Ventricular tachycardia after myocardial infarction: from arrhythmia surgery to catheter ablation.

Ventricular tachycardia due to prior myocardial infarction is caused by reentry. Intraoperative mapping at the time of arrhythmia surgery has shown that the reentry circuits are diverse in size and location. Many circuits are large, extending over several square centimeters. Endocardial excision guided by activation sequence mapping, fractionated sinus rhythm electrograms, or visual identification of scarred subendocardium renders 69% to 95% of patients free from inducible ventricular tachycardia, but with an operative mortality that exceeds 8% at most centers. Catheter ablation is difficult due to limitations of catheter mapping, relatively small size of lesions produced with current techniques, and limited access to intramural and epicardial portions of the reentry circuits. Many problems need to be overcome for catheter ablation to achieve success comparable to that of surgery. At present, only hemodynamically tolerated ventricular tachycardias can be mapped. Progress is being made, and it is likely that catheter ablation will become a viable therapy for subgroups of patients with postmyocardial infarction ventricular tachycardia.