Investigation of the Effect of Obstructive Sleep Apnea Hypopnea Syndrome (OSAHS)on Vascular Endothelial Function in Coronary Slow Flow (CSF) Patients

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Background and Objective: Obstructive sleep apnea–hypopnea syndrome (OSAHS) is one of the most recognized sleep apneas which are induced by complete or partial blocking of the upper airway. Multiple consequences of OSAHS have been identified clinically, most notably cardiovascular disease. We aim to explore the effect of OSAHS on the function of cardiac endothelia in coronary slow flow (CSF) patients. Methods: We retrospectively analyzed 90 patients who were diagnosed with having CSF but displayed normal coronary angiography (CAG). Based on nocturnal polysomnography (PSG) results, patients were divided into 2 groups – an OSAHS (OSAHS/CSF) group (n=39) and a non-OSAHS (CSF) group (n=51). The brachial artery endothelium-dependent flow mediated dilation (FMD) as well as the plasma levels of nitric oxide (NO), endothelin-1 (ET-1),high sensitivity C-reactive protein (hsCRP), and tumor necrosis factor-α (TNF-α) were determined and compared between the two groups. Results: Our results indicated that compared to the control group, OSAHS patients had lower levels of FMD and NO (p<0.05), but significantly increased hs-CRP, TNF-α and ET-1 levels in the plasma (p<0.05). Furthermore, amongst OSAHS patients, the apnea hypopnea index (AHI) and time of oxygen saturation (SaO2 ) <90% score were negatively correlated with FMD, while the lowest pulse oxygen saturation (LSpO2 ) score was positively correlated with FMD. Conclusion: OSAHS can significantly impair vascular endothelial function in CSF patients.