Evidence map›Paper›PMID 41562153›Full record

ArticleCoronary artery disease2026

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

Hehe Zhang, Jing Zhang, Yun Lin, Yuanni Jiao, Shuang Li, Hao Wu, Xin Xi, Jiang Xie

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Article in Coronary artery disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Hehe ZhangDepartment of Respiratory and Critical Medicine, Beijing Anzhen Hospital.
Jing ZhangInstitute of Heart, Lung and Blood Vessel Diseases.
Yun LinDepartment of Cardiovascular Medicine, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Yuanni JiaoDepartment of Respiratory and Critical Medicine, Beijing Anzhen Hospital.
Shuang LiDepartment of Respiratory and Critical Medicine, Beijing Anzhen Hospital.
Hao WuBeijing Anzhen Hospital Centre for Sleep Medicine and Science.
Xin XiBeijing Anzhen Hospital Centre for Sleep Medicine and Science.
Jiang XieDepartment of Respiratory and Critical Medicine, Beijing Anzhen Hospital.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObstructive 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.

methodsThis 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.

resultsAmong 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.

conclusionOSA 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.

Indexed as

Coronary Artery DiseaseCoronary StenosisEndothelial Progenitor CellsHypoxiaSleep Apnea, ObstructiveAgedAngina, UnstableCoronary AngiographyFemaleFlow CytometryHumansLinear ModelsMaleMiddle AgedPolysomnographyProspective Studiescoronary artery diseaseendothelial progenitor cellsobstructive sleep apneasleep apnea–specific hypoxic burden

Identifiers

PMID41562153
PMCPMC13299031

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.