The Role of Obstructive Sleep Apnea and Diabetes Mellitus in the Development of Cerebrovascular Complications: A Narrative Review

Background: Cerebrovascular accidents (stroke) remain a leading global cause of death and disability, with its burden increasingly overlapping the rising prevalence of obstructive sleep apnea (OSA) and diabetes mellitus (DM). These highly prevalent cardiometabolic conditions frequently coexist and may jointly amplify cerebrovascular risk through shared and interacting pathophysiologic pathways. This narrative review synthesizes current evidence on the independent and combined contributions of OSA and DM to cerebrovascular complications, with emphasis on mechanisms, stroke outcomes and implications for screening and integrated management. Methods: A narrative review was conducted using PubMed, MEDLINE, and the Cochrane Library to identify English-language articles published between January 2000 and December 2024. Search terms combined OSA or sleep-disordered breathing with stroke or cerebrovascular disease and DM or hyperglycemia. Secondary searches targeted mechanistic domains including intermittent hypoxia, insulin resistance, metabolic syndrome, atrial fibrillation, hypercoagulability, and bariatric surgery. Priority was given to systematic reviews and meta-analyses, randomized controlled trials, and large prospective cohort studies, with smaller studies included when mechanistically informative. Findings were synthesized thematically across OSA-related mechanisms, DM-related mechanisms, bidirectional interactions, combined risk through metabolic syndrome, stroke outcomes, and clinical management considerations. Results: OSA is associated with increased cerebrovascular risk through intermittent hypoxemia-related oxidative stress and inflammation, sympathetic activation with blood pressure surges and sustained hypertension, endothelial dysfunction and atherosclerosis, impaired cerebral autoregulation, arrhythmogenesis, particularly atrial fibrillation and prothrombotic changes. DM increases stroke risk via accelerated atherosclerosis, cerebral small vessel disease, endothelial injury, hypercoagulability, glycemic variability, and cardioembolic mechanisms. Evidence indicates that coexisting OSA and DM are common and associated with greater vascular injury markers, higher rates of cerebrovascular events, and poorer post-stroke recovery. Conclusions: OSA and DM contribute to cerebrovascular complications through convergent mechanisms centered on metabolic syndrome, obesity, inflammation, vascular dysfunction, and thrombosis. These findings support proactive screening and coordinated management strategies to reduce cerebrovascular risk and improve outcomes.