·綜述·

慢性完全閉塞性病變血運(yùn)重建后臨床獲益的影響因素

劉鑫王齊兵

(復(fù)旦大學(xué)附屬中山醫(yī)院心內(nèi)科， 上海200032)

Factors Influencing on Clinical Benefit after Chronic Total Occlusion RevascularizationLIUXinWANGQibing

DepartmentofCardiology,ZhongshanHospital,FudanUniversity,Shanghai200032,China

慢性完全閉塞(chronic total occlusion,CTO)是指冠狀動(dòng)脈在粥樣硬化的基礎(chǔ)上由于血栓形成、機(jī)化導(dǎo)致其管腔完全閉塞，且閉塞的病程超過(guò)3個(gè)月。CTO冠狀動(dòng)脈造影靶血管前向血流消失,心肌梗死溶栓治療臨床試驗(yàn)(TIMI)分級(jí)為0級(jí)或1級(jí)，0級(jí)為絕對(duì)性CTO，1級(jí)為功能性CTO[1]。國(guó)外有文獻(xiàn)[2]報(bào)道，CTO在冠心病患者中的發(fā)生率約為18.4%；64%CTO的患者選擇藥物治療，26%選擇冠狀動(dòng)脈旁路移植術(shù)(CABG)，10%選擇冠狀動(dòng)脈介入術(shù)(PCI)。研究[3-6]證實(shí)，CTO病變開(kāi)通后可以帶來(lái)多項(xiàng)臨床獲益，包括患者左心室功能、生命質(zhì)量(SAQ量表)、心絞痛等改善，生存率提高，但心肌活性、缺血程度、側(cè)枝循環(huán)等因素可影響CTO血運(yùn)重建的獲益率。選擇獲益率較高的患者群進(jìn)行CTO血運(yùn)重建治療可降低醫(yī)療費(fèi)用、減少并發(fā)癥，進(jìn)而提高獲益率。

1影響CTO血運(yùn)重建治療獲益率的因素

1.1心肌活性多項(xiàng)研究[5，7-10]表明，CTO病變開(kāi)通后左室射血分?jǐn)?shù)(LVEF)提高，并且提高程度隨著心肌活性的下降而下降，CTO病變血管支配區(qū)域無(wú)陳舊性心肌梗死但存在左心室功能減退的患者LVEF提高更明顯。研究[10]表明，CTO血運(yùn)重建后LVEF的改善與MRI強(qiáng)化透壁梗死范圍(transmural extent of infarction,TEI)的基線值相關(guān)；TEI<25%時(shí)，CTO-PCI后病變局部室壁厚度(segmental wall thickeness,SWT)增加、心肌節(jié)段收縮功能明顯改善；TEI >75%時(shí)，PCI后SWT、心肌節(jié)段收縮功能改善不明顯；TEI 為25%~75%時(shí)，收縮功能改善率較小。而另有研究[5, 11]綜合應(yīng)用MRI中的多項(xiàng)指標(biāo)如TEI、SWT、多巴酚丁胺負(fù)荷MRI等評(píng)估心肌活性，并選擇適于進(jìn)行CTO-PCI的患者，發(fā)現(xiàn)術(shù)后左心室功能的改善率提高。MRI多項(xiàng)指標(biāo)聯(lián)合應(yīng)用在TEI 為25%~75%患者的心肌活性評(píng)估中顯得尤為重要。但一項(xiàng)小樣本研究[12]表明，即使CTO病變支配區(qū)域缺乏活性心肌，CTO血運(yùn)重建治療仍可帶來(lái)臨床獲益，CTO-PCI治療可輕度提高LVEF，減小左心室舒張末期容積?？傊?，心肌活性對(duì)于CTO血運(yùn)重建治療后的獲益十分重要，存活心肌的數(shù)量與臨床獲益相關(guān)。當(dāng)CTO病變血管支配區(qū)域存活心肌范圍較大時(shí)，應(yīng)更加積極地進(jìn)行血運(yùn)重建治療。

1.2心肌缺血程度心肌缺血程度與心肌活性緊密相關(guān)。一般存在心絞痛等臨床癥狀及運(yùn)動(dòng)試驗(yàn)陽(yáng)性常提示心肌缺血，同時(shí)提示缺血局部存在活性心肌，這是因?yàn)樾募〈婊钍切募∪毖那疤?，無(wú)臨床癥狀可能意味著心肌已完全壞死，而心肌梗死后的瘢痕組織不會(huì)引起心絞痛等癥狀。不合并其他冠狀動(dòng)脈狹窄的單支冠狀動(dòng)脈CTO者，可由臨床癥狀及運(yùn)動(dòng)試驗(yàn)來(lái)推斷心肌缺血程度。但若患者存在其他冠狀動(dòng)脈病變時(shí)，則不能確定臨床癥狀是由哪支病變血管引起的，不能僅根據(jù)臨床癥狀的輕重來(lái)判斷心肌活性及心肌缺血程度，行經(jīng)冠狀動(dòng)脈介入治療(PCI)前需行核素灌注掃描、負(fù)荷超聲心動(dòng)圖、心臟MRI等檢查，以進(jìn)一步明確CTO病變血管支配區(qū)域的心肌缺血程度。目前常用靜息和負(fù)荷時(shí)的心肌灌注程度來(lái)評(píng)估心肌缺血程度，無(wú)灌注缺陷提示不存在心肌缺血，可逆性灌注缺陷提示存在心肌缺血，而不可逆的灌注缺損常提示存在瘢痕組織[13]。值得注意的是，如急性心肌梗死后再灌注治療較晚，導(dǎo)致心肌完全壞死，核素灌注顯像等檢查可能正常，但增強(qiáng)心臟MRI檢查不能發(fā)現(xiàn)存活心肌[5]時(shí)，此時(shí)行CTO血運(yùn)重建治療的臨床獲益可能不大。一項(xiàng)研究[14]對(duì)成功實(shí)施前降支PCI的CTO患者按照術(shù)前核素顯像的結(jié)果進(jìn)行分層分析，發(fā)現(xiàn)不論是可逆性灌注缺陷還是不可逆性灌注缺陷，術(shù)后1年均有明顯臨床獲益，其中可逆性灌注缺陷組的獲益更大，而術(shù)前無(wú)灌注缺陷的患者未發(fā)現(xiàn)臨床獲益。另一項(xiàng)研究[15]納入301例行CTO-PCI的患者，分別于術(shù)前和術(shù)后(12±3)個(gè)月行靜息/負(fù)荷心肌灌注顯像，評(píng)估心肌缺血程度，將缺血心肌百分比下降5%定義為有意義的臨床獲益，發(fā)現(xiàn)缺血心肌百分比超過(guò)12.5%的患者術(shù)后缺血心肌百分比下降較明顯，而缺血心肌百分比小于6.5%的患者術(shù)后缺血心肌百分比則可能增加。另一項(xiàng)冠狀動(dòng)脈核素顯像研究[16]也提示，中重度的心肌缺血(缺血心肌百分比>10%)能從CTO血運(yùn)重建治療(CTO-PCI或CABG)中獲益，患者生存率提高。因此，冠狀動(dòng)脈CTO患者行CTO-PCI前檢查心肌缺血程度是必要的，心肌缺血百分比>10%可作為是否有臨床獲益可能的切點(diǎn)。

1.3臨床癥狀研究[2]表明，約50%的CTO患者有急性冠狀動(dòng)脈綜合征的臨床表現(xiàn)，其中呼吸困難比胸痛更常見(jiàn)、更特異；13%的患者無(wú)癥狀或僅有輕微臨床癥狀(加拿大心血管學(xué)會(huì)勞力型心絞痛分級(jí)0或1級(jí))；>50%的患者左心室功能正常，17%的患者有嚴(yán)重的左心室功能減退。研究[17]發(fā)現(xiàn)，有臨床癥狀的CTO患者中CTO-PCI成功組的心絞痛發(fā)作頻率、活動(dòng)耐力、生命質(zhì)量比CTO-PCI失敗組改善明顯；而在無(wú)臨床癥狀的CTO患者中，CTO-PCI成功與否和心絞痛發(fā)作頻率、活動(dòng)耐力、生命質(zhì)量無(wú)明顯相關(guān)性。但該項(xiàng)研究中治療失敗組的抗心絞痛藥物應(yīng)用量低于治療成功組，這可能影響試驗(yàn)結(jié)果的準(zhǔn)確性。對(duì)于無(wú)臨床癥狀或臨床癥狀輕微的冠狀動(dòng)脈CTO患者的臨床獲益尚需進(jìn)一步的研究。對(duì)于無(wú)明顯臨床癥狀的CTO患者，心肌梗死、心源性死亡、靶血管再次血運(yùn)重建等指標(biāo)或許能更客觀地評(píng)價(jià)CTO-PCI的臨床獲益。因此，對(duì)于臨床癥狀較明顯的CTO患者，應(yīng)更積極地進(jìn)行CTO血運(yùn)重建治療；而對(duì)于無(wú)臨床癥狀的CTO患者，是否行PCI治療應(yīng)參考心肌活性、心肌缺血程度等指標(biāo)。

1.4側(cè)枝循環(huán)側(cè)枝循環(huán)的形成是機(jī)體對(duì)CTO病變的代償性改變。在存在明顯血流動(dòng)力學(xué)改變的動(dòng)脈粥樣硬化病變患者中，約有35%可以形成良好的側(cè)枝循環(huán)[18-19]。側(cè)枝循環(huán)的形成與多種因素有關(guān)，如C1q/TNF相關(guān)蛋白、血清趨化因子、炎性反應(yīng)等都可能影響側(cè)枝循環(huán)的形成[20]。但是，側(cè)枝循環(huán)的形成不能為CTO病變血管支配區(qū)域心肌提供足夠的血供，易出現(xiàn)心肌缺血[21-22]。有研究[7]表明，良好的側(cè)枝循環(huán)與相應(yīng)區(qū)域的心肌活性無(wú)相關(guān)性，而良好的微循環(huán)對(duì)于心肌活性的作用可能更大；但由于微血管的管徑較小，冠狀動(dòng)脈造影常不能顯示。研究[22]對(duì)CTO患者行血流儲(chǔ)備分?jǐn)?shù)(fractional flow reserve,FFR)檢查，結(jié)果表明，病變相應(yīng)區(qū)域不論是否存在廣泛的側(cè)枝循環(huán)、CTO病變位置如何、無(wú)創(chuàng)檢查結(jié)果是否陽(yáng)性，大多存在明顯的血流動(dòng)力學(xué)改變及心肌缺血，良好的側(cè)枝循環(huán)不能為心肌提供足夠的血供。良好的側(cè)枝循環(huán)還可能增加心血管不良事件的風(fēng)險(xiǎn)，比如發(fā)生急性心肌梗死時(shí)，常出現(xiàn)更大面積的梗死和更高水平的心肌酶升高，從而更易導(dǎo)致心源性休克[23]。因此，不能依據(jù)是否存在良好的側(cè)枝循環(huán)來(lái)決定是否行CTO血運(yùn)重建治療，但較好的側(cè)枝血管為PCI中逆向?qū)б摻z技術(shù)提供了可能，提高了CTO-PCI的成功率。

1.5CTO病變位置研究[2]表明，約47%的CTO位于右冠狀動(dòng)脈，20%位于前降支，16%位于左旋支，有17%的患者CTO病變出現(xiàn)在多支冠狀動(dòng)脈；多數(shù)CTO病變位于冠狀動(dòng)脈的近端或中段。有兩項(xiàng)研究發(fā)現(xiàn)CTO病變位置與患者預(yù)后有關(guān)。一項(xiàng)研究[24]納入2 608例行CTO-PCI治療的患者，隨訪5年，發(fā)現(xiàn)只有前降支CTO病變患者中CTO-PCI成功組生存率比失敗組高，而右冠狀動(dòng)脈及左旋支CTO病變患者中兩組生存率差異無(wú)統(tǒng)計(jì)學(xué)意義。另一項(xiàng)研究[25]納入1 734例患者，發(fā)現(xiàn)前降支和左旋支CTO病變患者中CTO-PCI成功組生存率均高于失敗組，而右冠狀動(dòng)脈CTO病變患者中兩組生存率差異無(wú)統(tǒng)計(jì)學(xué)意義。產(chǎn)生上述差異的可能原因有：(1)前降支CTO病變可以引起心臟自主神經(jīng)紊亂，而自主神經(jīng)紊亂如副交感神經(jīng)活性增強(qiáng)可增加室性心律失常的發(fā)生率，而開(kāi)通前降支CTO血管后可以改善心臟自主神經(jīng)功能并減少室速、室顫等嚴(yán)重心律失常的發(fā)生，進(jìn)而提高患者生存率[26]；(2)前降支血管支配心肌范圍較廣，對(duì)心臟功能的影響更大。

1.6心肌梗死在ST段抬高型心肌梗死(STEMI)患者中，約10%合并非梗死血管的CTO病變，此類患者常存在多支冠狀動(dòng)脈病變。非梗死血管的CTO病變常與STEMI患者的不良預(yù)后相關(guān)；且伴非梗死血管CTO病變者常伴更多的合并癥、心血管危險(xiǎn)因素，心肌酶及心肌壞死程度也高于不合并CTO病變的患者。在TAPAS和HORIZONS-AMI試驗(yàn)的子研究中發(fā)現(xiàn)，合并非梗死血管CTO病變的STEMI患者ST段回落程度、心肌灌注顯像、治療后梗死相關(guān)血管的TIMI血流分級(jí)均明顯差于不合并CTO病變的患者[27-29]。在非ST段抬高型心肌梗死患者中也有類似的報(bào)道[30]。雖然已有研究[31-34]證明，完全性血運(yùn)重建治療較不完全性血運(yùn)重建能更好地提高患者的生存率、改善其臨床癥狀，但是，CTO-PCI治療的難度較大、手術(shù)時(shí)間較長(zhǎng)，在急性心肌梗死患者中直接PCI對(duì)非梗死相關(guān)血管CTO病變行血運(yùn)重建治療能否帶來(lái)臨床獲益，以及對(duì)該類患者是選擇PCI治療還是CABG治療，目前尚無(wú)定論。

1.7冠狀動(dòng)脈多支病變CTO常出現(xiàn)在有多支冠狀動(dòng)脈病變的患者中，而CTO-PCI的臨床獲益可能與患者病變血管數(shù)量及病變程度相關(guān)。有研究[9, 35-36]表明，只有1處CTO病變的單支血管病變患者的病死率低，而病死率與CTO-PCI的成功與否無(wú)關(guān)；CTO合并冠狀動(dòng)脈多支病變的患者中，CTO-PCI成功組的生存率明顯高于失敗組。也有研究[37]表明，對(duì)于CTO合并冠狀動(dòng)脈多支病變的患者，完全血運(yùn)重建治療可以提高生存率；僅1支CTO病變血管且未開(kāi)通的患者的病死率沒(méi)有增加；而1支非CTO病變血管未治療的患者或2支血管(不論其是否為CTO病變)未治療的患者，其病死率均增加。研究[38-39]表明，在行左主干病變PCI治療的患者中，合并右冠狀動(dòng)脈CTO病變者的長(zhǎng)期預(yù)后明顯差于右冠狀動(dòng)脈正?；蛴夜跔顒?dòng)脈非CTO病變的患者；并且，在合并左主干非CTO病變的患者中，右冠狀動(dòng)脈CTO-PCI成功組的病死率低于失敗組或未治療組。這些研究提示，CTO合并存在其他需要血運(yùn)重建治療的冠脈血管時(shí)，CTO病變血管的血運(yùn)重建可進(jìn)一步提高臨床獲益。因此，當(dāng)合并有多支血管病變時(shí)，尤其對(duì)于合并有左主干病變的右冠狀動(dòng)脈CTO病變，可優(yōu)先處理CTO病變，后期再處理非CTO病變，以進(jìn)一步提高臨床獲益，降低PCI手術(shù)風(fēng)險(xiǎn)，這也是臨床上常用的PCI治療策略。

2CTO病變治療方案的選擇

目前，CTO病變患者中，約64%選擇藥物治療，26%選擇CABG，10%選擇PCI治療。雖然目前多項(xiàng)臨床研究證實(shí)CTO病變開(kāi)通后可以帶來(lái)左心室功能、生命質(zhì)量(SAQ量表)、心絞痛改善及生存率提高等多項(xiàng)臨床獲益，但由于這些研究為回顧性研究，并且大多未提供患者詳細(xì)的藥物治療情況，且進(jìn)行藥物治療者未采用最佳治療方案和藥物劑量，所以，CTO病變的血運(yùn)重建治療相對(duì)于最佳藥物治療的獲益尚存在爭(zhēng)議。而CABG、CTO-PCI技術(shù)要求較高，費(fèi)用高，且存在一定風(fēng)險(xiǎn)。因此，對(duì)于CTO病變，目前多數(shù)患者選擇藥物治療。

CABG和PCI均可以改善CTO患者的臨床預(yù)后，但研究[40-41]顯示，CABG比CTO-PCI的成功率略高，尤其是在心臟外科與介入治療狹窄冠狀動(dòng)脈研究評(píng)分(SYNTAX評(píng)分)、日本CTO病變多中心注冊(cè)研究評(píng)分(J-CTO評(píng)分)為中重度病變的患者中。另有研究[4,35,42]表明，CABG術(shù)后的靶血管再次血運(yùn)重建治療(target vessel revascularization,TVR)不良事件發(fā)生率低于CTO-PCI術(shù)后。因此多項(xiàng)臨床指南對(duì)于復(fù)雜血管病變、多支血管病變、左主干冠狀動(dòng)脈病變等仍優(yōu)先推薦CABG治療[43]。但是，近年來(lái)隨著CTO專用導(dǎo)管、導(dǎo)絲的出現(xiàn)，逆向?qū)б摻z技術(shù)的應(yīng)用以及術(shù)者技術(shù)經(jīng)驗(yàn)的提升，CTO-PCI的成功率也明顯提高。

3小結(jié)

多項(xiàng)因素可影響CTO病變經(jīng)血運(yùn)重建治療的獲益率，這些因素包括心肌活性、心肌缺血程度、臨床癥狀、側(cè)枝循環(huán)、病變位置、是否合并冠狀動(dòng)脈多支病變、是否合并心肌梗死等。對(duì)于CTO病變，是選擇最佳藥物治療還是血運(yùn)重建治療，目前仍無(wú)定論。在選擇CTO治療方案時(shí)需綜合評(píng)估上述影響因素，并選擇血運(yùn)重建獲益率較高的患者行CTO血運(yùn)重建治療。當(dāng)決定行血運(yùn)重建治療時(shí)，需進(jìn)一步根據(jù)病變復(fù)雜程度、SYNTAX評(píng)分、J-CTO評(píng)分、患者全身情況等決定選擇CABG還是CTO-PCI。

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中圖分類號(hào)R541.4

文獻(xiàn)標(biāo)識(shí)碼A

通訊作者王齊兵，E-mail:wang.qibing@zs-hospital.sh.cn