My research interest is to determine mechanisms responsible for ventricular arrhythmias and sudden cardiac death. We study mouse models and human induced pluripotent stem cell models of human arrhythmia syndromes to identify arrhythmia mechanisms. Current focus is on human gene mutations that alter (1) sarcoplasmic reticulum calcium handling and (2) contractile proteins. My basic and translational research program has identified alterations in the function of myofilaments and calcium release channels as new molecular arrhythmia mechanisms in heart muscle diseases. Based on these discoveries, I have tested new antiarrhythmic therapies in animal models and in patients. My goal is to identify new pathways for drug treatment of ventricular arrhythmias, a leading cause of death in the industrialized world.