Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
Peripheral arterial disease (PAD) constitutes a major public health burden. The incidence of PAD increases with age and is associated with other comorbid cardiovascular disorders. Atherosclerosis which underlies PAD is associated with increased arterial stiffness and an enhanced inflammatory state as evidenced by increased levels of pro-inflammatory cytokines and markers. One the earliest signs of cardiovascular disease is endothelial dysfunction which is characterized by a decreased vasodilatory capacity of the vascular endothelium and this lesion predates the development of clinical atherosclerosis. Endothelial dysfunction has been shown to be widely prevalent in PAD. It is postulated that endothelial dysfunction is due to enhanced sympathetic drive, diminished parasympathetic drive, chronic inflammatory state all of which leads to reduced nitric oxide synthase activity in the vascular endothelium with subsequent loss of vasodilatory capacity. Studies have shown endothelial dysfunction to be reversible with pharmaco-therapeutic interventions, though these interventions are associated with their own adverse effects. Stimulation of Vagal nerve increases the parasympathetic activity while suppressing sympathetic drive, decreases inflammation and enhancing nitric oxide synthase activity. Recent experimental and clinical data suggest that low-level tragus nerve stimulation (by stimulating the auricular branch of the vagus nerve located at the tragus of the external ear) may produce the same desired neuromodulator effect compared to vagus nerve stimulation. It is however unknown if Transcutaneous Vagal Stimulation (TVS) would lead to improved endothelial function as measured by flow mediated dilatation (FMD) and laser speckle contrast imaging(LSCI), a non-invasive method of measuring endothelial function or decrease in arterial stiffness as measured by Pulse Wave Analysis (PWA), in patients with PAD. The objective of this study is to determine the impact of TVS on endothelial dysfunction as measured by FMD & LSCI and arterial stiffness. Study population will include patients with established diagnosis of PAD. After performing baseline FMD, LSCI and PWA patients will be randomized to TVS and sham stimulation with cross over. The patient randomized to TVS stimulation will obtain stimulation for 1 hour followed by measurement of FMD,LSCI and PWA. There will be a washout period of at least 24 hours with patient crossing over to the other arms thus serving as their self-control.
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
| Label | Type | Description | Intervention Names |
|---|---|---|---|
| Interventional Arm | Experimental | Active TVS will be performed by use of a Tragus stimulator device with electrodes attached to the tragus of the ear. Stimulator will be applied continuously for 1 hour. |
|
| Control | Sham Comparator | Sham TVS will be performed by use of a Tragus stimulator device with electrodes attached to the ear lobule. Stimulator will be applied continuously for 1 hour. |
|
| Name | Type | Description | Arm Group Labels | Other Names |
|---|---|---|---|---|
| TVS | Device | Active TVS will be performed by use of a Tragus stimulator device with electrodes attached to the tragus of the ear. Stimulator will be applied continuously for 1 hour |
| Measure | Description | Time Frame |
|---|---|---|
| Flow mediated vasodilatation | Flow mediated vasodilatation will be tested. A change in the maximal diameter of the brachial artery(in mm) will be assessed immediately(within 10 minutes) after TVNS/sham stimulation. | Change from baseline to post stimulation(within 10 minutes of stimulation) with TVS/Sham stimulation |
| Measure | Description | Time Frame |
|---|---|---|
| Endothelial function in microcirculation | LSCI based calculation of perfusion unit before and after TVS/Sham stimulation | Change from baseline to post stimulation(within 20-30 minutes of stimulation) with TVS/Sham stimulation |
| Pulse wave analysis |
Not provided
Inclusion Criteria:
Exclusion Criteria:
Not provided
Not provided
Not provided
Not provided
Not provided
| Name | Affiliation | Role |
|---|---|---|
| Tarun Dasari, MD, MPH | University of Oklahoma | Principal Investigator |
| Facility | Status | City | State | ZIP | Country | Contacts |
|---|---|---|---|---|---|---|
| University of Oklahoma Health Sciences Center | Oklahoma City | Oklahoma | 73117 | United States |
Not provided
Not provided
Not provided
Not provided
Not provided
Not provided
| ID | Term |
|---|---|
| D058729 | Peripheral Arterial Disease |
| ID | Term |
|---|---|
| D050197 | Atherosclerosis |
| D001161 | Arteriosclerosis |
| D001157 | Arterial Occlusive Diseases |
| D014652 | Vascular Diseases |
Not provided
Not provided
This is a pilot study.
Not provided
Not provided
Blinding will be done so the investigator performing the FMD, LSCI and PWA testing will be blinded to the allocation of TVS
| Sham TVS | Device | Device will be applied but not to the Tragus of the ear but will be attached to the ear lobule. |
|
Arterial elasticity. Augmentation pressure (AP) will be calculated which is expressed as a percentage of the aortic pulse pressure (PP) which is the difference of systolic and diastolic BP(mm Hg).
| Change from baseline to post stimulation(within 15-20 minutes) with TVS/Sham stimulation. |
| D002318 |
| Cardiovascular Diseases |
| D016491 | Peripheral Vascular Diseases |