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.