Supported in part by National Institutes of Health grants P01 HL78931, R01 HL78932, 71140, R21 HL106554; a Heart Rhythm Society Fellowship in Cardiac Pacing and Electrophysiology (M.J.S.); a Nihon Kohden/St. Jude Medical Electrophysiology fellowship (M. M.); Medtronic-Zipes Endowments (P.-S.C.); and an American Heart Association Established Investigator Award (S.-F.L.).
Heart Failure Decreases Nerve Activity in the Right Atrial Ganglionated Plexus
Article first published online: 28 OCT 2011
© 2012 Wiley Periodicals, Inc.
Journal of Cardiovascular Electrophysiology
Volume 23, Issue 4, pages 404–412, April 2012
How to Cite
SHINOHARA, T., SHEN, M. J., HAN, S., MARUYAMA, M., PARK, H.-W., FISHBEIN, M. C., SHEN, C., CHEN, P.-S. and LIN, S.-F. (2012), Heart Failure Decreases Nerve Activity in the Right Atrial Ganglionated Plexus. Journal of Cardiovascular Electrophysiology, 23: 404–412. doi: 10.1111/j.1540-8167.2011.02204.x
Dr. Chen reports receiving support in the form of research equipment from St. Jude Medical, Medtronic, Cyberonics, and CryoCath. Other authors: No disclosures.
- Issue published online: 19 APR 2012
- Article first published online: 28 OCT 2011
- Manuscript received 28 March 2011; Revised manuscript received 15 August 2011; Accepted for publication 23 August 2011.
- heart failure;
- nervous system;
- sinoatrial node
Reduced Vagal Control in Heart Failure.
Objective: We tested the hypothesis that heart failure (HF) results in right atrial ganglionated plexus (RAGP) denervation that contributes to sinoatrial node dysfunction.
Background: HF is associated with sinoatrial node dysfunction. However, the detailed mechanisms remain unclear.
Methods: We recorded nerve activity (NA) from the RAGP, right stellate ganglion (SG), and right vagal nerve in 7 ambulatory dogs at baseline and after pacing-induced HF. We also determined the effects of RAGP stimulation in isolated normal and HF canine RA.
Results: NAs in both the SG and vagal were significantly higher in HF than at baseline. The relationship between 1-minute integrated NAs of vagal and RAGP showed either a positive linear correlation (Group 1, n = 4) or an L-shaped correlation (Group 2, n = 3). In all dogs, a reduced heart rate was observed when vagal-NA was associated with simultaneously increased RAGP-NA. On the other hand, when vagal-NA was not associated with increased RAGP-NA, the heart rate was not reduced. The induction of HF significantly decreased RAGP-NA in all dogs (P < 0.05). Stimulating the superior RAGP in isolated RA significantly reduced the sinus rate in normal but not the HF hearts. Immunohistochemical staining revealed lower densities of tyrosine hydroxylase- and choline acetyltransferase-positive nerve tissues in HF RAGP than normal (P < 0.001 and P = 0.001, respectively).
Conclusions: The RAGP-NA is essential for the vagal nerve to counterbalance the SG in sinus rate control. In HF, RAGP denervation and decreased RAGP-NA contribute to the sinus node dysfunction.