Why Sleep Matters in COPD: Cluster-Derived Sleep Phenotypes Reveal Distinct Physiological, Comorbidity and Survival Profiles.
6 affiliations
- 1Centre for Sleep Research, Department of Internal Medicine and Clinical Nutrition, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
- 2Department of Respiratory Medicine and Allergology, Sahlgrenska University Hospital, Gothenburg, Sweden.
- 3Department of Public Health and Clinical Medicine, The OLIN and Sunderby Research Unit, Umeå University, Umeå, Sweden.
- 4Krefting Research Centre, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
- 5COPD centre, Sahlgrenska University Hospital and Institute of Medicine, University of Gothenburg, Gothenburg, Sweden.
- 6Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.
Abstract
Background
Sleep disturbances are highly prevalent in chronic obstructive pulmonary disease (COPD) but are not incorporated into current phenotypic classifications. We examined whether multidimensional sleep data identify clinically relevant patterns in COPD and whether these patterns are associated with all-cause mortality.Methods
In a clinical cohort of 205 patients with COPD, home-based sleep assessment was performed using the WatchPAT™ device. Fifteen complementary variables reflecting sleep duration and architecture, nocturnal oxygenation, sleep-disordered breathing, and daytime sleepiness were analysed using Partitioning Around Medoids clustering. The resulting phenotypes were characterised by pulmonary function, gas exchange, functional capacity, systemic biomarkers, and comorbidity burden. Longitudinal follow-up was available for 199 participants; survival was assessed using Kaplan-Meier analysis and Cox regression adjusted for age, sex, post-bronchodilator FEV₁ and positive airway pressure (PAP) treatment.Results
Five distinct sleep phenotypes were identified: preserved sleep physiology (good sleepers, 20.5%), curtailed sleep duration (short sleepers, 33%), altered sleep architecture with REM suppression (light sleepers, 18.5%), predominant nocturnal hypoxaemia (hypoxic sleepers, 20%), and severe sleep-disordered breathing (apnoeic sleepers, 8%). Despite similar airflow limitation and COPD symptom burden, phenotypes differed in gas exchange, functional capacity, systemic inflammation, and cardiometabolic comorbidities. During a median follow-up of 4.2 years, 56 participants (28.1%) died. Compared with good sleepers, hypoxic sleepers had a higher hazard of death after adjustment for age, sex, and FEV₁ (HR 2.80, 95% CI 1.05-7.44). Following adjustment for PAP treatment, a higher mortality hazard was also observed among untreated apnoeic sleepers (HR 6.16, 95% CI 1.56-24.38).Conclusion
Multidimensional sleep phenotyping identified clinically distinct clusters of patients with COPD beyond conventional spirometric severity and apnoea-hypopnoea index (AHI)-defined sleep-disordered breathing. These findings support sleep as a clinically relevant dimension of COPD heterogeneity, and warrant prospective validation of sleep-related traits and their clinical outcomes.
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BibTeX
@article{hansson2026sleep,
title = {{Why Sleep Matters in COPD: Cluster-Derived Sleep Phenotypes Reveal Distinct Physiological, Comorbidity and Survival Profiles.}},
author = {Daniel Hansson and Daniil Lisik and Anders Andersson and Ding Zou and Jan Hedner and Lowie E G W Vanfleteren and Ludger Grote},
journal = {International journal of chronic obstructive pulmonary disease},
year = {2026},
month = oct,
doi = {10.2147/copd.s608140},
url = {https://europepmc.org/article/MED/42903829},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Why Sleep Matters in COPD: Cluster-Derived Sleep Phenotypes Reveal Distinct Physiological, Comorbidity and Survival Profiles.
AU - Daniel Hansson
AU - Daniil Lisik
AU - Anders Andersson
AU - Ding Zou
AU - Jan Hedner
AU - Lowie E G W Vanfleteren
AU - Ludger Grote
PY - 2026
DA - 2026/10/16
JO - International journal of chronic obstructive pulmonary disease
DO - 10.2147/copd.s608140
UR - https://europepmc.org/article/MED/42903829
AB - Background Sleep disturbances are highly prevalent in chronic obstructive pulmonary disease (COPD) but are not incorporated into current phenotypic classifications. We examined whether multidimensional sleep data identify clinically relevant patterns in COPD and whether these patterns are associated with all-cause mortality.Methods In a clinical cohort of 205 patients with COPD, home-based sleep assessment was performed using the WatchPAT™ device. Fifteen complementary variables reflecting sleep duration and architecture, nocturnal oxygenation, sleep-disordered breathing, and daytime sleepiness were analysed using Partitioning Around Medoids clustering. The resulting phenotypes were characterised by pulmonary function, gas exchange, functional capacity, systemic biomarkers, and comorbidity burden. Longitudinal follow-up was available for 199 participants; survival was assessed using Kaplan-Meier analysis and Cox regression adjusted for age, sex, post-bronchodilator FEV₁ and positive airway pressure (PAP) treatment.Results Five distinct sleep phenotypes were identified: preserved sleep physiology (good sleepers, 20.5%), curtailed sleep duration (short sleepers, 33%), altered sleep architecture with REM suppression (light sleepers, 18.5%), predominant nocturnal hypoxaemia (hypoxic sleepers, 20%), and severe sleep-disordered breathing (apnoeic sleepers, 8%). Despite similar airflow limitation and COPD symptom burden, phenotypes differed in gas exchange, functional capacity, systemic inflammation, and cardiometabolic comorbidities. During a median follow-up of 4.2 years, 56 participants (28.1%) died. Compared with good sleepers, hypoxic sleepers had a higher hazard of death after adjustment for age, sex, and FEV₁ (HR 2.80, 95% CI 1.05-7.44). Following adjustment for PAP treatment, a higher mortality hazard was also observed among untreated apnoeic sleepers (HR 6.16, 95% CI 1.56-24.38).Conclusion Multidimensional sleep phenotyping identified clinically distinct clusters of patients with COPD beyond conventional spirometric severity and apnoea-hypopnoea index (AHI)-defined sleep-disordered breathing. These findings support sleep as a clinically relevant dimension of COPD heterogeneity, and warrant prospective validation of sleep-related traits and their clinical outcomes.
SN - 1176-9106
SN - 1178-2005
ER -