Ganglionitis and Genetic Cardiac Arrhythmias

Moss, Arthur J.; Ryan, Daniel; Yeaney, Gabrielle

doi:10.1161/circep.114.001589

Cited by 5 publications

(4 citation statements)

References 13 publications

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“…Other etiologies may include circulating neurohormonal signals such as angiotensin II (18,19) or brainstem-mediated increases in efferent sympathetic outflow (20), all of which have been described in CMY and heart failure states. Cardiac inflammation and oxidative stress induced by repeated defibrillation might also contribute to ganglion pathology (21). The possible relationship between ganglion inflammation and cardiac arrhythmias was previously reported (22,23); however, the suggested mechanisms were viral or unknown.…”

Section: L I N I C a L M E D I C I N Ementioning

confidence: 96%

Inflammation, oxidative stress, and glial cell activation characterize stellate ganglia from humans with electrical storm

et al. 2017

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Section: L I N I C a L M E D I C I N Ementioning

confidence: 96%

Inflammation, oxidative stress, and glial cell activation characterize stellate ganglia from humans with electrical storm

et al. 2017

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“…They proposed that T-cell–mediated cytotoxicity toward ganglion cells may prompt an increase in sympathetic efferent activity toward the heart, therefore acting as a trigger and/or an enhancer of electrical instability in patients already predisposed to arrhythmias, as it occurs in LQTS and CPVT patients. Of note, as pointed out by Moss et al (64) in the editorial comments of the paper, all patients had either recurrent syncopal episodes or many ICD shocks before the ganglionectomy, although the time frame between the last events and LCSD was not provided by the authors. Syncopal events are associated with transient generalized hypoperfusion, while ICD shocks can damage the myocardium and the neuronal fibers (65).…”

Section: Antiarrhythmic Rationale and Mechanisms Of Action Of Cardiacmentioning

confidence: 97%

Cardiac Sympathetic Denervation in Channelopathies

Dusi

Ferrari

Pugliese

et al. 2019

Front. Cardiovasc. Med.

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Left cardiac sympathetic denervation (LCSD) is a surgical antiadrenergic intervention with a strong antiarrhythmic effect, supported by preclinical as well as clinical data. The mechanism of action of LCSD in structurally normal hearts with increased arrhythmic susceptibility (such as those of patients with channelopathies) is not limited to the antagonism of acute catecholamines release in the heart. LCSD also conveys a strong anti-fibrillatory action that was first demonstrated over 40 years ago and provides the rationale for its use in almost any cardiac condition at increased risk of ventricular fibrillation. The molecular mechanisms involved in the final antiarrhythmic effect of LCSD turned out to be much broader than anticipated. Beside the vagotonic effect at different levels of the neuraxis, other new mechanisms have been recently proposed, such as the antagonism of neuronal remodeling, the antagonism of neuropeptide Y effects, and the correction of neuronal nitric oxide synthase (nNOS) imbalance. The beneficial effects of LCSD have never been associated with a detectable deterioration of cardiac performance. Finally, patients express a high degree of satisfaction with the procedure. In this review, we focus on the rationale, results and our personal approach to LCSD in patients with channelopathies such as long QT syndrome and catecholaminergic polymorphic ventricular tachycardia.

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“…Moreover, although the origin of inflammatory infiltrates remains unknown, Rizzo et al ( 162 ) put forward the hypothesis of a viral (however not herpes-virus DNA was found in specimens) or autoimmune pathogenesis. As concerns this latter mechanism, Moss et al ( 166 ) underlined how all patients had recurrent syncope and/or many defibrillator shocks, and both transient hypoperfusion and recurrent shocks could cause ganglionic cell injury with protein damage putatively resulting in a secondary autoimmune reaction with manifestations of ganglionitis. In any case, independently whether ganglionitis is a primary event or a phenomenon secondarily occurring after first severe arrhythmic episodes (thus triggering a self-aggravating loop), it is conceivable that it may have played a role in precipitating life-threatening tachyarrhythmias since stellectomy induced rhythm stabilization in almost all patients.…”

Section: Do Inflammation and Immunity Play A Role In Congenital Lqts?mentioning

confidence: 99%

Long QT Syndrome: An Emerging Role for Inflammation and Immunity

Lazzerini

Capecchi

Laghi‐Pasini

2015

Front. Cardiovasc. Med.

137

131

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The long QT syndrome (LQTS), classified as congenital or acquired, is a multi-factorial disorder of myocardial repolarization predisposing to life-threatening ventricular arrhythmias, particularly torsades de pointes. In the latest years, inflammation and immunity have been increasingly recognized as novel factors crucially involved in modulating ventricular repolarization. In the present paper, we critically review the available information on this topic, also analyzing putative mechanisms and potential interplays with the other etiologic factors, either acquired or inherited. Accumulating data indicate inflammatory activation as a potential cause of acquired LQTS. The putative underlying mechanisms are complex but essentially cytokine-mediated, including both direct actions on cardiomyocyte ion channels expression and function, and indirect effects resulting from an increased central nervous system sympathetic drive on the heart. Autoimmunity represents another recently arising cause of acquired LQTS. Indeed, increasing evidence demonstrates that autoantibodies may affect myocardial electric properties by directly cross-reacting with the cardiomyocyte and interfering with specific ion currents as a result of molecular mimicry mechanisms. Intriguingly, recent data suggest that inflammation and immunity may be also involved in modulating the clinical expression of congenital forms of LQTS, possibly triggering or enhancing electrical instability in patients who already are genetically predisposed to arrhythmias. In this view, targeting immuno-inflammatory pathways may in the future represent an attractive therapeutic approach in a number of LQTS patients, thus opening new exciting avenues in antiarrhythmic therapy.

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Ganglionitis and Genetic Cardiac Arrhythmias

Cited by 5 publications

References 13 publications

Inflammation, oxidative stress, and glial cell activation characterize stellate ganglia from humans with electrical storm

Inflammation, oxidative stress, and glial cell activation characterize stellate ganglia from humans with electrical storm

Cardiac Sympathetic Denervation in Channelopathies

Long QT Syndrome: An Emerging Role for Inflammation and Immunity

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