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Hypotension, Orthostatic clinical trials

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NCT ID: NCT03970551 Active, not recruiting - Syncope Clinical Trials

Lower Body Muscle Pre-activation in Initial Orthostatic Hypotension

IOH
Start date: July 1, 2019
Phase: N/A
Study type: Interventional

This study is aimed primarily at providing a simple and effective form of treatment to reduce the symptoms of Initial Orthostatic Hypotension (IOH) and prevent syncope. We will first characterize the physiology of IOH, and then we will study four sit-to-stand maneuvers, each with a different stress tests to identify the role of sympathetic activity vs. simple muscle contraction in IOH. Then we will complete an additional two sit-to-stands with interventions designed to decrease the blood pressure drop (and hopefully symptoms) with initial stand. These consist of physical counter maneuvers, which may be a possible treatment that can be used to mitigate the drop in blood pressure (BP) seen in IOH during a stand and relieve presyncope symptoms.

NCT ID: NCT03924388 Not yet recruiting - Clinical trials for Spinal Cord Injuries

Spinal Cord Stimulation and Autonomic Response in People With SCI.

Start date: February 1, 2020
Phase: N/A
Study type: Interventional

Despite being studied less than half as frequently, autonomic dysfunction is a greater priority than walking again in spinal cord injury. One autonomic condition after spinal cord injury is orthostatic hypotension, where blood pressure dramatically declines when patients assume the upright posture. Orthostatic hypotension is associated with all-cause mortality and cardiovascular incidents as well as fatigue and cognitive dysfunction, and it almost certainly contributes to an elevated risk of heart disease and stroke in people with spinal cord injury. In addition, autonomic dysfunction leads to bladder, bowel, sexual dysfunctions, which are major contributors to reduced quality and quantity of life. Unfortunately, the available options for treating this condition, are primarily limited to pharmacological options, which are not effective and are associated with various side effects. It has been recently demonstrated that spinal cord stimulation can modulate autonomic circuits and improve autonomic function in people living with spinal cord injury. Neuroanatomically, the thoracolumbar sympathetic pathways are the primary spinal cord segments involved in blood pressure control. Recently, a pilot study has been published demonstrating that transcutaneous spinal cord stimulation of thoracolumbar afferents can improve cardiovascular function. However, some studies have shown that lumbosacral transcutaneous spinal cord stimulation can also elicit positive cardiovascular effects. Therefore, there is no consensus on the optimal strategy in order to deliver transcutaneous spinal cord stimulation to improve the function of the autonomic system, and it may be that lumbosacral (i.e. the stimulation site being used most commonly for restoring leg function is sufficient). Another key knowledge gap in terms of transcutaneous spinal cord stimulation is whether or not the current is directly or indirectly activating these spinal circuits. Last but not least, the effects of epidural spinal cord stimulation on the function of cardiovascular, bladder, bowel and sexual system in spinal cord injury have been investigated in no study yet. AIMS AND HYPOTHESES: Aim 1. To examine the effects of short-term (one session) transcutaneous spinal cord stimulation on the frequency and severity of episodes of orthostatic hypotension/autonomic dysfunction, and bladder, bowel, and sexual functions. These effects will be compared at two sites of stimulation. Hypothesis 1.1: Short-term transcutaneous mid-thoracic cord stimulation will mitigate the severity and frequency of orthostatic hypotension/autonomic dysfunction. Hypothesis 1.2: Lumbosacral transcutaneous spinal cord stimulation will improve bladder, bowel, and sexual functions. Aim 2. To examine the effects of long-term (one month) transcutaneous spinal cord stimulation on the severity and frequency of orthostatic hypotension/autonomic dysfunction. Hypothesis 2.1: Long-term stimulation of the mid-thoracic cord will result in sustained improvements in mitigated severity and frequency of orthostatic hypotension/autonomic dysfunction that is not dependent on active stimulation. Hypothesis 2.2: Long-term lumbosacral transcutaneous spinal cord stimulation will result in sustained improvements in bowel, bladder, and sexual function that is not dependent on active stimulation. Aim 3: To examine the effects of short-term (one session) epidural spinal cord stimulation on the severity and frequency of orthostatic hypotension/autonomic dysfunction, and bladder, bowel, and sexual functions. Hypothesis 3.1: Epidural spinal cord stimulation will mitigate the severity and frequency of orthostatic hypotension/autonomic dysfunction and improve bladder, bowel, and sexual function. Hypothesis 3.3: There is no significant difference between immediate effects of lumbosacral transcutaneous spinal cord stimulation and epidural spinal cord stimulation on bladder, bowel, and sexual function. For aim 1, 14 participants with spinal cord injury and no implanted electrodes on the spinal cord will be recruited. Participants will randomly receive one-hour stimulation under each of the two stimulation conditions in a crossover manner: Mid-thoracic and Lumbosacral. For aim 2, 28 individuals with spinal cord injury and no implanted electrode will be pseudo-randomized (1:1) to one of two stimulation sites. Participants will receive one-hour stimulation, five sessions per week for four weeks. Cardiovascular and neurological outcomes will be measured before the first stimulation session and after the last stimulation session. For aim 3, 4 participants with spinal cord injury with implanted electrodes on the spinal cord will be recruited to study the immediate effects of invasive epidural spinal cord stimulation. All outcomes will be measured in two positions: a) Supine, b) ~ 70° upright tilt-test. Additionally, bowel, bladder, and sexual functions in project 2 will be assessed weekly.

NCT ID: NCT03900000 Completed - Parkinson Disease Clinical Trials

Improved Orthostatic Tolerance = Better Cognitive Function in Parkinson's Disease

PaKogOH
Start date: May 2014
Phase: N/A
Study type: Interventional

Study on orthostatic Hypotension in Parkinson's disease

NCT ID: NCT03829657 Terminated - Clinical trials for Parkinson's Disease (PD)

Phase 3 Clinical Effect Durability of TD-9855 for Treating Symptomatic nOH in Subjects With Primary Autonomic Failure

REDWOOD
Start date: February 22, 2019
Phase: Phase 3
Study type: Interventional

A Phase 3, 22-week, Multi-center, Randomized Withdrawal Study of ampreloxetine in Treating Symptomatic Neurogenic Orthostatic Hypotension in Subjects with Primary Autonomic Failure

NCT ID: NCT03759574 Recruiting - Clinical trials for Postoperative Complications

Pathophysiologic Hemodynamics After Primary Unilateral Total Hip Arthroplasty (THA)

Start date: March 18, 2019
Phase:
Study type: Observational

Incidence and pathophysiologic hemodynamics of orthostatic intolerance and orthostatic hypotension in patients undergoing unilateral THA

NCT ID: NCT03750552 Completed - Clinical trials for Symptomatic Neurogenic Orthostatic Hypotension

Clinical Effect of Ampreloxetine (TD-9855) for Treating Symptomatic nOH in Subjects With Primary Autonomic Failure

SEQUOIA
Start date: January 24, 2019
Phase: Phase 3
Study type: Interventional

A Phase 3 study to evaluate efficacy, safety, and tolerability of ampreloxetine (TD-9855) in subjects with primary autonomic failures (MSA, PD, or PAF) and symptomatic nOH with up to 4 weeks of treatment.

NCT ID: NCT03743116 Completed - Clinical trials for Postoperative Complications

Postoperative Orthostatic Intolerance and Hypotension in Unilateral TKA

Start date: November 13, 2018
Phase:
Study type: Observational

Incidence of Postoperative Orthostatic Intolerance and Postoperative Orthostatic Hypotension in Patients Undergoing Unilateral Total Knee Arthroplasty

NCT ID: NCT03732716 Recruiting - Sarcopenia Clinical Trials

Sarcopenia and Orthostatic Hypotension

Start date: September 10, 2018
Phase:
Study type: Observational

Elderly patients generally have a tendency for having sarcopenia which refers to muscle loss that may be related to many factors. These patients also have a tendency to falls and injuries. Whether elderly sarcopenic patients have abrupt blood pressure drops upon standing remains unknown. Therefore, in this study, we sought to determine the incidence of orthostatic hypotension in sarcopenic elderly patients and compare it with elderly patients with no sarcopenia.

NCT ID: NCT03721393 Completed - Clinical trials for Orthostatic Hypotension

Data Collection - Of Syncope Tilt Table Testing Study

COST3
Start date: October 4, 2019
Phase:
Study type: Observational

To characterize the impact of orthostatic hypotension (OH) and reflex syncope on signals measured using a wearable cardiac monitor prototype device. To evaluate the relationship of signals measured from the wearable cardiac monitor prototype device with reported symptom severity of orthostatic intolerance per standard data collection, analysis, and questionnaires.

NCT ID: NCT03674541 Completed - Fibromyalgia Clinical Trials

The Exercise Response to Pharmacologic Cholinergic Stimulation in Myalgic Encephalomyelitis / Chronic Fatigue Syndrome

Start date: January 14, 2020
Phase: Phase 2
Study type: Interventional

Myalgic encephalomyelitis/Chronic fatigue syndrome (ME/CFS), otherwise known as Chronic fatigue syndrome (CFS) or myalgic encephalomyelitis (ME), is an under-recognized disorder whose cause is not yet understood. Suggested theories behind the pathophysiology of this condition include autoimmune causes, an inciting viral illness, and a dysfunctional autonomic nervous system caused by a small fiber polyneuropathy. Symptoms include fatigue, cognitive impairments, gastrointestinal changes, exertional dyspnea, and post-exertional malaise. The latter two symptoms are caused in part by abnormal cardiopulmonary hemodynamics during exercise thought to be due to a small fiber polyneuropathy. This manifests as low biventricular filling pressures throughout exercise seen in patients undergoing an invasive cardiopulmonary exercise test (iCPET) along with small nerve fiber atrophy seen on skin biopsy. After diagnosis, patients are often treated with pyridostigmine (off-label use of this medication) to enhance cholinergic stimulation of norepinephrine release at the post-ganglionic synapse. This is thought to improve venoconstriction at the site of exercising muscles, leading to improved return of blood to the heart and increasing filling of the heart to more appropriate levels during peak exercise. Retrospective studies have shown that noninvasive measurements of exercise capacity, such as oxygen uptake, end-tidal carbon dioxide, and ventilatory efficiency, improve after treatment with pyridostigmine. To date, there are no studies that assess invasive hemodynamics after pyridostigmine administration. It is estimated that four million people suffer from ME/CFS worldwide, a number that is thought to be a gross underestimate of disease prevalence. However, despite its potential for debilitating symptoms, loss of productivity, and worldwide burden, the pathophysiology behind ME/CFS remains unknown and its treatment unclear. By evaluating the exercise response to cholinergic stimulation, this study will shed further light on the link between the autonomic nervous system and cardiopulmonary hemodynamics, potentially leading to new therapeutic targets.