Cellular substrates of arrhythmogenicity in inherited and acquired cardiomyopathies

In this thesis, we describe various inherited and acquired cardiomyopathies focusing on the cellular substrates of arrhythmogenicity. The complex interactions between electrical activity, calcium handling, contractility, electromechanical cell coupling, and conduction require various research approaches to better understand the mechanisms of arrhythmias. Developments in cellular models have led to translational and patient-specific research, but further improvements in techniques and interdisciplinary research are necessary to justify the reduced use of animal models. The described patient populations in this thesis are highly suitable for reducing the number of future cardiac disease patients. Research focused on CKD patients or family members of patients with (potentially) inherited cardiomyopathies can be very successful in reducing arrhythmias in these patient groups. However, this will also introduce new and complicated situations where decisions need to be made regarding the clinical treatment of these (sometimes not yet symptomatic) individuals.