Plasma adenosine and neurally mediated syncope: ready for clinical use

Area of Science:

• Cardiology
• Neuroscience
• Biochemistry

Background:

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

Purpose of the Study:

• To investigate the biochemical profile of a specific syncope phenotype.
• To explore the potential therapeutic role of adenosine receptor antagonism.

Main Methods:

• Characterization of patients with syncope, normal heart function, and absence of prodromes.
• Analysis of plasma adenosine levels, A2A receptor expression, and A2A receptor gene polymorphism (c.1364 C>T).
• Review of case series and observational controlled studies on theophylline treatment.

Main Results:

• Patients with this syncope phenotype exhibit low plasma adenosine and low A2A receptor expression.
• A predominance of the TC variant in the A2A receptor gene polymorphism was observed.
• Theophylline treatment showed promise in preventing syncopal recurrences in case studies.

Conclusions:

• The low-adenosine phenotype is characterized by purinergic alterations opposite to vasovagal syncope.
• Patients with low adenosine levels are susceptible to endogenous adenosine, suggesting a therapeutic target.
• Theophylline, as a non-selective adenosine receptor antagonist, is a potential treatment to prevent syncope recurrence.