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The procedures were performed either under general anesthesia or under concious sedation with propofol and fentanyl. Endocardial LV mapping was preferentially performed by a transseptal access although the retroaortic approach was also used when considered necessary. For those cases in which an epicardial involvement was suspected, an epicardial access was obtained using the technique described by Sosa et al.14
A complete substrate mapping of the chamber/s of interest was initially obtained during the baseline patient’s rhythm and using either a linear (Smart-Touch, Biosense Webster) or a multielectrode catheter (PentaRay, Biosense Webster). Low voltage areas as well as late potentials were registered and tagged. Scar was defined as areas with bipolar voltage < 0.5 mV. Upon completion of the substrate mapping, a standardized PVS protocol was used to induce VT in all patients included in the study. This protocol consisted in a 8 beats basal train at three different cycle lengths (600, 500 and 400 ms) followed by up to 4 extraestimmuli with a minimun coupling interval of 200 ms or until ventricular refractoriness from the right ventricular apex, right ventricular outflow tract, or different LV sites. If a stable and hemodynamically tolerated SMVT was induced, activation mapping of the VT was performed and entrainment maneuvers were used whenever possible to clearly define the VT mechanism and circuit. In case of hemodynamic inestability VT was paced terminated or cardioverted. In this last scenario, the 12-lead ECG QRS morphology of the induced tachycardia was used as a reference during pacemapping. When the initially induced VT was mapped and/or terminated (spontaneously, pace-terminated, shocked or during radiofrequency ablation), PVS was performed again aiming for induction of additional VTs.
Once the areas of interest were identified, a contact force ablation catheter (Smart Touch, Biosense Webster) was used for radiofrequency (RF) delivery. In patients with a hemodynamically stable VT, RF was applied during tachycardia to evaluate the response to RF ablation. In case of VT interruption during RF application, additional lessions were administered to eliminate the substrate and then a new PVS protocol was used to test VT inducibility. In the case of non-inducibility and presence of abnormal signals (late potentials) additional lessions were applied until all the abnormal signals were abolished. Meanwhile, in all patients with hemodynamically unstable VT a substrate ablation strategy (±pacemapping as an adjunctive strategy whenever possible) was performed targeting all the sites with abnormal signals registered during the initial substrate mapping. Patients with baseline non-inducibility underwent substrate ablation exclusively.