2.3 Ablation procedure
All antiarrhythmic drugs were discontinued for at least 5 half-lives
before the ablation. In our hospital, all AADs were discontinued before
PVI because the previous study demonstrated AADs, in particular
Na+ channel blocker, suppressed extra systole from
pulmonary vein.18 Anticoagulation therapy was started
at least 3 weeks before the ablation procedure. A bolus infusion of 25mg
of hydroxyzine pamoate and 15mg of pentazocine were intravenously
administered before the ablation procedure. The ablation procedure was
performed under mild sedation obtained with propofol and dexmedetomidine
and the patients received adaptive servoventilation. An esophagus
temperature monitoring catheter via the nose was placed. A duo-decapolar
catheter (BeeAT, Japan Lifeline Co., Tokyo, Japan) was placed in the
coronary sinus through the right internal jugular vein. If the patient
was in AF, internal atrial cardioversion was performed with 15–20J of
biphasic energy. We performed a transseptal puncture under guidance with
the SoundStar 3D Ultrasound Catheter (Biosense Webster, Diamond Bar, CA,
USA) from the right atrium. After the transseptal puncture, 2 long
sheaths (8.5Fr SL0, Abbott, Chicago, IL, USA) were inserted into the
left atrium. A 100 IU/kg body weight bolus of heparin was administered
following the transseptal puncture and heparinized saline was
continuously infused to maintain the activated clotting time at 300-350
second. One circular mapping catheter was deployed in the superior and
inferior PVs and the left-sided then right-sided ipsilateral PVs were
circumferentially ablated guided by three-dimensional left atrium
mapping (CARTO3, Biosense-Webster, Diamond Bar, CA, USA). The PVI was
performed with a 3.5 mm ablation catheter with an externally-irrigated
tip (ThermoCool® SmartTouch® Catheter, Biosense-Webster, Diamond Bar,
CA, USA). Radiofrequency current was delivered with a power of up to 30W
and limited to 20W near the esophagus for 25 seconds. The PVI was
considered successful when all ostial PV potentials were abolished
during coronary sinus pacing and was also confirmed by PV pacing under
an isoproterenol (under increasing heart rate) and ATP bolus
administration (40mg). Cavo-tricuspid isthmus block was performed when
isthmus dependent atrial flutter was clinically confirmed or under the
operators’ judgement. When AF persisted after the PVI or firing sites of
atrial premature contraction triggers were detected, a substrate
modification was sequentially performed.