19. How to Map Autonomic Activity

  1. Mohammad Shenasa MD6,
  2. Gerhard Hindricks MD7,
  3. Martin Borggrefe MD8,
  4. Günter Breithardt MD9 and
  5. Mark E. Josephson MD10
  1. Eue-Keun Choi1,
  2. Mark J. Shen2,
  3. Shien-Fong Lin3,
  4. Michael C. Fishbein4,
  5. Lan S. Chen5 and
  6. Peng-Sheng Chen3

Published Online: 18 DEC 2012

DOI: 10.1002/9781118481585.ch19

Cardiac Mapping, Fourth Edition

Cardiac Mapping, Fourth Edition

How to Cite

Choi, E.-K., Shen, M. J., Lin, S.-F., Fishbein, M. C., Chen, L. S. and Chen, P.-S. (2013) How to Map Autonomic Activity, in Cardiac Mapping, Fourth Edition (eds M. Shenasa, G. Hindricks, M. Borggrefe, G. Breithardt and M. E. Josephson), Wiley-Blackwell, Oxford, UK. doi: 10.1002/9781118481585.ch19

Editor Information

  1. 6

    Attending Physician, Department of Cardiovascular Services, O'Connor Hospital, Heart & Rhythm Medical Group, San Jose, California, USA

  2. 7

    Professor of Medicine (Cardiology), University Leipzig, Heart Center, Director, Department of Electrophysiology, Leipzig, Germany

  3. 8

    Professor of Medicine (Cardiology), Head, Department of Cardiology, Angiology and Pneumology, University Medical Center, Mannheim Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany

  4. 9

    Professor Emeritus of Medicine and Cardiology, Department of Cardiology and Angiology, Hospital of the University of Münster, Münster, Germany

  5. 10

    Chief, Cardiovascular Medicine Division, Director, Harvard-Thorndike Electrophysiology Institute and Arrhythmia Service, Beth Israel Deaconess Medical Center, Herman C. Dana Professor of Medicine, Harvard Medical School, Boston, Massachusetts, USA

Author Information

  1. 1

    Department of Internal Medicine, Seoul National University Hospital, Seoul, Republic of Korea

  2. 2

    Department of Internal Medicine, University of Illinois at Chicago / Advocate Christ Medical Center, Chicago, IL, USA

  3. 3

    Krannert Institute of Cardiology, Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA

  4. 4

    Department of Pathology and Laboratory Medicine at David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA

  5. 5

    Department of Neurology, Indiana University School of Medicine, Indianapolis, IN, USA

Publication History

  1. Published Online: 18 DEC 2012
  2. Published Print: 10 JAN 2013

ISBN Information

Print ISBN: 9780470670460

Online ISBN: 9781118481585



  • nerve recording;
  • autonomic nervous system;
  • ganglionated plexi;
  • sympathetic;
  • vagal;
  • tachyarrhythmias;
  • atrial fibrillation;
  • neural remodeling;
  • neural modulation;
  • ablation;
  • nerve stimulation


The heart is highly innervated by extrinsic and intrinsic cardiac autonomic nervous system. Both sympathetic and parasympathetic nervous system may contribute to the induction of cardiac arrhythmia. It is feasible to map nerve activities by directly recording from nerve structures in ambulatory animals. Most intrinsic cardiac nerve activity (ICNA) showed a close temporal relationship with extrinsic cardiac nerve activity (ECNA), whereas some ICNA activated without a temporal relationship with ECNA, suggesting that ICNA may be independently arrhythmogenic. Sympathovagal co-activation is the most common ECNA pattern associated with paroxysmal atrial tachyarrhythmias. However, when ICNA is recorded, we found that all episodes of paroxysmal atrial tachyarrhythmias were preceded by ICNA sometimes even without extrinsic nerve activity. Furthermore, the balance between sympathetic and parasympathetic nerve activities was shown to have an impact on progression from paroxysmal atrial fibrillation (AF) to persistent AF induced by intermittent rapid atrial pacing. Reducing the autonomic nerve activity by ablation of the stellate ganglion and cardiac branch of vagal nerve may reduce paroxysmal atrial tachyarrhythmias in ambulatory dogs. In addition, low-level vagus nerve stimulation (LL-VNS) can induce stellate ganglion remodeling, reducing stellate ganglion nerve activity (SGNA) and reduce the incidences of paroxysmal atrial tachyarrhythmias. We conclude that mapping autonomic nerve activity is feasible, and may provide new insights into cardiac arrhythmogenesis.