[Zero-fluoroscopy catheter ablation for idiopathic premature ventricular contractions from the aortic sinus cusp].

OBJECTIVE: To compare the safety, feasibility, and efficacy of a completely nonfluoroscopic approach to radiofrequency catheter ablation (RFCA) using CARTO3 and ablation with conventional fluoroscopic guidance for treatment of idiopathic premature ventricular contractions from the aortic sinus cusp (ASC-PVCs). METHODS: From April 2013 to October 2015, we prospectively enrolled 52 consecutive patients with ASC-PVCs scheduled for either CARTO3 mapping-guided zero-fluoroscopy ablation (group A, n=23) or conventional fluoroscopic ablation (group B, n=29). The success rates, rates of complications, rates of recurrences, number of radiofrequency applications, procedure time, mapping time and fluoroscopy time were compared between the 2 groups. RESULTS: s No significant differences were found in the success rates between the 2 groups [22/23 (96%) vs 24/29 (83%), P=0.21]. No major complications occurred during the procedures in either group. There was no significant difference with regard to the procedure time between the two groups (79.6∓8.8 vs 77.4∓7.2 min, P=0.332). The procedure was completed without any fluoroscopy use in group A, while the mean fluoroscopy time in group B was 23.1∓6.0 min. Group A showed a shorter mapping time than group B (4.3∓1.7 vs 7.8∓2.6 min, P<0.01) with significantly fewer radiofrequency applications (4.8∓1.1 vs 7.9∓3.2, P<0.01). The recurrence rates were comparable between the two groups over a follow-up period of 5 to 20 months. CONCLUSION: Compared with the conventional fluoroscopic technique, the zero-fluoroscopy approach can shorten the total procedure time and the ablation time with significantly reduced RF applications to eliminate ionizing radiation exposure in RFCA. RFCA guided by CARTO3 system without fluoroscopy is feasible, safe, and effective for treatment of ASC-PVCs.

[Correlation of Tp-e interval and Tp-e/Q-T ratio with malignant ventricular arrhythmia in patients with implantable cardioverter-defibrillator for primary prevention].

OBJECTIVE: To investigate whether Tpeak-Tend interval (Tp-e) and Tp-e/QT ratio are associated with malignant ventricular arrhythmia in patients with implantable cardioverter-defibrillator (ICD) for primary prevention. METHODS: A cohort of 68 consecutive patients with chronic heart failure undergoing standard ICD for primary prevention indications (NYHA function class II-III, left ventricular ejection fraction ≤35%, systolic cardiomyopathy without prior malignant ventricular arrhythmia) were enrolled in this study. The patients were followed up for 18-48 months and were divided into high-risk group and low-risk group according to the occurrence of the endpoint events of sudden cardiac death (SCD), ventricular tachycardia (VT), or ventricular fibrillation (VF). Electrocardiographic and echocardiographic characteristics, Tp-e, and Tp-e/QT ratio were analyzed in all cases before ICD implantation. RESULTS: During the follow-up, ICD shock for sustained ventricular tachycardia or ventricular fibrillation occurred in 11 patients; nonsustained ventricular tachycardia (NSVT) that did not require therapy was detected by ICD in 7 patients (high-risk group, 18 cases). ICD did not detect ventricular tachycardia or ventricular fibrillation in 50 patients (low-rsk group). Compared with the low-rsik group, the high-risk group had an increased Tp-e/QT ratio (0.27±0.04 vs 0.22±0.05 P<0.01) and an increased Tp-e (105±15 vs 90±17 ms P<0.01). ROC analysis revealed that a Tp-e/QT ratio ≥0.255 had a sensitivity of 72.2% and a specificity of 65.9%, and a Tp-e ≥103 ms had a sensitivity of 66.7% and a specificity of 67.9% for predicting VT and VF in these patients. CONCLUSION: Increased Tp-e and Tp-e/QT ratio are associated with increased risks of ventricular arrhythmias in patients with ICD for primary prevention.

[Functional analysis of a novel SCN5A mutation G1712C identified in Brugada syndrome].

OBJECTIVE: To elucidate the molecular and electrophysiological mechanisms of Brugada syndrome through functional analysis of a novel SCN5A gene mutation G1712C. METHODS: A recombinant plasmid pRc