A common sleep disorder known as obstructive sleep apnea (OSA) is when a person sleeps, their upper airway repeatedly closes completely or partially. About 13% of middle-aged men and 6% of middle-aged women are thought to have moderate to severe disease if they experience at least 15 apneas or hypopneas per hour of sleep. OSA is associated with a wide range of adverse health outcomes, including cardiovascular disease, diabetes, neurodegenerative disorders, hypertension, and mortality. Frequently cited as OSA symptoms are loud snoring, witnessed apneas, and nocturnal gasping. Other symptoms include excessive sleepiness, sleep disturbances, and general fatigue. Due to the fact that OSA etiology, symptoms, and outcomes vary greatly from patient to patient, atypical symptom profiles are under-recognized. Consequently, a number of recent studies have attempted to better define OSA patients' clinical subtypes in terms of demographics, disease severity, symptoms, and comorbidities. In order to tailor and improve clinical administration, a more precise depiction and determination of OSA is essential.

The Icelandic Sleep Apnea Cohort (ISAC)'s moderate-to-severe OSA patients were the subject of the first major attempt to identify clinical presentation subtypes. The three distinct clusters that were found were as follows: a group with excessive sleepiness, a group with few symptoms, and a group with insomnia and restless sleep. Later research in Greece, Italy, France, and Europe suggested OSA clusters. These studies cannot be easily compared due to differences in sample characteristics (such as the inclusion of controls) and cluster-defining variables (such as the inclusion of the apnea hypopnea index, or AHI). However, several studies found clusters of patients with relatively low symptom burden, as well as clusters of patients with predominant symptoms of sleep disturbance or daytime sleepiness, in the original ISAC study. To better understand individual differences in clinical presentation, this article focuses on the clinical symptoms of patients with moderate-to-severe OSA.

Race and ethnicity play a role in OSA's etiology, according to recent research. Asian patients, for instance, are less likely to be obese and have more prevalent craniofacial risk factors when compared to Caucasians with similar disease severity. Similar to Caucasians, young African-Americans are found to have OSA with a higher severity than Caucasians. Due to these differences in disease risk factors and etiology, which may result in distinct symptom profiles and disease outcomes among ethnicities, the robustness and generalizability of OSA clusters previously identified within a single ethnic group are questioned. Also important is figuring out if the findings in Iceland are typical of OSA or unique to Iceland, possibly due to cultural norms or referral patterns. As a result of this knowledge, both our comprehension of OSA and clinicians' capacity to identify the most significant disease characteristics in particular patient populations would improve. The current study first attempted to confirm the existence of the three OSA clinical clusters that were initially identified by ISAC in a brand-new Icelandic cohort and a diverse international cohort of ethnic origin in order to accomplish this objective. Second, we attempted to determine the optimal number of clinical groups within the larger ethnically diverse partner outside of Iceland. We assumed that the ethnically diverse international cohort would exhibit similar OSA clusters and that the previously identified OSA clusters would be confirmed in Iceland.