Procedural approach
Endo-/epicardial CA was performed in the electrophysiology laboratory,
under general anesthesia. Patients were studied during AF; in case of
sinus rhythm at the beginning of the procedure, AF/atrial tachycardia
was induced using burst stimulation.
We performed an extensive ablation procedure in each patient, starting
from the LA endocardium, which was accessed with a single transseptal
puncture. Unfractionated heparin was administered in order to maintain
activated clotting time values >300 s. Procedures were
guided by electroanatomical mapping system (CARTO, Biosense
Webster)-derived three-dimensional reconstructions of the atria.
Biatrial endocardial maps were obtained with a circular mapping catheter
(Lasso, Biosense Webster), whereas biatrial epicardial replica were
obtained using the ablation catheter (Thermocool Smarttouch, Biosense
Webster). CA was guided by ablation index, targeting values higher than
550 in every site, apart from the posterior wall of the LA and the
epicardium, where values higher than 500 were
obtained.12
The procedural approach is represented in figure 1. The endocardial
phase of the procedure aimed at insulating pulmonary veins and closing
LA and right atrial (RA) anatomical isthmuses. Endocardial steps
included antral PVI, followed by linear lesions on the roof of the LA
connecting right and left superior PVs, on the anterior wall of the LA
connecting the roof line with mitral valve annulus, in the septal aspect
of the posterior wall of the right atrium (RA) connecting superior and
inferior venae cavae, and cavotricuspid isthmus ablation.
After completing this lesion set, access was gained to the epicardium,
by creating a small (2-3 cm) pericardial window, through which a
steerable introducer (Agilis EPI, Abbott) was placed into the
pericardial space. The pericardial window was performed in collaboration
with a cardiac surgeon. We preferred such an approach to the classic
pericardial puncture described by Sosa et al.,13because of the more favorable catheter manipulability with the
epicardial window.
In the epicardium, BB and the LOM were ablated first according to their
anatomic location (in the floor of the transverse sinus close to the
interatrial septum, and between the LA appendage and pulmonary veins,
respectively), followed by the eventual completion of roof and anterior
linear lesions in the proximity of the mitral valve in case of absence
of lesion transmurality. In case of ongoing AF, further ablation lesions
were delivered in the atria from the endocardium, targeting
complex/fractionated atrial electrograms in both left and right atria.
In case patients developed atrial tachycardia at any step during the
procedure, the arrhythmia was mapped and ablated, using a high-density
catheter (PentaRay, Biosense Webster). If sinus rhythm was not restored
at this point, patients were electrically cardioverted. Bidirectional
conduction block across all linear lesions and PV circumferential
entrance and exit blocks were verified in sinus rhythm by pacing
techniques, as described elsewhere.14 At the end,
burst pacing was performed to confirm loss of arrhythmia inducibility
from two different sites (coronary sinus and LA appendage), until
refractoriness was reached, or an arrhythmia induced. In case of atrial
tachycardia induction, the latter was mapped and ablated, aiming to
restore sinus rhythm; in case of AF induction, we performed electrical
cardioversion. AF termination, lack of arrhythmia inducibility, and
validation of conduction block through ablation lines were the acute
procedural endpoints.
Class III or Ic antiarrhythmic drugs were prescribed for the first three
months after CA and suspended thereafter in case of absence of
arrhythmia recurrences.