An interventional study of Neuromodulation in Acute Decompensated Heart Failure, sponsored by University of Oklahoma. Recruiting at 1 site in United States. Open to participants aged 18 Years to 80 Years. Per ClinicalTrials.gov, last updated 2025-05-28.
Sponsored by University of Oklahoma · Not applicable, Interventional, and Treatment
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. heart rate variability may also be abnormal in ADHF. The objective of this proposal is to determine the impact of LLTS on inflammatory cytokines, heart failure biomarkers(Pro BNP) and HRV in patients with ADHF.In addition we will study the impact on dyspnea resolution and change in renal function during hospitalization.
Patients will be randomized to either active or sham stimulation (2 hours daily). Serum collected will (post-admission and discharge day) will be used for cytokine measurement. We will also measure daily ECG to assess HRV and patient assessed dyspnea scale.This investigation will likely establish the first evidence of the effects of LLTS on the suppression of inflammation and improvement in dyspnea, natriuretic peptides, renal function and HRV in patients presenting with ADHF.
Acute Decompensated Heart Failure (ADHF) is a major cause of morbidity and mortality. It is associated with increased systemic inflammation and poor outcomes.
Previous studies have demonstrated increased inflammation 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 via stimulation of teh Tragus (LLTS) 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. Recent experimental and clinical data suggest that low level tragus nerve stimulation (LLTS) may produce the same desired neuromodulator effect compared to LLVNS.
It is however unknown if LLTS in ADHF will directly lead to sympathetic tone reduction and increase in parasympathetic tone, or neuromodulation and lead to 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.
Autonomic tone could be assessed using heart rate variability. The objective of this proposal is to determine the impact of LLTS on inflammatory cytokines and HRV in patients with ADHF.
Patients will be randomized to either active or sham stimulation (2 hours daily).
Serum collected will (post admission and discharge day) will be used for cytokine and biomarker measurement. We will also measure 10-15 minute ECG to assess HRV. Dyspnea will be determined using patient assessment tool(visual analog scale).This investigation will likely establish the first evidence of effects of LLTS on suppression of inflammation and improvement in dyspnea scale, renal function and HRV in patients presenting with ADHF.
5,701 studies on the registry are indexed under Heart Failure; 1,219 are open to participants now.
This study's planned enrollment of 100 is above the median of 72 across 3,733 interventional studies indexed under Heart Failure.
Browse Heart Failure studies →University of Oklahoma is the lead sponsor of 424 studies on the registry; 99 are open to participants now.
Of its 42 completed or terminated interventional studies of FDA-regulated products, 16 (38%) have results posted.
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Patients admitted with ADHF
Exclusion Criteria:
In this group patients will receive neuromodulation for 2 hours daily
Device: Neuromodulation
Sham neuromodulation will be done
Active LLTS will be performed by use of a transcutaneous electrical nerve stimulation Parasym neuromodulation system with electrodes attached to the ear. Neuromodulation will be applied continuously for 2 hours daily.
Change in Interleukin (IL) levels
Interleukin level
Time frame: From admission to discharge- over average 3-6 days
Change in TNF-alpha levels
TNF level
Time frame: From admission to discharge- over average 3-6 days
Change in CRP levels
CRP level
Time frame: From admission to discharge- over average 3-6 days
Change in Pro BNP and renal function(creatinine) levels
Pro BNP level
Time frame: From admission to discharge- over average 3-6 days
Change in HRV
Heart rate variability measures such time and frequency domains
Time frame: From admission to discharge- over average 3-6 days
Change in level of dyspnea
Dyspnea will be determined using simple tool called visual analog scale
Time frame: From admission to discharge- over average 3-6 days
Plan to share: No
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University of Oklahoma