Endocardial Autonomic Denervation of the Left Atrium to Treat Vasovagal Syncope

Yao, Yan; Shi, Rui; Wong, Tom; Zheng, Lihui; Chen, Wensheng; Yang, Lifen; Huang, Wen; Bao, Jingru; Zhang, Shu

doi:10.1161/circep.111.966465

Cited by 134 publications

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“…Endocardial GP ablation has been increasingly used to treat severe vagal-related arrhythmias. [8][9][10][11][12][13][14] Although the guidelines 20 indicate pacemaker implantation for cases of symptomatic bradycardia and atrioventricular block, the fact that these patients are mostly young and otherwise healthy individuals encourages a more conservative approach.…”

Section: Discussionmentioning

confidence: 99%

“…The diverse GP-mapping strategies used by different authors (1, high-frequency endocardial stimulation [2][3][4][5][6][8][9][10][11][12] ; 2, purely anatomic location 7,13 ; and 3, atrial electrogram characteristics 1,10,14,15 ) emerged as potential alternatives, with each one proposing specific end points (1, evoked reflex abolition; 2, ablation of all anatomic GP sites achieved; and 3, elimination of all fragmented potentials, respectively). However, some important questions still remain whichever technique is chosen:…”

Section: See Editorial By Mulpuru and Shenmentioning

confidence: 99%

“…Ganglionated plexus (GP) ablation for the treatment of vagal-related atrial fibrillation [1][2][3][4][5][6][7] and symptomatic bradycardia, [8][9][10][11][12][13][14] such as cardioinhibitory vasovagal syncope, has been widely studied, and although convincing results had been reported by some authors, no consensus still exists on the most adequate technique to identify the critical targets or end points indicating clinical vagal attenuation.…”

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confidence: 99%

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Targets and End Points in Cardiac Autonomic Denervation Procedures

Rivarola

Hachul

et al. 2017

Circ: Arrhythmia and Electrophysiology

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Background-Autonomic denervation is an alternative approach for patients with symptomatic bradycardia. No consensus exists on the critical targets and end points of the procedure. The aim of this study was to identify immediate end points and critical atrial regions responsible for vagal denervation. Methods and Results-We enrolled 14 patients (50% men; age: 34.0±13.8 years) with cardioinhibitory syncope, advanced atrioventricular block or sinus arrest, and no structural heart disease. Anatomic mapping of ganglionated plexuses was performed, followed by radiofrequency ablation. Heart rate, sinus node recovery time, Wenckebach cycle length, and atrial-His (AH) interval were measured before and after every radiofrequency pulse. Wilcoxon signed-rank test was used for comparison. Significant shortening of the R-R interval (P=0.0009), Wenckebach cycle length (P=0.0009), and AH intervals (P=0.0014) was observed after ablation. The heart rate elevation was 23.8±12.5%, and the Wenckebach cycle length and AH interval shortening was 18.1±11% and 24.6±19%, respectively. Atropine bolus injection (0.04 mg/kg) did not increase heart rate further. Targeting a single spot of the left side (64% of the patients) or right side (36%) of the interatrial septum was observed to be responsible for ≥80% of the final R-R and AH interval shortening during ablation. Conclusions-Targeting specific sites of the interatrial septum is followed by an increase in heart rate and atrioventricular nodal conduction properties and might be critical for vagal attenuation. The R-R interval, Wenckebach cycle length, and AH interval shortening, associated with a negative response to atropine, could be considered immediate end points of the procedure.

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Section: Discussionmentioning

confidence: 99%

Section: See Editorial By Mulpuru and Shenmentioning

confidence: 99%

mentioning

confidence: 99%

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Targets and End Points in Cardiac Autonomic Denervation Procedures

Rivarola

Hachul

et al. 2017

Circ: Arrhythmia and Electrophysiology

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“…The results of Yao et al 4 illustrate another example of the emerging paradigm of autonomic modulation for the treatment of cardiac arrhythmias and other cardiovascular diseases. The conventional wisdom to treat a disease caused by tissue hyperactivity is to injure (eg, ablate) that tissue.…”

Section: Article See P 279mentioning

confidence: 93%

Autonomic Modulation

Stavrakis

Scherlag

2012

Circ: Arrhythmia and Electrophysiology

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A variety of experimental and clinical reports have engendered a different approach to cardiac arrhythmias as well as other cardiovascular conditions. The focus of a new paradigm is the autonomic nervous system and its important role in various pathological states. From an overall standpoint, this new paradigm can be encompassed by the term "autonomic modulation," which would include autonomic nerve stimulation or autonomic denervation to modulate the autonomic activity in physiological or pathophysiological functions of the heart as well as other visceral organ systems. Article see p 279Vaso-vagal syncope is the most common form of neurally mediated syncope. 1 The pathophysiology of vaso-vagal syncope is still controversial, but it is thought to be related to prolonged orthostatic stress, which causes increased peripheral venous pooling with a subsequent fall in venous return to the heart. This in turn causes a hypercontractile state, which leads to activation of ventricular mechanoreceptors and a sudden increase in the afferent neural traffic to the brain. The result is sympathetic withdrawal and parasympathetic enhancement that manifests as hypotension (vasodepressor type), bradycardia (cardioinhibitory type), and syncope. 1 In other words, vaso-vagal syncope is a disorder caused by an abnormally amplified autonomic reflex involving both sympathetic and parasympathetic components. Over the past 2 decades, ␤-blockers, ␣-agonists, mineralocorticoids, selective serotonin reuptake inhibitors, and dual-chamber pacemaker implantation all produced initial promising but later disappointing results. 1-3 Vaso-vagal syncope continues to be a vexing clinical arrhythmia.In this issue of Circulation Arrhythmia and Electrophysiology, Yao et al 4 reported 10 patients who had drug-refractory, frequent, and highly symptomatic vaso-vagal syncope. Based on the hypothesis that vaso-vagal syncope is related to enhanced parasympathetic activity, the authors performed autonomic denervation by targeting the 4 major atrial ganglionated plexi (GP), guided by high-frequency stimulation as described by the Oklahoma group (Po et al 5 ). The left superior GP, right anterior GP and left inferior GP were identified and ablated in 10 (100%), 5 (50%), and 3 (30%) patients, respectively. Surprisingly, the right inferior GP, often referred to as the atrioventricular nodal GP, did not respond to high-frequency stimulation in any patient and was therefore not ablated. The authors did not show the presumed right inferior GP area where high-frequency stimulation was delivered. However, location of the right anterior GP as shown in Figure 1 in the article is not the typical location of the right anterior GP (at the left atrial septum, near the carina of the right pulmonary veins). 5 It is possible that high-frequency stimulation might not have been delivered to the correct location of the right inferior GP. Another technical problem is that ablation was performed using an 8-mm, nonirrigated catheter, which carries a significant risk for thromboemboli...

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“…There have been reports of success in control or elimination of vasovagal attacks by catheter ablation using radiofrequency energy endocardially to ablate ganglionic plexi in close anatomical relation to the left and right atria on the surface of the heart [24,25]. This is a difficult technique even for an experienced operator and must be considered to offer risk to the patient despite the reports not indicating complications.…”

Section: Catheter Ablationmentioning

confidence: 99%

Treatment of Reflex Syncope

Sutton

2013

J Med Diagn Meth

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This review assesses the role of all types of therapy for reflex syncope including physical counter-measures, diet, behavior, drugs and implantable devices. There are no drugs currently demonstrated to have convincingly beneficial effect by randomized controlled trial. However, provided that the patient experiences warning of an impending attack physical counter-measures are demonstrably effective. Implantable cardiac pacemakers have a role in a carefully selected minority of patients with vasovagal syncope. Pacing, dual chamber of cardio-inhibitory Carotid Sinus Syndrome is the treatment of choice. Modification of lifestyle in terms of fluid, caffeine and salt consumption is necessary in many cases but has little scientific background. Educating and reassuring the patient is an important part of management. The patient must understand that attacks are not as dangerous as they might seem in most cases and learning to anticipate those permits evasive measures.

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Endocardial Autonomic Denervation of the Left Atrium to Treat Vasovagal Syncope

Cited by 134 publications

References 28 publications

Targets and End Points in Cardiac Autonomic Denervation Procedures

Targets and End Points in Cardiac Autonomic Denervation Procedures

Autonomic Modulation

Treatment of Reflex Syncope

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