With respect to risk factors for arrhythmia incidence during hospitalization for COVID-19, we could identify age and previous cardiovascular disease as predictors for the occurrence of any arrhythmia. These baseline characteristics have previously been shown to predispose for the development of arrhythmia in the general population without association with infectious diseases [24]. Thus, they may reflect a subgroup of greater general susceptibility to additional proarrhythmic effects. In patients with arrhythmia in our cohort, QTc duration was longer at admission, albeit within normal range in the majority of patients. Dynamic changes of the QTc interval under therapy with hydroxychloroquine and azithromycin cannot be evaluated as repeated ECGs during hospital stay were not systematically available in all patients. Thus, proarrhythmic effects of these drugs cannot be excluded in this cohort. Previous reports point towards significant prolongation of the QTc interval by hydroxychloroquine in COVID-19 which is even more enhanced in combination with azithromycin therapy [25,26]. However, the rate of associated ventricular arrhythmia has been low in these studies. Similarly, no typical “torsades des pointes” were seen in our cohort: in three of five patients with ventricular arrhythmias pre-existent cardiovascular disease was present, and only one of the remaining two patients received QTc-prolonging medication. Thus, rather than induced by direct effects of administered medication, ventricular arrhythmias may have been due to other predisposing risk factors in our cohort.