Annals of the American Thoracic Society · 2026
Comorbid Insomnia and Sleep Apnea Is Associated with Uncontrolled Hypertension in a Middle-aged Population.
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Kobayashi Frisk Mio, Bergqvist Joel, Svedmyr Sven, Diamantis Philippe, Bergström Göran, Zou Ding
Аннотация
RATIONALE: Comorbid insomnia and sleep apnea (COMISA) has been linked to poorer health outcomes and increased allcause mortality compared with either insomnia or obstructive sleep apnea (OSA) alone.
OBJECTIVE: We investigated the relationship between COMISA and uncontrolled hypertension in SCAPIS (Swedish CardioPulmonary BioImage Study).
METHODS: A cross-sectional analysis including participants from the SCAPIS Gothenburg cohort (n = 3,832; 46% males; aged 57.564.3 yr; body mass index, 26.664.3 kg/m2) was performed. Subjects underwent a comprehensive examination, including functional tests and a home polygraph sleep recording. COMISA was defined as an apnea-hypopnea index (AHI) >10 events/h and an Insomnia Severity Index score ⩾15. Blood pressure (BP) status was characterized as uncontrolled hypertension (office systolic BP ⩾140 mm Hg or diastolic BP ⩾90 mm Hg), controlled hypertension (antihypertensive medication-treated hypertension with systolic/diastolic BP <140/90 mm Hg) or normotension with systolic/diastolic BP <140/90 mm Hg.
RESULTS: The prevalence of COMISA was 3.1% in the population and 14.5% among patients with OSA (AHI, >10 events/h). AHI was comparable between patients with OSA only and patients with COMISA (18 ± 9 vs. 19 ± 9 events/h; P = 0.86). Uncontrolled hypertension was found in 4.4%, 4.5%, 7.9%, and 10.2% of the control group, insomnia-only, OSA-only, and COMISA groups, respectively (P < 0.001). Compared with the control group, the risk of uncontrolled hypertension was significantly increased in the OSA-only group (odds ratio [95% confidence interval], 1.31 [1.05-1.64]; P = 0.02) and the COMISA group (1.88 [1.23-2.89]; P = 0.004) after controlling for anthropometrics, lifestyle, comorbidities, Epworth Sleepiness Scale score, and nocturnal hypoxic exposure (T90 [percentage recording time with oxygen saturation ⩽90%]). T90 was found to be a significant mediator of uncontrolled hypertension in the relationship between both OSA and COMISA.
CONCLUSIONS: This study is the first to demonstrate an independent association between COMISA and uncontrolled hypertension in the general population. These findings provide novel insights for identifying subgroups of patients with OSA at risk of adverse cardiovascular consequences. Furthermore, our results underscore the importance of recognizing sleep health as a multidimensional construct and advocate for personalized treatment strategies to effectively combat the burden of this common sleep disorder. (See the data supplement for graphical abstract and summary of key findings).
OBJECTIVE: We investigated the relationship between COMISA and uncontrolled hypertension in SCAPIS (Swedish CardioPulmonary BioImage Study).
METHODS: A cross-sectional analysis including participants from the SCAPIS Gothenburg cohort (n = 3,832; 46% males; aged 57.564.3 yr; body mass index, 26.664.3 kg/m2) was performed. Subjects underwent a comprehensive examination, including functional tests and a home polygraph sleep recording. COMISA was defined as an apnea-hypopnea index (AHI) >10 events/h and an Insomnia Severity Index score ⩾15. Blood pressure (BP) status was characterized as uncontrolled hypertension (office systolic BP ⩾140 mm Hg or diastolic BP ⩾90 mm Hg), controlled hypertension (antihypertensive medication-treated hypertension with systolic/diastolic BP <140/90 mm Hg) or normotension with systolic/diastolic BP <140/90 mm Hg.
RESULTS: The prevalence of COMISA was 3.1% in the population and 14.5% among patients with OSA (AHI, >10 events/h). AHI was comparable between patients with OSA only and patients with COMISA (18 ± 9 vs. 19 ± 9 events/h; P = 0.86). Uncontrolled hypertension was found in 4.4%, 4.5%, 7.9%, and 10.2% of the control group, insomnia-only, OSA-only, and COMISA groups, respectively (P < 0.001). Compared with the control group, the risk of uncontrolled hypertension was significantly increased in the OSA-only group (odds ratio [95% confidence interval], 1.31 [1.05-1.64]; P = 0.02) and the COMISA group (1.88 [1.23-2.89]; P = 0.004) after controlling for anthropometrics, lifestyle, comorbidities, Epworth Sleepiness Scale score, and nocturnal hypoxic exposure (T90 [percentage recording time with oxygen saturation ⩽90%]). T90 was found to be a significant mediator of uncontrolled hypertension in the relationship between both OSA and COMISA.
CONCLUSIONS: This study is the first to demonstrate an independent association between COMISA and uncontrolled hypertension in the general population. These findings provide novel insights for identifying subgroups of patients with OSA at risk of adverse cardiovascular consequences. Furthermore, our results underscore the importance of recognizing sleep health as a multidimensional construct and advocate for personalized treatment strategies to effectively combat the burden of this common sleep disorder. (See the data supplement for graphical abstract and summary of key findings).