It should come as no surprise that agents capable of modifying conduction and refractoriness would be capable of converting an arrhythmogenic substrate into one that is less arrhythmogenic. It should also come as no surprise that such agents might change the substrate in such a way as to potentiate the development of arrhythmias. It is now axiomatic that all drugs capable of interrupting or preventing ventricular arrhythmias should be considered capable of causing ventricular arrhythmias.