Evidence map›Paper›PMID 26607063›Full record

ArticleHeart rhythm2016

Intermittent left cervical vagal nerve stimulation damages the stellate ganglia and reduces the ventricular rate during sustained atrial fibrillation in ambulatory dogs.

Kroekkiat Chinda, Wei-Chung Tsai, Yi-Hsin Chan, Andrew Y-T Lin, Jheel Patel, Ye Zhao, Alex Y Tan, Mark J Shen, Hongbo Lin, Changyu Shen and 7 more

Abstract read
In one paragraph

Article in Heart rhythm, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.0field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Autonomic Neuromodulation Acutely Ameliorates Left Ventricular Strain in Humans.Journal of cardiovascular translational research · 2019
    Trial
  4. Autonomic dysregulation and atrial arrhythmias.American journal of physiology. Cell physiology · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Autonomic Modulation of Atrial Fibrillation.JACC. Basic to translational science · 2023
    Review
  9. Article
  10. Review
  11. Article
  12. Neural Mechanisms and Therapeutic Opportunities for Atrial Fibrillation.Methodist DeBakey cardiovascular journal · 2021
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Neuromodulation for the Treatment of Heart Rhythm Disorders.JACC. Basic to translational science · 2019
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 9 institutions in 4 countries.

Kroekkiat ChindaThe Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand; Department of Physiology, Faculty of Medical Science, Naresuan University, Phitsanulok, Thailand.
Wei-Chung TsaiThe Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
Yi-Hsin ChanThe Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Division of Cardiology, The First Department of Medicine, Chang-Gung Memorial Hospital, Taipei, Taiwan.
Andrew Y-T LinThe Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana.
Jheel PatelThe Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana.
Ye ZhaoThe Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Department of Cardiac Surgery, The First Affiliated Hospital of China Medical University, Shenyang, People's Republic of China.
Alex Y TanDivision of Cardiology, Hunter Holmes McGuire VA Medical Center, Virginia Commonwealth University, Richmond, Virginia.
Mark J ShenThe Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana.
Hongbo LinDepartment of Biostatistics, Indiana University School of Medicine and the Fairbanks School of Public Health, Indianapolis, Indiana.
Changyu ShenDepartment of Biostatistics, Indiana University School of Medicine and the Fairbanks School of Public Health, Indianapolis, Indiana.
Nipon ChattipakornCardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Michael Rubart-von der LoheDepartment of Pediatrics, Riley Heart Research Center, Indianapolis, Indiana.
Lan S ChenThe Department of Neurology, Indiana University School of Medicine, Indianapolis, Indiana.
Michael C FishbeinDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California.
Shien-Fong LinThe Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Institute of Biomedical Engineering, National Chiao-Tung University, Hsin-Chu, Taiwan.
Zhenhui ChenThe Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana.
Peng-Sheng ChenThe Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana. Electronic address: chenpp@iu.edu.
Indiana University School of MedicineChang Gung Memorial Hospital · TWChiang Mai University · THFirst Hospital of China Medical University · CNKaohsiung Medical University · TWNational Yang Ming Chiao Tung University · TWRiley Hospital for Children · USUniversity of California, Los Angeles · USVirginia Commonwealth University · US

Funding

Indiana Clinical and Translational Sciences InstituteUL1TR001108 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI DENNE, SCOTT C., SHEKHAR, ANANTHA · 2013 to 2017
$23.3M
WAVE DYNAMICS IN NORMAL AND DISEASED RABBIT HEARTSP01HL078931 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WEISS, JAMES · 2005 to 2015
$20.7M
Thoracic Veins and Sustained Atrial FibrillationR01HL071140 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI CHEN, PENG-SHENG · 2002 to 2014
$4.7M
Interactive Vagal Stimulation and Atrial FibrillationR21HL106554 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI LIN, SHIEN-FONG · 2011 to 2012
$424k
Sympathetic Nerve Activity Recorded From the Skin and Cardiac ArrhythmiasR41HL124741 · NHLBI · ARRHYTHMOTECH, LLC · PI EVERETT, THOMAS H · 2014 to 2014
$213k
NCATS NIH HHS UL1 TR001108NHLBI NIH HHS P01 HL078931NHLBI NIH HHS P01 HL78931NHLBI NIH HHS R01 HL071140NHLBI NIH HHS R01HL71140NHLBI NIH HHS R21 HL106554NHLBI NIH HHS R21HL106554NHLBI NIH HHS R41 HL124741NHLBI NIH HHS R41HL124741
6 · The paper itself

Abstract

backgroundThe effects of intermittent open-loop vagal nerve stimulation (VNS) on the ventricular rate (VR) during atrial fibrillation (AF) remain unclear.

objectiveThe purpose of this study was to test the hypothesis that VNS damages the stellate ganglion (SG) and improves VR control during persistent AF.

methodsWe performed left cervical VNS in ambulatory dogs while recording the left SG nerve activity (SGNA) and vagal nerve activity. Tyrosine hydroxylase (TH) staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining were used to assess neuronal cell death in the SG.

resultsWe induced persistent AF by atrial pacing in 6 dogs, followed by intermittent VNS with short ON-time (14 seconds) and long OFF-time (66 seconds). The integrated SGNA and VR during AF were 4.84 mV·s (95% confidence interval [CI] 3.08-6.60 mV·s) and 142 beats/min (95% CI 116-168 beats/min), respectively. During AF, VNS reduced the integrated SGNA and VR, respectively, to 3.74 mV·s (95% CI 2.27-5.20 mV·s; P = .021) and 115 beats/min (95% CI 96-134 beats/min; P = .016) during 66-second OFF-time and to 4.07 mV·s (95% CI 2.42-5.72 mV·s; P = .037) and 114 beats/min (95% CI 83-146 beats/min; P = .039) during 3-minute OFF-time. VNS increased the frequencies of prolonged (>3 seconds) pauses during AF. TH staining showed large confluent areas of damage in the left SG, characterized by pyknotic nuclei, reduced TH staining, increased percentage of TH-negative ganglion cells, and positive TUNEL staining. Occasional TUNEL-positive ganglion cells were also observed in the right SG.

conclusionVNS damaged the SG, leading to reduced SGNA and better rate control during persistent AF.

Indexed as

ElectrocardiographyAnimalsAtrial FibrillationCardiac Pacing, ArtificialDisease Models, AnimalDogsHeart AtriaHeart RateStellate GanglionVagus Nerve StimulationAtrial fibrillationExcitotoxicityVagal nerve stimulation

Identifiers

PMID26607063
PMCPMC4762711
OpenAlexW2182335687

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.