Since epigenetic mechanisms determining cardiac potassium and calcium channel activity have not yet been well characterized, one might speculate that the effects of class I HDAC inhibition by Entinostat on potassium and calcium channel activity critically depend on transcription factors and key regulators of potassium channel expression and activity that are induced or repressed as a result of the development of cardiac failure induced by rapid ventricular pacing. This evidence concerns the gene KCNA3 and heart failure.