K. Wirth and M. Böhm share senior authorship.
Effects of Electrical Stimulation of Carotid Baroreflex and Renal Denervation on Atrial Electrophysiology
Version of Record online: 2 MAY 2013
© 2013 Wiley Periodicals, Inc.
Journal of Cardiovascular Electrophysiology
Volume 24, Issue 9, pages 1028–1033, September 2013
How to Cite
LINZ, D., MAHFOUD, F., SCHOTTEN, U., UKENA, C., NEUBERGER, H.-R., WIRTH, K. and BÖHM, M. (2013), Effects of Electrical Stimulation of Carotid Baroreflex and Renal Denervation on Atrial Electrophysiology. Journal of Cardiovascular Electrophysiology, 24: 1028–1033. doi: 10.1111/jce.12171
D.L. is supported by HOMFOR2013. M.B. is supported by the Deutsche Forschungsgemeinschaft (KFO 196). F.M is supported by the Deutsche Hochdruckliga. Other authors: No disclosures.
- Issue online: 9 SEP 2013
- Version of Record online: 2 MAY 2013
- Accepted manuscript online: 12 APR 2013 03:02PM EST
- Manuscript Revised: 2 APR 2013
- Manuscript Accepted: 2 APR 2013
- Manuscript Received: 19 FEB 2013
- atrial fibrillation;
- baroreflex stimulation;
- renal denervation
Renal Denervation and Baroreflex Stimulation
This study was designed to compare the effect of electrical baroreflex stimulation (BRS) at an intensity used in hypertensive patients and renal denervation (RDN) on atrial electrophysiology. BRS and RDN reduce blood pressure and global sympathetic drive in patients with resistant hypertension. Whereas RDN decreases sympathetic renal afferent nerve activity, leading to decreased central sympathetic drive, BRS modulates autonomic balance by activation of the baroreflex, resulting in both reduced sympathetic drive and increased vagal activation. Increased vagal tone potentially shortens atrial refractoriness resulting in a stabilization of reentry circuits perpetuating atrial fibrillation (AF).
Methods and Results
In normotensive anesthetized pigs (n = 12), we compared the acute effect of BRS and RDN on blood pressure, atrial effective refractory period (AERP), and inducibility of AF. Electrical BRS was titrated to result in comparable heart rate and blood pressure reduction compared to irreversible RDN. BRS resulted in a rapid and pronounced shortening of AERP (from 162 ± 8 milliseconds to 117 ± 16 milliseconds, P = 0.001) associated with increased AF-inducibility from 0% to 82%. This shortening in AERP was completely reversible after stopping BRS. After administration of atropine, AF-inducibility during BRS was attenuated. Ventricular repolarization was not modulated by BRS. In RDN, AF was not inducible; however, it did not prevent BRS-induced shortening of AERP.
RDN and BRS resulting in comparable blood pressure and heart rate reductions differently influence atrial electrophysiology. Vagally mediated shortening of AERP, resulting in increased AF-inducibility, was observed with BRS but not with RDN.