A recent study from Prof. David Paterson and Prof. Dan Li’s team (first author Dr. Ni Li) at the University of Oxford highlights how human-derived neuro-cardiac microtissues can uncover new mechanisms behind inherited arrhythmias.
Using hiPSC-derived cardiomyocytes and sympathetic neurons, the researchers investigated catecholaminergic polymorphic ventricular tachycardia (CPVT) and showed that the disease is not solely driven by cardiomyocytes. Dysfunctional sympathetic neurons were able to trigger arrhythmogenic activity even in otherwise healthy cardiomyocytes, underscoring the critical role of neuro-cardiac interactions in arrhythmia development.
To study these interactions, the team combined microelectrode array (MEA) electrical mapping with optical mapping. MEA enables simultaneous multi-site electrophysiological recordings, providing quantitative parameters such as field potential duration, conduction velocity, and rhythm dynamics. Optical mapping complements this by visualizing calcium signaling and excitation propagation across cardiac tissues with fine spatial and temporal resolution, providing deeper insight into cardiac electrophysiology.
These mapping approaches were applied across both 2D and 3D neuro-cardiac models, including hiPSC-derived cardiomyocyte monolayers, neuron–cardiomyocyte co-cultures, and engineered microtissues. Together, they enable researchers to quantify activation patterns, calcium transient dynamics, conduction velocity, and arrhythmogenic activity, providing powerful tools to study cardiac disease mechanisms and evaluate potential therapeutic strategies.
More info: https://pubmed.ncbi.nlm.nih.gov/41691612/
#arrhythmia #electrophysiology #cardiology #CPVT #cardiacneurons #opticalmapping #MEA #iPSC #calcium


