Computer simulations are now an established tool in cardiology, linking ion channels to cellular excitation, tissue conduction, and arrhythmia risk, and increasingly shaping drug discovery and patient-specific prediction. After a brief overview of the state of the art, I will showcase our soon-to-be-published human virtual cardiomyocyte, T-World, and explain how it pushes generality and applicability far beyond currently available approaches.

Through my experience of integrating simulations with wet-lab experiments, I have identified nuclear calcium signalling as a major blind spot and a promising new frontier in cardiac pathophysiology. I will present pilot data supporting our hypothesis that the nucleus is far more than a passive recipient of cytosolic signals, instead functioning as a highly autonomous organelle with locally regulated calcium dynamics. Strikingly, our results suggest that nuclear calcium can act as a previously unrecognised driver of arrhythmia during myocardial infarction, a leading cause of sudden death.

Finally, I will outline how we aim to dissect this phenotype mechanistically and leverage these insights to develop next-generation virtual cardiomyocytes that dynamically remodel in response to stress, enabling in silico studies of progressive cardiac disease.