標題: Ganglionated plexi and ligament of Marshall ablation reduces atrial vulnerability and causes stellate ganglion remodeling in ambulatory dogs
作者: 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 H.
分子醫學與生物工程研究所
Institute of Molecular Medicine and Bioengineering
關鍵字: Ablation;Superior left ganglion plexi;Ligament of;Marshall;Atrial fibrillation
公開日期: Oct-2016
摘要: 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 mu V (95% confidence interval [CI] 1.2-3.3 mu V) and 80 bpm (95% CI 68-92 bpm) at baseline, to 3.0 mu V (95% CI 2.6-3.4 mu V, P = .046) and 90 bpm (95% CI 75-108 bpm, P = .026) after ablation, and to 3.1 mu V (95% CI 1.7-4.5 mu V, 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%) TUN EL-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.
URI: http://dx.doi.org/10.1016/j.hrthm.2016.07.014
http://hdl.handle.net/11536/132887
ISSN: 1547-5271
DOI: 10.1016/j.hrthm.2016.07.014
期刊: HEART RHYTHM
Volume: 13
Issue: 10
起始頁: 2083
結束頁: 2090
Appears in Collections:Articles