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Vaseghi M, Salavatian S, Rajendran PS, et al. Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction. JCI Insight. 2017;2(16)doi: 10.1172/jci.insight.86715.
Vaseghi, M., Salavatian, S., Rajendran, P. S., Yagishita, D., Woodward, W. R., Hamon, D., Yamakawa, K., Irie, T., Habecker, B. A., & Shivkumar, K. (2017). Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction. JCI insight, 2(16), . https://doi.org/10.1172/jci.insight.86715
Vaseghi, Marmar, et al. "Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction." JCI insight vol. 2,16 (2017). doi: https://doi.org/10.1172/jci.insight.86715
Vaseghi M, Salavatian S, Rajendran PS, Yagishita D, Woodward WR, Hamon D, Yamakawa K, Irie T, Habecker BA, Shivkumar K. Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction. JCI Insight. 2017 Aug 17;2(16). doi: 10.1172/jci.insight.86715. eCollection 2017 Aug 17. PMID: 28814663; PMCID: PMC5621871.
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JCI Insight. 2017 Aug 17;2(16). doi: 10.1172/jci.insight.86715. eCollection 2017 Aug 17.

Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction.

JCI insight

Marmar Vaseghi, Siamak Salavatian, Pradeep S Rajendran, Daigo Yagishita, William R Woodward, David Hamon, Kentaro Yamakawa, Tadanobu Irie, Beth A Habecker, Kalyanam Shivkumar

Affiliations

  1. Cardiac Arrhythmia Center.
  2. Neurocardiology Research Center of Excellence, and.
  3. Molecular Cellular and Integrative Physiology Interdepartmental Program, UCLA, Los Angeles, California, USA.
  4. Department of Physiology & Pharmacology and.
  5. Department of Medicine Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon, USA.

PMID: 28814663 PMCID: PMC5621871 DOI: 10.1172/jci.insight.86715

Abstract

Myocardial infarction causes sympathetic activation and parasympathetic dysfunction, which increase risk of sudden death due to ventricular arrhythmias. Mechanisms underlying parasympathetic dysfunction are unclear. The aim of this study was to delineate consequences of myocardial infarction on parasympathetic myocardial neurotransmitter levels and the function of parasympathetic cardiac ganglia neurons, and to assess electrophysiological effects of vagal nerve stimulation on ventricular arrhythmias in a chronic porcine infarct model. While norepinephrine levels decreased, cardiac acetylcholine levels remained preserved in border zones and viable myocardium of infarcted hearts. In vivo neuronal recordings demonstrated abnormalities in firing frequency of parasympathetic neurons of infarcted animals. Neurons that were activated by parasympathetic stimulation had low basal firing frequency, while neurons that were suppressed by left vagal nerve stimulation had abnormally high basal activity. Myocardial infarction increased sympathetic inputs to parasympathetic convergent neurons. However, the underlying parasympathetic cardiac neuronal network remained intact. Augmenting parasympathetic drive with vagal nerve stimulation reduced ventricular arrhythmia inducibility by decreasing ventricular excitability and heterogeneity of repolarization of infarct border zones, an area with known proarrhythmic potential. Preserved acetylcholine levels and intact parasympathetic neuronal pathways can explain the electrical stabilization of infarct border zones with vagal nerve stimulation, providing insight into its antiarrhythmic benefit.

Keywords: Cardiology

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