Low-Level Tragus Stimulation forAtrial Fibrillation: A Glimpse of Hope for Neuromodulation?*

摘要

The pathogenesis of atrial fibrillation (AF) is commonly known to involve triggers and JL substrates, but it also requires a complex interplay with the modulator-the autonomic nervous system (ANS), which via various activity patterns can promote the initiation and maintenance of AF (2). With enhanced automaticity and afterdepolarization, sympathetic input leads to increased focal activity (2), whereas parasympathetic input facilitates re-entry by shortening atrial effective refractory period and increasing dispersion of refractoriness (2). Shifts in the sympathovagal balance can set off the trigger, modify the substrate, and alter the milieu to perpetuate AF. Recent work has shown interesting results that low-level vagal nerve stimulation (LLVNS) (i.e., vagal nerve stimulation delivered at a lower voltage than that is needed to reduce the sinus rate) may have both anticholinergic and antiadrenergic effects (3). Preclinical work has shown that LLVNS can blunt the sinus rate responsiveness to autonomic stimulation and increase the threshold for AF induction (3). Additionally, through the cholinergic antiinflammatory pathway, LLVNS can reduce systemic inflammation known to promote AF (4). Although direct vagal stimulation has been used in early studies, it is invasive, technically challenging, and not entirely reproducible in its effects (5,6). This has in turn increased the interest in percutaneous stimulation via the auricular vagal branch.