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.