田　塬　柯永勝

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血管內(nèi)超聲在左主干病變介入治療中的應(yīng)用

田塬柯永勝

241000安徽省皖南醫(yī)學(xué)院第一附屬醫(yī)院弋磯山醫(yī)院心內(nèi)科

【摘要】冠狀動(dòng)脈造影只能提供血管腔的二維圖像，對(duì)于左主干病變的診斷有局限性。血管內(nèi)超聲作為目前應(yīng)用最廣泛、最成熟的血管內(nèi)成像技術(shù)，可提供血管壁、內(nèi)徑、斑塊負(fù)荷等信息，有助于術(shù)者判斷臨界病變，并選擇最佳的治療策略及手術(shù)器械，從而優(yōu)化左主干病變的介入治療，預(yù)防和減少并發(fā)癥。

【關(guān)鍵詞】左主干；血管內(nèi)超聲；經(jīng)皮冠狀動(dòng)脈介入治療；藥物洗脫支架

冠狀動(dòng)脈(冠脈)造影(CAG)一直被認(rèn)為是診斷冠狀動(dòng)脈粥樣硬化性心臟病(冠心病)的“金標(biāo)準(zhǔn)”，然而CAG只能提供管腔的二維圖像，造影結(jié)果常受到左主干長(zhǎng)度、直徑變異大、無(wú)參照血管、三分叉掩蓋左主干遠(yuǎn)端開(kāi)口等的限制，而無(wú)法精確地評(píng)價(jià)冠脈管腔真實(shí)直徑、斑塊負(fù)荷、血管鈣化及成角等解剖特點(diǎn)，對(duì)于左主干病變的診斷具有局限性。左主干為前降支(LAD)和回旋支(LCX)供血，是最重要的冠脈血管段，因此左主干病變預(yù)后最差。隨著經(jīng)皮冠脈介入治療(PCI)和藥物洗脫支架(DES)的發(fā)展，無(wú)保護(hù)左主干(unprotect left main coronary artery，ULMCA)病變PCI手術(shù)量快速增加[1]。2009年美國(guó)心臟病學(xué)會(huì)/美國(guó)心臟協(xié)會(huì)(ACC/AHA)指南指出，在預(yù)測(cè)接受外科手術(shù)預(yù)后差和PCI相關(guān)并發(fā)癥發(fā)生率較低的解剖學(xué)情況下，PCI由原本的Ⅲ類適應(yīng)證升級(jí)為Ⅱb類[2]，因此左主干的PCI治療有廣闊的前景，如何優(yōu)化ULMCA病變的PCI策略尤為重要。血管內(nèi)超聲(IVUS)作為目前應(yīng)用最廣泛、最成熟的血管內(nèi)成像技術(shù)，可提供包括血管壁、內(nèi)徑、斑塊負(fù)荷及其形態(tài)和組成等信息，尤其可以直觀而精確地呈現(xiàn)左主干及其分支的斑塊分布及性質(zhì)，有助于術(shù)者選擇最佳治療策略及手術(shù)器械，尤其適用于復(fù)雜左主干病變的診治[3]。

1判斷臨界病變

如何判斷臨界病變一直是冠心病診治的困境，由于CAG很難判斷相對(duì)正常的血管，尤其難以區(qū)分40%～70%的狹窄在血流動(dòng)力學(xué)方面究竟是臨界病變還是中度病變[4-5]。左主干較短，病變彌漫性時(shí)CAG無(wú)法判斷血管真實(shí)直徑，此時(shí)IVUS的高分辨率圖像就顯得尤其重要[6-7]。最小管腔面積(minimal luminal area，MLA)是最常用的左主干病變狹窄嚴(yán)重程度的替代指標(biāo)，也是左主干病變晚期主要心血管不良事件(MACE)的重要預(yù)測(cè)指標(biāo)[8]，臨床上可以參考MLA來(lái)決定是否對(duì)左主干病變進(jìn)行干預(yù)或者延期治療。

IVUS結(jié)合冠脈血流儲(chǔ)備分?jǐn)?shù)(franctional flow reserve，F(xiàn)FR)的功能學(xué)評(píng)價(jià)對(duì)臨界病變的判斷更為精確。研究發(fā)現(xiàn)FFR>0.75時(shí)推遲介入是合理的，而且FFR值與MLA具有高度的相關(guān)性[9-11]。

一項(xiàng)針對(duì)55例穩(wěn)定的左主干狹窄患者的單中心研究發(fā)現(xiàn)，與FFR<0.75相關(guān)性最好的MLA臨界值是5.9 mm2[11]；之后的前瞻性多中心LITRO研究入選了345例左主干臨界病變的患者，其中MLA≥6 mm2的患者推遲血運(yùn)重建，MLA<6 mm2的患者則接受血運(yùn)重建。結(jié)果顯示，未接受血運(yùn)重建組的2年無(wú)事件生存率是97.7%，而血運(yùn)重建組是94.5%(P=0.5)，因此認(rèn)為MLA>6.0 mm2的患者延期血運(yùn)重建的風(fēng)險(xiǎn)較低[12]。近期的一項(xiàng)單中心研究將112例ULMCA病變的患者隨機(jī)分為兩組，以FFR=0.80作為判斷MLA的臨界值，結(jié)果顯示對(duì)于左主干口部和體部的狹窄，MLA≤ 4.5 mm2是 FFR≤0.80的獨(dú)立影響因素(敏感度77%，特異度82%，OR=0.83, 95%CI: 0.759～0.960，P<0.001)，故建議MLA=4.5 mm2作為臨界病變是否需要即刻或延遲血運(yùn)重建的新標(biāo)準(zhǔn)[13]。然而左主干直徑變異大，該臨界值顯然不能完全適用于所有患者，且根據(jù)該試驗(yàn)提供的數(shù)據(jù)也不難看出，當(dāng)MLA調(diào)整至6 mm2時(shí)可以得到更高的FFR值。2015年一項(xiàng)評(píng)估MLA精確性的meta分析入選了2項(xiàng)針對(duì)左主干病變的研究(n=110)，結(jié)果顯示MLA臨界值為5.4 mm2(5.1～5.6 mm2)[14]。另一項(xiàng)薈萃分析同樣入選了這兩個(gè)研究，結(jié)果發(fā)現(xiàn)，相比FFR，IVUS對(duì)左主干復(fù)雜病變的預(yù)測(cè)更精確[15]。雖然MLA的臨界值一直沒(méi)有定論，但根據(jù)各項(xiàng)研究結(jié)果，目前的美國(guó)專家共識(shí)仍建議決策左主干病變血運(yùn)重建策略為MLA<6.0 mm2[16]。

IVUS對(duì)于左主干臨界病變的評(píng)判標(biāo)準(zhǔn)仍需更多大樣本臨床數(shù)據(jù)來(lái)說(shuō)明。需要指出的是，并不能完全依賴IVUS顯示的管腔面積大小來(lái)評(píng)估心肌是否缺血，因?yàn)槌芮幻娣e外，心肌缺血還受病變長(zhǎng)短、側(cè)支循環(huán)以及遠(yuǎn)端微血管損傷等因素的影響。因此McDaniel等[17]提議，對(duì)于經(jīng)IVUS測(cè)得MLA<6 mm2的左主干病變患者，應(yīng)通過(guò)FFR或其他無(wú)創(chuàng)檢查評(píng)估心肌是否缺血，而MLA>6 mm2者應(yīng)推遲血運(yùn)重建。

2指導(dǎo)PCI過(guò)程

PCI術(shù)前，IVUS可以測(cè)量管腔直徑及病變長(zhǎng)度以指導(dǎo)支架的選擇；PCI術(shù)后，IVUS可評(píng)估PCI并發(fā)癥及支架置入效果，對(duì)于左主干病變尤其具有不可替代的參考價(jià)值。2011年美國(guó)心臟病學(xué)會(huì)/美國(guó)心臟協(xié)會(huì)/美國(guó)心血管造影和介入學(xué)會(huì)(ACC/AHA/SCAI)PCI指南指出，左主干PCI中使用IVUS是Ⅱb類適應(yīng)證[18]， 2014年新指南更加強(qiáng)調(diào)了其必要性[19]。

左主干病變分為口部、體部及末端分叉病變，其中分叉病變約占60%，非分叉病變約40%。左主干開(kāi)口病變支架置入后需要IVUS來(lái)判斷支架膨脹狀態(tài)和有無(wú)夾層，并確定開(kāi)口是否被完全覆蓋。左主干末端分叉病變的介入治療是技術(shù)難點(diǎn)，可先行IVUS進(jìn)行預(yù)判，如發(fā)現(xiàn)鈣化程度較重，可先采用旋磨術(shù)旋切鈣化斑塊，幫助支架通過(guò)；當(dāng)判斷一側(cè)血管閉塞可能性較小時(shí)，多采用單支架術(shù)式。研究表明，LCX開(kāi)口病變不明顯時(shí)，單支架技術(shù)的遠(yuǎn)期效果優(yōu)于雙支架技術(shù)，但如果LCX開(kāi)口病變明顯，單支架會(huì)對(duì)預(yù)后產(chǎn)生不利影響，因?yàn)閱沃Ъ軓腖AD跨越至左主干，尤其當(dāng)LAD、LCX分叉角度較小時(shí)，有使LCX開(kāi)口發(fā)生幾何形態(tài)改變的風(fēng)險(xiǎn)，主要與隆脊移位(carina shift)、MLA縮小等有關(guān)，而非斑塊移位(plaque shift)所致[20-23]。當(dāng)單支架跨越LAD和左主干時(shí)，如造影提示累及LCX開(kāi)口>50%，則必須行IVUS或FFR對(duì)分支血管口部結(jié)構(gòu)及功能學(xué)進(jìn)行評(píng)估，幫助術(shù)者決定是否需要干預(yù)邊支[24]。如需干預(yù)邊支但不置入支架，當(dāng)行最終對(duì)吻擴(kuò)張(final kissing inflation)以保證邊支安全。雙支架術(shù)式主要包括Crush、Cullotte、T支架術(shù)式，當(dāng)一側(cè)血管閉塞率較高時(shí)使用。需強(qiáng)調(diào)的是，無(wú)論采用何種雙支架術(shù)式，最后都必須使用高壓球囊進(jìn)行對(duì)吻擴(kuò)張，并用IVUS來(lái)判斷支架膨脹狀況。

Kang等[25]對(duì)左主干單支架和雙支架(Crush和T支架技術(shù))術(shù)后患者(n=403)隨訪9個(gè)月發(fā)現(xiàn)，IVUS測(cè)定的最小支架面積(MSA)可預(yù)測(cè)支架內(nèi)再狹窄，臨界值分別為 5.0 mm2(LCX開(kāi)口處)、6.3 mm2(LAD開(kāi)口處)、7.2 mm2(分支匯合處)和8.2 mm2(分支匯合處以上臨近部位的左主干)。CROSS研究和PERFECT研究的亞組分析顯示，最終對(duì)吻擴(kuò)張是預(yù)測(cè)邊支無(wú)狹窄(<50%)的單支架術(shù)后患者支架內(nèi)再狹窄的獨(dú)立影響因素[26]，而IVUS是唯一能夠提高最終對(duì)吻擴(kuò)張質(zhì)量的方法。

IVUS指導(dǎo)DES置入的優(yōu)勢(shì)在于減少圍手術(shù)期并發(fā)癥，如邊支閉塞、支架邊緣夾層及血腫、支架膨脹不全、支架不完全重疊等。通過(guò)IVUS評(píng)價(jià)支架膨脹不全、異位、不完全覆蓋病變以及斑塊的殘留可以預(yù)測(cè)DES置入后支架血栓的形成[27-30]。

對(duì)2 193例DES置入患者的薈萃分析顯示，與冠脈造影指導(dǎo)下相比，IVUS預(yù)先指導(dǎo)下支架置入患者的MLA更大，支架內(nèi)再狹窄概率更小(OR= 0.64， 95% CI:0.42 ～0.96，P=0.02)，再次血運(yùn)重建減少(OR=0.66，95% CI: 0.48～0.91，P=0.004)。但相對(duì)于降低再狹窄或再次血運(yùn)重建，IVUS指導(dǎo)DES置入似乎與減少心肌梗死的發(fā)生和降低死亡風(fēng)險(xiǎn)的相關(guān)度更高[31]。

另一項(xiàng)薈萃分析總結(jié)了近年來(lái)的3項(xiàng)大型臨床隨機(jī)研究及14項(xiàng)觀察性研究(包含2項(xiàng)左主干病變研究)，總計(jì)26 503例DES置入患者，其中14 004例在IVUS指導(dǎo)下置入支架，12 499例在冠脈造影指導(dǎo)下置入支架，主要的臨床終點(diǎn)是死亡率、心肌梗死、支架內(nèi)血栓以及靶病變血運(yùn)重建(target lesion revascularization，TLR)。結(jié)果顯示，IVUS指導(dǎo)的PCI置入的支架更多、更長(zhǎng)、內(nèi)徑更大，TLR風(fēng)險(xiǎn)顯著降低(OR=0.81,95%CI：0.66～1.00，P=0.046)，死亡率(OR=0.61,95%CI：0.48～0.79，P<0.001)、心肌梗死(OR=0.57,95%CI：0.44～0.75，P<0.001)以及支架內(nèi)血栓形成(OR=0.59,95%CI：0.47～0.75，P<0.001)均顯著降低[32]。另一項(xiàng)薈萃分析(n=24 849)得出了類似的結(jié)論，即IVUS指導(dǎo)的DES置入較造影指導(dǎo)不僅減少了21%的MACE事件和36%的死亡風(fēng)險(xiǎn)，也減少了心肌梗死和TLR等并發(fā)癥的發(fā)生[33]。

IVUS指導(dǎo)下的ULMCA患者行PCI是否能長(zhǎng)期獲益目前仍沒(méi)有定論。MAIN-COMPARE研究入選了相互匹配的201對(duì)ULMCA的患者，與單純?cè)煊敖M相比，IVUS指導(dǎo)組3年的死亡率有降低的趨勢(shì)(6.0%對(duì)13.6%，P=0.063)，尤其是對(duì)置入DES的患者，IVUS指導(dǎo)組相比造影組3年死亡率顯著降低(4.7%對(duì)16.0%,P=0.048)。而對(duì)于置入金屬裸支架的患者，IVUS組與造影組的死亡率無(wú)明顯差異(8.6%對(duì)10.8%,P=0.35)[34]。

最近一項(xiàng)針對(duì)ULMCA的薈萃分析入選了4項(xiàng)注冊(cè)試驗(yàn)，共1 670例ULMCA病變并接受DES置入的患者。對(duì)比分析后認(rèn)為，IVUS組術(shù)后3年內(nèi)未發(fā)生死亡、心肌梗死和TLR的患者占88.7%，非IVUS組為83.6%(P=0.04)；在左主干遠(yuǎn)端病變亞組中，IVUS術(shù)后3年內(nèi)未發(fā)生死亡、心肌梗死、TLR的患者比例占90.0%，非IVUS組為80.7%(P=0.03)，且IVUS組支架內(nèi)血栓發(fā)生率明顯較低(0.6%對(duì)2.2%，P= 0.04)。IVUS指導(dǎo)的血運(yùn)重建是預(yù)測(cè)術(shù)后主要不良事件的獨(dú)立影響因素(HR=0.70, 95%CI: 0.52～0.99，P=0.04)。該研究還發(fā)現(xiàn)，IVUS并沒(méi)有減少TLR的發(fā)生，僅在置入雙支架的患者中，TLR的發(fā)生率有降低的趨勢(shì)[35]。

3展望

IVUS可通過(guò)預(yù)先評(píng)估病變指導(dǎo)PCI策略，通過(guò)優(yōu)化DES的置入來(lái)保證PCI的成功，從而改善患者預(yù)后。然而，對(duì)于功能學(xué)的評(píng)估仍是FFR更有優(yōu)勢(shì)，故目前更主張結(jié)合IVUS、FFR共同優(yōu)化左主干的PCI策略，而IVUS是否可使ULMCA患者長(zhǎng)期獲益則有待進(jìn)一步的隨機(jī)對(duì)照研究來(lái)證實(shí)。

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(收稿：2015-12-07修回：2016-04-10)

(本文編輯：梁英超)

通信作者：柯永勝，Email：keyongsheng@163.com

doi:10.3969/j.issn.1673-6583.2016.03.004