Massachusetts General Hospital pathologist James Stone can tell that most of the hearts he’s examined from COVID-19 patients are damaged from the first moment he holds them. They’re enlarged. They’re heavy. They’re uneven.

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What he can’t tell—at least until he starts looking at samples of the tissue under a microscope—is exactly how those hearts were damaged, and whether it is a direct result of SARS-CoV-2 infection.

Early in the pandemic, other clinicians noted that even some patients who didn’t have preexisting heart conditions experienced cardiovascular damage while fighting COVID-19 infections, pointing to a possible causative link. Researchers had found, for example, that 8% to 12% of hospitalized COVID-19 patients had elevated levels of muscle contraction-regulating proteins called troponins—a sign of heart damage—and that these patients had an increased risk of mortality compared with those who didn’t have excess troponins. And early observations of patients in China who suffered reduced ejection fraction—the amount of blood getting pumped out of the heart each time it contracts—led researchers to suggest that these individuals were likely experiencing myocarditis, a severe form of inflammation that can weaken the heart and is commonly associated with infections.