Circumferential Pulmonary Vein Isolation in Paroxysmal AF
Circumferential Pulmonary Vein Isolation in Paroxysmal AF
The study population consisted of 109 (70 males, 58.7 ± 10.8 years) with drug-refractory PAF undergoing CPVI in our center (Table 1). The exclusion criteria included: contraindication to anticoagulation, isoproterenol or ATP, LA thrombus, and previous AF ablation. PAF was defined as recurrent AF (≥2 episodes) that terminates spontaneously within 7 days. This study was approved by the institutional review board, and informed consent was obtained from all patients.
From April, 2010 to July, 2012, 226 consecutive patients referred for PAF ablation were screened and 109 PAF patients consented to participate in this study. All antiarrhythmic drugs except amiodarone were discontinued for ≥5 half-lives before ablation. Warfarin was stopped 3 days before ablation and low-molecular-weight heparin was administered until the day before ablation. Transesophageal echocardiography was performed the day before ablation. All procedures were performed under conscious sedation with fentanyl and midazolam. Deep sedation that may affect AF inducibility was avoided in all patients.
Group-1 consists of the first 92 consecutive patients enrolled into this study (60 males, 58.5 ± 10.7 years old). A flow chart summarizes the designs and results of the Group-1 patients (Fig. 1). After the PV ostium was determined by PV angiography, a multipolar circular catheter (Lasso™, Biosense Webster, Diamond Bar, CA, USA) and ablation catheter (Navi-star Thermo-Cool, Biosense Webster) were positioned at the ostium of the RSPV and LSPV, respectively. The coronary sinus (CS) catheter was positioned to record the CS and LA between the LIPV and mitral annulus. AF was present at the onset of the procedure in 11/92 patients. For the remaining 81 patients presented with sinus rhythm (SR), 20 mg of ATP was rapidly injected intravenously during continuous infusion of ISP (20 μg/min) to provoke Rap-F and AF. ISP+ATP was administered again if no Rap-F or AF was induced. Rap-F was defined as a short (<300 ms) average cycle length of the first 10 beats of spontaneous discharge. It was considered to originate from the PV if the timing of the onset of the rapid discharges was earliest in the PV or at the PV-LA junction. Sustained AF was defined as >30 minutes.
(Enlarge Image)
Figure 1.
Flow chart for the Group-1 patients showing the design and results. †Patients with sustained AF induced by ISP+ATP before CPVI. AF = atrial fibrillation; ATP = adenosine triphosphate; ISP = isoproterenol; SR = sinus rhythm.
Intravenous heparin, 5,000 U, was immediately given as a bolus after successful transseptal puncture. The second transseptal access was obtained by advancing the ablation catheter through the initial puncture site guided by a long wire positioned in the LSPV through the transseptal site, followed by 1,000 U/h during the remainder of the procedure. CPVI was guided by the Lasso catheter and electroanatomic mapping. Electrograms of surface ECG leads, CS catheter, and Lasso catheter were recorded simultaneously. Radiofrequency energy was delivered at a distance 5–10 mm from the PV ostia at 45 °C (maximal wattage = 35W, irrigated flow rate = 17–25 mL/min). Each target site was ablated for 20–30 seconds. Circumferential ablation lines around the left-sided and right-sided PVs were performed subsequently. Complete isolation was confirmed by placing the circular mapping catheter within the circumferential lines that showed no PV potential or the presence of dissociated PV potential. Isolation was reconfirmed after 5 minutes waiting and before the end of the procedure.
After successful CPVI, ISP+ATP was co-administered again to provoke Rap-F or AF in patients who was in SR. If AF continued despite complete CPVI, non-PV areas, such as superior vena cava (SVC), CS ostium, LA, ligament of Marshall (LOM), right atrium, and interatrial septum were mapped to identify the sites showing the shortest cycle length, the potential driver for AF, to serve as the ablation targets.
Clinical follow-up after ablation was performed at 1, 3, 6, 12, and 24 months, including 12-lead ECGs and 24-hour Holter monitoring at each visit and at the time of symptoms suggestive of arrhythmia.
This group consists of the last 17 patients of this study as a supplement to Group-1 and was started after the study of Group-1 has been completed. The rationale of including Group-2 is that the results of Group-1 showing marked suppression of PV-F after CPVI could be falsely positive due to the absence of spontaneous depolarization within the circumferential lines after successful CPVI. ATP+ISP alone may not be capable of inducing Rap-F as it may require the presence of spontaneous depolarization such as a long-short sequence or a pause to initiate Rap-F. Seventeen patients in whom PV-F was induced by ISP+ATP before CPVI were enrolled. After successful CPVI, we positioned a Lasso catheter in the already isolated PVs and then attempted to induce rapid PV-F using the following pacing schemes: (1) pacing (S1-S1) at a constant drive cycle length equal to the sinus cycle length before AF was induced before CPVI. If no PV-F was induced, pacing was repeated in the presence of ISP+ATP administration; (2) programmed stimulation (S1-S1 = 1,000 ms, n = 8): a premature extrastimulus (S2) initially coupled at 600 ms, by 10 ms decrements until refractoriness was reached; (3) burst pacing: 30-second burst pacing at cycle length of 200 ms to help accumulate intracellular Ca to facilitate triggered firing. In general, the output of stimulation was between 4 and 25 mA and the pulse width was between 2 and 10 ms.
Continuous variables were presented as mean ± standard deviation. Comparison of PV-F inducibility before and after CPVI was performed using the chi-square test or Fisher's exact test. The statistical significance for all tests was accepted at P < 0.05.
Methods
Study Population
The study population consisted of 109 (70 males, 58.7 ± 10.8 years) with drug-refractory PAF undergoing CPVI in our center (Table 1). The exclusion criteria included: contraindication to anticoagulation, isoproterenol or ATP, LA thrombus, and previous AF ablation. PAF was defined as recurrent AF (≥2 episodes) that terminates spontaneously within 7 days. This study was approved by the institutional review board, and informed consent was obtained from all patients.
EP Study and Ablation Procedure
From April, 2010 to July, 2012, 226 consecutive patients referred for PAF ablation were screened and 109 PAF patients consented to participate in this study. All antiarrhythmic drugs except amiodarone were discontinued for ≥5 half-lives before ablation. Warfarin was stopped 3 days before ablation and low-molecular-weight heparin was administered until the day before ablation. Transesophageal echocardiography was performed the day before ablation. All procedures were performed under conscious sedation with fentanyl and midazolam. Deep sedation that may affect AF inducibility was avoided in all patients.
Group-1
Group-1 consists of the first 92 consecutive patients enrolled into this study (60 males, 58.5 ± 10.7 years old). A flow chart summarizes the designs and results of the Group-1 patients (Fig. 1). After the PV ostium was determined by PV angiography, a multipolar circular catheter (Lasso™, Biosense Webster, Diamond Bar, CA, USA) and ablation catheter (Navi-star Thermo-Cool, Biosense Webster) were positioned at the ostium of the RSPV and LSPV, respectively. The coronary sinus (CS) catheter was positioned to record the CS and LA between the LIPV and mitral annulus. AF was present at the onset of the procedure in 11/92 patients. For the remaining 81 patients presented with sinus rhythm (SR), 20 mg of ATP was rapidly injected intravenously during continuous infusion of ISP (20 μg/min) to provoke Rap-F and AF. ISP+ATP was administered again if no Rap-F or AF was induced. Rap-F was defined as a short (<300 ms) average cycle length of the first 10 beats of spontaneous discharge. It was considered to originate from the PV if the timing of the onset of the rapid discharges was earliest in the PV or at the PV-LA junction. Sustained AF was defined as >30 minutes.
(Enlarge Image)
Figure 1.
Flow chart for the Group-1 patients showing the design and results. †Patients with sustained AF induced by ISP+ATP before CPVI. AF = atrial fibrillation; ATP = adenosine triphosphate; ISP = isoproterenol; SR = sinus rhythm.
Intravenous heparin, 5,000 U, was immediately given as a bolus after successful transseptal puncture. The second transseptal access was obtained by advancing the ablation catheter through the initial puncture site guided by a long wire positioned in the LSPV through the transseptal site, followed by 1,000 U/h during the remainder of the procedure. CPVI was guided by the Lasso catheter and electroanatomic mapping. Electrograms of surface ECG leads, CS catheter, and Lasso catheter were recorded simultaneously. Radiofrequency energy was delivered at a distance 5–10 mm from the PV ostia at 45 °C (maximal wattage = 35W, irrigated flow rate = 17–25 mL/min). Each target site was ablated for 20–30 seconds. Circumferential ablation lines around the left-sided and right-sided PVs were performed subsequently. Complete isolation was confirmed by placing the circular mapping catheter within the circumferential lines that showed no PV potential or the presence of dissociated PV potential. Isolation was reconfirmed after 5 minutes waiting and before the end of the procedure.
After successful CPVI, ISP+ATP was co-administered again to provoke Rap-F or AF in patients who was in SR. If AF continued despite complete CPVI, non-PV areas, such as superior vena cava (SVC), CS ostium, LA, ligament of Marshall (LOM), right atrium, and interatrial septum were mapped to identify the sites showing the shortest cycle length, the potential driver for AF, to serve as the ablation targets.
Clinical follow-up after ablation was performed at 1, 3, 6, 12, and 24 months, including 12-lead ECGs and 24-hour Holter monitoring at each visit and at the time of symptoms suggestive of arrhythmia.
Group-2
This group consists of the last 17 patients of this study as a supplement to Group-1 and was started after the study of Group-1 has been completed. The rationale of including Group-2 is that the results of Group-1 showing marked suppression of PV-F after CPVI could be falsely positive due to the absence of spontaneous depolarization within the circumferential lines after successful CPVI. ATP+ISP alone may not be capable of inducing Rap-F as it may require the presence of spontaneous depolarization such as a long-short sequence or a pause to initiate Rap-F. Seventeen patients in whom PV-F was induced by ISP+ATP before CPVI were enrolled. After successful CPVI, we positioned a Lasso catheter in the already isolated PVs and then attempted to induce rapid PV-F using the following pacing schemes: (1) pacing (S1-S1) at a constant drive cycle length equal to the sinus cycle length before AF was induced before CPVI. If no PV-F was induced, pacing was repeated in the presence of ISP+ATP administration; (2) programmed stimulation (S1-S1 = 1,000 ms, n = 8): a premature extrastimulus (S2) initially coupled at 600 ms, by 10 ms decrements until refractoriness was reached; (3) burst pacing: 30-second burst pacing at cycle length of 200 ms to help accumulate intracellular Ca to facilitate triggered firing. In general, the output of stimulation was between 4 and 25 mA and the pulse width was between 2 and 10 ms.
Statistical Analysis
Continuous variables were presented as mean ± standard deviation. Comparison of PV-F inducibility before and after CPVI was performed using the chi-square test or Fisher's exact test. The statistical significance for all tests was accepted at P < 0.05.