Low Level Tragus Stimulation in Acute Decompensated Heart Failure

Acute Decompensated Heart Failure (ADHF) is a major cause of morbidity and mortality. It is
associated with increased systemic inflammation. Previous studies have demonstrated increased
levels of cytokines such as C-reactive protein (CRP), interleukin-1 (IL-1), interleukin-6
(IL-6), interleukin-10 (IL-10) and Tumor Necrosis Factor alpha (TNFα) in patients with heart
failure (HF). Increased activity of sympathetic nervous system in ADHF is linked to
inflammation. Previous anti-inflammatory drug therapies in HF have demonstrated no
significant impact on cardiovascular outcomes. Low-level vagus nerve stimulation (LLVNS) is a
non-invasive way to modulate autonomic tone and thereby inflammation. Vagal nerve stimulation
is thought to increase the parasympathetic activity and suppress the sympathetic activity.
Clinical studies of vagal stimulation in chronic HF have been negative. Recent experimental
and clinical data suggest that low level tragus nerve stimulation (LLTNS) may produce the
same desired neuromodulator effect compared to LLVNS. It is however unknown if LLTNS in ADHF
will directly lead to a reduction in the levels of pro-inflammatory cytokines (CRP, IL-1,
IL-6 and TNF-α) and an increase in the level of anti-inflammatory marker IL-10.The objective
of this proposal is to determine the impact of LLTS on inflammatory cytokines in patients
with ADHF.

Patients will be randomized to either active or no stimulation(~8 hours daily). Serum
collected will (post admission and on days 2, 3 and 4 post admission) will be used for
cytokine measurement. This investigation will likely establish the first evidence of effects
of LLTS on suppression of inflammation in patients presenting with ADHF.