Heart failure (HF) is defined when the heart is unable to circulate sufficient blood to meet the systemic metabolic need. Although it is one of the leading death causes, there remain unanswered questions with regard to the fundamental pathophysiological processes. HF can be caused by a genetic disorder, but recent data shows that it can also be triggered by inflammation. The ongoing covid-19 pandemic stresses the link between inflammation and life-threatening arrhythmia. Besides acutely developed arrhythmia, the delayed effects of inflammation-associated arrhythmia will emerge as a post-covid 19 health issue. The aim of my project is to reveal the role of the immune system, more specifically the macrophages, on electrical remodelling of cardiomyocytes. Using human-induced pluripotent stem cell- derived cardiomayocytes (hiPSC-CMs) and macrophages (hiPSC-MPs) an in vitro model, it will be possible to evaluate the 3 main pathways through which macrophages cause electrical remodeling of cardiomyocytes. Electrical remodeling is proposed to be driven by: 1) the secreted cytokines, 2) macrophage’s “inflammatory soup” including proteases and other non-cytokine components, and 3) through a direct interaction between macrophages and cardiomyocytes via gap-junctions. Since many variables have been unaddressed, delineating the specific role of these 3 pathways in a hiPSC-based human cell model will provide a better understanding of the role of macrophages in electrical remodelling.