Introduction: More Than Just Snoring

Obstructive sleep apnea (OSA) is a common and underdiagnosed sleep disorder marked by recurrent episodes of upper airway collapse during sleep, leading to intermittent hypoxia and fragmented sleep architecture. Although frequently dismissed as “just snoring,” OSA is a serious medical condition with far-reaching systemic effects. Epidemiological data suggest that up to 20% of adults may have OSA, with a large proportion remaining undiagnosed. When left untreated, OSA is associated with heightened systemic inflammation, metabolic dysfunction, and significantly elevated risks of hypertension, stroke, heart failure, and overall mortality.1

The hallmark cycles of oxygen desaturation and reoxygenation in OSA activate the inflammasome pathway and promote the release of proinflammatory cytokines, accelerating cardiovascular and neurocognitive deterioration. Additionally, OSA is a recognized contributor to insulin resistance and metabolic syndrome. Early recognition and appropriate management are therefore essential to mitigate long-term systemic complications.2，3

Clinical Presentation and Diagnostic Challenges

OSA often manifests through symptoms such as loud snoring, gasping or choking during sleep, excessive daytime fatigue, and cognitive impairment. However, the condition is frequently underrecognized—particularly in women and non-obese individuals—who may present with atypical complaints like insomnia or mood disturbances. These subtleties contribute to delayed or missed diagnoses.4

The diagnostic gold standard remains overnight polysomnography (PSG), a comprehensive assessment of neurophysiological and respiratory variables during sleep. Home sleep apnea testing (HSAT) offers a more accessible alternative for patients with high clinical suspicion, though it may be less accurate in complex or comorbid cases. Several barriers impede timely diagnosis, including limited awareness among both patients and providers, perceived stigma around CPAP therapy, and reduced access to sleep centers—especially in resource-limited settings. Additionally, the complexity and perceived inconvenience of sleep studies often discourage patients from seeking evaluation. Addressing these gaps is vital for improving diagnostic rates and initiating timely treatment.5，6

Pathophysiology: How Sleep Apnea Affects the Body

At the core of OSA lies repetitive upper airway obstruction during sleep, leading to cycles of intermittent hypoxia and reoxygenation. This triggers a cascade of pathophysiological responses. Sympathetic nervous system overactivation results in elevated blood pressure and heart rate, increasing cardiovascular workload. Intermittent hypoxia promotes oxidative stress, which damages cellular structures and exacerbates systemic inflammation.

These events lead to endothelial dysfunction, arterial stiffness, and the progression of atherosclerosis. Concurrently, systemic inflammation amplifies metabolic disturbances, including insulin resistance and dyslipidemia, linking OSA to an increased risk of type 2 diabetes. Anatomical factors such as craniofacial structure, soft tissue laxity, and impaired neuromuscular tone compound these effects, illustrating the multifactorial impact of OSA on systemic health.7，8

Cardiovascular Consequences: The Hidden Risk

OSA has been firmly established as an independent risk factor for a spectrum of cardiovascular diseases. It contributes to the development and exacerbation of hypertension—particularly resistant forms—as well as atrial fibrillation, coronary artery disease, heart failure, and stroke. Large-scale studies, including the Sleep Heart Health Study, have shown that 40–80% of patients with cardiovascular disease may also have undiagnosed OSA.9

The central mechanism linking OSA to cardiovascular pathology is nocturnal hypoxemia, which fuels sympathetic activation, oxidative stress, and systemic inflammation. These factors promote cardiac remodeling, left ventricular hypertrophy, and myocardial fibrosis, increasing the risk of arrhythmias. Notably, the severity of nocturnal oxygen desaturation, rather than the apnea-hypopnea index (AHI) alone, has emerged as a more precise predictor of adverse cardiovascular outcomes.10

Intermittent hypoxia also accelerates endothelial dysfunction and atherogenesis, heightening the risk for cerebrovascular and coronary events. While continuous positive airway pressure (CPAP) remains the cornerstone of treatment, its impact on cardiovascular endpoints has varied in clinical trials, underscoring the need for better risk stratification and patient selection. Nevertheless, early identification and effective management of OSA are essential components of cardiovascular disease prevention.11

Frontier Research: Biomarkers, AI, and Personalized Risk Stratification

Advances in sleep medicine are shifting toward personalized diagnostics and risk profiling, driven by innovations in biomarkers and artificial intelligence (AI). AI-based algorithms are now integrated into PSG systems and wearable technologies to automate sleep staging and respiratory event detection, enhancing efficiency and reducing diagnostic variability.12

Wearable devices capable of real-time monitoring of oxygen saturation and respiration enable continuous tracking of hypoxic burden—a metric that may better predict cardiovascular risk than AHI. Concurrently, research into systemic biomarkers, including interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and C-reactive protein (CRP), offers promise for identifying patients at highest risk for cardiovascular complications.13

Genomic and proteomic studies are revealing gene-sleep interactions. For instance, individuals carrying the APOE4 allele appear particularly vulnerable to cognitive decline when OSA is present, emphasizing the need for precision-based management. AI is also being leveraged to integrate multi-modal data—combining sleep metrics, genomics, and imaging—to stratify patients more effectively and personalize interventions.14

Together, these frontiers represent a paradigm shift in the management of OSA, moving from a reactive to a proactive and tailored model of care.

Conclusion

OSA is far more than a sleep disturbance—it is a multisystem disorder with significant public health implications. The underrecognition of its systemic impact, particularly on cardiovascular and metabolic health, has contributed to diagnostic and treatment gaps. As AI, biomarker research, and digital health technologies continue to evolve, the opportunity to reframe OSA as a chronic, treatable condition with significant systemic consequences is within reach. Recognizing and addressing the full burden of sleep apnea is essential not only for improving sleep health but also for reducing the global burden of non-communicable disease.

References:

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