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NCT Number: NCT04720547

Sleep and Breathing in the General Population - Chemical Stimuli

Central sleep apnea (CSA) is a common condition and its treatment remains elusive. The focus of this proposal is to identify the role of the physiologic path involving cortical arousals in CSA by decreasing arousal frequency using the pharmacological agent zolpidem. The goal is to identify the acute effects of administering zolpidem on sleep and respiratory outcomes, and subsequently, its effect on the severity of CSA and propensity to develop CSA. This study will shed light on the mechanisms underlying CSA that involve cortical arousals and will guide future therapeutic interventions for CSA.

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Key information

Conditions

Sleep-Disordered Breathing Apnea Dyssomnias Nervous System Diseases Respiration Disorders Respiratory Tract Diseases Sleep Apnea Syndromes Sleep Apnea, Central Sleep Disorders, Intrinsic Sleep Wake Disorders

Age range

18 year–89 year

Sex eligibility

All sexes

Study type

Interventional

Phase

Phase 4

Primary location

John D. Dingell VA Medical Center

Detroit, Michigan, 48201, United States

About this study

The literature suggests that zolpidem may be effective in the treatment of central sleep apnea (CSA). However, evidence regarding the efficacy of zolpidem and the underlying mechanisms involved in its effect on CSA are not well-studied. Furthermore, respiratory-related arousals are hypothesized to contribute CSA symptoms and severity. The aim of the study is to determine the effect of decreasing respiratory-related arousals on the propensity to develop central apnea. The investigators hypothesize that administration of the nonbenzodiazepine hypnotic zolpidem will decrease the frequency of respiratory-related arousals, lower the central apnea-hypopnea index, and widen the CO2 reserve during sleep in patients with CSA compared to no treatment. Participants will complete a night study on a low dose of zolpidem and another night study without zolpidem in a crossover manner. The order of night studies is randomized. The results will help unveil the role of arousals in CSA and the acute effect of zolpidem on CSA severity and the propensity to CSA.

Who can participate

Healthy volunteers accepted: Yes

Only the study team can determine whether someone qualifies for participation.

Inclusion criteria

  • Men and women Veterans with central sleep apnea, defined as Apnea Hypopnea Index (AHI)>15/hour with CAHI>5/hour, will be included in the experiments.

Exclusion criteria

  • less than 18 years old
  • pregnant or breastfeeding female
  • have severe respiratory disease that require to be on oxygen
  • recent health event that may affect the ability to participate in the study,
  • Body Mass Index (BMI) is >40 kg/m2
  • significant insomnia
  • mental instability
  • recent health event that may affect sleep
  • if at any time the principal investigator (PI) identifies that a certain drug is not suitable, or are unable to use the device that is used to treat sleep apnea, will be not be allowed to participate in the study

Treatment and study plan

zolpidem

Drug

A nonbenzodiazepine hypnotic

Other names: Ambien

No treatment

Other

The Control condition in which participants do not receive medication.

Primary outcomes

  1. The Central Apnea-hypopnea Index

    Time frame: one night

    The number of central apneas and hypopneas per hour of sleep was obtained from polysomnography studies.

  2. Respiratory Arousal Index

    Time frame: one night

    A measure of the frequency of respiratory-related arousals during sleep

Secondary outcomes

  1. CO2 Reserve

    Time frame: one night

    CO2 reserve is the requisite change to induce central apnea is referred to as the CO2 reserve, which can be positive or negative. CO2 reserve is defined as the difference between the eupneic end-tidal CO2 pressure and the end-tidal CO2 pressure induced by the ventilation protocol that is sufficient to trigger a central apnea as defined by the American Academy of Sleep Medicine.

  2. Controller Gain

    Time frame: one night

    Controller gain is a ventilatory response to changes in end-tidal PCO2. Controller gain was calculated by dividing the difference in minute ventilation between the post-mechanical ventilation induced by the ventilation protocol and steady-state respiration by the difference in the end-tidal CO2 pressure between the mechanical ventilation and steady-state respiration.

  3. Stead-State Plant Gain (mmHg

    Time frame: one night

    Plant gain is a blood gas response to a change in ventilation. This measure represents the effectiveness of the "plant" in eliminating CO2. Steady-state plant gain was calculated from the ratio of end-tidal CO2 to minute ventilation during stable respiration.

  4. Respiratory Arousal Threshold

    Time frame: one night

    The nadir pressure in the upper airway (supra-glottic pressure) prior to the occurrence of an arousal

Sponsors and collaborators

Lead sponsor

Wayne State University

Other

Collaborators

  • National Heart, Lung, and Blood Institute (NHLBI)
  • National Institutes of Health (NIH)

Registry information

Official study title

Sleep and Breathing in Health and Disease (Part 2A - Chemical Stimuli, Sleep and Breathing in the General Population)

Important dates

Study start
2018
Primary completion
2020
Study completion
2020
First posted
Jan 22, 2021
Registry last updated
Dec 6, 2023

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

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