Background: The relationship between obstructive sleep apnea (OSA) and platelet reactivity in patients undergoing percutaneous coronary intervention (PCI) has not been defined. The present prospective, single-center study explored the relationship between platelet reactivity and OSA in patients with PCI.
Methods: A total of 242 patients were finally included in the study. OSA was screened overnight by polysomnography. Platelet reactivity was assessed with a sequential platelet counting method, and the platelet maximum aggregation ratio (MAR) and average aggregation ratio were calculated. All patients were assigned per apnea-hypopnea index (AHI) to non-OSA (n = 128) and OSA (n = 114) groups. The receiver operating characteristic curve analysis was used to evaluate the accuracy of AHI for high platelet reactivity (HPR) on aspirin and clopidogrel, and multivariable logistic regression was used to determine the independent predictors of HPR on aspirin and clopidogrel.
Results: Median AHI was significantly higher in the OSA group than in the non-OSA group (34.5 events/h vs. 8.1 events/h, Z = -13.422, P < 0.001). Likewise, median arachidonic acid- and adenosine diphosphate-induced maximum aggregation rate (MAR) in the OSA group was significantly higher than those in the non-OSA group (21.1% vs. 17.7%, Z = -3.525, P < 0.001 and 45.8% vs. 32.2%, Z = -5.708, P < 0.001, respectively). Multivariable logistic regression showed that OSA was the only independent predictor for HPR on aspirin (odds ratio [OR]: 1.055, 95% confidence interval [CI]: 1.033-1.077, P < 0.001) and clopidogrel (OR: 1.036, 95% CI: 1.017-1.056, P < 0.001). The cutoff value of AHI for HPR on aspirin was 45.2 events/h (sensitivity 47.1% and specificity 91.3%), whereas cutoff value of AHI for HPR on clopidogrel was 21.3 events/h (sensitivity 68.3% and specificity 67.7%).
Conclusion: Platelet reactivity appeared to be higher in OSA patients with PCI despite having received a loading dose of aspirin and clopidogrel, and OSA might be an independent predictor of HPR on aspirin and clopidogrel.
阻塞性睡眠呼吸暂停对经皮冠脉支架介入治疗患者血小板活性的影响摘要背景：目前阻塞性睡眠呼吸暂停与经皮冠脉支架介入治疗（PCI）患者血小板活性之间的关系尚未明确报道。本前瞻性单中心研究主要探究这两者之间的潜在联系。 方法：本研究最终纳入242名患者。利用多导睡眠监测仪检测睡眠呼吸暂停现象，并使用连续血小板检测的方法评估血小板功能，计算最大血小板聚集率（MAR）和平均血小板聚集率（AAR）。按照呼吸暂停低通气指数（AHI）将患者分为睡眠呼吸暂停（OSA）组（n=114）和非睡眠呼吸暂停（non-OSA）组（n=128）。使用ROC曲线评估AHI对阿司匹林和氯吡格雷高血小板反应性的诊断准确度，运用多元回归分析来确定阿司匹林和氯吡格雷高血小板反应性的独立预测因子。 结果：在OSA组中，AHI的中位数显著高于non-OSA组（34.5 events/h vs. 8.1 events/h, Z=-13.422, P<0.001）。而且，OSA组的AA和ADP诱导的最大血小板聚集率同样显著高于non-OSA组(分别为21.1% vs. 17.7%, Z=-3.525, P<0.001; 以及45.8% vs. 32.2%, Z=-5.708, P<0.001)。多元logistic回归分析显示OSA为阿司匹林和氯吡格雷高血小板反应性的独立预测因子（OR: 1.055, 95% CI: 1.033-1.077, P<0.001；以及OR: 1.036, 95% CI: 1.017-1.056, P<0.001）。预测阿司匹林高血小板反应性的AHI截断值为45.2 events/h (敏感性 47.1%, 特异性 91.3%)，而预测氯吡格雷高血小板反应性的AHI截断值为21.3 events/h (敏感性 68.3%, 特异性 67.7%)。 结论：PCI患者虽然在术前接受了负荷剂量的阿司匹林和氯吡格雷，但OSA患者的血小板活性仍处于较高水平。OSA可能是阿司匹林和氯吡格雷高血小板反应性的独立预测因子。.
Keywords: Antiplatelet Drugs; Maximum Aggregation Rate; Obstructive Sleep Apnea; Percutaneous Coronary Intervention; Platelet Reactivity.