The autonomic nervous system plays an essential role in the initiation and maintenance of arrhythmias. My lab has a keen interest in understanding fundamental mechanisms behind cardiac autonomic dysfunction in cardiovascular disease and developing novel neuromodulatory therapies. We have demonstrated important changes throughout the peripheral sympathetic and parasympathetic nervous system that result from cardiac injury and contribute to arrhythmias and worsening heart failure in patients with ischemic and non-ischemic cardiomyopathy. To better evaluate mechanisms behind this neural remodeling that leads to sympathoexcitation and parasympathetic dysfunction, my lab has developed and has a decade of experience using a porcine model of myocardial infarction and ventricular trachycardia, an experimental model with electrical and neural changes akin to humans, and utilizing genetic mouse models of heart failure and cardiomyopathy. We use detailed multi-electrode high resolution electrophysiological recordings, neural recordings and network analysis, tissue clearing and confocal/super-resolution imaging, and tracer and viral tracer techniques and genetic analysis/RNAseq to improve our understanding of the substrate of arrhythmias. In addition, as the Director of Clinical and Translational Research at the UCLA Cardiac Arrhythmia Center, I oversee several human mechanistic and multicenter clinical studies, a role that fosters a bench-to-bedside and back approach, with a focus on discovering novel therapeutic pathways that can be directly translated to patients.