Obstructive Sleep ApneaNCT05387122
The Effect of Mandibular Advancement Devices on Markers of Cardiovascular Health in Obstructive Sleep Apnea Patients
An observational study of Obstructive Sleep Apnea, run by University of Alberta at 1 site in Canada.
Trial summary
Obstructive sleep apnea (OSA) is a type of disordered breathing defined by the repetitive obstruction of airflow during sleep due to upper airway collapse. Each obstructive event contributes to decreased blood oxygen, or hypoxia. Read more about this study
- Who is it for?
- Ages 18 to 70 years
- Conditions the study is for
- Obstructive Sleep Apnea
- What is being tested?
- mandibular advancement device (MAD)
- Type of treatment
- Pill or oral medicine, Medical device
- How many people
- 4 participants
- Where
- 1 siteCanada
- Study dates
- 11 Jul 2021to 9 Sep 2024
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 70 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Volunteers with mild to moderate OSA will be recruited with the assistance of referring dentists who are certified to provide MADs under the Alberta Dental Association \& College guidelines. Participants will be included if they are between the ages of 18-70 years, initiating adjustable MAD therapy with their provider and no medical history of heart failure, cardiopulmonary and renal disease
Who may be able to join
- Between ages of 18-70
- Diagnosed with Obstructive Sleep Apnea and prescribed with Mandibular Advancement Device
- No medical history of cardiovascular, pulmonary, renal diseases
Who cannot join
- Any known cardiovascular, respiratory or pulmonary disease
- Have a history of smoking regularly in past 6 months
- Pre-existing symptomatic non-respiratory sleep disorder (restless leg syndrome, chronic insomnia)
- if more than 50% of their observed apneas are due to sleep apnea
Trial locations and contacts
1 site in 1 country.
About this study
Official title: The Effect of Mandibular Advancement Devices on Markers of Cardiovascular Health in Mild to Moderate Obstructive Sleep Apnea Patients Who Are Non-Compliant With Continuous Positive Airway Pressure Therapy
Obstructive sleep apnea (OSA) is a type of disordered breathing defined by the repetitive obstruction of airflow during sleep due to upper airway collapse. Each obstructive event contributes to decreased blood oxygen, or hypoxia. OSA has been associated with various cardiovascular diseases, including hypertension, stroke, heart failure, and coronary artery disease. A factor in this association may be the decrease in blood vessel health and the marked over activation of the sympathetic nervous system that is observed in OSA due to nighttime hypoxia. The sympathetic nervous system is responsible for maintaining heart and blood vessel (cardiovascular) balance. Elevated sympathetic nervous activity (SNA) is a likely cause of hypertension and subsequent cardiovascular disease.
Continuous positive airway pressure (CPAP) therapy is the most accepted treatment for OSA and has been shown to improve high blood pressure and SNA in patients. An alternative therapy for OSA is a type of removable oral appliance known as a mandibular advancement device (MAD). Currently, there is no research directly measuring SNA in OSA patients using MADs. In addition to other cardiovascular markers, the investigators would like to directly assess SNA during a MAD intervention using the gold standard technique of microneurography. The investigators believe this will provide important information for the management of OSA, as levels of SNA are known to respond to both acute and chronic levels of hypoxia. Improved heart and blood vessel markers could further support MAD use, providing an important alternative therapy for those that can not tolerate CPAP.
Read the detailed description
In OSA the obstruction of breathing can be either partial (hypopnea) or complete (apnea), and each obstructive event contributes to decreased blood oxygen, or hypoxia. Sleep disordered breathing and nighttime hypoxia have both been identified as independent risk factors of death. Specifically, OSA is estimated to affect 34% of men and 17% of women and when inadequately treated patients present with daytime sleepiness, depression, workplace accidents and cardiovascular disease.
The severity of OSA is determined by the apnea-hypopnea index (AHI) which is the average number of airway obstructions experienced per hour of sleep. CPAP therapy has been shown to improve high blood pressure, AHI and SNA in patients. However, benefits of CPAP therapy are dose-dependent and are largely affected by patient compliance. Unfortunately, due to various discomforts associated with the use of CPAP therapy, less than fifty percent of patients adhere to long-term therapy.
MADs have increased compliance in comparison to CPAP, and improve some patient's symptoms of sleepiness. Yet, MAD interventions have shown smaller improvements in AHI values when compared to CPAP. However, AHI has been criticized for being an overly simplistic measurement of nocturnal hypoxia. In contrast, SNA is known to respond both acutely and chronically to varying levels of blood oxygen. Therefore, MAD interventions may not produce changes in AHI equal to that of a CPAP intervention; however, they may change levels of SNA and other specific CV markers of blood vessel health. This would further support the use of MADs and provide additional insight into the underlying cardiovascular mechanisms involved in OSA therapy. Understanding and validating additional therapies for OSA is of great importance, due to the significant health consequences of the disease.
Objectives
The proposed investigation aims to determine the following in mild to moderate OSA patients who fail to comply with CPAP therapy:
Does MAD therapy improve AHI in mild to moderate severity OSA?
Does MAD therapy lower basal SNA in mild to moderate severity OSA?
Does MAD therapy improve vascular function, blood pressure, heart rate variability and blood markers of elevated SNA in mild to moderate severity OSA?
Research Method/ Procedures
Methodology
To address this hypothesis, the investigators propose a prospective case series examining subjects at baseline, at 3 months and again at 6 months after a MAD intervention. A 2020 study by Ruzicka et al. found no changes in SNA after a CPAP intervention of 6 weeks. Another study by Henderson et al, 2016, found a significant reduction in SNA during a CPAP intervention of 6 months and 12 months. In 2009, Kuramoto et al measured changes in SNA indirectly during a 3 month CPAP intervention and did not see significant results. Our methodology involves direct measurement of SNA during MAD therapy, therefore, testing intervals at baseline, 3 months and 6 months of MAD therapy have been selected.
- Conditions
- Obstructive Sleep Apnea
- Being tested
- mandibular advancement device (MAD)
- Medical subject headings
- Sleep Apnea, Obstructive
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
mandibular advancement device (MAD)Device
mandibular advancement device (MAD) is a removable oral appliance. It is an alternative therapy for patients of Obstructive Sleep Apnea who are non compliant to Continuous positive airway pressure(CPAP) which is the most accepted therapy for Obstructive Sleep Apnea.
What is being measured
The primary outcome is the main question the study is designed to answer.
Difference in Sympathetic Nerve Activity
Muscle sympathetic nerve activity. Direct multi-unit postganglionic muscle sympathetic nerve activity (MSNA) will be obtained via microneurography. A sterile Tungsten recording microelectrode (35 mm long, 200 μm in diameter, tapered to a 1- to 5-μm uninsulated tip) will be inserted into a muscle nerve fascicle of a sympathetic nerve bundle, of the peroneal nerve. A reference electrode will also be inserted subcutaneously 1-3 cm from the recording electrode. MSNA will be obtained by manually manipulating the microelectrode until a characteristic bursting pattern is observed A trained researcher will record and analyze to quantify sympathetic activity as: burst frequency (bursts/min), burst incidence (bursts/ 100 heart beats), burst amplitude (normalized to largest resting amplitude), and total activity (burst frequency multiplied by mean normalized burst amplitude)
Measured: 3 months
Difference in Cardiovascular markers - Heart Rate
All cardiovascular parameters will be acquired using an analog-to-digital converter (Powerlab/16SP ML 880; ADInstruments, Colorado Springs, CO, USA) interfaced with a personal computer. Commercially available software will be used to analyze ventilatory and cardiovascular variables (LabChart V7.1, ADinstruments, Colorado Springs, CO, USA). Throughout all procedures, heart rate will be determined from a standard lead III electrocardiogram (ML 132, ADInstruments, Colorado Springs, CO, USA). Heart Rate will be recorded in beats/ minute
Measured: 3 months
Difference in Cardiovascular markers- Blood Pressure
All cardiovascular parameters will be acquired using an analog-to-digital converter (Powerlab/16SP ML 880; ADInstruments, Colorado Springs, CO, USA) interfaced with a personal computer. Commercially available software will be used to analyze ventilatory and cardiovascular variables (LabChart V7.1, ADinstruments, Colorado Springs, CO, USA). Throughout all procedures, Blood pressure will be recorded beat-by-beat by finger pulse photoplethysmograph; mmHg.
Measured: 3 months
Fasted blood sample- Neurotransmitters
Fasted blood samples (~30ml) will be analyzed for sympathetic nervous system neurotransmitters (Norepinephrine, Epinephrine,)
Measured: 3 months
Fasted blood sample- Sex Hormones
Fasted blood samples (~30ml) will be analyzed for sex hormones (estrogen, progesterone, testosterone)
Measured: 3 months
Endothelial function- time to peak dilation
Flow Mediated Dilation: This will be assessed in the brachial artery, using an ultrasound system. A sphygmomanometer cuff will be placed and inflated around the forearm to a supra-systolic pressure (250 mmHg) to occlude forearm blood flow for 5 min. After this time period, the cuff will be rapidly deflated (~1 s). Baseline brachial artery blood flow velocity and diameter will be recorded for 1 minute before cuff inflation, and for 3.5 min beginning 30 s prior to cuff release. (FMD, time to maximal dilation; s)
Measured: 3 months
Endothelial function- Flow mediated dilation
Flow Mediated Dilation: This will be assessed in the brachial artery, using an ultrasound system. A sphygmomanometer cuff will be placed and inflated around the forearm to a supra-systolic pressure (250 mmHg) to occlude forearm blood flow for 5 min. After this time period, the cuff will be rapidly deflated (~1 s). Baseline brachial artery blood flow velocity and diameter will be recorded for 1 minute before cuff inflation, and for 3.5 min beginning 30 s prior to cuff release. Percent change in artery diameter will be calculated.
Measured: 3 months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted24 May 2022
- Study start11 Jul 2021
- Primary completion9 Sep 2024
- Study completion9 Sep 2024
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (15)Papers the sponsor has linked to this study.
- Other trials for Obstructive Sleep ApneaStudies of the same condition, open and under way.
- More trials run by University of AlbertaThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case only
- Time perspective
- Prospective
- Enrolment
- 4 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of Alberta
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
- Investigators
- Carlos F Mir, DSc, Principal investigator, University of AlbertaCraig Steinback, PhD, Principal investigator, University of Alberta
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05387122
- Sponsor's protocol ID
- Pro00108618
- Status last verified
- Sep 2024
- First submitted
- 29 Mar 2022
- Last updated
- 19 Sep 2024
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Publications
Somers VK, Dyken ME, Clary MP, Abboud FM. Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest. 1995 Oct;96(4):1897-904. doi: 10.1172/JCI118235.
PubMed 7560081Henderson LA, Fatouleh RH, Lundblad LC, McKenzie DK, Macefield VG. Effects of 12 Months Continuous Positive Airway Pressure on Sympathetic Activity Related Brainstem Function and Structure in Obstructive Sleep Apnea. Front Neurosci. 2016 Mar 10;10:90. doi: 10.3389/fnins.2016.00090. eCollection 2016.
PubMed 27013952de Vries GE, Wijkstra PJ, Houwerzijl EJ, Kerstjens HAM, Hoekema A. Cardiovascular effects of oral appliance therapy in obstructive sleep apnea: A systematic review and meta-analysis. Sleep Med Rev. 2018 Aug;40:55-68. doi: 10.1016/j.smrv.2017.10.004. Epub 2017 Oct 26.
PubMed 29195726Ferguson KA, Cartwright R, Rogers R, Schmidt-Nowara W. Oral appliances for snoring and obstructive sleep apnea: a review. Sleep. 2006 Feb;29(2):244-62. doi: 10.1093/sleep/29.2.244.
PubMed 16494093Imes CC, Baniak LM, Choi J, Luyster FS, Morris JL, Ren D, Chasens ER. Correlates of Endothelial Function in Older Adults With Untreated Obstructive Sleep Apnea and Cardiovascular Disease. J Cardiovasc Nurs. 2019 Jan/Feb;34(1):E1-E7. doi: 10.1097/JCN.0000000000000536.
PubMed 30303893Lopez-Jimenez F, Sert Kuniyoshi FH, Gami A, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. Chest. 2008 Mar;133(3):793-804. doi: 10.1378/chest.07-0800. No abstract available.
PubMed 18321908Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet. 2005 Mar 19-25;365(9464):1046-53. doi: 10.1016/S0140-6736(05)71141-7.
PubMed 15781100Meah VL, Busch SA, Jones KE, Davenport MH, Steinback CD. A review of acute responses, after-effects and chronic complications related to microneurography. Clin Neurophysiol. 2019 Oct;130(10):1781-1788. doi: 10.1016/j.clinph.2019.06.228. Epub 2019 Jul 15.
PubMed 31401486Ning Y, Zhang TS, Wen WW, Li K, Yang YX, Qin YW, Zhang HN, Du YH, Li LY, Yang S, Yang YY, Zhu MM, Jiao XL, Zhang Y, Zhang M, Wei YX. Effects of continuous positive airway pressure on cardiovascular biomarkers in patients with obstructive sleep apnea: a meta-analysis of randomized controlled trials. Sleep Breath. 2019 Mar;23(1):77-86. doi: 10.1007/s11325-018-1662-2. Epub 2018 Apr 22.
PubMed 29682699Peppard PE, Young T, Barnet JH, Palta M, Hagen EW, Hla KM. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol. 2013 May 1;177(9):1006-14. doi: 10.1093/aje/kws342. Epub 2013 Apr 14.
PubMed 23589584Phillips CL, Grunstein RR, Darendeliler MA, Mihailidou AS, Srinivasan VK, Yee BJ, Marks GB, Cistulli PA. Health outcomes of continuous positive airway pressure versus oral appliance treatment for obstructive sleep apnea: a randomized controlled trial. Am J Respir Crit Care Med. 2013 Apr 15;187(8):879-87. doi: 10.1164/rccm.201212-2223OC.
PubMed 23413266Punjabi NM, Caffo BS, Goodwin JL, Gottlieb DJ, Newman AB, O'Connor GT, Rapoport DM, Redline S, Resnick HE, Robbins JA, Shahar E, Unruh ML, Samet JM. Sleep-disordered breathing and mortality: a prospective cohort study. PLoS Med. 2009 Aug;6(8):e1000132. doi: 10.1371/journal.pmed.1000132. Epub 2009 Aug 18.
PubMed 19688045Thijssen DHJ, Bruno RM, van Mil ACCM, Holder SM, Faita F, Greyling A, Zock PL, Taddei S, Deanfield JE, Luscher T, Green DJ, Ghiadoni L. Expert consensus and evidence-based recommendations for the assessment of flow-mediated dilation in humans. Eur Heart J. 2019 Aug 7;40(30):2534-2547. doi: 10.1093/eurheartj/ehz350.
PubMed 31211361Zinchuk A, Yaggi HK. Phenotypic Subtypes of OSA: A Challenge and Opportunity for Precision Medicine. Chest. 2020 Feb;157(2):403-420. doi: 10.1016/j.chest.2019.09.002. Epub 2019 Sep 17.
PubMed 31539538Yamamoto U, Nishizaka M, Tsuda H, Tsutsui H, Ando SI. Crossover comparison between CPAP and mandibular advancement device with adherence monitor about the effects on endothelial function, blood pressure and symptoms in patients with obstructive sleep apnea. Heart Vessels. 2019 Oct;34(10):1692-1702. doi: 10.1007/s00380-019-01392-3. Epub 2019 Mar 29.
PubMed 30927057
Study at a glance
From the registry record, last updated by the sponsor on 19 Sep 2024. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- The Effect of Mandibular Advancement Devices on Markers of Cardiovascular Health in Mild to Moderate Obstructive Sleep Apnea Patients Who Are Non-Compliant With Continuous Positive Airway Pressure Therapy
- ClinicalTrials.gov ID
- NCT05387122
- Acronym / sponsor ID
- Pro00108618
- Conditions
- Obstructive Sleep Apnea
- Study type
- Observational
- Recruitment status
- Completed
- Enrolment
- 4 participants (actual)
- Lead sponsor
- University of AlbertaUniversity, hospital or other
- Study start
- 11 Jul 2021 (actual)
- Primary completion
- 9 Sep 2024 (actual)
- Study completion
- 9 Sep 2024 (actual)
- First posted
- 24 May 2022 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Obstructive sleep apnea (OSA) is a type of disordered breathing defined by the repetitive obstruction of airflow during sleep due to upper airway collapse. Each obstructive event contributes to decreased blood oxygen, or hypoxia. OSA has been associated with various cardiovascular diseases, including hypertension, stroke, heart failure, and coronary artery disease. A factor in this association may be the decrease in blood vessel health and the marked over activation of the sympathetic nervous system that is observed in OSA due to nighttime hypoxia. The sympathetic nervous system is responsible for maintaining heart and blood vessel (cardiovascular) balance. Elevated sympathetic nervous activity (SNA) is a likely cause of hypertension and subsequent cardiovascular disease.
Continuous positive airway pressure (CPAP) therapy is the most accepted treatment for OSA and has been shown to improve high blood pressure and SNA in patients. An alternative therapy for OSA is a type of removable oral appliance known as a mandibular advancement device (MAD). Currently, there is no research directly measuring SNA in OSA patients using MADs. In addition to other cardiovascular markers, the investigators would like to directly assess SNA during a MAD intervention using the gold standard technique of microneurography. The investigators believe this will provide important information for the management of OSA, as levels of SNA are known to respond to both acute and chronic levels of hypoxia. Improved heart and blood vessel markers could further support MAD use, providing an important alternative therapy for those that can not tolerate CPAP.
Detailed description
In OSA the obstruction of breathing can be either partial (hypopnea) or complete (apnea), and each obstructive event contributes to decreased blood oxygen, or hypoxia. Sleep disordered breathing and nighttime hypoxia have both been identified as independent risk factors of death. Specifically, OSA is estimated to affect 34% of men and 17% of women and when inadequately treated patients present with daytime sleepiness, depression, workplace accidents and cardiovascular disease.
The severity of OSA is determined by the apnea-hypopnea index (AHI) which is the average number of airway obstructions experienced per hour of sleep. CPAP therapy has been shown to improve high blood pressure, AHI and SNA in patients. However, benefits of CPAP therapy are dose-dependent and are largely affected by patient compliance. Unfortunately, due to various discomforts associated with the use of CPAP therapy, less than fifty percent of patients adhere to long-term therapy.
MADs have increased compliance in comparison to CPAP, and improve some patient's symptoms of sleepiness. Yet, MAD interventions have shown smaller improvements in AHI values when compared to CPAP. However, AHI has been criticized for being an overly simplistic measurement of nocturnal hypoxia. In contrast, SNA is known to respond both acutely and chronically to varying levels of blood oxygen. Therefore, MAD interventions may not produce changes in AHI equal to that of a CPAP intervention; however, they may change levels of SNA and other specific CV markers of blood vessel health. This would further support the use of MADs and provide additional insight into the underlying cardiovascular mechanisms involved in OSA therapy. Understanding and validating additional therapies for OSA is of great importance, due to the significant health consequences of the disease.
Objectives
The proposed investigation aims to determine the following in mild to moderate OSA patients who fail to comply with CPAP therapy:
Does MAD therapy improve AHI in mild to moderate severity OSA?
Does MAD therapy lower basal SNA in mild to moderate severity OSA?
Does MAD therapy improve vascular function, blood pressure, heart rate variability and blood markers of elevated SNA in mild to moderate severity OSA?
Research Method/ Procedures
Methodology
To address this hypothesis, the investigators propose a prospective case series examining subjects at baseline, at 3 months and again at 6 months after a MAD intervention. A 2020 study by Ruzicka et al. found no changes in SNA after a CPAP intervention of 6 weeks. Another study by Henderson et al, 2016, found a significant reduction in SNA during a CPAP intervention of 6 months and 12 months. In 2009, Kuramoto et al measured changes in SNA indirectly during a 3 month CPAP intervention and did not see significant results. Our methodology involves direct measurement of SNA during MAD therapy, therefore, testing intervals at baseline, 3 months and 6 months of MAD therapy have been selected.
Study design
- Observational model
- Case only
- Time perspective
- Prospective
Who may qualify
- Ages
- 18 to 70 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Volunteers with mild to moderate OSA will be recruited with the assistance of referring dentists who are certified to provide MADs under the Alberta Dental Association \& College guidelines. Participants will be included if they are between the ages of 18-70 years, initiating adjustable MAD therapy with their provider and no medical history of heart failure, cardiopulmonary and renal disease
Key inclusion criteria (3 listed)
- Between ages of 18-70
- Diagnosed with Obstructive Sleep Apnea and prescribed with Mandibular Advancement Device
- No medical history of cardiovascular, pulmonary, renal diseases
Key exclusion criteria (4 listed)
- Any known cardiovascular, respiratory or pulmonary disease
- Have a history of smoking regularly in past 6 months
- Pre-existing symptomatic non-respiratory sleep disorder (restless leg syndrome, chronic insomnia)
- if more than 50% of their observed apneas are due to sleep apnea
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| mandibular advancement device (MAD)mandibular advancement device (MAD) is a removable oral appliance. It is an alternative therapy for patients of Obstructive Sleep Apnea who are non compliant to Continuous positive airway pressure(CPAP) which is the most accepted therapy for Obstructive Sleep Apnea. | Device | – |
Primary outcome
Difference in Sympathetic Nerve Activity
Time frame: 3 months
Muscle sympathetic nerve activity. Direct multi-unit postganglionic muscle sympathetic nerve activity (MSNA) will be obtained via microneurography. A sterile Tungsten recording microelectrode (35 mm long, 200 μm in diameter, tapered to a 1- to 5-μm uninsulated tip) will be inserted into a muscle nerve fascicle of a sympathetic nerve bundle, of the peroneal nerve. A reference electrode will also be inserted subcutaneously 1-3 cm from the recording electrode. MSNA will be obtained by manually manipulating the microelectrode until a characteristic bursting pattern is observed A trained researcher will record and analyze to quantify sympathetic activity as: burst frequency (bursts/min), burst incidence (bursts/ 100 heart beats), burst amplitude (normalized to largest resting amplitude), and total activity (burst frequency multiplied by mean normalized burst amplitude)
Difference in Cardiovascular markers - Heart Rate
Time frame: 3 months
All cardiovascular parameters will be acquired using an analog-to-digital converter (Powerlab/16SP ML 880; ADInstruments, Colorado Springs, CO, USA) interfaced with a personal computer. Commercially available software will be used to analyze ventilatory and cardiovascular variables (LabChart V7.1, ADinstruments, Colorado Springs, CO, USA). Throughout all procedures, heart rate will be determined from a standard lead III electrocardiogram (ML 132, ADInstruments, Colorado Springs, CO, USA). Heart Rate will be recorded in beats/ minute
Difference in Cardiovascular markers- Blood Pressure
Time frame: 3 months
All cardiovascular parameters will be acquired using an analog-to-digital converter (Powerlab/16SP ML 880; ADInstruments, Colorado Springs, CO, USA) interfaced with a personal computer. Commercially available software will be used to analyze ventilatory and cardiovascular variables (LabChart V7.1, ADinstruments, Colorado Springs, CO, USA). Throughout all procedures, Blood pressure will be recorded beat-by-beat by finger pulse photoplethysmograph; mmHg.
Fasted blood sample- Neurotransmitters
Time frame: 3 months
Fasted blood samples (~30ml) will be analyzed for sympathetic nervous system neurotransmitters (Norepinephrine, Epinephrine,)
Fasted blood sample- Sex Hormones
Time frame: 3 months
Fasted blood samples (~30ml) will be analyzed for sex hormones (estrogen, progesterone, testosterone)
Endothelial function- time to peak dilation
Time frame: 3 months
Flow Mediated Dilation: This will be assessed in the brachial artery, using an ultrasound system. A sphygmomanometer cuff will be placed and inflated around the forearm to a supra-systolic pressure (250 mmHg) to occlude forearm blood flow for 5 min. After this time period, the cuff will be rapidly deflated (~1 s). Baseline brachial artery blood flow velocity and diameter will be recorded for 1 minute before cuff inflation, and for 3.5 min beginning 30 s prior to cuff release. (FMD, time to maximal dilation; s)
Endothelial function- Flow mediated dilation
Time frame: 3 months
Flow Mediated Dilation: This will be assessed in the brachial artery, using an ultrasound system. A sphygmomanometer cuff will be placed and inflated around the forearm to a supra-systolic pressure (250 mmHg) to occlude forearm blood flow for 5 min. After this time period, the cuff will be rapidly deflated (~1 s). Baseline brachial artery blood flow velocity and diameter will be recorded for 1 minute before cuff inflation, and for 3.5 min beginning 30 s prior to cuff release. Percent change in artery diameter will be calculated.
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 19 Sep 2024.
- Background: PubMed 7560081Somers VK, Dyken ME, Clary MP, Abboud FM. Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest. 1995 Oct;96(4):1897-904. doi: 10.1172/JCI118235.
- Background: PubMed 27013952Henderson LA, Fatouleh RH, Lundblad LC, McKenzie DK, Macefield VG. Effects of 12 Months Continuous Positive Airway Pressure on Sympathetic Activity Related Brainstem Function and Structure in Obstructive Sleep Apnea. Front Neurosci. 2016 Mar 10;10:90. doi: 10.3389/fnins.2016.00090. eCollection 2016.
- Results publication: PubMed 29195726de Vries GE, Wijkstra PJ, Houwerzijl EJ, Kerstjens HAM, Hoekema A. Cardiovascular effects of oral appliance therapy in obstructive sleep apnea: A systematic review and meta-analysis. Sleep Med Rev. 2018 Aug;40:55-68. doi: 10.1016/j.smrv.2017.10.004. Epub 2017 Oct 26.
- Results publication: PubMed 16494093Ferguson KA, Cartwright R, Rogers R, Schmidt-Nowara W. Oral appliances for snoring and obstructive sleep apnea: a review. Sleep. 2006 Feb;29(2):244-62. doi: 10.1093/sleep/29.2.244.
- Results publication: PubMed 30303893Imes CC, Baniak LM, Choi J, Luyster FS, Morris JL, Ren D, Chasens ER. Correlates of Endothelial Function in Older Adults With Untreated Obstructive Sleep Apnea and Cardiovascular Disease. J Cardiovasc Nurs. 2019 Jan/Feb;34(1):E1-E7. doi: 10.1097/JCN.0000000000000536.
- Results publication: PubMed 18321908Lopez-Jimenez F, Sert Kuniyoshi FH, Gami A, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. Chest. 2008 Mar;133(3):793-804. doi: 10.1378/chest.07-0800. No abstract available.
- Results publication: PubMed 15781100Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet. 2005 Mar 19-25;365(9464):1046-53. doi: 10.1016/S0140-6736(05)71141-7.
- Results publication: PubMed 31401486Meah VL, Busch SA, Jones KE, Davenport MH, Steinback CD. A review of acute responses, after-effects and chronic complications related to microneurography. Clin Neurophysiol. 2019 Oct;130(10):1781-1788. doi: 10.1016/j.clinph.2019.06.228. Epub 2019 Jul 15.
- Results publication: PubMed 29682699Ning Y, Zhang TS, Wen WW, Li K, Yang YX, Qin YW, Zhang HN, Du YH, Li LY, Yang S, Yang YY, Zhu MM, Jiao XL, Zhang Y, Zhang M, Wei YX. Effects of continuous positive airway pressure on cardiovascular biomarkers in patients with obstructive sleep apnea: a meta-analysis of randomized controlled trials. Sleep Breath. 2019 Mar;23(1):77-86. doi: 10.1007/s11325-018-1662-2. Epub 2018 Apr 22.
- Results publication: PubMed 23589584Peppard PE, Young T, Barnet JH, Palta M, Hagen EW, Hla KM. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol. 2013 May 1;177(9):1006-14. doi: 10.1093/aje/kws342. Epub 2013 Apr 14.
- Results publication: PubMed 23413266Phillips CL, Grunstein RR, Darendeliler MA, Mihailidou AS, Srinivasan VK, Yee BJ, Marks GB, Cistulli PA. Health outcomes of continuous positive airway pressure versus oral appliance treatment for obstructive sleep apnea: a randomized controlled trial. Am J Respir Crit Care Med. 2013 Apr 15;187(8):879-87. doi: 10.1164/rccm.201212-2223OC.
- Results publication: PubMed 19688045Punjabi NM, Caffo BS, Goodwin JL, Gottlieb DJ, Newman AB, O'Connor GT, Rapoport DM, Redline S, Resnick HE, Robbins JA, Shahar E, Unruh ML, Samet JM. Sleep-disordered breathing and mortality: a prospective cohort study. PLoS Med. 2009 Aug;6(8):e1000132. doi: 10.1371/journal.pmed.1000132. Epub 2009 Aug 18.
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Apnea, Sleep Disorders
Not yet recruitingPhase 2
Supplemental Oxygen for Sleep-Disordered Breathing in Adults With Chronic Opioid Use.
Sleep-disordered Breathing, Chronic Opioid Use
Recruiting
Nightly Wearable Monitoring During Home-Based Submental Electrical Stimulation for Obstructive Sleep Apnea
Obstructive Sleep Apnea
RecruitingPhase 1/2
DRonabinol Treatment of OSA
Obstructive Sleep Apnea
Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Carlos F Mir, DSc principal investigator
University of Alberta
Craig Steinback, PhD principal investigator
University of Alberta
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Obstructive Sleep Apnea, run by University of Alberta at 1 site in Canada.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 3 inclusion and 4 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 19 Sep 2024. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Canada. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Difference in Sympathetic Nerve Activity (time frame: 3 months). The study lists 7 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT05387122, which also lists 15 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 19 Sep 2024.