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目的 观察阻塞性睡眠呼吸暂停（OSA）对急性冠脉综合征（ACS）患者成功接受冠状动脉支架置入后支架再狭窄的影响及血浆高敏C反应蛋白（hsCRP）的变化。方法 2008年1月至2010年12月本院心内科收治的ACS患者并植入药物支架66例。所有患者入院后行多导睡眠仪监测后分两组，①OSA组：ACS合并OSA患者21例，②对照组：ACS不合并OSA患者45例。术前患者抽血查血糖、血脂及hsCRP ，术后6个月随访时复查血糖、血脂、hsCRP并进行冠状动脉血管造影复查。结果 OSA 组基线水平的总胆固醇（TC）及低密度脂蛋白（LDL）较对照组增高（ P ＜0．05）；经过他汀调脂治疗6个月后复查两组 TC及LDL差异无显著性（ P＞0．05）。OSA组基线时和随访时 hsCRP均较对照组显著增高（ P ＜ 0．01）。在6个月随访时，在OSA组支架再狭窄率较对照组明显增高（ P ＜0．01）。AHI与hsCRP及再狭窄严重程度呈正相关（ P＜0．05）。hsCRP与再狭窄严重程度呈正相关（ P ＜0．05）。结论 OSA促进ACS冠脉支架术后再狭窄，其可能机制为OSA患者的A HI增高导致的低氧血症，促进血浆hsCRP增高，导致血管内皮炎症反应加重及支架内再狭窄的发生率增高。“,”Objective] To observe the effect of obstructive sleep apnea(OSA ) on restenosis and plasma high‐sensitivity C‐reactive protein(hsCRP) in patients with acute coronary syndrome(ACS) after successful coronary artery stent implantation .[Methods] A total of 66 patients with ACS undergoing coronary artery stent implantation in cardiology department of our hospital from Jan .2008 to Dec .20100 CS) were selected . After polysomnography ,all patients were divided into OSA group( n = 21 ,ACS combined with OSA) and control group( n=45 ,ACS without OSA) .Blood samples were collected for detecting blood glucose ,lipids and hsCRP before operation .Blood glucose ,lipids and hsCRP were reexamined and coronary angiography was performed again at 6‐month follow up after operation .[Results]Compared with control group ,total cholester‐ol(TC) and low density lipoprotein(LDL) in OSA group at baseline were increased( P0 .05) .Compared with control group ,hsCRP in OSA group at baseline and follow up was significantly in‐creased( P<0 .01) .Compared with control group ,the rate of stent restenosis in OSA group was obviously in‐creased at 6‐month follow‐up( P <0 .01) .AHI was positively correlated with stent restenosis and hsCRP ( P<0 .05) .hsCRP was positively correlated with stent restenosis( P<0 .05) .[Conclusion]OSA promotes coro‐nary stent restenosis of patients with ACS .The mechanism may be that hypoxemia caused by AHI in OSA pa‐tients promotes the increasing of plasma hsCRP ,which leads to aggravate vascular endothelial inflammation and raise the occurrence of in‐stent restenosis .