Case Presentation: A 22-year-old man with recent diagnosis of COVID-19 after developing shortness of breath was admitted to our hospital on day 5 of symptoms with acute worsening of dyspnea and new onset chest pain. On admission, he was tachycardic to the 120s, febrile to 38.6°C and hypotensive with systolic pressures in the 80s. On exam he was ill-appearing and confused. His initial labs were significant for white blood cells 22 K/uL, troponin 2.9 ng/mL, blood urea nitrogen/creatinine of 55/6.3 mmol/L, d-dimer 3.5 mcg/mL, mildly elevated liver enzymes and rising lactate to 14 mmol/L. His EKG showed sinus tachycardia. Chest x-ray showed cardiomegaly but no diffuse pulmonary edema or infiltrates. Echocardiogram demonstrated severe biventricular failure with ejection fraction of 20-25%. He had rapidly increased pressor requirements despite IV fluids, was urgently intubated and cannulated for extracorporeal membrane oxygenation(ECMO) and Impella in the ICU. In addition, he received high dose methylprednisolone for his myocarditis. Workup for other causes, including toxic and infectious etiologies was negative.His condition improved and his Impella and ECMO were removed by day 12 of his disease course, and then extubated. His repeat echocardiogram on day 19 showed return to normal ventricular function with an ejection fraction of 55-60%. His COVID test returned negative on day 22 and he was subsequently discharged.

Discussion: Myocarditis is an inflammatory disease of cardiac muscle that can be caused by both noninfectious and infectious agents, including COVID-19. A combination of clinical presentation and noninvasive diagnostic findings may be used to make a diagnosis of “clinically suspected” myocarditis. While histology remains the gold standard for establishing the diagnosis, patients may be diagnosed with “clinically suspected myocarditis” on the basis of a compatible clinical presentation. Patients with COVID-19 commonly present with signs of myocardial injury, particularly troponin elevation. A recent study reported that 12% of COVID-19 patients had associated acute cardiac injury, the majority being in those with pre-existing heart disease and patients >50 years old. Here we present a young patient with no medical history who developed myocarditis and heart failure secondary to COVID-19. Additional diagnostic tools such as cardiac MRI and biopsy were limited due to the renal failure and instability of the patient. He was treated for clinically suspected myocarditis with methylprednisolone and improved. Remarkably he did not appear to have severe lung disease and never required supplemental oxygenation for respiratory failure. Upon review of the literature, only one other patient of this age group has been reported with COVID myocarditis, a 21-year-old South Korean woman. Her clinical course was not reported. In a study that predated COVID-19, 26.6% of patients admitted with suspected acute myocarditis had either left ventricular ejection fraction <50 percent, sustained ventricular arrhythmias, or a low cardiac output syndrome. Patients who presented with these complications had worse long-term outcomes. COVID-19 patients with myocarditis are associated with a high risk of mortality during hospitalization. Those with greater frequency and magnitude of troponin elevations had worse outcomes.

Conclusions: COVID-19 myocarditis is an important presentation that is rarely found in young patients. Continued research on the prevalence and treatment of this new viral disease is needed.