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Adenosine and neurohumoral syncope.

Jean C Deharo1,2, Michele Brignole3,4, Regis Guieu5,6

  • 1Department of Cardiology, Institut National de la Santé et de la Recherche Médicale - INSERM, Hôpital La Timone Adultes, Aix-Marseille University, Marseille, France - jean-claude.deharo@ap-hm.fr.

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A newly identified low-adenosine form of neurohumoral syncope involves low adenosine levels and specific gene variants. Theophylline treatment is proposed to prevent recurrent syncope in affected patients.

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Area of Science:

  • Cardiology
  • Neuroscience
  • Biochemistry

Background:

  • Neurally mediated syncope often involves baroreceptor reflex or neurohumoral alterations.
  • Understanding biochemical mechanisms can lead to targeted therapies for neurohumoral syncope.
  • A specific low-adenosine phenotype of neurohumoral syncope has been recently identified.

Purpose of the Study:

  • To investigate the biochemical profile of a specific syncope phenotype.
  • To explore the potential of adenosine receptor antagonism for treating this syncope form.

Main Methods:

  • Characterization of patients with syncope, no prodromes, and normal heart function.
  • Analysis of plasma adenosine levels, A2A receptor expression, and A2A receptor gene polymorphism (c.1364 C>T).
  • Evaluation of theophylline as a non-selective adenosine receptor antagonist.

Main Results:

  • Patients exhibited a purinergic profile opposite to vasovagal syncope, with very low plasma adenosine.
  • Low A2A receptor expression and a predominance of the TC variant in the A2A receptor gene were observed.
  • The typical syncope mechanism involved atrioventricular block or bradycardia, often with sinus arrest.

Conclusions:

  • The identified low-adenosine phenotype suggests susceptibility to endogenous adenosine.
  • Chronic theophylline treatment is hypothesized to prevent syncopal recurrences in these patients.
  • Case series and controlled studies support the efficacy of theophylline for this condition.