Evidence map›Paper›PMID 29327943›Full record

ArticleAmerican journal of respiratory and critical care medicine2018

Phenotyping Pharyngeal Pathophysiology using Polysomnography in Patients with Obstructive Sleep Apnea.

Scott A Sands, Bradley A Edwards, Philip I Terrill, Luigi Taranto-Montemurro, Ali Azarbarzin, Melania Marques, Lauren B Hess, David P White, Andrew Wellman

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07577661 (Combination Upper-Airway Electrical and Pharmacological Stimulation for Obstructive Sleep Apnea), which is not on this map. Cited by 155 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
155citing papers in PubMed, 1 pooled it
12.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT07577661 phase1 / phase2not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Combination Upper-Airway Electrical and Pharmacological Stimulation for Obstructive Sleep Apnea: A Randomized-Controlled Trial.

TypeinterventionalSponsorBrigham and Women's HospitalRan2026 to 2027Enrolled24ConditionsObstructive Sleep Apnea, Sleep-disordered BreathingArmsCombination device and drug: Unilateral hypoglossal nerve stimulation & atomoxetine-plus-oxybutynin (HGNS+AtoOxy), Unilateral hypoglossal nerve stimulation (HGNS), active comparator condition, Atomoxetine-plus-oxybutynin (80/5 mg) (AtoOxy), active comparator condition, Placebo, placebo comparator condition
3 · Its place in the literature

Who cites it

155 citing papers in PubMed, 1 synthesis or guideline pooled it, 260 citations in OpenAlex.

  1. Effect of norepinephrine reuptake inhibitors combined with antimuscarinic agents vs monotherapy for OSA: a systematic review and meta-analysis.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2024
    Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Trial
  6. Trial
  7. Cognitive behavioral therapy for insomnia is associated with reduced sleep apnea severity but not its endotype traits in those with comorbid insomnia and sleep apnea.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2025
    Trial
  8. Trial
  9. Trial
  10. Trial
  11. The norepinephrine reuptake inhibitor reboxetine alone reduces obstructive sleep apnea severity: a double-blind, placebo-controlled, randomized crossover trial.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2023
    Trial
  12. Trial
  13. Trial
  14. Trial
  15. Trial
  16. Trial
  17. Trial
  18. Trial
  19. Trial
  20. A randomized controlled trial of oxygen therapy for patients who do not respond to upper airway surgery for obstructive sleep apnea.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2021
    Trial

95 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 6 countries.

Scott A Sands1 Division of Sleep and Circadian Disorders, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.ORCID 0000-0003-3752-0328
Bradley A Edwards1 Division of Sleep and Circadian Disorders, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
Philip I Terrill6 School of Information Technology and Electrical Engineering, University of Queensland, Brisbane, Queensland, Australia; and.
Luigi Taranto-Montemurro1 Division of Sleep and Circadian Disorders, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
Ali Azarbarzin1 Division of Sleep and Circadian Disorders, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
Melania Marques1 Division of Sleep and Circadian Disorders, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
Lauren B Hess1 Division of Sleep and Circadian Disorders, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
David P White1 Division of Sleep and Circadian Disorders, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
Andrew Wellman1 Division of Sleep and Circadian Disorders, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts.
Brigham and Women's Hospital · USQueensland University of Technology · AU

Funding

Harvard Clinical and Translational Science CenterUL1TR001102 · NCATS · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2013 to 2017
$106.2M
Wakefulness and Forebrain Activation by Orexin NeuronsP01HL095491 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WELLMAN, DAVID ANDREW · 2010 to 2019
$25.1M
Understanding the relationship between obesity and tongue fat in humans and ratsP01HL094307 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI PACK, ALLAN I · 2009 to 2020
$23.7M
Validation of a Phenotype Model to Predict Response to Alternative OSA TreatmentsR01HL102321 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI WELLMAN, DAVID ANDREW · 2011 to 2025
$7.3M
Determination of the site of pharyngeal collapse in Obstructive Sleep Apnea patients from snoring soundsR01HL128658 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI WELLMAN, DAVID ANDREW · 2016 to 2025
$4.3M
NCATS NIH HHS UL1 TR001102NHLBI NIH HHS P01 HL094307NHLBI NIH HHS P01 HL095491NHLBI NIH HHS R01 HL102321NHLBI NIH HHS R01 HL128658
6 · The paper itself

Abstract

rationaleTherapies for obstructive sleep apnea (OSA) could be administered on the basis of a patient's own phenotypic causes ("traits") if a clinically applicable approach were available.

objectivesHere we aimed to provide a means to quantify two key contributors to OSA-pharyngeal collapsibility and compensatory muscle responsiveness-that is applicable to diagnostic polysomnography.

methodsBased on physiological definitions, pharyngeal collapsibility determines the ventilation at normal (eupneic) ventilatory drive during sleep, and pharyngeal compensation determines the rise in ventilation accompanying a rising ventilatory drive. Thus, measuring ventilation and ventilatory drive (e.g., during spontaneous cyclic events) should reveal a patient's phenotypic traits without specialized intervention. We demonstrate this concept in patients with OSA (N = 29), using a novel automated noninvasive method to estimate ventilatory drive (polysomnographic method) and using "gold standard" ventilatory drive (intraesophageal diaphragm EMG) for comparison. Specialized physiological measurements using continuous positive airway pressure manipulation were employed for further comparison. The validity of nasal pressure as a ventilation surrogate was also tested (N = 11). MEASUREMENTS AND MAIN

resultsPolysomnography-derived collapsibility and compensation estimates correlated favorably with those quantified using gold standard ventilatory drive (R = 0.83, P < 0.0001; and R = 0.76, P < 0.0001; respectively) and using continuous positive airway pressure manipulation (R = 0.67, P < 0.0001; and R = 0.64, P < 0.001; respectively). Polysomnographic estimates effectively stratified patients into high versus low subgroups (accuracy, 69-86% vs. ventilatory drive measures; P < 0.05). Traits were near-identical using nasal pressure versus pneumotach (N = 11, R ≥ 0.98, both traits; P < 0.001).

conclusionsPhenotypes of pharyngeal dysfunction in OSA are evident from spontaneous changes in ventilation and ventilatory drive during sleep, enabling noninvasive phenotyping in the clinic. Our approach may facilitate precision therapeutic interventions for OSA.

Indexed as

AdultFemaleHumansMaleMiddle AgedPharyngeal DiseasesPhenotypePolysomnographySleep Apnea, Obstructiveendotypepathophysiologypersonalized medicine

Identifiers

PMID29327943
PMCPMC6019932
OpenAlexW2783783250

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.