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Abstract Sleep apnea (SA) is associated with risk of cardiovascular disease, cognitive decline, and accidents due to sleepiness, yet the majority (over 80%) of patients remain undiagnosed. Inertial measurement units (IMUs) are built into modern wearable devices and are capable of long-term continuous measurement with low power consumption. We examined if SA can be detected by an IMU embedded in a wristwatch device. In 122 adults who underwent polysomnography (PSG) examinations, triaxial acceleration and triaxial gyro signals from the IMU were recorded during the PSG. Subjects were divided into a training group and a test groups (both n = 61). In the training group, an algorithm was developed to extract signals in the respiratory frequency band (0.13–0.70 Hz) and detect respiratory events as transient (10–90 s) decreases in amplitude. The respiratory event frequency estimated by the algorithm correlated with the apnea–hypopnea index (AHI) of the PSG with r = 0.84 in the test group. With the cutoff values determined in the training group, moderate-to-severe SA (AHI ≥ 15) was identified with 85% accuracy and severe SA (AHI ≥ 30) with 89% accuracy in the test group. SA can be quantitatively detected by the IMU embedded in wristwatch wearable devices in adults with suspected SA.

Objective: To examine the associations of self-efficacy and outcome expectancy with adherence to continuous positive airway pressure (CPAP) therapy among Japanese men with obstructive sleep apnea (OSA) using objective adherence data for CPAP therapy. Methods: We conducted a retrospective study of 497 Japanese men with OSA who were receiving CPAP therapy. Good adherence was defined as CPAP use of ≥4 hours per night for ≥70% of nights. Logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for the associations of good adherence to CPAP therapy with self-efficacy and outcome expectancy (measured with the CPAP Self-Efficacy Questionnaire for Sleep Apnea in Japanese). The models were adjusted for age, duration of CPAP therapy, body mass index, apnea–hypopnea index, Epworth Sleepiness Scale score, and comorbidities (diabetes mellitus and hypertension). Results: In total, 53.5% of participants had good adherence to CPAP therapy. The mean CPAP use was 5.18±1.53 hours/night. After adjusting for related factors, we found significant associations of good adherence to CPAP therapy with self-efficacy scores (OR, 1.10; 95% CI, 1.05–1.13; p

Objectives: Continuous positive airway pressure (CPAP) is the first line of therapy for obstructive sleep apnea (OSA). Adherence to CPAP, however, is known to be problematic, and its associations with the comorbidities of hypertension and diabetes mellitus have not been sufficiently evaluated. Thus, we investigated the associations of CPAP therapy adherence with comorbidities of hypertension and diabetes mellitus. Methods: We conducted a retrospective study among 497 male patients with OSA on CPAP therapy. Participants with pretreatment Apnea–Hypopnea Index (AHI) data based on overnight polysomnographic recordings completed a questionnaire. Adherence data for CPAP therapy were collected using a smart card system. We classified CPAP use of ≥4 hours per night and ≥70% of nights as good adherence; other CPAP use was categorized as poor adherence. Logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (CIs) for poor adherence to CPAP therapy in the hypertension and diabetes mellitus groups, compared with the no comorbidity group, adjusting for body mass index, duration of CPAP therapy, AHI, and Epworth Sleepiness Scale score. Results: In the no comorbidity, hypertension, and diabetes mellitus groups, 43.4%, 44.7%, and 56.0%, respectively, had poor adherence to CPAP therapy. Being in the diabetes mellitus group was significantly associated with poor adherence to CPAP therapy (OR=1.86, 95% CI: 1.18–2.92, p=0.007); there was no association for the hypertension group. Conclusion: Our results indicate that comorbidity of diabetes mellitus is associated with poor adherence to CPAP therapy in male patients with OSA.

Objectives: Obstructive sleep apnea syndrome (OSAS) affects patients' vital prognosis. Although adenotonsillar hypertrophy is linked to the pathogenesis of OSAS in children, the etiological role of childhood adenotonsillar hypertrophy in the later development of OSAS in the Japanese general population is unknown. Methods: We evaluated 1121 male factory workers aged ≥20 years who underwent home portable monitoring for screening examinations of OSAS in Japan. The relative risk of developing OSAS among patients with a history of adenotonsillar hypertrophy in childhood and the relative risk reduction associated with treatment were estimated. Results: We identified 85 men with OSAS (prevalence, 7.2%). The relative risk of OSAS in patients with untreated adenotonsillar hypertrophy was 2.92 (95% confidence interval [CI], 1.42–6.13). The relative risk reduction for treatment of adenotonsillar hypertrophy with OSAS was estimated as 78.3% (95% CI, 4.7–95.3) in men with a history of adenotonsillar hypertrophy and 11.9% (95% CI, 4.4–21.5) in the whole male population with and without a history of adenotonsillar hypertrophy. Conclusions: The findings of this study suggest a large relative risk reduction of adult OSAS in patients who have undergone treatment of adenotonsillar hypertrophy in childhood.

Objectives: Obstructive sleep apnea syndrome (OSAS) is an important cause of medical morbidity and mortality. Although adenotonsillar hypertrophy is linked to the pathogenesis of OSAS in children, the potential role of childhood adenotonsillar hypertrophy in the etiology of adult OSAS has not yet been examined. Methods: We retrospectively evaluated 1,369 men aged ≥20 years with suspected OSAS who had undergone polysomnography at Fujita Health University Hospital in Japan. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated after adjusting for age and body mass index to evaluate the risk of development of OSAS in men with a history of adenotonsillar hypertrophy in childhood. The reference category for OSAS was non-OSAS. Results: In total, 988 men were diagnosed with OSAS and 561 were diagnosed with severe OSAS (apnea–hypopnea index of ≥30). The adjusted ORs for a history of untreated adenotonsillar hypertrophy with OSAS and severe OSAS were 3.13 (95% CI, 1.18–8.27) and 4.31 (1.56–11.90), respectively. The adjusted ORs for a history of treated adenotonsillar hypertrophy with OSAS and severe OSAS were 1.31 (0.69–2.50) and 0.87 (0.41–1.90), respectively. Conclusions: This study confirmed the risk of untreated childhood adenotonsillar hypertrophy in the development of adult OSAS. Our data also support the idea that abnormal dentofacial morphology induced by adenotonsillar hypertrophy in childhood is a critical factor in the pathogenesis of OSAS in adulthood.