Ectopic atrial arrhythmias arising from canine thoracic veins during in vivo stellate ganglia stimulation

Alex Y. Tan, Shengmei Zhou, Chun Jung Byung, Masahiro Ogawa, Lan S. Chen, Michael C. Fishbein, Peng Sheng Chen

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

The purpose of the present study was to determine whether thoracic veins may act as ectopic pacemakers and whether nodelike cells and rich sympathetic innervation are present at the ectopic sites. We used a 1,792-electrode mapping system with 1-mm resolution to map ectopic atrial arrhythmias in eight normal dogs during in vivo right and left stellate ganglia (SG) stimulation before and after sinus node crushing. SG stimulation triggered significant elevations of transcardiac norepinephrine levels, sinus tachycardia in all dogs, and atrial tachycardia in two of eight dogs. Sinus node crushing resulted in a slow junctional rhythm (51 ± 6 beats/min). Subsequent SG stimulation induced 20 episodes of ectopic beats in seven dogs and seven episodes of pulmonary vein tachycardia in three dogs (cycle length 273 ± 35 ms, duration 16 ± 4 s). The ectopic beats arose from the pulmonary vein (n = 11), right atrium (n = 5), left atrium (n = 2), and the vein of Marshall (n = 2). There was no difference in arrhythmogenic effects of left vs. right SG stimulation (13/29 vs. 16/29 episodes, P = nonsignificant). There was a greater density of periodic acid Schiff-positive cells (P < 0.05) and sympathetic nerves (P < 0.05) at the ectopic sites compared with other nonectopic atrial sites. We conclude that, in the absence of a sinus node, thoracic veins may function as subsidiary pacemakers under heightened sympathetic tone, becoming the dominant sites of initiation of focal atrial arrhythmias that arise from sites with abundant sympathetic nerves and periodic acid Schiff-positive cells.

Original languageEnglish (US)
Pages (from-to)H691-H698
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume295
Issue number2
DOIs
StatePublished - Aug 1 2008

Fingerprint

Stellate Ganglion
Canidae
Cardiac Arrhythmias
Veins
Thorax
Sinoatrial Node
Dogs
Periodic Acid
Pulmonary Veins
Heart Atria
Tachycardia
Sinus Tachycardia
Norepinephrine
Electrodes

Keywords

  • Atrial tachycardia
  • Autonomic nervous system
  • Computerized mapping
  • Electrophysiology
  • Sympathetic nerves

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)
  • Cardiology and Cardiovascular Medicine

Cite this

Ectopic atrial arrhythmias arising from canine thoracic veins during in vivo stellate ganglia stimulation. / Tan, Alex Y.; Zhou, Shengmei; Byung, Chun Jung; Ogawa, Masahiro; Chen, Lan S.; Fishbein, Michael C.; Chen, Peng Sheng.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 295, No. 2, 01.08.2008, p. H691-H698.

Research output: Contribution to journalArticle

Tan, Alex Y. ; Zhou, Shengmei ; Byung, Chun Jung ; Ogawa, Masahiro ; Chen, Lan S. ; Fishbein, Michael C. ; Chen, Peng Sheng. / Ectopic atrial arrhythmias arising from canine thoracic veins during in vivo stellate ganglia stimulation. In: American Journal of Physiology - Heart and Circulatory Physiology. 2008 ; Vol. 295, No. 2. pp. H691-H698.
@article{dd97f6e646af45368f1924d3a258495a,
title = "Ectopic atrial arrhythmias arising from canine thoracic veins during in vivo stellate ganglia stimulation",
abstract = "The purpose of the present study was to determine whether thoracic veins may act as ectopic pacemakers and whether nodelike cells and rich sympathetic innervation are present at the ectopic sites. We used a 1,792-electrode mapping system with 1-mm resolution to map ectopic atrial arrhythmias in eight normal dogs during in vivo right and left stellate ganglia (SG) stimulation before and after sinus node crushing. SG stimulation triggered significant elevations of transcardiac norepinephrine levels, sinus tachycardia in all dogs, and atrial tachycardia in two of eight dogs. Sinus node crushing resulted in a slow junctional rhythm (51 ± 6 beats/min). Subsequent SG stimulation induced 20 episodes of ectopic beats in seven dogs and seven episodes of pulmonary vein tachycardia in three dogs (cycle length 273 ± 35 ms, duration 16 ± 4 s). The ectopic beats arose from the pulmonary vein (n = 11), right atrium (n = 5), left atrium (n = 2), and the vein of Marshall (n = 2). There was no difference in arrhythmogenic effects of left vs. right SG stimulation (13/29 vs. 16/29 episodes, P = nonsignificant). There was a greater density of periodic acid Schiff-positive cells (P < 0.05) and sympathetic nerves (P < 0.05) at the ectopic sites compared with other nonectopic atrial sites. We conclude that, in the absence of a sinus node, thoracic veins may function as subsidiary pacemakers under heightened sympathetic tone, becoming the dominant sites of initiation of focal atrial arrhythmias that arise from sites with abundant sympathetic nerves and periodic acid Schiff-positive cells.",
keywords = "Atrial tachycardia, Autonomic nervous system, Computerized mapping, Electrophysiology, Sympathetic nerves",
author = "Tan, {Alex Y.} and Shengmei Zhou and Byung, {Chun Jung} and Masahiro Ogawa and Chen, {Lan S.} and Fishbein, {Michael C.} and Chen, {Peng Sheng}",
year = "2008",
month = "8",
day = "1",
doi = "10.1152/ajpheart.01321.2007",
language = "English (US)",
volume = "295",
pages = "H691--H698",
journal = "American Journal of Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "2",

}

TY - JOUR

T1 - Ectopic atrial arrhythmias arising from canine thoracic veins during in vivo stellate ganglia stimulation

AU - Tan, Alex Y.

AU - Zhou, Shengmei

AU - Byung, Chun Jung

AU - Ogawa, Masahiro

AU - Chen, Lan S.

AU - Fishbein, Michael C.

AU - Chen, Peng Sheng

PY - 2008/8/1

Y1 - 2008/8/1

N2 - The purpose of the present study was to determine whether thoracic veins may act as ectopic pacemakers and whether nodelike cells and rich sympathetic innervation are present at the ectopic sites. We used a 1,792-electrode mapping system with 1-mm resolution to map ectopic atrial arrhythmias in eight normal dogs during in vivo right and left stellate ganglia (SG) stimulation before and after sinus node crushing. SG stimulation triggered significant elevations of transcardiac norepinephrine levels, sinus tachycardia in all dogs, and atrial tachycardia in two of eight dogs. Sinus node crushing resulted in a slow junctional rhythm (51 ± 6 beats/min). Subsequent SG stimulation induced 20 episodes of ectopic beats in seven dogs and seven episodes of pulmonary vein tachycardia in three dogs (cycle length 273 ± 35 ms, duration 16 ± 4 s). The ectopic beats arose from the pulmonary vein (n = 11), right atrium (n = 5), left atrium (n = 2), and the vein of Marshall (n = 2). There was no difference in arrhythmogenic effects of left vs. right SG stimulation (13/29 vs. 16/29 episodes, P = nonsignificant). There was a greater density of periodic acid Schiff-positive cells (P < 0.05) and sympathetic nerves (P < 0.05) at the ectopic sites compared with other nonectopic atrial sites. We conclude that, in the absence of a sinus node, thoracic veins may function as subsidiary pacemakers under heightened sympathetic tone, becoming the dominant sites of initiation of focal atrial arrhythmias that arise from sites with abundant sympathetic nerves and periodic acid Schiff-positive cells.

AB - The purpose of the present study was to determine whether thoracic veins may act as ectopic pacemakers and whether nodelike cells and rich sympathetic innervation are present at the ectopic sites. We used a 1,792-electrode mapping system with 1-mm resolution to map ectopic atrial arrhythmias in eight normal dogs during in vivo right and left stellate ganglia (SG) stimulation before and after sinus node crushing. SG stimulation triggered significant elevations of transcardiac norepinephrine levels, sinus tachycardia in all dogs, and atrial tachycardia in two of eight dogs. Sinus node crushing resulted in a slow junctional rhythm (51 ± 6 beats/min). Subsequent SG stimulation induced 20 episodes of ectopic beats in seven dogs and seven episodes of pulmonary vein tachycardia in three dogs (cycle length 273 ± 35 ms, duration 16 ± 4 s). The ectopic beats arose from the pulmonary vein (n = 11), right atrium (n = 5), left atrium (n = 2), and the vein of Marshall (n = 2). There was no difference in arrhythmogenic effects of left vs. right SG stimulation (13/29 vs. 16/29 episodes, P = nonsignificant). There was a greater density of periodic acid Schiff-positive cells (P < 0.05) and sympathetic nerves (P < 0.05) at the ectopic sites compared with other nonectopic atrial sites. We conclude that, in the absence of a sinus node, thoracic veins may function as subsidiary pacemakers under heightened sympathetic tone, becoming the dominant sites of initiation of focal atrial arrhythmias that arise from sites with abundant sympathetic nerves and periodic acid Schiff-positive cells.

KW - Atrial tachycardia

KW - Autonomic nervous system

KW - Computerized mapping

KW - Electrophysiology

KW - Sympathetic nerves

UR - http://www.scopus.com/inward/record.url?scp=52449122892&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=52449122892&partnerID=8YFLogxK

U2 - 10.1152/ajpheart.01321.2007

DO - 10.1152/ajpheart.01321.2007

M3 - Article

C2 - 18539751

AN - SCOPUS:52449122892

VL - 295

SP - H691-H698

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6135

IS - 2

ER -