Patients with arrhythmias during hospitalization showed elevated cardiac biomarkers and elevated levels of IL-6. Myocardial injury in COVID-19 has been reported by multiple studies, however, the underlying mechanisms have yet to be elucidated [2,4]. In our cohort, arrhythmia itself may have promoted a more pronounced increase in hsTNT and NTproBNP by an additional shift in myocardial oxygen demand under a restricted respiratory function and by increasing atrial and ventricular load. In particular, among patients with pre-existent cardiovascular disease a myocardial supply-demand-imbalance of oxygen may become evident during arrhythmia. On the other hand, myocardial injury or ischemia-especially in the light of a higher prevalence of cardiovascular disease in this subgroup-may have exerted proarrhythmic effects in addition to the inflammatory state. Such additional inflammatory influences are implicated by the pronounced increase in IL-6 in patients with arrhythmias in our cohort. In COVID-19 a state of hyperinflammation is commonly observed and correlates with both respiratory failure and myocardial injury [27]. Based on our observations, it may additionally constitute a risk factor for the incidence of arrhythmia but distinct molecular mechanisms have yet to be investigated in experimental studies and larger, prospective patient cohorts. Estimating optimal cut-off values is associated with uncertainty and is affected by the study population. Therefore, the calculated cut-offs for the biomarkers in this study should be interpreted with caution.