Nearly 80% of patients with coronary artery disease who have map-directed surgery for control of ventricular tachycardias require no drug therapy to prevent recurrences, while fewer than 50% of patients undergoing catheter ablation have similar outcomes. Catheter ablation will fail if arrhythmogenic sites are incompletely ablated by lesions that are too small or too far away from the reentrant pathway or if all arrhythmogenic sites are not identified. The underlying assumptions used to guide site selection are that: (a) ventricular tachycardias arise from reentrant mechanisms; (b) monomorphic ventricular tachycardias with similar QRS morphologies arise from the same pathway; (c) the ventricular tachycardia initiated during the procedure represents the patient's spontaneous arrhythmia; (d) the endocardial site that should be ablated can be identified from cardiac activation maps produced during induced ventricular tachycardia or from ancillary techniques; and (e) the patient has only one or two reentrant pathways. Relying on incorrect assumptions may account for the difference in success rates. Patients may have similar appearing ventricular tachycardias that arise from different pathways, and the entire thin layer of viable tissue between the infarct and the endocardium may contain many reentrant pathways. Some ventricular tachycardias may arise from the myocardium away from the endocardium, while others may arise from the epicardium. Small lesions may not be large enough to eliminate all possible reentrant pathways. Catheter ablation may be less successful because the lesions are inadequate, the assumptions guiding the selection of arrhythmogenic tissue are incorrect, or all arrhythmogenic sites are not identified. The primary reason catheter ablation is less successful than surgery in the treatment of ventricular tachycardias is that catheter ablation does not ablate as much tissue as is removed by surgery. The success rate of catheter ablation probably can be improved if the amount of tissue ablated is increased.

The decreased number of activation fronts and the longer delay following the shock for the earliest epicardial appearance of those activation fronts that do occur may be responsible for the increased defibrillation efficacy for biphasic shocks.