scholarly journals Mechanism of ventricular premature beats elicited by left stellate ganglion stimulation during acute ischaemia of the anterior left ventricle

2020 ◽  
Author(s):  
Bastiaan J D Boukens ◽  
Michael Dacey ◽  
Veronique M F Meijborg ◽  
Michiel J Janse ◽  
Joseph Hadaya ◽  
...  

Abstract Aims Enhanced sympathetic activity during acute ischaemia is arrhythmogenic, but the underlying mechanism is unknown. During ischaemia, a diastolic current flows from the ischaemic to the non-ischaemic myocardium. This ‘injury’ current can cause ventricular premature beats (VPBs) originating in the non-ischaemic myocardium, especially during a deeply negative T wave in the ischaemic zone. We reasoned that shortening of repolarization in myocardium adjacent to ischaemic myocardium increases the ‘injury’ current and causes earlier deeply negative T waves in the ischaemic zone, and re-excitation of the normal myocardium. We tested this hypothesis by activation and repolarization mapping during stimulation of the left stellate ganglion (LSG) during left anterior descending coronary artery (LAD) occlusion. Methods and results In nine pigs, five subsequent episodes of acute ischaemia, separated by 20 min of reperfusion, were produced by occlusion of the LAD and 121 epicardial local unipolar electrograms were recorded. During the third occlusion, left stellate ganglion stimulation (LSGS) was initiated after 3 min for a 30-s period, causing a shortening of repolarization in the normal myocardium by about 100 ms. This resulted in more negative T waves in the ischaemic zone and more VPBs than during the second, control, occlusion. Following the decentralization of the LSG (including removal of the right stellate ganglion and bilateral cervical vagotomy), fewer VPBs occurred during ischaemia without LSGS. During LSGS, the number of VPBs was similar to that recorded before decentralization. Conclusion LSGS, by virtue of shortening of repolarization in the non-ischaemic myocardium by about 100 ms, causes deeply negative T waves in the ischaemic tissue and VPBs originating from the normal tissue adjacent to the ischaemic border.


Author(s):  
Nam Van Tran ◽  
Samuel Rotman ◽  
Patrice Carroz ◽  
Etienne Pruvot

Abstract Background We report an unusual case of non-sustained ventricular tachycardia (NSVT) from the epicardial part of the right ventricular outflow tract (RVOT). Case summary A 37-year-old woman who underwent in 2006 an ablation for idiopathic ventricular premature beats (VPBs) from the RVOT presented with pre-syncopal NSVT in 2016. A cardiac workup showed no coronary disease, normal biventricular function, and no enhancement on cardiac magnetic resonance imaging. A metabolic positron emission tomography scan excluded inflammation. Biopsies revealed normal desmosomal proteins. An endocardial mapping revealed an area of low voltage potential (<0.5 mV) at the antero-septal aspect of the RVOT corresponding to the initial site of ablation from 2006. Activation mapping revealed poor prematurity and pace-mapping showed unsatisfactory morphologies in the RVOT, the left ventricle outflow tract and the right coronary cusp. An epicardial map revealed a low voltage area at the antero-septal aspect of the RVOT with fragmented potentials opposite to the endocardial scar. Pace-mapping demonstrated perfect match. An NSVT was induced and local electrocardiogram showed mid-diastolic potentials. Ablation was applied epicardially and endocardially without any complication. The patient was arrhythmia free at 4-year follow-up. Discussion Cardiac workup allowed to exclude specific conditions such as arrhythmogenic cardiomyopathy, tetralogy of Fallot, sarcoidosis, or myocarditis as a cause for NSVT from the RVOT. The epi and endocardial map showed residual scar subsequent to the first ablation which served as substrate for the re-entrant NSVT. This is the first case which describes NSVT from the epicardial RVOT as a complication from a previous endocardial ablation for idiopathic VPB.



1965 ◽  
Vol 209 (4) ◽  
pp. 751-756 ◽  
Author(s):  
Vincent V. Glaviano ◽  
Mary Ann Klouda

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.



1988 ◽  
Vol 66 (4) ◽  
pp. 419-421 ◽  
Author(s):  
Réginald Nadeau ◽  
Daniel Lamontagne ◽  
René Cardinal ◽  
Jacques de Champlain ◽  
J. Andrew Armour

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.



1997 ◽  
Vol 273 (4) ◽  
pp. H1696-H1698 ◽  
Author(s):  
Cheuk-Wah Wong

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.







1964 ◽  
Vol 207 (2) ◽  
pp. 325-333 ◽  
Author(s):  
Robert L. Hamlin ◽  
David L. Smetzer ◽  
C. Roger Smith

A semiorthogonal lead system for recording electrocardiograms from horses was designed. The X, Y, and Z axes of the body were monitored by leads I, aVF, and V10 (the unipolar lead taken from the dorsal spinous process of the seventh thoracic vertebra), respectively. Records were taken from 15 standing horses. Ventricular premature beats were elicited by pricking foci on the right and left ventricular epicardium. For normally conducted beats, two major vectors represented forces generating the QRS complex. Vector 1, probably representing excitation of the apical third of the interventricular septum from left to right, was relatively low in magnitude, and was oriented dextrad, ventrad, and craniad. Vector 2, probably representing depolarization of the basilar third of the interventricular septum from left to right and in an apicobasilar direction, was of greater magnitude and was oriented ventrad, sinistrad, and craniad. Occasionally a vector intermediate between vectors 1 and 2 was oriented caudad and dorsad. The origin of this vector is equivocal. Left ventricular premature beats generated vectors of great magnitude oriented dextrad and craniad. Right ventricular premature beats generated vectors of magnitude between those of sinus or left ventricular origin, and directed predominantly sinistrad.





1997 ◽  
Vol 36 (04/05) ◽  
pp. 257-260 ◽  
Author(s):  
H. Saitoh ◽  
T. Yokoshima ◽  
H. Kishida ◽  
H. Hayakawa ◽  
R. J. Cohen ◽  
...  

Abstract:The frequency of ventricular premature beats (VPBs) has been related to the risk of mortality. However, little is known about the temporal pattern of occurrence of VPBs and its relationship to autonomic activity. Hence, we applied a general correlation measure, mutual information, to quantify how VPBs are generated over time. We also used mutual information to determine the correlation between VPB production and heart rate in order to evaluate effects of autonomic activity on VPB production. We examined twenty subjects with more than 3000 VPBs/day and simulated ran-( dom time series of VPB occurrence. We found that mutual information values could be used to characterize quantitatively the temporal patterns of VPB generation. Our data suggest that VPB production is not random and VPBs generated with a higher value of mutual information may be more greatly affected by autonomic activity.



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