raffo, M., Tomasoni, D., Cani, D.S., Cerini, M., Farina, D., Gavazzi, E., et al. (2020). Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19). JAMA Cardiol.
  6. Madjid, M., Safavi-Naeini, P., Solomon, S.D., and Vardeny, O. (2020). Potential Effects of Coronaviruses on the Cardiovascular System: A Review. JAMA Cardiol.
  7. Oudit, G.Y., Kassiri, Z., Jiang, C., Liu, P.P., Poutanen, S.M., Penninger, J.M., and Butany, J. (2009). SARS-coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS. Eur. J. Clin. Invest. 39, 618–625.
  8. Ruan, Q., Yang, K., Wang, W., Jiang, L., and Song, J. (2020). Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China. Intensive Care Med.
  9. Xu, Z., Shi, L., Wang, Y., Zhang, J., Huang, L., Zhang, C., Liu, S., Zhao, P., Liu, H., Zhu, L., et al. (2020). Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med.

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