Implications for the Care of Patients With COVID-19 and Inflammatory Myocardial Disease To the Editor Cardiologists are quickly learning about the effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on the heart. Inciardi et al 1 describe a case that may well represent a myocardium-centered extreme of the wide coronavirus disease 2019 (COVID-19) clinical spectrum. In the midst of the COVID-19 outbreak in Italy, a 53-year-old woman presented afebrile 1 week after mild respiratory symptoms with a clinical picture of acute myopericarditis and heart failure but no respiratory tract symptoms and signs of infection. On circumstantial evidence from positive results on SARS-CoV-2 assay, she was treated with hydroxychloroquine, lopinavir/ritonavir, and intravenous methylprednisolone, besides dobutamine and heart failure drugs, and experienced clinical and pump function recovery. 1 A cytokine storm associated with SARS-CoV-2 infection likely plays a role in the development of severe lung involvement and acute respiratory distress syndrome. The early shortterm use of high-dose corticosteroids directed at curtailing this hyperinflammatory response has been recommended as beneficial in these patients. 2 Myopericarditis is an inflammatory disease that may be triggered by different stimuli. Postviral inflammation, linked to parvovirus B12, coxsackie, cytomegalovirus, and, so far sporadically, coronaviruses, is the most frequent pathway. To date, the routine use of immunosuppressants, other than in autoimmune myocarditis, is strictly discouraged if active infection has not been ruled out by negative results on viral genome testing on endomyocardial biopsy. 3 Case reports described clinical and hemodynamic improvement and no evidence of virusrelated adverse events with immunosuppression in patients with lymphocytic myocarditis in whom viral genome presence was not assessed, questioning the stringent need for systematic viral genome search. Two incoming studies are testing immunosuppression in patients with virus-negative myocarditis in the absence of viral genome, 4 but in the pre-COVID-19 era, patient series were small. The SARS-CoV-2 pandemic will sadly offer an unprecedented large number of concurrent cases that span over the range of severe cardiac and lung viral involvement. 1,5