Effects of Renal Artery Denervation on Ventricular Arrhythmias in a Postinfarct Model

Author:

Jackson Nicholas1,Gizurarson Sigfús1,Azam Mohammed Ali1,King Benjamin1,Ramadeen Andrew1,Zamiri Nima1,Porta-Sánchez Andreu1,Al-Hesayen Abdul1,Graham John1,Kusha Marjan1,Massé Stéphane1,Lai Patrick F.H.1,Parker John1,John Rohan1,Kiehl Tim-Rasmus1,Nair Govind Krishna Kumar1,Dorian Paul1,Nanthakumar Kumaraswamy1

Affiliation:

1. From the Hull Family Cardiac Fibrillation Management Laboratory, Division of Cardiology (N.J., S.G., M.A.A., B.K., N.Z., A.P.-S., M.K., S.M., P.F.H.L., G.K.K.N., K.N.) and Department of Pathology (R.J., T.-R.K.), University Health Network, Toronto, Ontario, Canada; St Michael’s Hospital, Toronto, Ontario, Canada (A.R., A.A.-H., J.G., P.D.); University of Newcastle, Australia (N.J.); and Mount Sinai Hospital, Toronto, Ontario, Canada (J.P.).

Abstract

Background— The therapeutic potential of renal denervation (RDN) for arrhythmias has not been fully explored. Detailed mechanistic evaluation is in order. The objective of the present study was to determine the antiarrhythmic potential of RDN in a postinfarct animal model and to determine whether any benefits relate to RDN-induced reduction of sympathetic effectors on the myocardium. Methods and Results— Pigs implanted with single-chamber implantable cardioverter defibrillators to record ventricular arrhythmias (VAs) were subjected to percutaneous coronary occlusion to induce myocardial infarction. Two weeks later, a sham or real RDN treatment was performed bilaterally using the St Jude EnligHTN basket catheter. Parameters of ventricular remodeling and modulation of cardio–renal sympathetic axis were monitored for 3 weeks after myocardial infarction. Histological analysis of renal arteries yielded a mean neurofilament score of healthy nerves that was significantly lower in the real RDN group than in sham controls; damaged nerves were found only in the real RDN group. There was a 100% reduction in the rate of spontaneous VAs after real RDN and a 75% increase in the rate of spontaneous VAs after sham RDN ( P =0.03). In the infarcted myocardium, presence of sympathetic nerves and tissue abundance of neuropeptide-Y, an indicator of sympathetic nerve activities, were significantly lower in the RDN group. Peak and mean sinus tachycardia rates were significantly reduced after RDN. Conclusions— RDN in the infarcted pig model leads to reduction of postinfarction VAs and myocardial sympathetic effectors. This may form the basis for a potential therapeutic role of RDN in postinfarct VAs.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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