On March 12, 2020, the National Basketball Association suspended its 2020 season after two players tested positive for the novel SARS-CoV-2 (COVID-19) virus. Fears of rapid viral spread, amongst not just athletes but spectators as well, were motivating concerns for halting play. Shortly thereafter, the National Collegiate Athletic Association (NCAA) canceled the 2020 "March Madness" national basketball championship. A significant factor in the decision to cancel sporting events were concerns of myocardial involvement and injury associated with COVID-19 infection. Early observational studies described some degree of cardiac involvement in up to 78% of infected patients, ranging from troponin elevations to features of myocarditis and myopericarditis on cardiac MRI.1 The uncertain risks for myocarditis, a leading cause of sports related sudden cardiac death, and heightened risks for transmission among athletes with limited ability to don personal protective equipment, factored heavily in the decision to halt play during the early months of the pandemic. The first two reported case series of athletes recovering from COVID-19 appeared to validate these concerns.2, 3 (Table) While these initial studies were relatively small in size, cardiac findings were common, occurring in approximately 40% of athletes. Notably, in the first study by Rajpal et al.2, 4 athletes out 26 (15%) had cardiac MRI findings suggestive of myocarditis based on elevated T2 signal and presence of late gadolinium enhancement (LGE), while 8 athletes had evidence for LGE in isolation. No athlete had elevated serum troponin levels, and T1 signals were similar between those with and without suspected myocarditis. In contrast, Brito et al3 found COVID-infected athletes had primarily pericardial involvement by MRI with no cases of suspected myocarditis. Three athletes had abnormal echocardiograms with impaired global longitudinal strain or reduced ejection fraction (< 50%). Only one athlete had elevated troponin levels.
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