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Combination Therapy to Treat Sleep Apnea

This study has been completed.
Sponsor:
Collaborator:
National Heart, Lung, and Blood Institute (NHLBI)
Information provided by (Responsible Party):
David Andrew Wellman, Brigham and Women's Hospital
ClinicalTrials.gov Identifier:
NCT01633827
First received: June 25, 2012
Last updated: January 11, 2017
Last verified: January 2017
  Purpose
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.

Condition Intervention
Sleep Apnea, Obstructive Drug: Placebo pill Drug: Sedative Other: Room air Other: Oxygen

Study Type: Interventional
Study Design: Allocation: Randomized
Intervention Model: Crossover Assignment
Masking: Single Blind (Participant)
Primary Purpose: Basic Science
Official Title: Combination Therapy for the Treatment of Obstructive Sleep Apnea

Resource links provided by NLM:


Further study details as provided by David Andrew Wellman, Brigham and Women's Hospital:

Primary Outcome Measures:
  • 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)



Secondary Outcome Measures:
  • Apnea-Hypopnea Index [ Time Frame: Subjects will be assessed on day 1 (visit 1) and up to 1 month (visit 2) ]
    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).


Enrollment: 22
Study Start Date: August 2012
Study Completion Date: December 2014
Primary Completion Date: December 2014 (Final data collection date for primary outcome measure)
Arms Assigned Interventions
Placebo Comparator: Placebo
Subjects will receive both a sugar pill and room air during their overnight sleep studies
Drug: Placebo pill
Subjects will receive a sugar pill (in combination with room air) during their placebo arm studies
Other Name: sugar pill
Other: Room air
Subjects will receive room air (in combination with a sugar pill) during their placebo arm studies
Active Comparator: Treatment
Subjects will receive both Lunesta (eszopiclone) and medical grade oxygen during their overnight sleep studies
Drug: Sedative
Subjects will receive eszopiclone (in combination with medical oxygen) during their treatment arm studies
Other Name: Lunesta
Other: Oxygen
Subjects will receive medical grade oxygen (in combination with eszopiclone) during their treatment arm studies

  Show Detailed Description

  Eligibility

Ages Eligible for Study:   18 Years to 79 Years   (Adult, Senior)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Criteria

Inclusion Criteria:

  • 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)

Exclusion Criteria:

  • 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
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT01633827

Locations
United States, Massachusetts
Brigham and Women's Hospital
Boston, Massachusetts, United States, 02115
Sponsors and Collaborators
Brigham and Women's Hospital
National Heart, Lung, and Blood Institute (NHLBI)
Investigators
Principal Investigator: David A Wellman, MD Brigham & Womens Hospital
  More Information

Publications automatically indexed to this study by ClinicalTrials.gov Identifier (NCT Number):
Responsible Party: David Andrew Wellman, Principal Investigator, Brigham and Women's Hospital
ClinicalTrials.gov Identifier: NCT01633827     History of Changes
Other Study ID Numbers: BWH-2012P000956
5R01HL102321-02 ( U.S. NIH Grant/Contract )
Study First Received: June 25, 2012
Results First Received: January 13, 2016
Last Updated: January 11, 2017
Individual Participant Data (IPD) Sharing Statement:
Plan to Share IPD: Undecided

Additional relevant MeSH terms:
Apnea
Sleep Apnea Syndromes
Sleep Apnea, Obstructive
Respiration Disorders
Respiratory Tract Diseases
Signs and Symptoms, Respiratory
Signs and Symptoms
Sleep Disorders, Intrinsic
Dyssomnias
Sleep Wake Disorders
Nervous System Diseases
Hypnotics and Sedatives
Eszopiclone
Central Nervous System Depressants
Physiological Effects of Drugs

ClinicalTrials.gov processed this record on July 24, 2017