Limitations of pharmacological therapy for VT have led to great interest in alternative nonpharmacological therapies. The appeal of a curative therapy for VT initially led to the search for operative techniques to identify and destroy the underlying substrate, and more recently, has resulted in the development of catheter techniques to achieve the same goal in the electrophysiology laboratory. Investigations into the pathophysiology of VT have resulted in the recognition that this arrhythmia reflects a mechanistically and anatomically heterogeneous set of disorders. Recent growth in our understanding of these distinctions has both led to, and resulted from, simultaneous advances in catheter ablation techniques. The clinical electrophysiology laboratory has served as a testing ground for theories derived from in vitro and animal experiments while also providing its own set of human experimental data regarding the pathophysiology and treatment of VT. As a result of this process, several distinct forms of VT that are amenable to catheter ablation have been characterized. This article will summarize current knowledge of the pathophysiology of various VT subtypes and of techniques for catheter mapping and ablation.