Catheter ablation protocol
All patients underwent the procedure under arterial blood pressure and O2 saturation monitoring. Conscious sedation or general anesthesia were used according to the operator’s discretion and with anesthesiologist support. Antiarrhythmic drugs (AAD) were stopped at least 48 hours before the procedure when applicable. The choice of the VT ablation access (endocardial vs epicardial vs combined) was decided according to the etiology, previous VT ablation site and imaging information regarding scar localization. Systemic anticoagulation with intravenous heparin targeted a minimum activation clotting time of 300 s during each left ventricular endocardial ablation, with protamine reversal (1mg/100U) at the end of the procedure. Systemic anticoagulation was also reversed with protamine before percutaneous epicardial access when necessary. Epicardial access was obtained through the subxiphoid space under fluoroscopic guidance as previously described by Sosa et all6. A mapping multipolar catheter was placed in the coronary sinus via femoral vein and standard transvenous multipolar catheters were placed into the appropriate cardiac chambers under study. Left ventricular mapping was performed via the retrograde aortic or transseptal route. Endocardial and epicardial electroanatomical mapping was obtained with the CARTO® (Biosense Webster, Diamond Bar, CA, USA), the EnSite NavX® (St Jude Medical, St Paul, MN, USA) or with the Rhythmia® (Boston Scientific, Marlborough, Massachusetts, USA) systems and included activation and voltage mapping acquired in sinus rhythm, ventricular pacing or during hemodynamically stable VT. Intracardiac signals were filtered at 30 to 500 Hz. Normal tissue was defined by a voltage threshold greater than 1.5 mV while dense scare as tissue under a threshold of 0.5 mV in bipolar substrate map. A first attempt to induce the clinical VT was always performed at the beginning of each procedure. Activation and entrainment-mapping techniques were performed in all hemodynamically tolerated VTs, and if not possible, ablation was guided by substrate, pace mapping and identification of delayed and fractionated potentials. Coronary angiography was performed when deemed necessary before epicardial radiofrequency applications. Epicardial phrenic nerve capture was identified by bipolar pacing from the ablation catheter at 20 mA with a pulse width of 10 ms. Radiofrequency (RF) was delivered with a 3.5-mm open irrigated tip catheter in power control mode through the use of a Stockert generator, with power set to 30-50 W and irrigation set to 17-30 ml/min. The procedure was deemed as successful if no VT was induced with a standard stimulation protocol of up to 3 extrastimuli at a 200ms cycle length in 2 different sites, excluding induction of VF or fast polymorphic VT.