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Increased sympathetic activity precipitates ventricular tachyarrhythmias and sudden cardiac death in long-QT syndrome type 1 (LQT1). Renal sympathetic denervation (RDN) has emerged as a new approach to reduce sympathetic activity. This study aimed to investigate whether RDN could prevent ventricular tachycardia in a canine model of drug-induced LQT1.
Fourteen adult beagle dogs were randomly assigned into control group (n=7) and RDN group (n=7). ECGs, blood pressure and left stellate ganglion (LSG) neural activity were continuously recorded. The LQT1 model was constructed by infusion of the slowly-activating delayed-rectifier K+ current (IKs) blocker HMR1556 (0.05 mg/kg/min). In RDN group, RDN was performed 30 minutes before the administration of HMR1556 by radiofrequency ablation of the adventitial surface of the renal artery. In both groups, ventricular effective refractory period (ERP), action potential duration (APD), and APD restitution properties were determined at baseline and 15 min after infusion of HMR1556, and then bolus injections of isoproterenol (2.5 ug/kg) were performed to trigger torsades de pointes (TdP).
In both groups, infusion of HMR1556 for 15 minutes significantly prolonged the QT interval, ventricular ERP and APD. Besides, in the control group, infusion of HMR1556 dramatically increased the spatial dispersion of repolarization (Tpeak-Tend interval) and the maximal slopes of the APD restitution curves (Smax), which, however, were attenuated by RDN. Bolus injection of isoproterenol significantly increased LSG neural activity, evoked paradoxical repolarization prolongation during heart rate accelerations, and triggered the occurrence of TdP in the control group. However, RDN also significantly attenuated the activation of LSG and the occurrence of TdP during bolus injection of isoproterenol when compared to the control group.
RDN could prevent ventricular tachycardia in this model of drug-induced LQT1.