Left posterior fascicular block: a new endpoint of ablation for verapamil-sensitive idiopathic ventricular tachycardia

Background Verapamil-sensitive, idiopathic left ventricular tachycardia （ILVT） with right bundle branch block configuration and left-axis deviation is known to be due to re-entry mechanism but the exact nature of reentrant circuit in ILVT is not fully elucidated. Radiofrequency （RF） ablation was applied during ventricular tachycardia （VT） and termination of the VT or abolishing the inducibility of the tachycardia was used as an endpoint for successful RF. In this study, the left posterior fascicular block in surface electrocardiogram （ECG） was used as a new endpoint of ablation to cure ILVT. Methods Electrophysiological studies and radiofrequency ablation were performed in 39 consecutive patients [30 men, 9 women; age ranging from 10 to 64 years, mean （29± 16） years] with verapamil-sensitive ILVT and structurally normal hearts. VT could be terminated by the intravenous adininistration of verapamil in all patients. The target site was the midseptum of LV where the earliest Purkinje potentials were recorded during VT. RF current was applied to the target site with or without late diastolic potential （LDP） during sinus rhythm in 37 patients and during VT in 2 patients to meet the ablation endpoint： the left posterior fascicuiar block in the surface ECG. Results Thirty-seven patients with ILVT had been treated by RF ablation during sinus rhythm and two had been treated during VT. All of them met the endpoint of the left posterior fascicuiar block. Thirty-eight cases were symptom-free without medications during the follow-up period （range from 3 to 95 months, median 17 months）. One patient developed a clinical recurrence and the left posterior fascicuiar block in surface ECG disappeared. The patient received another treatment. The endpoint was met and the procedure was successful. Conclusions The left posterior fascicuiar block in surface ECG used as an endpoint of RF ablation to treat ILVT is effective. It is important especially in those patients whose VT can not be induced or the inducible condition is unstable. The effective endpoint implied that the left posterior fascicle might be a critical part of the re-entrant circuit.

Beta2-adrenoceptor gene variant Arg16Gly is associated with idiopathic ventricular outflow-tract tachycardia

Background Imbalance of the sympathetic nervous system was involved in the pathogenesis of idiopathic ventricular outflow-tract tachycardia （IVOT）. We aimed to investigate whether the major genetic variants in β1-and β2-adrenoceptors and GNB3 C825T were associated with IVOT and verapamil sensitive idiopathic left ventricular tachycardia （ILVT）.Methods Patients with IVOT and ILVT from December 2005 to December 2007 were consecutively enrolled into this study. Controls were randomly selected from the community-based inhabitants. Five genetic variants, Ser49Gly and Gly389Arg in the β1-adrenoceptor, Arg16Gly and Gln27Glu in the β2-adrenoceptor and GNB3 C825T, were genotyped by polymerase chain reaction-restriction fragment length polymorphism analysis.Results A total of 227 patients with IVOT and 110 patients with ILVT were included. Genotyping revealed that the 16Gly allele of Arg16Gly variant of β2-adrenoceptor was associated with a higher risk of IVOT （OR：1.40, 95% CI： 1.12-1.75,P=0.003 in the addictive model and OR：. 1.62, 95% CI： 1.14-2.31, P=0.007 in the dominant model）. Patients with Gly16Gln27 haplotype also had a higher risk of IVOT （OR： 1.38, 95% CI： 1.11-1.73, P=0.012）. Other four variants,including Ser49Gly and Arg389Gly in β1-adrenoceptor, GIn27Glu in β2-adrenoceptor and GNB3 C825T, did not differ between patients with IVOT and controls. In patients with ILVT, no significant difference was found in these five variants compared with controls.Conclusions Arg16Gly in β2-adrenoceptor is significantly associated with IVOT in Chinese Han population. Major genetic variants in β1- and β2-adrenoceptor and GNB3 C825T may not be associated with ILVT. These data suggest a different arrhythmogenic mechanism in IVOT and ILVT.