抄録
Over the past ten years, electrophysiologic studies have improved our understanding of the basic mechanisms of a variety of arrhythmias. At present, the overwhelming weight of evidence suggests that sustained uniform ventricular tachycardia (VT), particularly that associated with coronary artery disease, is due to reentry1) -5) . In addition to establishing the mechanism of VT, the appropriate use of electrophysiologic studies, including both program-med stimulation and endocardial mapping, has allowed for the development of therapeutic modalities which can be based on objective endpoints. Therapeutic options available for the management of VT includes drugs, electrical devices, and surgery, or combinations of the above. One can consider VT the product of triggers which are usually premature ventricular complexes, and a substrate which is either functionally or anatomically determined, both of which can be modified by autonomic tone, heart rate, hemodynamics, ischemia, etc. (Fig.1) . Electrophysiologic testing is primarily directed at the substrate. It is the basic hypothesis that if the substrate can be rendered incapable of supporting sustained reentry, then no arrhythmia will result, regardless of the trigger or other factors involved.
