Ganglionated plexi and ligament of Marshall ablation reduces atrial vulnerability and causes stellate ganglion remodeling in ambulatory dogs

Ye Zhao, Zhaolei Jiang, Wei Chung Tsai, Yuan Yuan, Kroekkiat Chinda, Eue Keun Choi, Michael C. Fishbein, Shien-Fong Lin, Peng-Sheng Chen, Thomas Everett

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Background Simultaneous activation of the stellate ganglion (SG), the ligament of Marshall (LOM), and the ganglionated plexi often precedes the onset of paroxysmal atrial tachyarrhythmia (PAT). Objective The purpose of this study was to test the hypothesis that ablation of the LOM and the superior left ganglionated plexi (SLGP) reduces atrial vulnerability and results in remodeling of the SG. Methods Nerve activity was correlated to PAT and ventricular rate (VR) at baseline, after ablation of the LOM and SLGP, and after atrial fibrillation. Neuronal cell death was assessed with tyrosine hydroxylase and terminal deoxynucleotidyl transferase dUTP nick end label (TUNEL) staining. Results There were 4 ± 2 PAT episodes per day in controls. None were observed in the ablation group, even though SG nerve activity and VR increased from 2.2 µV (95% confidence interval [CI] 1.2–3.3 µV) and 80 bpm (95% CI 68–92 bpm) at baseline, to 3.0 µV (95% CI 2.6–3.4 µV, P = .046) and 90 bpm (95% CI 75–108 bpm, P = .026) after ablation, and to 3.1 µV (95% CI 1.7–4.5 µV, P = .116) and 95 bpm (95% CI 79–110 bpm, P = .075) after atrial fibrillation. There was an increase in tyrosine hydroxylase–negative cells in the ablation group and 19.7% (95% CI 8.6%–30.8%) TUNEL-positive staining in both the left and right SG. None were observed in the control group. Conclusion LOM and SLGP ablation caused left SG remodeling and cell death. There was reduced correlation of the VR response and PAT to SG nerve activity. These findings support the importance of SLGP and LOM in atrial arrhythmogenesis.

Original languageEnglish (US)
Pages (from-to)2083-2090
Number of pages8
JournalHeart Rhythm
Volume13
Issue number10
DOIs
StatePublished - Oct 1 2016

Fingerprint

Stellate Ganglion
Ligaments
Dogs
Confidence Intervals
Tachycardia
Atrial Fibrillation
Cell Death
Staining and Labeling
DNA Nucleotidylexotransferase
Tyrosine 3-Monooxygenase
Transferases
carbosulfan
Tyrosine
Control Groups

Keywords

  • Ablation
  • Atrial fibrillation
  • Ligament of Marshall
  • Superior left ganglion plexi

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Ganglionated plexi and ligament of Marshall ablation reduces atrial vulnerability and causes stellate ganglion remodeling in ambulatory dogs. / Zhao, Ye; Jiang, Zhaolei; Tsai, Wei Chung; Yuan, Yuan; Chinda, Kroekkiat; Choi, Eue Keun; Fishbein, Michael C.; Lin, Shien-Fong; Chen, Peng-Sheng; Everett, Thomas.

In: Heart Rhythm, Vol. 13, No. 10, 01.10.2016, p. 2083-2090.

Research output: Contribution to journalArticle

Zhao, Ye ; Jiang, Zhaolei ; Tsai, Wei Chung ; Yuan, Yuan ; Chinda, Kroekkiat ; Choi, Eue Keun ; Fishbein, Michael C. ; Lin, Shien-Fong ; Chen, Peng-Sheng ; Everett, Thomas. / Ganglionated plexi and ligament of Marshall ablation reduces atrial vulnerability and causes stellate ganglion remodeling in ambulatory dogs. In: Heart Rhythm. 2016 ; Vol. 13, No. 10. pp. 2083-2090.
@article{2382f14fcf774897a9cec04eedc9edde,
title = "Ganglionated plexi and ligament of Marshall ablation reduces atrial vulnerability and causes stellate ganglion remodeling in ambulatory dogs",
abstract = "Background Simultaneous activation of the stellate ganglion (SG), the ligament of Marshall (LOM), and the ganglionated plexi often precedes the onset of paroxysmal atrial tachyarrhythmia (PAT). Objective The purpose of this study was to test the hypothesis that ablation of the LOM and the superior left ganglionated plexi (SLGP) reduces atrial vulnerability and results in remodeling of the SG. Methods Nerve activity was correlated to PAT and ventricular rate (VR) at baseline, after ablation of the LOM and SLGP, and after atrial fibrillation. Neuronal cell death was assessed with tyrosine hydroxylase and terminal deoxynucleotidyl transferase dUTP nick end label (TUNEL) staining. Results There were 4 ± 2 PAT episodes per day in controls. None were observed in the ablation group, even though SG nerve activity and VR increased from 2.2 µV (95{\%} confidence interval [CI] 1.2–3.3 µV) and 80 bpm (95{\%} CI 68–92 bpm) at baseline, to 3.0 µV (95{\%} CI 2.6–3.4 µV, P = .046) and 90 bpm (95{\%} CI 75–108 bpm, P = .026) after ablation, and to 3.1 µV (95{\%} CI 1.7–4.5 µV, P = .116) and 95 bpm (95{\%} CI 79–110 bpm, P = .075) after atrial fibrillation. There was an increase in tyrosine hydroxylase–negative cells in the ablation group and 19.7{\%} (95{\%} CI 8.6{\%}–30.8{\%}) TUNEL-positive staining in both the left and right SG. None were observed in the control group. Conclusion LOM and SLGP ablation caused left SG remodeling and cell death. There was reduced correlation of the VR response and PAT to SG nerve activity. These findings support the importance of SLGP and LOM in atrial arrhythmogenesis.",
keywords = "Ablation, Atrial fibrillation, Ligament of Marshall, Superior left ganglion plexi",
author = "Ye Zhao and Zhaolei Jiang and Tsai, {Wei Chung} and Yuan Yuan and Kroekkiat Chinda and Choi, {Eue Keun} and Fishbein, {Michael C.} and Shien-Fong Lin and Peng-Sheng Chen and Thomas Everett",
year = "2016",
month = "10",
day = "1",
doi = "10.1016/j.hrthm.2016.07.014",
language = "English (US)",
volume = "13",
pages = "2083--2090",
journal = "Heart Rhythm",
issn = "1547-5271",
publisher = "Elsevier",
number = "10",

}

TY - JOUR

T1 - Ganglionated plexi and ligament of Marshall ablation reduces atrial vulnerability and causes stellate ganglion remodeling in ambulatory dogs

AU - Zhao, Ye

AU - Jiang, Zhaolei

AU - Tsai, Wei Chung

AU - Yuan, Yuan

AU - Chinda, Kroekkiat

AU - Choi, Eue Keun

AU - Fishbein, Michael C.

AU - Lin, Shien-Fong

AU - Chen, Peng-Sheng

AU - Everett, Thomas

PY - 2016/10/1

Y1 - 2016/10/1

N2 - Background Simultaneous activation of the stellate ganglion (SG), the ligament of Marshall (LOM), and the ganglionated plexi often precedes the onset of paroxysmal atrial tachyarrhythmia (PAT). Objective The purpose of this study was to test the hypothesis that ablation of the LOM and the superior left ganglionated plexi (SLGP) reduces atrial vulnerability and results in remodeling of the SG. Methods Nerve activity was correlated to PAT and ventricular rate (VR) at baseline, after ablation of the LOM and SLGP, and after atrial fibrillation. Neuronal cell death was assessed with tyrosine hydroxylase and terminal deoxynucleotidyl transferase dUTP nick end label (TUNEL) staining. Results There were 4 ± 2 PAT episodes per day in controls. None were observed in the ablation group, even though SG nerve activity and VR increased from 2.2 µV (95% confidence interval [CI] 1.2–3.3 µV) and 80 bpm (95% CI 68–92 bpm) at baseline, to 3.0 µV (95% CI 2.6–3.4 µV, P = .046) and 90 bpm (95% CI 75–108 bpm, P = .026) after ablation, and to 3.1 µV (95% CI 1.7–4.5 µV, P = .116) and 95 bpm (95% CI 79–110 bpm, P = .075) after atrial fibrillation. There was an increase in tyrosine hydroxylase–negative cells in the ablation group and 19.7% (95% CI 8.6%–30.8%) TUNEL-positive staining in both the left and right SG. None were observed in the control group. Conclusion LOM and SLGP ablation caused left SG remodeling and cell death. There was reduced correlation of the VR response and PAT to SG nerve activity. These findings support the importance of SLGP and LOM in atrial arrhythmogenesis.

AB - Background Simultaneous activation of the stellate ganglion (SG), the ligament of Marshall (LOM), and the ganglionated plexi often precedes the onset of paroxysmal atrial tachyarrhythmia (PAT). Objective The purpose of this study was to test the hypothesis that ablation of the LOM and the superior left ganglionated plexi (SLGP) reduces atrial vulnerability and results in remodeling of the SG. Methods Nerve activity was correlated to PAT and ventricular rate (VR) at baseline, after ablation of the LOM and SLGP, and after atrial fibrillation. Neuronal cell death was assessed with tyrosine hydroxylase and terminal deoxynucleotidyl transferase dUTP nick end label (TUNEL) staining. Results There were 4 ± 2 PAT episodes per day in controls. None were observed in the ablation group, even though SG nerve activity and VR increased from 2.2 µV (95% confidence interval [CI] 1.2–3.3 µV) and 80 bpm (95% CI 68–92 bpm) at baseline, to 3.0 µV (95% CI 2.6–3.4 µV, P = .046) and 90 bpm (95% CI 75–108 bpm, P = .026) after ablation, and to 3.1 µV (95% CI 1.7–4.5 µV, P = .116) and 95 bpm (95% CI 79–110 bpm, P = .075) after atrial fibrillation. There was an increase in tyrosine hydroxylase–negative cells in the ablation group and 19.7% (95% CI 8.6%–30.8%) TUNEL-positive staining in both the left and right SG. None were observed in the control group. Conclusion LOM and SLGP ablation caused left SG remodeling and cell death. There was reduced correlation of the VR response and PAT to SG nerve activity. These findings support the importance of SLGP and LOM in atrial arrhythmogenesis.

KW - Ablation

KW - Atrial fibrillation

KW - Ligament of Marshall

KW - Superior left ganglion plexi

UR - http://www.scopus.com/inward/record.url?scp=84994310809&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84994310809&partnerID=8YFLogxK

U2 - 10.1016/j.hrthm.2016.07.014

DO - 10.1016/j.hrthm.2016.07.014

M3 - Article

C2 - 27426436

AN - SCOPUS:84994310809

VL - 13

SP - 2083

EP - 2090

JO - Heart Rhythm

JF - Heart Rhythm

SN - 1547-5271

IS - 10

ER -