Customize your JAMA Network experience by selecting one or more topics from the list below.
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 al1 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 short-term 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 virus-related 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
From the front lines of the COVID-19 pandemic, cardiologists could gather a deeper understanding about the role of early corticosteroids as anti-inflammatory therapy in acute or fulminant myocarditis. Steroids are apparently well tolerated during acute COVID-19 infection, and these results might offer indirect evidence against the paradigm of withholding corticosteroids in viral disease, which will have to be confirmed in appropriately designed trials. Prospective assessment of the extent of residual myocardial injury in patients recovered from COVID-19 will be critical to evaluate the potentially impressive long-term burden of cardiovascular complications from COVID-19 and to estimate progression of myocardial dysfunction from postviral myocarditis toward inflammatory cardiomyopathy.
Corresponding Author: Renata De Maria, MD, CNR Institute of Clinical Physiology ASST Grande Ospedale Metropolitano Niguarda, Piazza Ospedale Maggiore 3, 20162 Milan, Italy (email@example.com).
Conflict of Interest Disclosures: None reported.
Published Online: August 19, 2020. doi:10.1001/jamacardio.2020.3389
Di Tano G, Iacovoni A, De Maria R. Implications for the Care of Patients With COVID-19 and Inflammatory Myocardial Disease. JAMA Cardiol. 2020;5(11):1305–1306. doi:10.1001/jamacardio.2020.3389
Coronavirus Resource Center
Create a personal account or sign in to: