42501272-E-男A(02中央單位02.(14國(guó)有企 06.外商投資企 11.高等院集體企 07.有限責(zé)任公 12.研究院私營(yíng)企 08.股份有限公 13.社會(huì)團(tuán)聯(lián)營(yíng)企 22689684574426％()認(rèn)定的高新技術(shù)企 高等院校辦的企 科研院所辦的企 無(wú)(2) .（PCI）是目前治療AMI的最有效方法，可使AMI的死亡率降低30％以上。急診PCI的主要作用是及時(shí)開(kāi)通閉塞的冠脈，減少心肌壞死，促進(jìn)心功能恢復(fù)，從而降低死亡率。恢復(fù)血流、實(shí)現(xiàn)心肌再灌注是急診PCI改善預(yù)后的關(guān)鍵，但根據(jù)傳統(tǒng)的TIMI血流分級(jí)方法所確定的冠脈血流恢復(fù)情況有時(shí)并不能反應(yīng)心肌再灌注的真實(shí)情況，臨床上常出現(xiàn)病人血流雖然恢復(fù)，但仍存在心電圖ST盾結(jié)果。因此研究者一直在尋找其它更可靠的再灌注評(píng)價(jià)方法。ECT及PET等方面進(jìn)行評(píng)價(jià)，1）胞、磷酸肌酸激酶（CK）、血糖、粘附分子、BP、RP、TNF等。這些指標(biāo)在心肌得到及時(shí)再灌注后也此除常規(guī)的循環(huán)靜脈血樣本之外，研究者還直接自冠狀靜脈竇和梗死相關(guān)動(dòng)脈分別取血標(biāo)本進(jìn)行檢測(cè)。血常規(guī)檢查：研究顯示發(fā)病時(shí)血白細(xì)胞升高的AMI患者急診PCI后的預(yù)后相對(duì)較差[1][3細(xì)胞也是炎癥的一個(gè)指標(biāo)，AMI發(fā)病時(shí)多形核細(xì)胞升高與PCI后的灌注不良相關(guān)[4]。血小板是動(dòng)脈血栓形成的關(guān)鍵因素，在AMI發(fā)病時(shí)血小板數(shù)量升高將導(dǎo)致冠脈灌注不良，并與PCI后6個(gè)月的死亡相關(guān)[5]。顯示SigmaSTR與MB(myocardialblush)均能很好地作為急診PCI術(shù)后的預(yù)后判斷指標(biāo)[17]、18]，而單純的的房撲和房顫是急診PCI后1年死亡的獨(dú)立預(yù)測(cè)指標(biāo)[25]。AMI還可出現(xiàn)QRS時(shí)程的增寬，并提示遠(yuǎn)期（2灌注顯影分級(jí)（TIMIMyocardialBlushGrade，MBG）。sofoITMIII級(jí)血流，急診PCI才可能使病人真正獲益。TIMI血流分級(jí)能夠較好地反應(yīng)梗死相關(guān)動(dòng)脈的開(kāi)通情況，并與預(yù)后有較好的相關(guān)性，一直沿用至今。但TIMI診PCI后IMI1、2]，0％TIMIST，TII]。TIMI血流幀數(shù)（TFC）：是反應(yīng)梗死相關(guān)動(dòng)脈血流恢復(fù)情況的更可靠指標(biāo)。計(jì)數(shù)自造影劑開(kāi)始充盈冠脈至標(biāo)準(zhǔn)化遠(yuǎn)端血管標(biāo)記顯影所需的幀數(shù)。標(biāo)準(zhǔn)化遠(yuǎn)端血管標(biāo)記因血管而異，前降支為其最遠(yuǎn)端分叉、回旋支為鈍緣支最遠(yuǎn)端分叉、右冠為左室后側(cè)支遠(yuǎn)端分叉，而前降支因血管較長(zhǎng)需除以.7來(lái)進(jìn)行校正。按國(guó)際上常用的標(biāo)準(zhǔn)化圖像采集速度30幀/秒，評(píng)價(jià)的標(biāo)準(zhǔn)是TII血流幀數(shù)<7幀為正常血流。在應(yīng)用硝酸鹽后由血管擴(kuò)張，TFC計(jì)數(shù)也要增加6幀進(jìn)行校正。TIMI血流幀數(shù)能夠使血流分級(jí)標(biāo)準(zhǔn)化而具有可比性，研究顯示與住院期間死亡率以及梗死相關(guān)動(dòng)脈再狹窄相關(guān)。TIMI心肌灌注分級(jí)（TMPG）：根據(jù)造影劑經(jīng)過(guò)微血管進(jìn)入心肌使其染色的能力，反應(yīng)心肌微血管灌注3：TPG級(jí)）1級(jí)、2級(jí)3后能夠消失）、3級(jí)（正常顯影，造影劑在3個(gè)心動(dòng)周期內(nèi)消失，與非梗死區(qū)相同）。TMPG強(qiáng)調(diào)造影劑進(jìn)入TMP與AI30TIMI心肌灌注顯影分級(jí)（MBG）：能夠反應(yīng)心肌組織灌注情況，最早由Van’tHof提出的主要針對(duì)PCI術(shù)血管內(nèi)超聲（IVUS）：血管內(nèi)超聲多應(yīng)用于擇期PCI冠脈內(nèi)超聲心肌聲學(xué)造影能夠直接檢測(cè)經(jīng)冠脈注射的聲學(xué)造影劑在心肌組織的分布情況，是反應(yīng)心肌在組織水平灌注的可靠方法。心肌聲學(xué)造影技術(shù)主要是運(yùn)用比紅細(xì)胞直徑還小的造影劑顆粒，在灌注區(qū)域和無(wú)灌注區(qū)域產(chǎn)生不同的超聲云霧狀影像增強(qiáng)，直接觀察心肌的灌注狀態(tài)。冠狀動(dòng)脈造影只能顯示心外膜直徑大于100um的小動(dòng)脈，并非真正意義上的微循環(huán)。選擇性心肌造影技術(shù)，即在冠狀動(dòng)脈造影時(shí)選擇性將造影劑注入目標(biāo)冠狀動(dòng)脈，通過(guò)超聲心動(dòng)圖顯示該冠狀動(dòng)脈供血區(qū)域造影劑顯示情況并進(jìn)行評(píng)分，完全顯影為1050PC發(fā)[肌聲學(xué)造影似乎具有相同價(jià)值[16]。9mTc-6h患者的再灌注時(shí)間和療效。當(dāng)患者明確為AMI時(shí)收住院，即刻注射99mTc-MIBI740MBq，之后，立即開(kāi)始手術(shù)和內(nèi)科治療，待患者病情平穩(wěn)后，行術(shù)前的心肌顯像，反映的是術(shù)前的心肌血流分布情況。～799mT-MIBI[1-6診檢查項(xiàng)目，為臨床療效判斷提供客觀指征。，18F-量進(jìn)一步減少，導(dǎo)致心肌細(xì)胞壞死，心肌代謝活動(dòng)停止，不能攝取葡萄糖和FDG。因此，PET是檢測(cè)心肌[7-11PC術(shù)即刻心肌再灌注情況的判斷，而是多作為術(shù)后心肌恢復(fù)情況以及預(yù)后的判斷指標(biāo)。對(duì)于局部心肌灌注和代謝圖像的分析，主要有兩類(lèi)，一類(lèi)為心肌灌注減低區(qū)對(duì)18F-FDG的攝取正常或明顯增加，稱(chēng)為“灌注-代謝不匹配(mismatch，MM)”，表明心肌存活；而另一類(lèi)為灌注減低區(qū)對(duì)18F-FDG攝取亦受損，稱(chēng)“灌注-代謝相匹配(match，M)”，表明心肌梗死[8~12](partialmismtch，PM)，對(duì)其臨床價(jià)值目前手術(shù)前后心肌灌注的變化和術(shù)后心肌代謝情況就能比較好地評(píng)價(jià)手術(shù)效果。，并24小時(shí)待命，隨時(shí)為AMI病人進(jìn)行急診手術(shù)。兩間專(zhuān)用導(dǎo)管室，配備有呼吸機(jī)、IABP、血管內(nèi)超聲等各種搶救和檢查設(shè)備。中心實(shí)驗(yàn)室配備有實(shí)驗(yàn)所需的流式細(xì)胞儀等各種設(shè)備，同位素室配備有最新的ECT、SPECT以及PET。5）、本課題將委托專(zhuān)業(yè)統(tǒng)計(jì)學(xué)人員處理所有數(shù)據(jù)，以保證結(jié)果的可靠性。建立專(zhuān)基礎(chǔ)。Comparan-NunezA,PalaciosJM,Jerjes-SanchezCD.Leucocytosisassociatedwithhigherincidenceofadversecardiovasculareventsinmyocardialinfarcts.ArchCardiolMex.2005;75Suppl3:S3-61-8.BlumA,MassachiR,MillerH.Thepredictivevalueofwhitebloodcellcountonthesuccessofprimaryinfarction.EurJInternMed.2004;15(3):176-180.KojimaS,SakamotoT,IshiharaM,KimuraK,MiyazakiS.Thewhitebloodcellcountisanindependentpredictorofno-reflowandmortalityfollowingacutemyocardialinfarctioninthecoronaryinterventionalera.AnnMed.LinkA,SchwerdtH,HennenB,BohmM.Polymorphonuclearneutrophilsinmyocardialischemiaandreperfusioninjury.Influenceofcoronaryintervention?ZKardiol.2004;93(8):605-11.HuczekZ,KochmanJ,FilipiakKJ,HorszczarukGJ,GrabowskiM.Meanplateletvolumeonadmissionpredictsimpairedreperfusionandlong-termmortalityinacutemyocardialinfarctiontreatedwithprimarypercutaneouscoronaryintervention.JAmCollCardiol.2005;46(2):284-90.HalkinA,StoneGW,GrinesCL,CoxDA,RutherfordBD.Prognosticimplicationsofcreatinekinaseelevationafterprimarypercutaneouscoronaryinterventionforacutemyocardialinfarction.JAmCollCardiol.2006;47(5):951-61.PrasadA,StoneGW,StuckeyTD,CostantiniCO,ZimetbaumPJ.ImpactofdiabetesmellitusonmyocardialTimmerJR,vanderHorstIC,OttervangerJP,HenriquesJP,HoorntjeJC.Prognosticvalueofadmissionglucoseinnon-diabeticpatientswithmyocardialinfarction.AmHeartJ.2004;148(3):399-404.IshiiH,IchimiyaS,KanashiroM,AmanoT,MatsubaraT,MuroharaT.Effectsofintravenousnicorandilbeforereperfusionforacutemyocardialinfarctioninpatientswithstresshyperglycemia.DiabetesCare.2006;29(2):202-6.congestiveheartfailureandpredictiveof30-dayuntowardclinicaloutcomesinpatientswithacutemyocardialinfarctionundergoingprimarypercutaneouscoronaryintervention.CircJ.2006;70(2):163-8.KatayamaT,NakashimaH,YonekuraT,HondaY,Suzuki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