Background-Conventional activation mapping is difficult without inducible, stable ventricular tachycardia (VT). Methods and Results-We evaluated 16 patients with drug refractory, unimorphic, unmappable VT. Nine patients had ischemic and 7 had nonischemic cardiomyopathy. All patients had implantable defibrillators and had experienced 6 to 55 VT episodes during the month before treatment. Patients underwent bipolar catheter mapping during baseline rhythm. The amount of endocardium with an abnormal electrogram amplitude was estimated using fluoroscopy in 3 patients and a magnetic mapping system (CARTO) in 13 patients. For the magnetic mapping, normal endocardium was defined by an amplitude Ͼ1.5 mV; this measurement was based on sinus rhythm maps in 6 patients who did not have structural heart disease. Radiofrequency point lesions extended linearly from the "dense scar," which had a voltage amplitude Ͻ0.5 mV, to anatomic boundaries or normal endocardium. To limit radiofrequency applications, 12-lead ECG during VT and pacemapping guided placement of linear lesions. No new antiarrhythmic drug therapy was added. The amount of endocardium demonstrating an abnormal electrogram amplitude ranged from 25 to 127 cm 2 . A total of 8 to 87 radiofrequency lesions (mean, 55) produced a median of 4 linear lesions that had an average length of 3.9 cm (range, 1.4 to 9.4 cm). Twelve patients (75%) have been free of VT during 3 to 36 months of follow-up (median, 8 months); 4 patients had VT episodes at 1, 3, 9, and 13 months, respectively. Only one of these patient had frequent VT. Conclusions-Radiofrequency linear endocardial lesions extending from the dense scar to the normal myocardium or anatomic boundary seem effective in controlling unmappable VT.
Background-Efficacy of endocardial ventricular tachycardia (VT) ablation in arrhythmogenic right ventricular cardiomyopathy/dysplasia may be limited by epicardial VT, right ventricular thickening, or both. We sought to characterize the endocardial versus epicardial substrate, measure right ventricular free wall thickness, and determine epicardial ablation efficacy in patients with right ventricular cardiomyopathy/dysplasia. Methods and Results-Thirteen consecutive patients (3 female; aged 43Ϯ15 years; range, 17 to 70 years) undergoing endocardial and epicardial sinus rhythm voltage mapping and epicardial VT ablation after failed endocardial VT ablation were included. In each patient, the low bipolar voltage area (Ͻ1.0 mV for epicardium and Ͻ1.5 mV for endocardium) was more extensive on the epicardium (95Ϯ47 versus 38Ϯ32 cm 2 ; PϽ0.001) and was uniformly marked by multicomponent and late electrograms. The basal right ventricular thickness assessed by electroanatomic map was Ͼ10 mm in 6 of 13 patients compared with 5 to 10 mm in 4 reference patients without structural disease. Twenty-seven VTs were targeted on the epicardium with the use of activation, entrainment, or pace mapping with focal/linear ablation and targeting of late potentials. Epicardial VTs were targeted opposite normal endocardium in 10 patients (77%) and/or opposite ineffective endocardial ablation sites in 11 patients (85%). During 18Ϯ13 months, 10 of the 13 patients (77%) had no VT, with 2 patients having only a single VT at 2 and 38 months, respectively.
Conclusions-Patients
Recurrent AF following selective PV isolation is overwhelmingly associated with PV electrical reconnection. Repeat PV isolation without linear ablation provides effective treatment for recurrent AF in patients in whom an initial PV isolation procedure failed, independent of clinical characteristics.
In this nonrandomized study, the risk-benefit ratio favored the suspension of OAT after successful AF ablation even in patients at moderate-high risk of TE. This conclusion needs to be confirmed by future large randomized trials.
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.
In patients with NICM and VT of epicardial origin, the substrate is characterized by areas of basal LV epicardial > endocardial bipolar low voltage. The electrograms in these areas are not only small (<1.0 mV) but wide (>80 ms), split, and/or late, and help identify the substrate targeted for successful ablation.
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