Mapping of ventricular tachycardia induced by thoracic neural stimulation in dogs

1986 ◽  
Vol 64 (4) ◽  
pp. 411-418 ◽  
Author(s):  
René Cardinal ◽  
Pierre Savard ◽  
J. Andrew Armour ◽  
Réginald Nadeau ◽  
D. Leigh Carson ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Stellate Ganglion ◽  
Sympathetic Ganglia ◽  
Posterior Aspect ◽  
Cardiac Nerve ◽  
Surface Ecg ◽  
Cervical Ganglion ◽  
Potential Gradients ◽  
The Right ◽  
Stimulation Of

To investigate ventricular tachycardias produced in healthy canine myocardium by stimulation of sympathetic ganglia or cardiac nerves, we simultaneously recorded a surface ECG and 63 ventricular electrograms in anesthetized open-chest dogs. Isochronal and isopotential maps were generated off-line by computer. Ventricular tachycardia with uniform beat-to-beat morphology was induced in 13 or 22 dogs by electrical stimulation of the left stellate ganglion (five experiments), the left middle cervical ganglion (four experiments), the left caudal pole cardiopulmonary nerve (two experiments), or the ventrolateral cardiac nerve (eight experiments). It was not inducible by stimulation of the right-sided major cardiopulmonary nerves or ganglia. In most instances the earliest measured electrical excitation occurred on the posterior aspect of the ventricles. Isochronal maps demonstrated a radial spread of the impulse away from the area of earliest excitation. Changes in the region of earliest excitation and (or) activation pattern were accompanied by changes in QRS morphology. The potential gradients measured between areas displaying positive and negative T waves on the anterior and left lateral aspects of the ventricles were significantly increased by ventrolateral cardiac nerve stimulation. However, the ventricular regions where these potential gradients existed differed from the regions of earliest excitation during ventricular tachycardia. These results demonstrate that the thoracic autonomic nervous system can induce repetitive ventricular excitation originating from consistent loci.

Sympathetic neural effects on regional atrial recovery properties and cardiac rhythm

1981 ◽  
Vol 240 (4) ◽  
pp. H590-H596
Author(s):  
F. A. Kralios ◽  
C. K. Millar
Keyword(s):  
Left Atrial ◽  
Sinus Node ◽  
Stellate Ganglion ◽  
Sympathetic Nerves ◽  
Substantial Effect ◽  
Cardiac Nerve ◽  
Anesthetized Dogs ◽  
Functional Distribution ◽  
The Right ◽  
Stimulation Of

The functional distribution of the cardiac sympathetic nerves to the atria and their arrhythmiogenic effects were determined in 16 open-chest pentobarbital-anesthetized dogs. Shortening of refractory periods at four right and two left atrial sites during stimulation of the nerves was taken as a criterion of their distribution. Stimulation of right stellate ganglion, craniovagal, and right stellate cardiac nerves produced localized shortening on the right atrium, particularly at the sinus node area, and invariably induced sinus tachycardia. The recurrent cardiac nerve produced little shortening at all sites and less arrhythmiogenic effect. The left stellate ganglion and ventrolateral cardiac nerve affected only left atrial sites and induced atrioventricular junctional rhythm. The ventromedial cardiac nerve affected all sites and had no consistent arrhythmiogenic effect. The innominate nerve had no substantial effect. We concluded that the functional distribution of the cardiac sympathetic nerves is localized, and that rate, rhythm, and refractory period changes induced by stimulation of these nerves are characteristic of the area of distribution.

Functional Analysis of the Cardioaugmentor and Cardioaccelerator Pathways in the Dog

1957 ◽  
Vol 191 (2) ◽  
pp. 213-217 ◽  
Author(s):  
Walter C. Randall ◽  
Howard McNally ◽  
Jerry Cowan ◽  
Lawrence Caliguiri ◽  
Wayne G. Rohse
Keyword(s):  
Spinal Cord ◽  
Stellate Ganglion ◽  
Heart Tissue ◽  
Nerve Fibers ◽  
Direct Electrical Stimulation ◽  
Cervical Ganglion ◽  
Cervical Ganglia ◽  
The Right ◽  
Upper Thoracic ◽  
Stimulation Of

The direct, electrical stimulation of the thoracic anterior roots, the communicating rami, and the upper thoracic sympathetic trunk in the dog reveals the preganglionic pathways followed by the cardiac accelerator and augmentor nerves. These nerve fibers are generally intermingled in each of the above pathways, but accelerator fibers are much more prominent on the right whereas augmentor fibers predominate on the left. The most significant pathways are via the T2 and T3 anterior roots and communicating rami, but significant responses were elicited from the T4 nerves and occasionally from the T1 and T5 nerves. Neither accelerator nor augmentor responses could be induced by stimulation of the C8 nerve nor by excitation of nerves below T5. It is concluded that preganglionic cardiomotor fibers enter the trunk between T1 and T5, course cephalad to the stellate ganglion where they may synapse or pass to the caudal cervical ganglion by way of the ansa subclavia. The stellate cardiac nerve furnishes a very important postganglionic augmentor and accelerator pathway, when it is present, but direct branches from the caudal cervical ganglia carry a majority of these fibers in most animals. Augmentor and accelerator fibers can not be functionally separated at any point in their anatomical pathways from the spinal cord to the heart. Responses seem to be determined rather, by the site of nerve terminations in heart tissue.

Functional and anatomical variability of canine cardiac sympathetic efferent pathways: implications for regional denervation of the left ventricle

1986 ◽  
Vol 64 (7) ◽  
pp. 958-969 ◽  
Author(s):  
R. D. Janes ◽  
D. E. Johnstone ◽  
J. C. Brandys ◽  
J. A. Armour
Keyword(s):  
Left Ventricle ◽  
Stellate Ganglion ◽  
Left Ventricular ◽  
Efferent Innervation ◽  
Cardiac Nerve ◽  
Cervical Ganglion ◽  
The Right ◽  
Inotropic Responses ◽  
Left Middle ◽  
Cardiac Nerves

To further elucidate the functional anatomy of canine cardiac innervation as well as to assess the feasibility of producing regional left ventricular sympathetic denervation, the chronotropic and (or) regional left ventricular inotropic responses produced by stellate or middle cervical ganglion stimulation were investigated in 22 dogs before and after sectioning of individual major cardiopulmonary or cardiac nerves. Sectioning the right or left subclavian ansae abolished all cardiac responses produced by ipsilateral stellate ganglion stimulation. Sectioning a major sympathetic cardiopulmonary nerve, other than the right interganglionic nerve, usually reduced, but seldom abolished, regional inotropic responses elicited by ipsilateral middle cervical ganglion stimulation. Sectioning the dorsal mediastinal cardiac nerves consistently abolished the left ventricular inotropic responses elicited by right middle cervical ganglion stimulation but minimally affected those elicited by left middle cervical ganglion stimulation. In contrast, cutting the left lateral cardiac nerve decreased the inotropic responses in lateral and posterior left ventricular segments elicited by left middle cervical ganglion stimulation but had little effect on the inotropic responses produced by right middle cervical ganglion stimulation. In addition, the ventral mediastinal cardiac nerve was found to be a significant sympathetic efferent pathway from the left-sided ganglia to the left ventricle. These results indicate that (i) the stellate ganglia project axons to the heart via the subclavian ansae and thus effective sympathetic decentralization can be produced by cutting the subclavian ansae; (ii) the right-sided cardiac sympathetic efferent innervation of the left ventricle converges intrapericardially in the dorsal mediastinal cardiac nerves; and (iii) the left-sided cardiac sympathetic efferent innervation of the left ventricle diverges to innervate the left ventricle by a number of nerves including the dorsal mediastinal, ventral mediastinal, and left lateral cardiac nerves. Thus consistent denervation of a region of the left ventricle can not be accomplished by sectioning an individual cardiopulmonary or cardiac nerve because of the functional and anatomical variability of the neural components in each nerve, as well as the fact that overlapping regions of the left ventricle are innervated by these different nerves.

scholarly journals Stimulation of left stellate ganglion prolongs Q-T interval in patients with palmar hyperhidrosis

1997 ◽  
Vol 273 (4) ◽  
pp. H1696-H1698 ◽  
Author(s):  
Cheuk-Wah Wong
Keyword(s):  
Heart Rate ◽  
Stellate Ganglion ◽  
Sympathetic Ganglia ◽  
Palmar Hyperhidrosis ◽  
The Third ◽  
Video Assisted ◽  
Stellate Ganglia ◽  
Left Stellate Ganglion ◽  
The Right ◽  
Stimulation Of

With the advent of transthoracic video-assisted endoscopic electrocautery of the second and the third sympathetic ganglia for the treatment of palmar hyperhidrosis, it is possible to approach the stellate ganglia with ease. To see whether stimulation of stellate ganglia in humans is similar to the case in dogs, we stimulated the sympathetic ganglia in 18 palmar hyperhidrosis patients with a coagulation power of 5 W at a frequency of three times every 2 s. We found that left stellate stimulation prolongs the Q-T interval and increases the heart rate, whereas right stellate stimulation affects the Q-T interval and heart rate insignificantly, just like the case in dogs in which the left stellate ganglion predominates the right one in determining the Q-T interval. Left stellate stimulation after destruction of the left second and third ganglia also prolongs the Q-T interval, suggesting that the left stellate ganglion is more important in determining the Q-T interval.

Abstract 5690: Idiopathic Catecholamine-sensitive Epicardial Ventricular Tachycardia At The Crux Of The Heart

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Harish Doppalapudi ◽  
Karthik Ramaswamy ◽  
Joon Ahn ◽  
Takumi Yamada ◽  
G Neal Kay
Keyword(s):  
Ventricular Tachycardia ◽  
Catheter Ablation ◽  
Coronary Sinus ◽  
Clinical Syndrome ◽  
Epicardial Surface ◽  
Surface Ecg ◽  
Coronary Venous System ◽  
The Right ◽  
Mean Cycle ◽  
Middle Cardiac Vein

Idiopathic ventricular tachycardia (VT) has been described from the epicardial surface of the left ventricle (LV), usually near the summit of the LV in the outflow tract. Ablation of these VTs may be possible by delivery of energy within the coronary venous system or directly on the epicardial surface. We describe a distinct syndrome of focal epicardial VT induced by catecholamine infusion that arises from the crux of the heart. Among 340 cases of idiopathic VT referred for catheter ablation, 4 patients were identified with a clinical syndrome of catecholamine sensitive VT that was mapped to the epicardial surface at the crux of the heart. There were 3 males and 1 female (age 31–79 yrs, mean 58). VT was sustained in all patients and associated with syncope or near syncope in 3 of 4 pts. The LVEF was >0.55 in 3 pts and mildly depressed (0.45) in 1 pt. In all pts VT could be induced with programmed stimulation or burst pacing from the right ventricular apex but required the infusion of isoproterenol for induction in 3. The VT was very rapid with a mean cycle length of 264 msec. The surface ECG during VT demonstrated a left superior axis QRS morphology in all pts, with an abrupt precordial tansition from V1 to V2 in 3 pts and R waves across the precordium in one. The precordial maximal deflection index was > 0.55 in all pts (mean 0.67). The site of earliest activation during intracardiac mapping occurred at the crux of the heart with activation in the middle cardiac vein or proximal coronary sinus recorded 20 –50 msec (mean −38 msec) prior to the onset of the surface QRS. Catheter ablation with irrigated RF was attempted within the middle cardiac vein or proximal coronary sinus in all pts and was successful in 1. In 2 of 3 remaining pts, percutaneous epicardial RF ablation was attempted and was successful. Simultaneous coronary angiography demonstrated the site of earliest activation within 5–10 mm of the proximal posterior descending coronary artery (PDA). There was no acute narrowing of the PDA in any pt following ablation. Idiopathic VT may arise from the epicardial surface at the crux of the heart in close proximity to the PDA. This syndrome can result in very rapid, catecholamine sensitive VT, and may require careful attention to the PDA during ablation.

Myocardial catecholamines and stimulation of the stellate ganglion in hemorrhagic shock

1965 ◽  
Vol 209 (4) ◽  
pp. 751-756 ◽  
Author(s):  
Vincent V. Glaviano ◽  
Mary Ann Klouda
Keyword(s):  
Blood Pressure ◽  
Hemorrhagic Shock ◽  
Stellate Ganglion ◽  
Myocardial Contraction ◽  
Cardiac Contraction ◽  
Cardiac Responses ◽  
Left Stellate Ganglion ◽  
Anesthetized Dogs ◽  
The Right ◽  
Stimulation Of

Cardiac responses to electrical stimulation of the right or left stellate ganglion were recorded from 16 open-chest anesthetized dogs in hemorrhagic shock. Shock was induced by bleeding the animals to a mean blood pressure of 40 mm Hg. This level of pressure was maintained for 4 hr, during which time blood pressure, heart rate, force of myocardial contraction, and intraventricular pressures were recorded. Stimulation of the stellate ganglion for 15–40 sec every 30 min after hemorrhage showed a gradual decrease in these parameters to levels below control. The reinfusion of blood and the infusion of exogenous l-norepinephrine did not restore an increase in force of cardiac contraction to stellate stimulation. Myocardial epinephrine and norepinephrine levels in shock were found not to differ from those in 14 normal dog hearts. In contrast to almost complete myocardial refractoriness to stellate stimulation in hemorrhagic shock, stimulation of the vagus nerve elicited bradycardia and eventual cardiac arrest. The decrease observed in force of cardiac contraction to stimulation of the stellate ganglion in hemorrhagic shock may be due to depletion of norepinephrine stores in the heart.

Coronary sinus norepinephrine concentrations during ventricular tachycardia induced by left stellate ganglion stimulation in dogs

1988 ◽  
Vol 66 (4) ◽  
pp. 419-421 ◽  
Author(s):  
Réginald Nadeau ◽  
Daniel Lamontagne ◽  
René Cardinal ◽  
Jacques de Champlain ◽  
J. Andrew Armour
Keyword(s):  
Ventricular Tachycardia ◽  
Coronary Sinus ◽  
Nerve Stimulation ◽  
Stellate Ganglion ◽  
Normal Myocardium ◽  
Sympathetic Stimulation ◽  
Sodium Thiopental ◽  
Cardiac Nerve ◽  
Left Stellate Ganglion ◽  
Ventricular Tachycardias

Coronary sinus catecholamine overflow was measured in open-chest dogs, anesthetized with sodium thiopental and α-chloralose, during left sympathetic stimulation. Uniform ventricular tachycardias were induced in 9 out of 16 dogs during either left stellate ganglion or left ventrolateral cardiac nerve stimulations. Significant increases in norepinephrine (8.1 ng/mL, plasma) and epinephrine (0.19 ng/mL, plasma) overflows were obtained after 30 and 90 s of stimulation, respectively. Maximum norepinephrine overflow was significantly higher in dogs with ventricular tachycardia than in those without it (16.0 vs. 7.4 ng/mL, p < 0.05). This suggests that the induction of ventricular tachycardia in the normal myocardium is related to the amount of local secretion of norepinephrine during nerve stimulation.

scholarly journals Outcome of a modified sympathicotomy for cardiac neuromodulation of untreatable ventricular tachycardia

EP Europace ◽  
2021 ◽  
Vol 23 (Supplement_3) ◽  
Author(s):  
FM Cauti ◽  
P Rossi ◽  
J Vannucci ◽  
M Polselli ◽  
C Rossi ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Stellate Ganglion ◽  
Case Series ◽  
Structural Heart Disease ◽  
Early Recurrence ◽  
Modified Technique ◽  
Funding Sources ◽  
Surgical Data ◽  
Procedural Complications ◽  
The Right

Abstract Funding Acknowledgements Type of funding sources: None. OBJECTIVES This study aimed to describe the results of a modified sympathicotomy (uniportal VATs with stellate ganglion sparing) for cardiac sympathetic denervation (CSD) in the setting of untreatable ventricular tachycardia. BACKGROUND. CSD, in patients with refractory ventricular tachycardia (VT), is comprehensively recognized as an important treatment option for patients with structural heart disease as well as congenital inherited arrhythmia syndrome. A recent case series demostrated  the feasibility of the modified technique. METHODS We consecutively enrolled 8 patients with refractory VT. Baseline demographic, medical, and surgical data as well as arrhythmia outcomes and procedural complications were evaluated. RESULTS A total of 8 patients ( 7 pts NIDCM, 1 pt IDCM with mean age:68+-8 years) were enrolled for the treatment of refractory VT with a modified CSD technique. Mean sympathicotomy length were 7.3 (SD 3) min per side. 3/8 patients underwent monolateral (LCSD) sympathicotomy due to strong adesion in the right pleural cavity. Mean follow up was 13 months (SD 6). No complication occurred during the sympathicotomy. An overall reduction in VT burden and VT number was observed after the CSD despite an in-hospital early recurrence in 3 patients. CONCLUSIONS A modified CSD (sympathicotomy T2–T5) with stellate ganglion sparing and the use of unipolar radiofrequency is feasible, effective, and safe in the setting of untreatable VT. Abstract Figure. VT trend

scholarly journals Recording Intrinsic Nerve Activity at the Sinoatrial Node in Normal Dogs with High-density Mapping

2021 ◽  
Author(s):  
Yufan Yang ◽  
Yuan Yuan ◽  
Johnson Wong ◽  
Michael C. Fishbein ◽  
Peng-Sheng Chen ◽  
...  
Keyword(s):  
Heart Rate ◽  
Sinoatrial Node ◽  
Stellate Ganglion ◽  
High Density ◽  
Nerve Activity ◽  
Density Mapping ◽  
Sinus Rate ◽  
Intrinsic Nerve ◽  
The Right ◽  
Stimulation Of

Background - It is known that autonomic nerve activity controls the sinus rate. However, the coupling between local nerve activity and electrical activation at the sinoatrial node (SAN) remains unclear. We hypothesized that we would be able to record nerve activity at the SAN to investigate if right stellate ganglion (RSG) activation can increase the local intrinsic nerve activity, accelerate sinus rate, and change the earliest activation sites (EASs). Methods - High-density mapping of the epicardial surface of the right atrium (RA) including the SAN was performed in 6 dogs during stimulation of the RSG, and after RSG stellectomy. A radiotransmitter was implanted into 3 additional dogs to record RSG and local nerve activity at the SAN. Results - Heart rate accelerated from 108±4 bpm at baseline to 125±7 bpm after RSG stimulation ( P =0.001), and to 132±7 bpm after apamin injection ( P <0.001). Both electrical RSG stimulation and apamin injection induced local nerve activity at the SAN with the average amplitudes of 3.60±0.72 µV and 3.86±0.56 µV, respectively. RSG stellectomy eliminated the local nerve activity and decreased the heart rate. In ambulatory dogs, local nerve activity at the SAN had a significantly higher average Pearson correlation to heart rate (0.72±0.02, P =0.001) than RSG nerve activity to HR (0.45±0.04 P =0.001). Conclusions - Local intrinsic nerve activity can be recorded at the SAN. Short bursts of these local nerve activities are present before each atrial activation during heart rate acceleration induced by stimulation of the right stellate ganglion.

Heart rate response to sympathetic stimulation before and after sodium pentobarbital

1975 ◽  
Vol 228 (5) ◽  
pp. 1568-1574 ◽  
Author(s):  
MJ Cowan ◽  
AM Scher ◽  
J Hildebrandt
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Stellate Ganglion ◽  
Sodium Pentobarbital ◽  
Sympathetic Stimulation ◽  
Initial Decrease ◽  
Before And After ◽  
The Right ◽  
Main Effects ◽  
Stimulation Of

Heart rate response to electrical stimulation of the right stellate ganglion of vagotomized cats was studied before and after the administration of sodium pentobarbital. The increase and decrease of heart rate with the initiation and cessation of sympathetic stimulation could be accurately described by separate exponential time functions. The time constants of rise and decline, the maximum steady-state heart rate, and the time between cessation of stimulation and initial decrease of heart rate (lag) were functions of the frequency and voltage of stimulation. The main effects of sodium pentobarbital were: 1) to prolong the rise of heart rate by 20-30 percent (P smaller than 0.0001),2) to prolong the decay of heart rate by 36-56 percent (P smaller than 0.005), and 3) to decrease the resting heart rate. The effects were observed 10 min after administration of the drug and lasted at least 4 h.

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