Ye Zhao1, Zhaolei Jiang2, Wei-Chung Tsai3, Yuan Yuan2, Kroekkiat Chinda4, Eue-Keun Choi5, Michael C Fishbein6, Shien-Fong Lin7, Peng-Sheng Chen8, Thomas H Everett9. 1. Krannert Institute of Cardiology, 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, Sheng Yang, China. 2. Krannert Institute of Cardiology, Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Department of Cardiothoracic Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. 3. Krannert Institute of Cardiology, 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. 4. Krannert Institute of Cardiology, Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Department of Physiology, Faculty of Medical Science, Naresuan University, Phitsanulok, Thailand. 5. Division of Cardiology, Department of Internal Medicine, Seoul National University Hospital, Seoul, Republic of Korea. 6. Department of Pathology and Laboratory Medicine, UCLA, Los Angeles, California. 7. Krannert Institute of Cardiology, Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Institute of Biomedical Engineering, National Chiao-Tung University, Hsin-Chu, Taiwan. 8. Krannert Institute of Cardiology, Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana. 9. Krannert Institute of Cardiology, Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana. Electronic address: theveret@iu.edu.
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.
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.
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