Concepts of antiarrhythmic therapy have undergone major changes in the past decade for a variety of reasons. First of all, electrophysiologic studies — ushered in by the observation1 that His-bundle activation could be recorded simply, safely, and reliably in human beings — have progressed from academic, research-oriented tools providing important data on mechanisms of arrhythmogenesis to procedures that yield useful clinical and therapeutic information. Tachyarrhythmias occurring infrequently can be initiated by cardiac stimulation in the laboratory; the electrophysiologic mechanisms can then be surmised, and the response to antiarrhythmic drugs evaluated. Preliminary information suggests that a drug that prevents the induction.
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