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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.