Why the study?
Does renal sympathetic denervation improve ventricular electrophysiology and reduce ischemia-induced ventricular arrhythmias in a canine model?
Does renal sympathetic denervation improve ventricular electrophysiology and reduce ischemia-induced ventricular arrhythmias in a canine model?
Renal sympathetic denervation stabilizes ventricular electrophysiological properties and reduces the occurrence of ventricular arrhythmias during acute myocardial ischemia in a canine model.
Leaves open clinical translation of RSD for ischemia-induced arrhythmias; extends canine evidence of electrophysiological stabilization.
New Findings What is the central question of this study? It is well known that modulation of the autonomic nervous system affects cardiac electrophysiology. Renal sympathetic denervation has been shown to reduce systemic sympathetic activity. However, it is unknown whether renal sympathetic denervation could modulate ventricular electrophysiology and decrease the occurrence of ventricular arrhythmias associated with ischaemia. What is the main finding and its importance? Our data show that renal sympathetic denervation stabilizes ventricular electrophysiological properties in normal hearts and reduces the occurrence of ventricular arrhythmia in hearts experiencing acute myocardial ischaemia. These findings suggest that renal sympathetic denervation may become a new treatment option for ventricular arrhythmia. Recently, a beneficial effect of renal sympathetic denervation (RSD) has been seen in patients with ventricular electrical storm. However, the effect of RSD on ventricular electrophysiology remains unclear. Thirty‐three mongrel dogs were included in the present study. Renal sympathetic denervation was performed by radiofrequency ablation of the adventitial surface of the renal artery. In group 1 ( n = 8), programmed stimulation was performed before and after RSD to determine the ventricular effective refractory period (ERP) and action potential duration (APD) restitution properties. The same parameters were measured in five other animals that underwent sham RSD to serve as controls. In group 2 ( n = 10), acute myocardial ischaemia (AMI) was induced by ligating the proximal left anterior descending coronary artery after the performance of RSD, and the incidence of ventricular arrhythmia (VA) was calculated during 1 h of recording. In another 10 dogs (group 3), AMI was induced and VA was measured with sham RSD. In group 1, RSD significantly prolonged ventricular ERP and APD, reduced the maximal slope ( S max ) of the restitution curve and suppressed APD alternans at each site. Renal sympathetic denervation also significantly decreased the spatial dispersion of ERP, APD and S max . In the five control animals, no significant electrophysiological change was detected after sham RSD. The occurrence of spontaneous VA during 1 h of AMI in group 2 was significantly lower than that in group 3. These data suggest that RSD stabilizes ventricular electrophysiological properties in normal hearts and reduces the occurrence of VA in hearts experiencing AMI.
No takes yet. Share an insight, caveat, or question.
Huang et al. (2014) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: