Phenylephrine (Neo-synephrine) Terminated Ventricular Tachycardia

Waxman, Menashe B.; Downar, Eugene; Berman, Neil D.; Felderhof, Clarence H.

doi:10.1161/01.cir.50.4.656

Cited by 38 publications

(3 citation statements)

References 24 publications

(2 reference statements)

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“…More relevant to the current topic are the few clinical studies examining the effects of reflexly induced vagal hyperactivity, mostly on ventricular arrhythmias. Waxman and colleagues provided the first evidence that some ventricular tachycardias (VTs) could respond to vagal activation, contrary to traditional belief [27,28], and that ventricular automaticity was decreased by vagal activity [29].…”

Section: Vagal Stimulation and Arrhythmias In Patientsmentioning

confidence: 99%

Vagus nerve stimulation: from pre-clinical to clinical application: challenges and future directions

2010

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Vagus nerve stimulation was performed experimentally for the first time more than 150 years ago. In the 1980s and 1990s, vagus nerve stimulation was shown, both in the anesthetized and in the conscious animal, to exert marked antiarrhythmic effects, particularly during acute myocardial ischemia. There is a strong rationale for a beneficial effect of augmented vagal activity in the setting of chronic heart failure. Studies in experimental models of heart failure showed that chronic vagus nerve stimulation exerts beneficial effects on left ventricular function and on survival. Vagus nerve stimulation is approved in man for refractory epilepsy and depression. The first-in-man study performed in 32 patients with chronic heart failure suggests that vagus nerve stimulation was safe and well tolerated. Six months of open-label treatment was associated with significant improvements (P < 0.001) in NYHA class, quality of life, 6-min walk test, LV ejection fraction (from 22 ± 7 to 29 ± 8%), and LV systolic volumes (P = 0.02). These improvements were maintained at 1 year. Mechanisms of action may include the following: heart rate, anti-adrenergic, anti-apoptotic, and anti-inflammatory effects as well as an increase in nitric oxide. Controlled clinical trials will start soon to assess whether vagus nerve stimulation can indeed represent a new non-pharmacological approach for the treatment of symptomatic heart failure.

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Section: Vagal Stimulation and Arrhythmias In Patientsmentioning

confidence: 99%

Vagus nerve stimulation: from pre-clinical to clinical application: challenges and future directions

2010

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“…In this view, micro-re-entry occurring in the right ventricle would be more plausible, but the effects of atrial pacing during tachycardia do not support this hypothesis. Anyhow, the role of vagal action in terminating the arrhythmia argues against a ventricular origin, though this proof is not definite (Waxman et al, 1974). Moreover, the latter explanation does not take into account the similarity between the preexcitation beats induced by atrial premature stimulation and those seen during tachycardia.…”

Section: Discussionmentioning

confidence: 97%

Re-entry via Mahaim fibres as a possible basis for tachycardia.

Touboul¹,

Vexler²,

Chatelain³

1978

Heart

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SUMMARY Paroxysmal tachycardia with widened QRS complexes was recorded in a 21-year-old man. In sinus rhythm there was no evidence of pre-excitation. His bundle studies revealed an abnormally short HV interval of 30 ms. Premature atrial stimuli produced an increased PR interval. At short coupling intervals the His bundle activity became incorporated within the QRS complex. Concurrently, a left bundle-branch block pattern appeared identical to that seen during tachycardia. Closely coupled ventricular extrastimuli initiated a tachycardia identical to the initial episode. A re-entry mechanism via anterograde Mahaim fibres and retrograde His bundle -AV node pathway is postulated.

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“…In contrast to sympathetic stimulation, VNS decreased the maximum slope of APD restitution, attenuated electrical alternans, and increased ventricular ERP and VF thresholds. 87 Waxman et al provided early clinical evidence, which demonstrated that VTs could respond to vagal activation, contrary to traditional belief, 88,89 and that ventricular automaticity was decreased by vagal activity. 90 Subsequently, experimental animal data in conscious dogs clearly demonstrated that increasing vagal tone by means of right vagus nerve stimulation can prevent ventricular tachyarrhythmias in a model with healed myocardial infarction, evaluated with exercise testing and intermittent ischaemia.…”

Section: Vagal Stimulation and Ventricular Electrophysiologymentioning

confidence: 97%

Device-Based Approaches to Modulate the Autonomic Nervous System and Cardiac Electrophysiology

Hucker

Singh

Parks

et al. 2014

Arrhythm Electrophysiol Rev

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The interplay between the central nervous system and cardiac electrophysiology is fundamental, and becomes obvious each time one's pulse quickens in response to stress. Normally, cardiac neurohormonal regulation is accomplished through the balanced effects of sympathetic and parasympathetic autonomic stimulation, along with the hormonal regulation of the renin-angiotensinaldosterone system (RAAS). Autonomic and hormonal input modulate multiple facets of cellular electrophysiology -action potential duration, ion channel kinetics and intracellular calcium dynamics (just to name a few) -which translate into macroscopic manifestations of autonomic modulation such as heart rate variability, atrioventricular (AV) conduction time and QT interval variability.1 Therefore, it is no surprise that neurohormonal regulation of cardiac electrophysiology is an area of active investigation for its potential antiarrhythmic effects. Recent reviews have focused on the efficacy of neurohormonal modulation, via non-pharmacological methods, to enhance heart failure treatment. 2,3 This review will attempt to provide a state-of-the-art on the potential antiarrhythmic efficacy of renal artery denervation, spinal cord stimulation and direct vagal stimulation. Neurohormonal Control in the Normal and Failing HeartAutonomic control of cardiac physiology is often conceptualised as parasympathetic (cholinergic) and sympathetic (adrenergic) innervation existing in a 'yin and yang' balance under normal circumstances; however, this concept may be over-simplified. 4 In reality, the intrinsic cardiac nervous system, composed of several ganglia located primarily posterior to the atria, likely acts as a 'little brain' of the heart -it provides efferent input to the myocardium, collects afferent signals on a beat-to-beat basis and performs some integrative functions on its own, all under the tonic modulation of extrinsic sympathetic and parasympathetic input (see Figure 1). 4-8The ganglia are predominantly composed of cholinergic neurons; however, sympathetic efferent neurons are also present. Due to the complex interconnectivity between the ganglia, afferent mechanosensory, nociceptive and chemosensory signals from all four chambers of the heart may be processed within a single ganglion. 4 Such interconnectivity implies that predicting the effect of stimulation or ablation of a particular ganglion may be difficult, because each ganglion performs multiple functions. 7,9Abstract Alterations in resting autonomic tone can be pathogenic in many cardiovascular disease states, such as heart failure and hypertension.Indeed, autonomic modulation by way of beta-blockade is a standard treatment of these conditions. There is a significant interest in developing non-pharmacological methods of autonomic modulation as well. For instance, clinical trials of vagal stimulation and spinal cord stimulation in the treatment of heart failure are currently underway, and renal denervation has been studied recently in the treatment of resistant hypertension. Notably, autonom...

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Phenylephrine (Neo-synephrine) Terminated Ventricular Tachycardia

Cited by 38 publications

References 24 publications

Vagus nerve stimulation: from pre-clinical to clinical application: challenges and future directions

Vagus nerve stimulation: from pre-clinical to clinical application: challenges and future directions

Re-entry via Mahaim fibres as a possible basis for tachycardia.

Device-Based Approaches to Modulate the Autonomic Nervous System and Cardiac Electrophysiology

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