Syncope and Idiopathic (Paroxysmal) AV Block

Brignole, Michele; Deharo, Jean‐Claude; Guieu, Régis

doi:10.1016/j.ccl.2015.04.012

Cited by 18 publications

(25 citation statements)

References 27 publications

(18 reference statements)

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“…This result may open the field to new diagnostic approaches, and treatments to avoid syncope recurrence in 2A HUT patients. Therefore, according to other authors, [ 18 – 22 ] we may propose ES as new diagnostic approach to reduce cardioreflex syncope recurrence. This treatment may change the historical course of the cardioreflex syncope, reducing syncope recurrence.…”

Section: Discussionmentioning

confidence: 94%

“…In our study, we supposed that, an autonomic dysfunction triggered a syncope event, [ 1 ] and an arrhythmic condition probably related to a cardiac reflex syncope. [ 21 , 22 ] These arrhythmic abnormalities may be more or less pronounced in the same clinical setting as the cardioreflex syncope event, and detectable by an ES. However, in this study, we focused on 2A HUT patients, and on the ES using to drive to successful interventional therapies, and to reduce syncope recurrence at follow-up in this population.…”

Section: Discussionmentioning

confidence: 99%

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ELectrophysiological mechanisms underlying the Inhibitory CArdiac syncope without asystolic significant pause

et al. 2018

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Background:The aim of this study was to investigate syncope recurrence in patients with a 2A cardioinhibitory response to the head up tilt testing (HUT).Methods:In this study, we enrolled 72 consecutive patients affected by syncope with cardioinhibitory response without asystolic significant pause to HUT (2A type). In these patients, we randomly performed electrophysiological study (ES). In case of sino-atrial node, atrio-ventricular node dysfunction, and sustained arrhythmias induction, the ES resulted positive. ES was positive in 9 patients (group A), then treated by catheter ablation, and/or by devices implants. Otherwise, ES resulted negative (group B), and these patients did not receive an interventional treatment. However, after ES, we evaluated syncope recurrence during 360 days follow-up.Results:There was a lower statistical significant syncope recurrence at follow-up, comparing group A to group B of patients [n of events 9 (40.9%) vs 8 (57.1%), P < .05]. At multivariate analysis, ES result was the only factor predicting syncope recurrence at follow-up (hazard ratio = 27.63, 95% confidence interval = 1.02–54.24, P < .005).Conclusion:The positivity to ES study, and successful interventional therapies may reduce the burden of syncope recurrence at 360 days follow-up in 2A HUT subjects.Clinical trial number: NCT02861274.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

ELectrophysiological mechanisms underlying the Inhibitory CArdiac syncope without asystolic significant pause

et al. 2018

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“…Interruption of tachycardia [89] AVB [92] AVB in low adenosine syncope patients [73,103] Asystole, myoclonic jerk [93] Fetal bradycardia [95] Atrial fibrillation [60] Atrial premature complex [62] Atrial ectopic beats [63] Flutter [62] Ventricular Level…”

Section: Supra Ventricular Levelmentioning

confidence: 99%

“…NHS is characterized by a partial (presyncope) or complete loss of consciousness due to a decrease in heart rate and systemic blood pressure in the absence of any heart structural abnormalities. Loss of consciousness is often preceded by prodromes, including discomfort, nausea, vomiting, abdominal pain, but sometimes the loss of consciousness occurs at outset, without or with very short prodromes [73,74,103]. Symptoms may be reproduced by the head up tilt test (HUT) [106] or sometimes by ATP or adenosine administration [107].…”

Section: Adenosine and Reflex (Neurohumoral) Syncopementioning

confidence: 99%

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Adenosine and the Cardiovascular System: The Good and the Bad

Guieu

Deharo

Maille

et al. 2020

JCM

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Adenosine is a nucleoside that impacts the cardiovascular system via the activation of its membrane receptors, named A1R, A2AR, A2BR and A3R. Adenosine is released during hypoxia, ischemia, beta-adrenergic stimulation or inflammation and impacts heart rhythm and produces strong vasodilation in the systemic, coronary or pulmonary vascular system. This review summarizes the main role of adenosine on the cardiovascular system in several diseases and conditions. Adenosine release participates directly in the pathophysiology of atrial fibrillation and neurohumoral syncope. Adenosine has a key role in the adaptive response in pulmonary hypertension and heart failure, with the most relevant effects being slowing of heart rhythm, coronary vasodilation and decreasing blood pressure. In other conditions, such as altitude or apnea-induced hypoxia, obstructive sleep apnea, or systemic hypertension, the adenosinergic system activation appears in a context of an adaptive response. Due to its short half-life, adenosine allows very rapid adaptation of the cardiovascular system. Finally, the effects of adenosine on the cardiovascular system are sometimes beneficial and other times harmful. Future research should aim to develop modulating agents of adenosine receptors to slow down or conversely amplify the adenosinergic response according to the occurrence of different pathologic conditions.

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