Estimating Apnea Phenotypes From Polysomnography: Oxygen

Sleep Apnea Clinical Trial

— PSGtraits-O2  

Official title:

Estimating Apnea Phenotypes From Routine Polysomnography: Application to Oxygen Therapy

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT01751971
• Other study ID #: 2005P001296-O2PSG
• Secondary ID: R01HL090897
• Status: Completed
• Phase: N/A
• First received: December 12, 2012
• Last updated: March 19, 2018
• Start date: November 2012
• Est. completion date: July 2016

Study information

• Verified date: March 2018
• Source: Brigham and Women's Hospital
• Contact: n/a
• Is FDA regulated: No
• Study type: Interventional

Clinical Trial Summary

This study seeks to employ advanced methods to estimate the individual factors contributing to sleep apnea from standard recordings made during routine clinical sleep studies. This study focuses on breathing control or "loop gain" as one of the factors contributing to sleep apnea. Increased levels of oxygen in the air is known to make breathing more stable by lowering "loop gain". Here, our goal is to use a new method capable of detecting a reduction in loop gain with oxygen. The investigators also aim to test whether a high loop gain measured at baseline/placebo predicts a greater improvement in sleep apnea with oxygen therapy.

Description:

In a single-blinded randomized crossover study, inspired oxygen/air (40%/21%) is delivered on two separate nights. Loop gain is measured from routine polysomnography using a novel mathematical method. A value of loop gain >1 reflects unstable breathing, and a value less than but approaching 1 denotes a system more prone to oscillate. Loop gain is measured as the changes in ventilatory drive/effort that arises subsequent to changes in ventilation (e.g. due to obstructive apnea). A simple chemoreflex model (gain, time constant, delay) is fit to surrogate ventilation data (derived from airflow) during sleep. The best model is one that best matches the elevated ventilatory drive (measured as ventilation in the absence of airflow obstruction) based on the prior apneic/hypopneic fall in ventilation. Loop gain is calculated from this model. We aim to use loop gain measured on and off oxygen to determine whether a strong response (reduction in apnea severity) can be predicted by a higher loop gain (in the sham arm) using our method. We also assessed whether assessing upper airway anatomy/collapsibility, dilator muscle responsiveness, and the arousal threshold helped to predict responses to treatment.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 47
• Est. completion date: July 2016
• Est. primary completion date: July 2016
• Accepts healthy volunteers: No
• Gender: All
• Age group: 20 Years to 79 Years

Eligibility

Inclusion Criteria:

• Apnea/hypopnea index >20 events per hour

• Age 20-79 years

Exclusion Criteria:

• COPD with desaturation (resting SpO2<96%)

• Use of respiratory stimulants or depressants

• Pregnancy

Related Conditions & MeSH terms

• Apnea
• Sleep Apnea

Intervention

Drug:
• Inspired oxygen (40%)
Supplemental oxygen at 40% inspired via venturi mask (15 L/min). Equivalent to 5 L/min via nasal cannula.

Other:
• Sham
Medical air with 21% oxygen via venturi mask (15 L/min).

Locations

Country	Name	City	State
United States	Brigham and Women's Hospital	Boston	Massachusetts

Sponsors (3)

Lead Sponsor	Collaborator
Brigham and Women's Hospital	American Heart Association, National Heart, Lung, and Blood Institute (NHLBI)

Country where clinical trial is conducted

United States, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Apnea-hypopnea Index	Apnea-hypopnea index (AHI) will be compared between oxygen and sham nights. Hypopneas are based on 30% reduction in airflow (no desaturation or arousal criteria). AHI data are exclusive to non-REM supine sleep.; The results presented here are for the AHI at each intervention ("per intervention") regardless of the sequence (preferred clinicaltrials.gov format).; Please note, however, that the a priori outcome measure was the reduction in AHI with oxygen as a percent of sham values, i.e. (AHI on sham - AHI on oxygen)/(AHI on sham) % (a comparison with greater statistical power), compared between patient subgroups (see Statistical Analysis section).; Subgroups were defined a priori as higher (>=0.7) versus lower loop gain (<0.7), but tests were also performed in subgroups defined by "favorable" versus "unfavorable" pathophysiology.	1 night
Secondary	Frequency of EEG Arousals (Events Per Hour)	Frequency of scored EEG arousals per hour of non-REM sleep. Note: Our objective was to describe changes in secondary outcomes within phenotypic subgroups. Overall effects (unselected patients / ignoring phenotypic subgroups) are first presented below, followed by effects in favorable vs. unfavorable subgroups.	1 night
Secondary	Overnight Change in Systolic Blood Pressure	The change in systolic blood pressure overnight. Two supine oscillometric measurements of blood pressure are made: just prior to lights out (evening), and after lights on (morning).	1 night
Secondary	Overnight Change in Diastolic Blood Pressure	The change in diastolic blood pressure overnight. Two supine oscillometric measurements of blood pressure are made: just prior to lights out (evening), and after lights on (morning).	1 night
Secondary	Subjective Sleep Quality (Oxygen vs Sham)	Better(+1)/Same(0)/Worse(-1) on oxygen vs sham, i.e. "a relative comparison between arms". When subjects had completed the entire study, they were asked to compare subjectively their sleep quality on the first versus second study.	1 night
Secondary	Subjective Sleepiness/Alertness (Stanford Sleepiness Scale)	Assessed in the morning after the single night of treatment. Minimum score: 1 (alert), maximum score: 7 (not alert).	1 night