Juyi Wan1, Mu Chen2, Yuan Yuan3, Zhuo Wang4, Changyu Shen5, Michael C Fishbein6, Zhenhui Chen7, Johnson Wong7, Maria B Grant8, Thomas H Everett7, Peng-Sheng Chen9. 1. Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Department of Cardiothoracic Surgery, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan Province, China. 2. Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Department of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. 3. Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Department of Cardiac Surgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. 4. Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China. 5. Richard and Susan Smith Center for Outcomes Research in Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts. 6. Department of Pathology and Laboratory Medicine, University of California, Los Angeles, California. 7. Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana. 8. Department of Ophthalmology, University of Alabama-Birmingham, Birmingham, Alabama. 9. Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana. Electronic address: chenpp@iu.edu.
Abstract
BACKGROUND: High output subcutaneous nerve stimulation (ScNS) remodels the stellate ganglia and suppresses cardiac arrhythmia. OBJECTIVE: The purpose of this study was to test the hypothesis that long duration low output ScNS causes cardiac nerve sprouting and increases plasma norepinephrine concentration and the duration of paroxysmal atrial tachycardia (PAT) in ambulatory dogs. METHODS: We prospectively randomized 22 dogs (11 males and 11 females) into 5 different output groups for 2 months of ScNS: 0 mA (sham) (n = 6), 0.25 mA (n = 4), 1.5 mA (n = 4), 2.5 mA (n = 4), and 3.5 mA (n = 4). RESULTS: As compared with baseline, the changes in the durations of PAT episodes per 48 hours were significantly different among different groups (sham, -5.0 ± 9.5 seconds; 0.25 mA, 95.5 ± 71.0 seconds; 1.5 mA, -99.3 ± 39.6 seconds; 2.5 mA, -155.3 ± 87.8 seconds; and 3.5 mA, -76.3 ± 44.8 seconds; P < .001). The 3.5 mA group had a greater reduction in sinus heart rate than did the sham group (-29.8 ± 15.0 beats/min vs -14.5 ± 3.0 beats/min; P = .038). Immunohistochemical studies showed that the 0.25 mA group had a significantly increased while 2.5 mA and 3.5 mA stimulation had significantly reduced growth-associated protein 43 nerve densities in both atria and ventricles. The plasma norepinephrine concentrations in the 0.25 mA group was 5063.0 ± 4366.0 pg/mL, which was significantly higher than that in the other groups of dogs (739.3 ± 946.3; P = .009). There were no significant differences in the effects of simulation between males and females. CONCLUSION: In ambulatory dogs, low output ScNS causes cardiac nerve sprouting and increases plasma norepinephrine concentration and the duration of PAT episodes while high output ScNS is antiarrhythmic.
BACKGROUND: High output subcutaneous nerve stimulation (ScNS) remodels the stellate ganglia and suppresses cardiac arrhythmia. OBJECTIVE: The purpose of this study was to test the hypothesis that long duration low output ScNS causes cardiac nerve sprouting and increases plasma norepinephrine concentration and the duration of paroxysmal atrial tachycardia (PAT) in ambulatory dogs. METHODS: We prospectively randomized 22 dogs (11 males and 11 females) into 5 different output groups for 2 months of ScNS: 0 mA (sham) (n = 6), 0.25 mA (n = 4), 1.5 mA (n = 4), 2.5 mA (n = 4), and 3.5 mA (n = 4). RESULTS: As compared with baseline, the changes in the durations of PAT episodes per 48 hours were significantly different among different groups (sham, -5.0 ± 9.5 seconds; 0.25 mA, 95.5 ± 71.0 seconds; 1.5 mA, -99.3 ± 39.6 seconds; 2.5 mA, -155.3 ± 87.8 seconds; and 3.5 mA, -76.3 ± 44.8 seconds; P < .001). The 3.5 mA group had a greater reduction in sinus heart rate than did the sham group (-29.8 ± 15.0 beats/min vs -14.5 ± 3.0 beats/min; P = .038). Immunohistochemical studies showed that the 0.25 mA group had a significantly increased while 2.5 mA and 3.5 mA stimulation had significantly reduced growth-associated protein 43 nerve densities in both atria and ventricles. The plasma norepinephrine concentrations in the 0.25 mA group was 5063.0 ± 4366.0 pg/mL, which was significantly higher than that in the other groups of dogs (739.3 ± 946.3; P = .009). There were no significant differences in the effects of simulation between males and females. CONCLUSION: In ambulatory dogs, low output ScNS causes cardiac nerve sprouting and increases plasma norepinephrine concentration and the duration of PAT episodes while high output ScNS is antiarrhythmic.
Authors: Moshe Swissa; Shengmei Zhou; Ignacio Gonzalez-Gomez; Che-Ming Chang; Angela C Lai; Adam W Cates; Michael C Fishbein; Hrayr S Karagueuzian; Peng-Sheng Chen; Lan S Chen Journal: J Am Coll Cardiol Date: 2004-03-03 Impact factor: 24.094
Authors: Yuan Yuan; Xiao Liu; Juyi Wan; Johnson Wong; Amanda A Bedwell; Scott A Persohn; Changyu Shen; Michael C Fishbein; Lan S Chen; Zhenhui Chen; Thomas H Everett; Paul R Territo; Peng-Sheng Chen Journal: Heart Rhythm Date: 2019-05-29 Impact factor: 6.343
Authors: Yuan Yuan; Ye Zhao; Johnson Wong; Wei-Chung Tsai; Zhaolei Jiang; Ryan A Kabir; Seongwook Han; Changyu Shen; Michael C Fishbein; Lan S Chen; Zhenhui Chen; Thomas H Everett; Peng-Sheng Chen Journal: Heart Rhythm Date: 2020-02-14 Impact factor: 6.343