Reduction in circulating endothelial progenitor cells caused by obstructive sleep apnea–related hypoxemia and its association with the severity of coronary artery disease

Background Obstructive sleep apnea (OSA) is a risk factor for coronary artery disease (CAD), while endothelial progenitor cells (EPCs) are critical for vascular repair. This study investigated the associations among OSA-related hypoxemia, circulating EPC, and CAD severity. Methods This prospective study enrolled patients with unstable angina undergoing coronary angiography. All participants underwent overnight polysomnography to determine the apnea–hypopnea index (AHI) and the sleep apnea–specific hypoxic burden (SASHB). Circulating EPCs were quantified using flow cytometry. CAD severity was assessed via angiography, with a Gensini score greater than or equal to 22 defining severe CAD and the presence of greater than or equal to 2 major vessels with greater than or equal to 50% diameter stenosis defining multivessel CAD. Results Among 80 included patients median age 59 years; 53 (66.3%) male, 42 (52.5%) had OSA (AHI ≥ 15 events/h). Patients with high SASHB exhibited more severe coronary artery lesions than those with low SASHB (Gensini: 33.0 vs. 19.5; P = 0.040). Multivariable linear regression confirmed log10-transformed SASHB as an independent predictor of reduced circulating EPC levels (count: standardized β = –0.37, P = 0.002; percentage: standardized β = –0.40, P < 0.001). Multivariable logistic regression analysis revealed low EPC count odds ratio (OR) = 3.41, 95% confidence interval (CI): 1.21–9.58, P = 0.020 and low EPC percentage (OR = 2.94, 95% CI: 1.00–8.78, P = 0.049) as independent risk factors for multivessel CAD. Conclusion OSA may promote CAD progression by depleting EPCs and hindering vascular repair. Incorporating hypoxemia metrics and EPC levels into risk assessment could help identify patients with OSA-related CAD.