Sleep Apnea, ObstructiveNCT01633827
Combination Therapy to Treat Sleep Apnea
A study testing Sedative, Room air and Oxygen in people with Sleep Apnea, Obstructive, run by Brigham and Women's Hospital at 1 site in United States.
Trial summary
In Obstructive sleep apnea (OSA), the upper airway closes over and over again during sleep. This leads to disrupted sleep (waking up during the night), daytime sleepiness, and an increased risk for developing high blood pressure. Read more about this study
- Who is it for?
- Ages 18 to 79 years
- Conditions the study is for
- Sleep Apnea, Obstructive
- What is being tested?
- Sedative, Room air and Oxygen
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 22 participants
- Where
- 1 siteUnited States
- Study dates
- Aug 2012to Dec 2014
- Phase
- Interventional
- Are there results?
- Yes, posted in the registrySummary in the doctors' view
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 79 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- Ages 18 - 79 years
- Documented OSA (AHI > 10 events/hr Non rapid eye movement sleep supine)
- If treated then, current CPAP use (>4 hrs CPAP/night for > 2 months)
Who cannot join
- Any uncontrolled medical condition
- Any other sleep disorder (Periodic leg movement syndrome, restless legs syndrome, insomnia, etc.)
- Use of medications known to affect sleep/arousal, breathing, or muscle physiology
- Allergy to lidocaine or Afrin
- Claustrophobia
- Alcohol consumption within 24 hours of PSG
Trial locations and contacts
1 site in 1 country.
United States1 site
Brigham and Women's Hospital
Boston, Massachusetts, 02115
About this study
Official title: Combination Therapy for the Treatment of Obstructive Sleep Apnea
In Obstructive sleep apnea (OSA), the upper airway closes over and over again during sleep. This leads to disrupted sleep (waking up during the night), daytime sleepiness, and an increased risk for developing high blood pressure. Currently, the best treatment for obstructive sleep apnea is sleeping with a mask that continuously blows air into the nose (i.e. Continuous positive airway pressure [CPAP] treatment). While CPAP treatment stops the upper airway from closing in most people, many people have difficulty sleeping with the mask in place and therefore do not use the CPAP treatment. This research study is being conducted to learn whether using a combination of therapies (i.e. a sedative and oxygen therapy) will improve OSA severity by altering some of the traits that are responsible for the disorder.
Read the detailed description
Obstructive sleep apnea (OSA) is characterized by repetitive collapse or 'obstruction' of the pharyngeal airway during sleep. These obstructions result in repetitive hypopneas/apneas and intermittent hypoxia/hypercapnia, as well as surges in sympathetic activity. Such processes disturb normal sleep and impair neurocognitive function, often resulting in excessive daytime sleepiness and decreased quality of life. Furthermore, OSA is associated with cardiovascular morbidity and mortality, making OSA a major health concern.
Current evidence suggests that OSA pathogenesis involves the interactions of at least four physiological traits comprising 1) the pharyngeal anatomy and its propensity towards collapse 2) the ability of the upper airway dilator muscles to activate and reopen the airway during sleep (i.e. neuromuscular compensation), 3) the arousal threshold from sleep (i.e. the propensity for hypopneas/apneas to lead to arousal and fragmented sleep) and 4) the stability of the ventilatory feedback loop (i.e. loop gain). Continuous positive airway pressure (CPAP) is the most common treatment for OSA but it is often poorly tolerated; only ~50% of patients diagnosed with OSA continue therapy beyond 3 months. Given this limitation, alternative approaches have been tested and have generally focused on the use of oral appliances, surgery, and more recently pharmacological agents.
However, these alternate therapies, when used alone as monotherapy, rarely abolish OSA completely. This is not that surprising given that these treatments focus primarily on correcting only one trait and ignore the fact that the pathogenesis of OSA is multi-factorial. Thus the investigators hypothesize that some patients could be treated without CPAP if more than one trait is targeted (i.e., the investigators take a multi-factorial treatment approach). Such a multi-factorial approach is not unusual in Medicine. Many disorders such as diabetes, asthma, hypertension, cancer and congestive heart failure are treated with more than one medication or modality. In our view, giving CPAP to all OSA patients is like treating every diabetic with insulin, or every asthmatic with oral steroids - these treatments, like CPAP, are poorly tolerated and ignore the complexity of the underlying biology.
The investigators recently published a technique that measures the four traits using repeated 'drops' in CPAP levels during sleep. Each trait is measured in a way that allows model-based predictions of the presence/absence of OSA. With this technique the investigators demonstrated in a small group of CPAP-treated OSA subjects that decreasing the sensitivity of the ventilatory feedback loop (i.e. reducing loop gain) by approximately 50% with either acetazolamide or oxygen reduces the apnea/hypopnea index (AHI) by half. Interestingly, our model allowed us to make the prediction that if, in addition to an agent that reduces loop gain, the investigators also gave a drug that increases the arousal threshold by at least 25%, then the investigators could potentially abolish OSA (rather than just reduce its severity by 50%). This is of great interest given that the investigators already have shown than eszopiclone increases the arousal threshold by approximately 30% and is associated with an improvement in the AHI. However, to date there has been no study examining the combination of an agent that reduces loop gain (i.e. oxygen) with one that increases the arousal threshold (i.e. eszopiclone) as a treatment for OSA.
To determine the effect of combination therapy on each of the four traits and how they contribute to our model prediction of OSA, as well as on apnea severity. Specifically the investigators will assess:
- The physiological traits responsible for OSA:
- Pharyngeal anatomy and its propensity towards collapse
- The ability of the upper airway dilator muscles to activate and reopen the airway during sleep (i.e. neuromuscular compensation)
- Arousal threshold from sleep (i.e. the propensity for hypopneas/apneas to lead to arousal and fragmented sleep).
- Stability of the ventilatory control system feedback loop (i.e. loop gain)
- The severity of OSA (apnea-hypopnea index (AHI), percent of time with unstable breathing, sleep quality)
STUDY DESIGN:
A single-blinded randomized control design will be used. Initially, participants will be randomized to either the treatment or placebo arm where they will have both a clinical and research polysomnography (PSG); these initial PSGs constitute what will be referred to as VISIT 1 (see outcome measures). The purpose of the clinical PSG is to determine the severity of OSA (i.e. AHI). The research PSG will measure the 4 physiological OSA traits.
During the treatment arm, in both PSGs (i.e. clinical and research) participants will be given eszopiclone (3mg by mouth) to take before bed and be placed on oxygen throughout the night. During the placebo arm, subjects will be given a placebo to take before bed and placed on room air while they sleep. Participants will then have at least a 1-week washout period and cross over to the other arm of the study whereby the clinical and research PSG will be repeated; these studies constitute what will be referred to asVISIT 2 (see outcome measures).
- Conditions
- Sleep Apnea, Obstructive
- Being tested
- Placebo pill, Sedative, Room air, Oxygen
- 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.
Placebo pillDrug
Also called sugar pill
Subjects will receive a sugar pill (in combination with room air) during their placebo arm studies
SedativeDrug
Also called Lunesta
Subjects will receive eszopiclone (in combination with medical oxygen) during their treatment arm studies
Room airOther
Subjects will receive room air (in combination with a sugar pill) during their placebo arm studies
OxygenOther
Subjects will receive medical grade oxygen (in combination with eszopiclone) during their treatment arm studies
| Study group | Role | What they receive |
|---|---|---|
| Placebo | Placebo comparator | Subjects will receive both a sugar pill and room air during their overnight sleep studies Receives: Drug: Placebo pill; Other: Room air |
| Treatment | Active comparator | Subjects will receive both Lunesta (eszopiclone) and medical grade oxygen during their overnight sleep studies Receives: Drug: Sedative; Other: Oxygen |
What is being measured
The primary outcome is the main question the study is designed to answer.
Model Prediction of Absence/Presence of OSA: Ventilation That Causes an Arousal From Sleep (Varousal)
Our published method estimates 4 important physiological traits causing OSA: 1) pharyngeal anatomy, 2) loop gain, 3) the ability of the upper airway to dilate/stiffen in response to increases in ventilatory drive, and 4) arousal threshold. Each individual's set of traits is then entered into a physiological model of OSA that graphically illustrates the relative importance of each trait in that individual.
In this table the investigators report the minimum ventilation that can be tolerated before an arousal from sleep (Varousal). It is calculated by slowly reducing the CPAP level from optimum to the minimum tolerable pressure. This trait is symbolized as Varousal (L/min)
Measured: Subjects will be assessed on day 1 (visit 1) and up to 1 month (visit 2)
Model Prediction of Absence/Presence of OSA: Ventilatory Control Sensitivity (Loop Gain)
Our published method estimates 4 important physiological traits causing OSA: 1) pharyngeal anatomy, 2) loop gain, 3) the ability of the upper airway to dilate/stiffen in response to increases in ventilatory drive, and 4) arousal threshold. Each individual's set of traits is then entered into a physiological model of OSA that graphically illustrates the relative importance of each trait in that individual and predicts OSA presence/absence.
In this table the investigators report the ventilatory control sensitivity value (Loop Gain). It is calculated dividing the increase in ventilatory drive by the steady state reduction in ventilation. The increase in ventilatory drive is measured as the ventilatory overshoot following a switch to optimal CPAP from the minimum tolerable CPAP. This trait is symbolized as steady state loop gain (LG, adimensional)
Measured: Subjects will be assessed on day 1 (visit 1) and up to 1 month (visit 2)
Model Prediction of Absence/Presence of OSA: Passive Collapsibility
Our published method estimates 4 important physiological traits causing OSA: 1) pharyngeal anatomy, 2) loop gain, 3) the ability of the upper airway to dilate/stiffen in response to increases in ventilatory drive, and 4) arousal threshold. Each individual's set of traits is then entered into a physiological model of OSA that graphically illustrates the relative importance of each trait in that individual and predicts OSA presence/absence.
The passive collapsibility of the upper airway is quantified as the ventilation on no CPAP (atmospheric pressure) at the eupneic level of ventilatory drive when upper airway dilator muscles are relatively passive. This trait is symbolized as Vpassive (L/min)
Measured: Subjects will be assessed on day 1 (visit 1) and up to 1 month (visit 2)
Model Prediction of Absence/Presence of OSA: Active Collapsibility (Vactive)
Our published method estimates 4 important physiological traits causing OSA: 1) pharyngeal anatomy, 2) loop gain, 3) the ability of the upper airway to dilate/stiffen in response to increases in ventilatory drive, and 4) arousal threshold. Each individual's set of traits is then entered into a physiological model of OSA that graphically illustrates the relative importance of each trait in that individual and predicts OSA presence/absence.
Active collapsibility is the ventilation on no CPAP when upper airway muscle are maximally activated. It is calculated by slowing reducing CPAP from the optimal to the minimum tolerable level and rapidly dropping the CPAP to 0 for a few breaths. This trait is symbolized as Vactive (L/min)
Measured: Subjects will be assessed on day 1 (visit 1) and up to 1 month (visit 2)
Secondary outcomes (1)
Apnea-Hypopnea Index
The Apnea-Hypopnea Index (AHI) is an index of sleep apnea severity that encompasses the frequency of apneas (cessations in breathing) and hypopneas (reductions in airflow).
Measured: Subjects will be assessed on day 1 (visit 1) and up to 1 month (visit 2)
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted4 Jul 2012 (estimated)
- Study startAug 2012
- Primary completionDec 2014
- Study completionDec 2014
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Posted resultsParticipant flow, outcome measures and adverse events reported by the sponsor.
- Publications (2)Papers the sponsor has linked to this study.
- Other trials for Sleep Apnea, ObstructiveStudies of the same condition, open and under way.
- More trials run by Brigham and Women's HospitalThe 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
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Single blind
- Who is masked
- Participant
- Enrolment
- 22 participants (actual)
Sponsor and investigators
- Lead sponsor
- Brigham and Women's Hospital
- Sponsor type
- University, hospital or other
- Collaborators
- National Heart, Lung, and Blood Institute (NHLBI)
- Responsible party
- Principal investigator, David Andrew Wellman, Brigham and Women's Hospital
- Investigators
- David A Wellman, MD, Principal investigator, Brigham & Womens Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT01633827
- Sponsor's protocol ID
- BWH-2012P000956
- Other IDs
- 5R01HL102321-02
- Status last verified
- Jan 2017
- First submitted
- 25 Jun 2012
- Last updated
- 3 Mar 2017
- Results posted
- Yes, on ClinicalTrials.gov
- Data monitoring committee
- No
- Individual data sharing
- Undecided
Publications
Landry SA, Joosten SA, Sands SA, White DP, Malhotra A, Wellman A, Hamilton GS, Edwards BA. Response to a combination of oxygen and a hypnotic as treatment for obstructive sleep apnoea is predicted by a patient's therapeutic CPAP requirement. Respirology. 2017 Aug;22(6):1219-1224. doi: 10.1111/resp.13044. Epub 2017 Apr 13.
PubMed 28409851Edwards BA, Sands SA, Owens RL, Eckert DJ, Landry S, White DP, Malhotra A, Wellman A. The Combination of Supplemental Oxygen and a Hypnotic Markedly Improves Obstructive Sleep Apnea in Patients with a Mild to Moderate Upper Airway Collapsibility. Sleep. 2016 Nov 1;39(11):1973-1983. doi: 10.5665/sleep.6226.
PubMed 27634790
Study at a glance
From the registry record, last updated by the sponsor on 3 Mar 2017. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Combination Therapy for the Treatment of Obstructive Sleep Apnea
- ClinicalTrials.gov ID
- NCT01633827
- Acronym / sponsor ID
- BWH-2012P000956
- Conditions
- Sleep Apnea, Obstructive
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 22 participants (actual)
- Lead sponsor
- Brigham and Women's HospitalUniversity, hospital or other
- Collaborators
- National Heart, Lung, and Blood Institute (NHLBI)
- Study start
- Aug 2012
- Primary completion
- Dec 2014 (actual)
- Study completion
- Dec 2014 (actual)
- First posted
- 4 Jul 2012 (estimated)
- Results
- Posted 3 Mar 2017
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
In Obstructive sleep apnea (OSA), the upper airway closes over and over again during sleep. This leads to disrupted sleep (waking up during the night), daytime sleepiness, and an increased risk for developing high blood pressure. Currently, the best treatment for obstructive sleep apnea is sleeping with a mask that continuously blows air into the nose (i.e. Continuous positive airway pressure [CPAP] treatment). While CPAP treatment stops the upper airway from closing in most people, many people have difficulty sleeping with the mask in place and therefore do not use the CPAP treatment. This research study is being conducted to learn whether using a combination of therapies (i.e. a sedative and oxygen therapy) will improve OSA severity by altering some of the traits that are responsible for the disorder.
Detailed description
Obstructive sleep apnea (OSA) is characterized by repetitive collapse or 'obstruction' of the pharyngeal airway during sleep. These obstructions result in repetitive hypopneas/apneas and intermittent hypoxia/hypercapnia, as well as surges in sympathetic activity. Such processes disturb normal sleep and impair neurocognitive function, often resulting in excessive daytime sleepiness and decreased quality of life. Furthermore, OSA is associated with cardiovascular morbidity and mortality, making OSA a major health concern.
Current evidence suggests that OSA pathogenesis involves the interactions of at least four physiological traits comprising 1) the pharyngeal anatomy and its propensity towards collapse 2) the ability of the upper airway dilator muscles to activate and reopen the airway during sleep (i.e. neuromuscular compensation), 3) the arousal threshold from sleep (i.e. the propensity for hypopneas/apneas to lead to arousal and fragmented sleep) and 4) the stability of the ventilatory feedback loop (i.e. loop gain). Continuous positive airway pressure (CPAP) is the most common treatment for OSA but it is often poorly tolerated; only ~50% of patients diagnosed with OSA continue therapy beyond 3 months. Given this limitation, alternative approaches have been tested and have generally focused on the use of oral appliances, surgery, and more recently pharmacological agents.
However, these alternate therapies, when used alone as monotherapy, rarely abolish OSA completely. This is not that surprising given that these treatments focus primarily on correcting only one trait and ignore the fact that the pathogenesis of OSA is multi-factorial. Thus the investigators hypothesize that some patients could be treated without CPAP if more than one trait is targeted (i.e., the investigators take a multi-factorial treatment approach). Such a multi-factorial approach is not unusual in Medicine. Many disorders such as diabetes, asthma, hypertension, cancer and congestive heart failure are treated with more than one medication or modality. In our view, giving CPAP to all OSA patients is like treating every diabetic with insulin, or every asthmatic with oral steroids - these treatments, like CPAP, are poorly tolerated and ignore the complexity of the underlying biology.
The investigators recently published a technique that measures the four traits using repeated 'drops' in CPAP levels during sleep. Each trait is measured in a way that allows model-based predictions of the presence/absence of OSA. With this technique the investigators demonstrated in a small group of CPAP-treated OSA subjects that decreasing the sensitivity of the ventilatory feedback loop (i.e. reducing loop gain) by approximately 50% with either acetazolamide or oxygen reduces the apnea/hypopnea index (AHI) by half. Interestingly, our model allowed us to make the prediction that if, in addition to an agent that reduces loop gain, the investigators also gave a drug that increases the arousal threshold by at least 25%, then the investigators could potentially abolish OSA (rather than just reduce its severity by 50%). This is of great interest given that the investigators already have shown than eszopiclone increases the arousal threshold by approximately 30% and is associated with an improvement in the AHI. However, to date there has been no study examining the combination of an agent that reduces loop gain (i.e. oxygen) with one that increases the arousal threshold (i.e. eszopiclone) as a treatment for OSA.
To determine the effect of combination therapy on each of the four traits and how they contribute to our model prediction of OSA, as well as on apnea severity. Specifically the investigators will assess:
- The physiological traits responsible for OSA:
- Pharyngeal anatomy and its propensity towards collapse
- The ability of the upper airway dilator muscles to activate and reopen the airway during sleep (i.e. neuromuscular compensation)
- Arousal threshold from sleep (i.e. the propensity for hypopneas/apneas to lead to arousal and fragmented sleep).
- Stability of the ventilatory control system feedback loop (i.e. loop gain)
- The severity of OSA (apnea-hypopnea index (AHI), percent of time with unstable breathing, sleep quality)
STUDY DESIGN:
A single-blinded randomized control design will be used. Initially, participants will be randomized to either the treatment or placebo arm where they will have both a clinical and research polysomnography (PSG); these initial PSGs constitute what will be referred to as VISIT 1 (see outcome measures). The purpose of the clinical PSG is to determine the severity of OSA (i.e. AHI). The research PSG will measure the 4 physiological OSA traits.
During the treatment arm, in both PSGs (i.e. clinical and research) participants will be given eszopiclone (3mg by mouth) to take before bed and be placed on oxygen throughout the night. During the placebo arm, subjects will be given a placebo to take before bed and placed on room air while they sleep. Participants will then have at least a 1-week washout period and cross over to the other arm of the study whereby the clinical and research PSG will be repeated; these studies constitute what will be referred to asVISIT 2 (see outcome measures).
Study design
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Single blind (participant)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Placebo | Placebo comparator | Drug: Placebo pill, Other: Room airSubjects will receive both a sugar pill and room air during their overnight sleep studies |
| Treatment | Active comparator | Drug: Sedative, Other: OxygenSubjects will receive both Lunesta (eszopiclone) and medical grade oxygen during their overnight sleep studies |
Who may qualify
- Ages
- 18 to 79 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (3 listed)
- Ages 18 - 79 years
- Documented OSA (AHI > 10 events/hr Non rapid eye movement sleep supine)
- If treated then, current CPAP use (>4 hrs CPAP/night for > 2 months)
Key exclusion criteria (6 listed)
- Any uncontrolled medical condition
- Any other sleep disorder (Periodic leg movement syndrome, restless legs syndrome, insomnia, etc.)
- Use of medications known to affect sleep/arousal, breathing, or muscle physiology
- Allergy to lidocaine or Afrin
- Claustrophobia
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 |
|---|---|---|
| Placebo pillAlso: sugar pillSubjects will receive a sugar pill (in combination with room air) during their placebo arm studies | Drug | Placebo |
| SedativeAlso: LunestaSubjects will receive eszopiclone (in combination with medical oxygen) during their treatment arm studies | Drug | Treatment |
| Room airSubjects will receive room air (in combination with a sugar pill) during their placebo arm studies | Other | Placebo |
| OxygenSubjects will receive medical grade oxygen (in combination with eszopiclone) during their treatment arm studies | Other | Treatment |
Primary outcome
Model Prediction of Absence/Presence of OSA: Ventilation That Causes an Arousal From Sleep (Varousal)
Time frame: Subjects will be assessed on day 1 (visit 1) and up to 1 month (visit 2)
Our published method estimates 4 important physiological traits causing OSA: 1) pharyngeal anatomy, 2) loop gain, 3) the ability of the upper airway to dilate/stiffen in response to increases in ventilatory drive, and 4) arousal threshold. Each individual's set of traits is then entered into a physiological model of OSA that graphically illustrates the relative importance of each trait in that individual. In this table the investigators report the minimum ventilation that can be tolerated before an arousal from sleep (Varousal). It is calculated by slowly reducing the CPAP level from optimum to the minimum tolerable pressure. This trait is symbolized as Varousal (L/min)
Model Prediction of Absence/Presence of OSA: Ventilatory Control Sensitivity (Loop Gain)
Time frame: Subjects will be assessed on day 1 (visit 1) and up to 1 month (visit 2)
Our published method estimates 4 important physiological traits causing OSA: 1) pharyngeal anatomy, 2) loop gain, 3) the ability of the upper airway to dilate/stiffen in response to increases in ventilatory drive, and 4) arousal threshold. Each individual's set of traits is then entered into a physiological model of OSA that graphically illustrates the relative importance of each trait in that individual and predicts OSA presence/absence. In this table the investigators report the ventilatory control sensitivity value (Loop Gain). It is calculated dividing the increase in ventilatory drive by the steady state reduction in ventilation. The increase in ventilatory drive is measured as the ventilatory overshoot following a switch to optimal CPAP from the minimum tolerable CPAP. This trait is symbolized as steady state loop gain (LG, adimensional)
Model Prediction of Absence/Presence of OSA: Passive Collapsibility
Time frame: Subjects will be assessed on day 1 (visit 1) and up to 1 month (visit 2)
Our published method estimates 4 important physiological traits causing OSA: 1) pharyngeal anatomy, 2) loop gain, 3) the ability of the upper airway to dilate/stiffen in response to increases in ventilatory drive, and 4) arousal threshold. Each individual's set of traits is then entered into a physiological model of OSA that graphically illustrates the relative importance of each trait in that individual and predicts OSA presence/absence. The passive collapsibility of the upper airway is quantified as the ventilation on no CPAP (atmospheric pressure) at the eupneic level of ventilatory drive when upper airway dilator muscles are relatively passive. This trait is symbolized as Vpassive (L/min)
Model Prediction of Absence/Presence of OSA: Active Collapsibility (Vactive)
Time frame: Subjects will be assessed on day 1 (visit 1) and up to 1 month (visit 2)
Our published method estimates 4 important physiological traits causing OSA: 1) pharyngeal anatomy, 2) loop gain, 3) the ability of the upper airway to dilate/stiffen in response to increases in ventilatory drive, and 4) arousal threshold. Each individual's set of traits is then entered into a physiological model of OSA that graphically illustrates the relative importance of each trait in that individual and predicts OSA presence/absence. Active collapsibility is the ventilation on no CPAP when upper airway muscle are maximally activated. It is calculated by slowing reducing CPAP from the optimal to the minimum tolerable level and rapidly dropping the CPAP to 0 for a few breaths. This trait is symbolized as Vactive (L/min)
1 secondary outcome
Apnea-Hypopnea Index
Time frame: Subjects will be assessed on day 1 (visit 1) and up to 1 month (visit 2)
Results and safety
Loading the posted results from ClinicalTrials.gov…
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 3 Mar 2017.
- Posted resultsParticipant flow, baseline, all outcome measures and adverse events.
- Derived from this study: PubMed 28409851Landry SA, Joosten SA, Sands SA, White DP, Malhotra A, Wellman A, Hamilton GS, Edwards BA. Response to a combination of oxygen and a hypnotic as treatment for obstructive sleep apnoea is predicted by a patient's therapeutic CPAP requirement. Respirology. 2017 Aug;22(6):1219-1224. doi: 10.1111/resp.13044. Epub 2017 Apr 13.
- Derived from this study: PubMed 27634790Edwards BA, Sands SA, Owens RL, Eckert DJ, Landry S, White DP, Malhotra A, Wellman A. The Combination of Supplemental Oxygen and a Hypnotic Markedly Improves Obstructive Sleep Apnea in Patients with a Mild to Moderate Upper Airway Collapsibility. Sleep. 2016 Nov 1;39(11):1973-1983. doi: 10.5665/sleep.6226.
- Individual participant dataSharing planned: Undecided
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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.
David A Wellman, MD principal investigator
Brigham & Womens Hospital
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Sedative, Room air and Oxygen in people with Sleep Apnea, Obstructive, run by Brigham and Women's Hospital at 1 site in United States.
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 6 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 3 Mar 2017. 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 United States. 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. Some participants in this study may receive a placebo. 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?
Yes. Results are posted in the registry (first posted 3 Mar 2017). A summary is in the For doctors view, and the full results are on ClinicalTrials.gov.
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?
Model Prediction of Absence/Presence of OSA: Ventilation That Causes an Arousal From Sleep (Varousal) (time frame: Subjects will be assessed on day 1 (visit 1) and up to 1 month (visit 2)). The study lists 4 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 NCT01633827, which also lists 2 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 3 Mar 2017.