It is critical to begin any discussion on ablation of unstable ventricular tachycardia with background information supporting the importance of the effort. First, stable, mappable ventricular tachycardias represent the tip of the arrhythmia iceberg. In order for any arrhythmia to be mappable it must be reliably inducible and hemodynamically tolerable. The ventricular tachycardia must also be stable in response to the catheter manipulation and pacing required to identify the appropriate site for ablative therapy during activation and entrainment mapping [1–4]. In a consecutive series of “ideal” patients presenting with hemodynamically tolerated ventricular tachycardia and referred for catheter ablation, 30% had only unmappable VT at the time of electrophysiological evaluation [5]. Secondly, ICD event monitoring after device implantation has documented rapid unmappable VT in most patients regardless of the clinical indication for initial device therapy [6–8]. Finally, in looking to the future, a strategy for prevention of sudden cardiac death that uses ablative therapy must target the substrate for unmappable ventricular tachycardia [9].

Background—A proarrhythmic consequence of pulmonary vein (PV) isolation can be a recurrent organized left atrial (LA) tachycardia after ablation. This arrhythmia is frequently referred to as “left atrial flutter,” but the mechanism and best ablation strategy have not been determined. Methods and Results—Isolation of arrhythmogenic PVs was initially performed by segmental ostial PV ablation guided by a circular mapping catheter in 341 patients. Patients whose predominant recurrent arrhythmia was a persistent organized tachycardia returned for mapping and ablation. Recurrent organized LA tachycardias (cycle length 253±33 ms, range 213 to 328 ms) occurred in 10 (2.9%) of 341 patients (age 59±9 years, 1 woman). Mapping was consistent with a focal origin in 8 patients and with macroreentry in 1 patient and was unclear in 1 patient owing to degeneration to atrial fibrillation. Focal tachycardias originated from reconnected segments of prior isolated PVs (6 patients), the posterior LA (1 patient), or the superior septum (1 patient). Focal atrial tachycardias were ablated with point lesions that targeted the earliest activation. All reconnected PVs were also reisolated. Reentrant LA flutter occurred around the left PVs in 1 patient. After 6.7±2.3 months of follow-up, 9 (90%) of 10 patients were arrhythmia free (4 of whom were taking antiarrhythmic drug therapy), and one was having recurrent atrial fibrillation. Conclusions—Recurrent organized LA tachycardia after PV isolation is uncommon and typically has a focal origin from reconnected PV ostia. Reisolation of the PV and ablation of non-PV foci are sufficient to treat this proarrhythmia. Linear lesions are only required when a macroreentrant mechanism is present.

Background— To gain insight into the pathogenesis of right ventricular (RV) cardiomyopathy and ventricular tachycardia (VT), we determined the clinical and electroanatomic characteristics and outcome of ablative therapy in consecutive patients with (1) RV dilatation, (2) multiple left bundle-branch block (LBBB)–type VTs, and (3) an abnormal endocardial substrate defined by contiguous electrogram abnormalities. Methods and Results— All 21 patients had detailed RV bipolar electrogram voltage mapping. Eighteen patients had simultaneous left ventricular (LV) mapping, including all 4 patients with right bundle-branch block (RBBB) VT. VT was ablated in 19 patients by use of focal and/or linear lesions with irrigated-tip catheters in 10 of 19 patients. Eighteen patients were men, age 47±18 years, and none had a family history of RV dysplasia. RV volume was 223±89 cm 3 . Electrogram abnormalities extended from perivalvular tricuspid valves (5 patients), pulmonic valves (6 patients), or both valves (10 patients). Electrogram abnormalities always involved free wall, spared the apex, and included the septum in 15 patients (71%). The area of abnormality was 55±37 cm 2 (range, 12 to 130 cm 2 ) and represented 34±19% of the RV. In 52 of 66 LBBB VTs, the origin was from the RV perivalvular region. LV perivalvular low-voltage areas noted in 5 patients were associated with a RBBB VT origin. No VT recurred after ablation in 17 patients (89%) during 27±22 months. Conclusions— In patients with RV cardiomyopathy and VT, (1) perivalvular electrogram abnormalities represent the commonly identified substrate and source of most VT, (2) LV perivalvular endocardial electrogram abnormalities and VT can occasionally be identified, and (3) aggressive ablative therapy provides long-term VT control.