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Objective: Acute myocardial infarction (AMI) remains a leading cause of morbidity and mortality worldwide. About half of sudden deaths from AMI are mainly because of malignant ventricular arrhythmias (VA) after AMI. The sodium channel gene SCN5A and potassium channel genes KCNQ1 and KCNH2 have been widely reported to be genetic risk factors for arrhythmia including Brugada syndrome and long QT syndrome (LQTS). A few studies reported the association of SCN5A variant with ventricular tachycardia (VT)/ventricular fibrillation (VF) complicating AMI. However, little is known about the role of KCNQ1 and KCNH2 in AMI with VA (AMI_VA). This study focuses on investigating the potential variants on SCN5A, KCNQ1, and KCNH2 contributing to AMI with VA in a Chinese population. Materials and Methods: In total, 139 patients with AMI_VA, and 337 patients with AMI only, were included. Thirty exonic sites were selected to be screened. Sanger sequencing was used to detect variants. A subsequent association study was also performed between AMI_VA and AMI. Results: Twelve variants [5 on KCNH2(NM_000238.3), 3 on KCNQ1(NM_000218.2), and 4 on SCN5A(NM_198056.2)] were identified in AMI_VA patients. Only 5 (KCNH2: c.2690A>C; KCNQ1: c.1927G>A, c.1343delC; SCN5A: c.1673A>G, c.3578G>A) of them are missense variants. Two (KCNQ1: c.1343delC and SCN5A: c.3578G>A) of the missense variants were predicted to be clinically pathogenic. All these variants were further genotyped in an AMI without VA group. The association study identified a statistically significant difference in genotype frequency of KCNH2: c.1539C>T and KCNH2: c.1467C>T between the AMI and AMI_VA groups. Moreover, 2 rare variants (KCNQ1: c.1944C>T and SCN5A: c.3621C>T) showed an elevated allelic frequency (more than 1.5-fold) in the AMI_VA group when compared to the AMI group. Conclusion: Twelve variants (predicting from benign/VUS to pathogenic) were identified on KCNH2, KCNQ1, and SCN5A in patients with AMI_VA. Genotype frequency comparison between AMI_VA and AMI identified 2 significant common variants on KCNH2. Meanwhile, the allelic frequency of 2 rare variants on KCNQ1 and SCN5A, respectively, were identified to be enriched in AMI_VA, although there was no statistical significance. The present study suggests that the ion-channel genes KCNH2, KCNQ1, and SCN5A may contribute to the pathogenesis of VA during AMI. [ABSTRACT FROM AUTHOR]

Aims: To summarize our experience of radiofrequency catheter ablation (RFCA) for recurrent drug-refractory ventricular tachycardias (VTs) due to arrhythmogenic right ventricular cardiomyopathy (ARVC) in our center over the past 11 years and its related factors. Methods and Results: We reviewed 48 adults (mean age 39.9 ± 12.9 years, range: 14 to 65) who met the present ARVC diagnostic criteria and accepted RFCA for VTs from December 2004 to April 2016. The patients received a total of 70 procedures using two ablation approaches, the endocardial approach in 52 RFCAs, and the combined epicardial and endocardial approach (the combined approach) in 18 RFCAs. Kaplan-Meier survival analysis showed that the combined approach achieved better acute procedural success (p = 0.003) and better long-term outcomes (p = 0.028) than the endocardial approach. Patients who obtained acute procedural success with non-inducibility had better long-term outcomes (p < 0.001). COX regression of multivariate analysis showed that procedural success was the only factor that benefited long-term outcome, irrespective of the endocardial or the combined approach (p = 0.001). The rate of sudden cardiac death (SCD) in patients without procedural success was significantly higher than that in patients with procedural success (p = 0.005). All patients without implantable cardioverter defibrillator (ICD) implantation who had successful final RFCA survived. Conclusions: The combined approach resulted in better procedural success and long-term VT-free survival compared with the endocardial approach in ARVC patients with recurrent VTs. Acute procedural success with non-inducibility was strongly related to better long-term VT-free survival and reduced SCD, irrespective of whether this was achieved by the endocardial approach or the combined approach. [ABSTRACT FROM AUTHOR]

Background: Idiopathic ventricular arrhythmias (VAs) originating from the pulmonary sinus cusp (PSC) have not been sufficiently clarified.Objectives: The goal of this study was to investigate the prevalence, electrocardiographic characteristics, mapping, and ablation of idiopathic VAs arising from the PSC.Methods: Data were analyzed from 218 patients undergoing successful endocardial ablation of idiopathic VAs with a left bundle branch block morphology and inferior axis deviation.Results: Twenty-four patients had VAs originating from the PSC. In the first 7 patients, initial ablation performed in the right ventricular outflow tract failed to abolish the clinical VAs but produced a small change in the QRS morphology in 3 patients. In all 24 patients, the earliest activation was eventually identified in the PSC, at which a sharp potential was observed preceding the QRS complex onset by 28.2 ± 2.9 ms. The successful ablation site was in the right cusp (RC) in 10 patients (42%), the left cusp (LC) in 8 (33%), and the anterior cusp (AC) in 6 (25%). Electrocardiographic analysis showed that RC-VAs had significantly larger R-wave amplitude in lead I and a smaller aVL/aVR ratio of Q-wave amplitude compared with AC-VAs and LC-VAs, respectively. The R-wave amplitude in inferior leads was smaller in VAs localized in the RC than in the LC but did not differ between VAs from the AC and LC.Conclusions: VAs arising from the PSC are not uncommon, and RC-VAs have unique electrocardiographic characteristics. These VAs can be successfully ablated within the PSC. [ABSTRACT FROM AUTHOR]