CAJ | 학술논문

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。
목적 관찰조새성수면호흡잠정（OSA）대급성관맥종합정（ACS）환자성공접수관상동맥지가치입후지가재협착적영향급혈장고민C반응단백（hsCRP）적변화。방법 2008년1월지2010년12월본원심내과수치적ACS환자병식입약물지가66례。소유환자입원후행다도수면의감측후분량조，①OSA조：ACS합병OSA환자21례，②대조조：ACS불합병OSA환자45례。술전환자추혈사혈당、혈지급hsCRP ，술후6개월수방시복사혈당、혈지、hsCRP병진행관상동맥혈관조영복사。결과 OSA 조기선수평적총담고순（TC）급저밀도지단백（LDL）교대조조증고（ P ＜0．05）；경과타정조지치료6개월후복사량조 TC급LDL차이무현저성（ P＞0．05）。OSA조기선시화수방시 hsCRP균교대조조현저증고（ P ＜ 0．01）。재6개월수방시，재OSA조지가재협착솔교대조조명현증고（ P ＜0．01）。AHI여hsCRP급재협착엄중정도정정상관（ P＜0．05）。hsCRP여재협착엄중정도정정상관（ P ＜0．05）。결론 OSA촉진ACS관맥지가술후재협착，기가능궤제위OSA환자적A HI증고도치적저양혈증，촉진혈장hsCRP증고，도치혈관내피염증반응가중급지가내재협착적발생솔증고。
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( P<0 .05) .There was no significant difference in TC and LDL between two groups at 6‐month follow up after lipid‐lowing treatment( P>0 .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 .