Histone deacetylase 2-dependent ventricular electrical remodeling in a porcine model of early heart failure

•Early heart failure is characterized by prolongation of QTc intervals and ventricular effective refractory periods•Delayed repolarization is linked to significant downregulation of HDAC2 in left ventricular tissue•In vitro, knock-down of Hdac2 causes AP prolongation and reduces Kcnh2/Kv11.1 K+ channel expression•Regulation of ventricular repolarization by HDAC2 serves as basis for mechanism-based antiarrhythmic therapy