Renal sympathetic denervation for treatment of ventricular arrhythmias: a review on current experimental and clinical findings.

Ventricular arrhythmias (VAs) remain the major cause of mortality and sudden cardiac death (SCD) in almost all forms of heart disease. Despite so many therapeutic advances, such as pharmacological therapies, catheter ablation, and arrhythmia surgery, management of VAs remains a great challenge for cardiologists. Evidence from histological studies and from direct nerve activity recordings have suggested that increased sympathetic nerve density and activity contribute to the generation of VAs and SCD. It is well known that renal sympathetic nerve (RSN), either afferent component or efferent component, plays an important role in modulation of central sympathetic activity. We have recently shown that RSN activation by electrical stimulation significantly increases cardiac and systemic sympathetic activity and promotes the incidence of acute ischemia-induced VAs, suggesting RSN has a role in the development of VAs. Initial experience of RSN denervation (RDN) in patients with resistant hypertension showed that this novel and minimally invasive device-based approach significantly reduced not only kidney but also whole-body norepinephrine spillover. In addition, experimental studies find that left stellate ganglion nerve activity is significantly decreased after RDN. Based on these observations, it is reasonable to conclude that RDN may be an effective therapy for the management of VAs. Indeed, RDN has provided a protection against VAs in both animal models and patients. In this article, we review the role of the RSN in the generation of VAs and SCD and the role of RDN as a potential treatment strategy for VAs and SCD.