Besides ventricular dysfunction, pathological enlargement of the atria, often accompanied by the occurrence of atrial fibrillation, is a frequently observed characteristic of heart failure. This atrial enlargement is related to what is known as "atrial cardiomyopathy", which is associated with an increased risk of atrial arrhythmias and a deterioration of the mechanical atrial function and thus ventricular filling. Atrial cardiomyopathy is also associated with increased mortality, independently of ventricular function per se. Atrial cardiomyopathy is particularly common in heart failure with reduced ejection fraction (HFrEF) and a hallmark feature of heart failure with preserved ejection fraction (HFpEF). The Hohendanner lab has previously described various relevant mechanisms in HFpEF and HFrEF animal models, but also in atrial cardiomyopathy in humans, and identified potential therapeutic targets. We, for example, only recently provided evidence for combined SGLT1/2 inhibition as a potential preventive drug in atrial fibrillation. Ongoing research addresses the interplay of ventricular and atrial changes (atrioventricular coupling), the presence of atrial cardiomyopathy and the development of atrial fibrillation in heart failure.

The treatment of atrial and ventricular arrhythmias is still an unmet clinical need. Beyond atrial cardiomyopathy, the Hohendanner lab aims to find new translational approaches to treat cardiac arrhythmias. As an example the group only recently developed a novel iPS-derived cardiomyocyte assay for precision medicine. This tool was used during the COVID-19 pandemic to test pharmacological approaches in severe disease related cardiac dysfunction with imminent translational potential.