Syncope without prodromes is associated with excessive plasma release of adenosine at the time of syncope during head-up tilt table test

Fragakis, Nikolaos; Antoniadis, Antonios; Sotiriadou, Melani; Virgiliou, Christina; Ballauri, Iris; Gika, Helen; Bougiouklis, Dimitrios; Gerou, Spyridon; Lazaridis, Charalampos; Vergopoulos, S; Bakogiannis, Constantinos; Γιαννόπουλος, Γεώργιος; Theodoridis, Georgios; Papadopoulos, Christodoulos; Karamitsos, Theodoros D; Vassilikos, Vassilios

doi:10.1016/j.ijcard.2022.06.045

Cited by 2 publications

(1 citation statement)

References 22 publications

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“…Thus, there is evidence that an adenosinergic disturbance is implicated in NES. In vasovagal syncope: high basal APL was reported with a significant increase during the HUT associated with fainting [ 11 ], while an increase in APL was also reported during HUT [ 11 , 21 , 22 ]. This increase may explain the lack of prodromes in this patient population.…”

Section: Role Of the Adenosinergic System In Nesmentioning

confidence: 99%

Adenosinergic System and Neuroendocrine Syncope: What Is the Link?

Guieu

Fromonot

Mottola

et al. 2023

Cells

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Although very common, the precise mechanisms that explain the symptomatology of neuroendocrine syncope (NES) remain poorly understood. This disease, which can be very incapacitating, manifests itself as a drop in blood pressure secondary to vasodilation and/or extreme slowing of heart rate. As studies continue, the involvement of the adenosinergic system is becoming increasingly evident. Adenosine, which is an ATP derivative, may be involved in a large number of cases. Adenosine acts on G protein-coupled receptors with seven transmembrane domains. A1 and A2A adenosine receptor dysfunction seem to be particularly implicated since the activation leads to severe bradycardia or vasodilation, respectively, two cardinal symptoms of NES. This mini-review aims to shed light on the links between dysfunction of the adenosinergic system and NHS. In particular, signal transduction pathways through the modulation of cAMP production and ion channels in relation to effects on the cardiovascular system are addressed. A better understanding of these mechanisms could guide the pharmacological development of new therapeutic approaches.

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