The Different Clinical Faces of Obstructive Sleep Apnea (OSA), OSA in Older Adults as a Distinctly Different Physiological Phenotype, and the Impact of OSA on Cardiovascular Events after Coronary Artery Bypass Surgery

Failure to appreciate the heterogeneity of obstructive sleep apnea (OSA) may impede its clinical recognition and management (1, 2). Using cluster analysis from a large, cross-sectional, clinically based cohort of adults with moderate-to-severe OSA, representative of the population of Iceland, Ye and colleagues identified subgroups with distinct combinations of symptoms (1). Included in the analysis were 822 subjects who were positive airway pressure naive. These were predominantly middle-aged obese males with severe OSA. Three distinct clusters were identified: (1) a “disturbed sleep” cluster (33%) with the highest probability of experiencing insomnia-related symptoms such as difficulty with sleep initiation and maintenance, nocturnal and early awakenings, nocturnal sweating, restless sleep, restless leg symptoms, and symptom of gasping for breath; (2) a “minimally symptomatic” cluster (25%) with the highest probability of feeling rested on awaking; and (3) an “excessive daytime sleepiness” cluster (42%) with a higher probability of daytime hypersomnolence (as measured by the Epworth Sleepiness Scale), the presence of daytime sleepiness-related symptoms (such as falling asleep unintentionally during the day, dozing off while driving), and symptoms of witnessed apneas and loud snoring. The identification of the “disturbed sleep” group in this study, underscores the presence of OSA in those with comorbid insomnia, suggesting that both the screening for OSA in those with insomnia as well as treatment with combination therapies (e.g., positive airway pressure and cognitive behavioral therapy for insomnia) may be beneficial in this population (3). Furthermore, the probabilities of having comorbid hypertension and cardiovascular disease were highest in the “minimally symptomatic” but lowest in the “excessive daytime sleepiness” group. The authors proposed that a potentially longer lag time between initial symptoms and diagnosis in minimally symptomatic compared with symptomatic patients may lead to a longer duration of exposure to untreated OSA and, thus, a higher probability of developing comorbidities. However, the crosssectional design of this study makes it impossible to infer causality, and as with any observational study, there are limitations related to unmeasured confounders such as depression or cognitive impairment. In addition, the study results are pertinent to the specific patient group evaluated, and extrapolation to other OSA cohorts may be inapplicable. Despite no statistical or clinically meaningful difference observed in sex, age, body mass index, apnea–hypopnea index, oxygen desaturation index, or minimal oxygen saturation among the three clusters, these important variables may account for different clinical presentations of OSA. Lastly, the use of type 3 portable monitors may have contributed to the underestimation of the apnea–hypopnea index in those with insomnia. As such, further validation in independent cohorts including a broader demographic profile and OSA severity is needed. Regardless of limitations, this study serves to highlight and increase physician awareness of the heterogeneity of OSA clinical presentation. It also provides clinicians with some guidance as to the differing OSA phenotypic presentations. In so doing it may facilitate early identification of OSA and lead to the development of personalized therapies. This may be of particular importance in those who are less symptomatic or who experience less common symptoms of OSA, although the need for treatment of minimally symptomatic patients remains uncertain at this time (4, 5). n

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