As I've pointed out, I'm not a physician and so am not in the best position to speculate on alternatives to the article's apparent hypothesis that the participant's inflammation resulted from their infection with COVID-19: "The global pandemic of coronavirus disease 2019 (COVID-19) continues to cause considerable morbidity and mortality worldwide." It is certainly possible that alternative hypotheses may more accurately describe the data, including the one you suggest that their treatment itself may have partly or completely accounted for the patients' heart tissue inflammation. It should be noted, though, that there are some indications which don't appear to be consistent with your alternative hypothesis. For one thing, it is well-established that viruses trigger heart damage, apart from any treatment: https://www.heartandstroke.ca/articles/how-do-viruses-trigger-heart-damage Yes, heart inflammation (myocarditis) apparently can result from a variety of causes, but they are apparently less likely sources of myocarditis, which seems to be apparent in the Mayo Clinic's statement on myocarditis: "A viral infection usually causes myocarditis, but it can result from a reaction to a drug or be part of a more general inflammatory condition." Another point regarding the German study which might be seen as inconsistent with your alternative hypothesis is that the study sample (n=100) ranged from asymptomatic to minor or moderate symptoms. And, of course, the asymptomatic patients were sent home, while the unwell patients (33) were hospitalized. The majority of the unwell patients received noninvasive ventilation and oxygen supplementation. The list of unwell patients receiving medication included 15 who received an antibiotic, 8 who received a steroid,1 who received an antiviral, and 1 who received hydrochloroquine. Only two patients underwent mechanical ventilation. There does not appear to be strong support in these data for the alternative hypothesis that treatment itself partly or wholly contributed to the "cardiac involvement" of 78 of the 100 patients or the ongoing myocardial inflammation (independent of preexisting conditions) in 60 of these patients. Again, I'm hardly an expert in heart disease or in its causes, diagnosis, or treatment. For all I know, your alternative hypothesis is correct. All I'm saying is that it doesn't appear to be very consistent with the study data.