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

Figures

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  Fig. 1. Association of OSA metrics with Gensini score. (a, c, and e) Spearman’s rank-correlation scatterplots of log10(AHI), log10(T90SpO₂), and log10(SASHB) with the Gensini score, respectively. (b, d, and f) Comparisons of Gensini scores between OSA and non-OSA, high and low T90SpO₂, and high and low SASHB groups, respectively. AHI, apnea–hypopnea index; log10: log10-transformed; OSA, obstructive sleep apnea; SASHB, sleep apnea–specific hypoxic burden; T90SpO₂, percentage of sleep time with oxygen saturation less than 90%.

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  Fig. 2. Correlations between OSA metrics and circulating EPC levels. (a, c, and e) Spearman’s rank-correlation scatterplots between log10(AHI), log10(T90SpO₂), and log10(SASHB) and the EPC count (CD45dimCD34⁺KDR⁺, cells/ml). (b, d, and f) The corresponding correlations with the EPC percentage (% of CD45+). AHI, apnea–hypopnea index; EPC, endothelial progenitor cell; log10, log10-transformed; OSA, obstructive sleep apnea; SASHB, sleep apnea–specific hypoxic burden; T90SpO₂, percentage of sleep time with oxygen saturation less than 90%.

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  Fig. 3. Multivariable logistic regression analysis of circulating EPC levels and CAD severity. *Univariate logistic regression model. †Model 1, adjusted for age and sex. ‡Model 2, adjusted for age, sex, hypertension history, glycated hemoglobin, low-density lipoprotein, and use of angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers. CAD, coronary artery disease; CI, confidence interval; EPC, endothelial progenitor cell; OR, odds ratio.

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  Fig. 4. Proposed mechanism linking OSA to multivessel CAD. OSA-induced chronic intermittent hypoxia, quantified as SASHB, leads to endothelial injury and EPC reduction both directly and through the mediation of oxidative stress, chronic inflammation, and reduced nitric oxide bioavailability. The resulting impairment in vascular repair capacity contributes to the progression of diffuse, multivessel CAD. CAD, coronary artery disease; EPC, endothelial progenitor cell; OSA, obstructive sleep apnea; SASHB, sleep apnea–specific hypoxic burden.