Coronary artery disease · 2026
Reduction in circulating endothelial progenitor cells caused by obstructive sleep apnea-related hypoxemia and its association with the severity of coronary artery disease.
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Zhang Hehe, Zhang Jing, Lin Yun, Jiao Yuanni, Li Shuang, Wu Hao, Xi Xin, Xie Jiang
Аннотация
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.
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.