



摘要:目的" 評(píng)估單側(cè)頸內(nèi)動(dòng)脈閉塞(ICAO)患者癥狀與腦灌注關(guān)系、閉塞時(shí)期及位置對(duì)腦灌注的影響。方法" 納入2021年9月~2023年3月在西安交通大學(xué)第二附屬醫(yī)院神經(jīng)內(nèi)科就診的符合納入排除標(biāo)準(zhǔn)的16例ICAO患者,通過(guò)Dr Brain's軟件動(dòng)脈自旋標(biāo)記模塊計(jì)算區(qū)域腦血流量(CBF)。比較癥狀性及無(wú)癥狀I(lǐng)CAO、急性及慢性ICAO、起始部及顱內(nèi)段閉塞患者全腦、雙側(cè)大腦中動(dòng)脈供血區(qū)、大腦前動(dòng)脈供血區(qū)、ASPECTS區(qū)域(尾狀核、豆?fàn)詈恕u帶、內(nèi)囊、M1、M2、M3、M4、M5、M6)、腦葉(額葉、頂葉、顳葉、島葉)的區(qū)域腦血流量在標(biāo)記后延遲時(shí)間(PLD)為1.5 s和2.5 s的差異。結(jié)果" 癥狀性及無(wú)癥狀、急性及慢性、起始部及顱內(nèi)段ICAO患者全腦CBF、非閉塞側(cè)半球各區(qū)域CBF在PLD 1.5 s 及 PLD 2.5 s的差異均無(wú)統(tǒng)計(jì)學(xué)意義(Pgt;0.05)。起始部和顱內(nèi)段ICAO患者閉塞側(cè)半球區(qū)域CBF在PLD 1.5 s及PLD 2.5 s的差異均無(wú)統(tǒng)計(jì)學(xué)意義(Pgt;0.05)。在PLD 1.5 s時(shí),癥狀性ICAO患者閉塞側(cè)M5區(qū)域CBF較無(wú)癥狀者明顯降低,閉塞側(cè)內(nèi)囊CBF較無(wú)癥狀者升高(Plt;0.05);在PLD 2.5 s時(shí),癥狀性及無(wú)癥狀I(lǐng)CAO患者各區(qū)域CBF的差異均無(wú)統(tǒng)計(jì)學(xué)意義(Pgt;0.05)。在PLD 1.5 s時(shí),急性ICAO患者閉塞側(cè)大腦中動(dòng)脈、M1、M5及額葉區(qū)域CBF較慢性ICAO者降低(Plt;0.05);在PLD 2.5 s時(shí),急性ICAO患者在閉塞側(cè)大腦中動(dòng)脈、M1、M5、M6及額葉的區(qū)域CBF較慢性ICAO者降低(Plt;0.05)。結(jié)論" 急性ICAO較慢性ICAO患者閉塞側(cè)大腦中動(dòng)脈供血區(qū)和部分ASPECTS皮質(zhì)區(qū)域腦灌注受損更加嚴(yán)重,癥狀性ICAO與閉塞側(cè)ASPECT部分區(qū)域灌注進(jìn)一步受損有關(guān),頸內(nèi)動(dòng)脈不同閉塞位置的腦灌注無(wú)差異。
關(guān)鍵詞:動(dòng)脈自旋標(biāo)記;頸內(nèi)動(dòng)脈閉塞;腦血流量;缺血性卒中;血流動(dòng)力學(xué)
Relationship between symptoms, occlusion period, and site with cerebral perfusion in patients with internal carotid artery occlusion
ZHANG Guirong, ZHANG Yanyan, LIANG Wenbin, DING Dun
Department of Medical Imaging, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China
Abstract: Objective To assess the relationship between symptoms and cerebral perfusion in patients with unilateral internal carotid artery occlusion (ICAO), and the influence of the occlusion period and location on cerebral perfusion. Methods Sixteen patients with ICAO who met the inclusion and exclusion criteria were enrolled in the Department of Neurology of the Second Affiliated Hospital of Xi'an Jiaotong University from September 2021 to March 2023. Regional cerebral blood flow (CBF) was measured by Dr Brain's software ASL module. Differences in regional CBF in global, middle cerebral artery (MCA) territory, anterior cerebral artery territory, Alberta Stroke Programme Early Computed Tomography Score (ASPECTS) regions (include caudate nucleus, lentiform nucleus, insula ribbon, internal capsule and M1-M6) and brain lobes (include frontal, parietal, temporal, insular lobe) of different subgroups (symptomatic and asymptomatic, acute and chronic, initial and intracranial ICAO) at PLD 1.5 s and PLD 2.5 s were evaluated. Results The CBF of symptomatic and asymptomatic, acute and chronic, initial and intracranial ICAO patients found no differences in the global and contralateral hemisphere at PLD 1.5 s and PLD 2.5 s (Pgt;0.05). The CBF of initial and intracranial ICAO patients found no differences in the ipsilateral hemisphere at PLD 1.5 s and PLD 2.5 s (Pgt;0.05). In the occluded hemisphere, the CBF of symptomatic ICAO was significantly lower than that of asymptomatic at PLD 1.5 s in M5, the CBF of symptomatic was significantly higher than that of asymptomatic at PLD 1.5 s in internal capsule (Plt;0.05). The CBF of symptomatic and asymptomatic ICAO found no differences in the ipsilateral hemisphere at PLD 2.5 s (Pgt;0.05). In the occluded hemisphere, the CBF of acute ICAO was significantly lower than that of chronic at PLD 1.5 s in middle cerebral artery territory, M1, M5, frontal lobe; the CBF of acute ICAO was significantly lower than that of chronic at PLD 2.5 s in middle cerebral artery territory, M1, M5, M6, frontal lobe (Plt;0.05). Conclusion Acute ICAO has further perfusion impairment than chronic ICAO in the middle cerebral artery territory and partly ASPECTS cortical areas of the occluded side. Symptomatic ICAO was associated with further perfusion impairment in partly ASPECT area of the occluded side. There was no significant difference in cerebral perfusion at different locations of internal carotid artery occlusion.
Keywords:" arterial spin labeling; internal carotid artery occlusion; cerebral blood flow; ischemic stroke; hemodynamic
動(dòng)脈粥樣硬化性頸內(nèi)動(dòng)脈閉塞(ICAO)是腦缺血事件的重要原因,栓塞和灌注不足是腦卒中的兩個(gè)重要機(jī)制[1, 2] 。腦灌注成像是評(píng)估腦血流動(dòng)力學(xué)變化的功能成像方法,三維動(dòng)脈自旋標(biāo)記(ASL)磁共振成像可實(shí)現(xiàn)腦血流量無(wú)創(chuàng)定量評(píng)估。臨床上頸內(nèi)動(dòng)脈閉塞人群的臨床癥狀、影像改變表現(xiàn)出巨大異質(zhì)性,但相關(guān)ASL灌注研究較少;且既往研究采用單一標(biāo)記后延遲時(shí)間(PLD)或手動(dòng)繪制區(qū)域興趣,使得腦血流量(CBF)測(cè)量耗時(shí)、費(fèi)力。隨著人工智能技術(shù)的發(fā)展,Dr Brain-ASL軟件可以實(shí)現(xiàn)快速全腦和解剖區(qū)域腦血流定量測(cè)量。
頸內(nèi)動(dòng)脈閉塞包括急性和慢性閉塞,既往研究顯示急性ICAO與臨床預(yù)后差有關(guān)[3, 4] 。ICAO患者可出現(xiàn)不同的臨床特征,從無(wú)癥狀到短暫性腦缺血發(fā)作(TIA)或急性嚴(yán)重卒中綜合征[5] 。有癥狀I(lǐng)CAO患者的缺血性事件復(fù)發(fā)率為每年10%~18%,但無(wú)癥狀I(lǐng)CAO患者的復(fù)發(fā)率相對(duì)較低[6] 。ICAO可發(fā)生在任何節(jié)段,顱內(nèi)段和顱外段頸內(nèi)動(dòng)脈閉塞具有不同的臨床和影像學(xué)特征[7] 。閉塞部位是與預(yù)后不良相關(guān)的變量之一[8] 。Alberta卒中項(xiàng)目早期CT評(píng)分(ASPECTS)是一種簡(jiǎn)單可靠的定性評(píng)分系統(tǒng),廣泛用于評(píng)估早期缺血性腦梗死的嚴(yán)重程度,是血管內(nèi)治療決策的重要篩選標(biāo)準(zhǔn)[9-12] ,有助于預(yù)測(cè)治療效果和預(yù)后。ASPECTS評(píng)分,現(xiàn)已從CT平掃延伸至MR的DWI/FLAIR等序列來(lái)進(jìn)行梗死評(píng)分,腦灌注成像較常規(guī)序列能更早識(shí)別梗死及缺血區(qū),但目前ASPECTS相關(guān)區(qū)域的灌注評(píng)價(jià)研究尚缺乏。本研究擬采用新CBF定量軟件分析方法評(píng)估包括常規(guī)前循環(huán)腦區(qū)以及ASPECTS區(qū)域在內(nèi)的腦灌注改變,旨在探討ICAO患者的癥狀與腦灌注的關(guān)系,閉塞時(shí)期和閉塞部位對(duì)腦灌注影響,進(jìn)一步細(xì)化ICAO患者腦灌注評(píng)估工作,為明確頸內(nèi)動(dòng)脈閉塞患者臨床和影像特征異質(zhì)性原因提供客觀證據(jù),加深臨床醫(yī)生對(duì)該類病變認(rèn)識(shí),進(jìn)而指導(dǎo)臨床決策,為后續(xù)研究提供基礎(chǔ)。
1" 資料與方法
1.1" 一般資料
本研究經(jīng)我院倫理學(xué)審批通過(guò)(審批號(hào):2022156)。選擇2021年9月~2023年3月在西安交通大學(xué)第二附屬醫(yī)院神經(jīng)內(nèi)科就診的頸內(nèi)動(dòng)脈閉塞患者。納入標(biāo)準(zhǔn):行數(shù)字減影血管造影檢查并確診單側(cè)ICAO的患者;同期行PLD 1.5 s、PLD 2.5 s的3D-pCASL成像。排除標(biāo)準(zhǔn):對(duì)側(cè)血管有中度或重度狹窄(≥50%);圖像質(zhì)量差或ASL使用單PLD或其它標(biāo)記后延遲時(shí)間掃描;患有腦損傷/手術(shù)/精神疾病/其他影響大腦的疾病。
36例ICAO患者中,排除對(duì)側(cè)頭頸部血管狹窄程度大于50%患者10例,排除伴有癲癇和既往顱腦手術(shù)患者2例,排除單PLD患者8例。最終16例ICAO患者(2例女性和14例男性;年齡57.06±11.24歲)納入本研究。患者分組如下:腦或視網(wǎng)膜缺血表現(xiàn)包括與同側(cè)頸內(nèi)動(dòng)脈閉塞(ICA)相關(guān)的短暫性或非致殘性癥狀,定義為有癥狀[13] ,否則定義為無(wú)癥狀患者,本組有癥狀I(lǐng)CAO患者11例,無(wú)癥狀I(lǐng)CAO患者5例。根據(jù)臨床和影像學(xué)的相關(guān)證據(jù),參考既往文獻(xiàn)[14, 15] ,將閉塞時(shí)間小于1周定義為急性ICAO,大于4周定義為慢性ICAO,本組8例為急性ICAO,8例為慢性ICAO。根據(jù)閉塞部位,8例為頸內(nèi)動(dòng)脈起始部閉塞,8例為頸內(nèi)動(dòng)脈顱內(nèi)段閉塞。各組間年齡、性別的差異無(wú)統(tǒng)計(jì)學(xué)意義(Pgt;0.05)。
1.2" MRI成像
全腦三維pCASL序列使用3.0T MR掃描儀(HDxt Signa,GE)掃描,配備8通道頭部線圈用于信號(hào)采集。參數(shù)為:TR 4599 ms(PLD=1525 ms),TR 5294 ms(PLD=2525 ms),回波時(shí)間10.86 ms,標(biāo)記時(shí)間1500 ms,視野24 cm×24 cm,層厚4.0 mm,36層,背景抑制。
1.3" 數(shù)據(jù)分析
將ASL序列原始數(shù)據(jù)包(PLD 1.5 s和PLD 2.5 s)脫敏后上傳至Dr Brain軟件ASL模塊(YIWEI醫(yī)療科技),基于Buxton血流動(dòng)力學(xué)模型,血液T1和腦組織T1常數(shù)分別為1650 ms和1165 ms,處理流程(圖1)。評(píng)估ICAO患者不同亞組的全腦、大腦前動(dòng)脈(ACA)、大腦中動(dòng)脈(MCA)供血區(qū)、ASPECTS區(qū)域(包括尾狀核、狀核、島帶、內(nèi)囊和M1-M6)、額葉、頂葉、顳葉、島葉區(qū)域CBF在不同PLD的差異。
1.4" 統(tǒng)計(jì)學(xué)分析
采用SPSS 21.0軟件進(jìn)行統(tǒng)計(jì)分析。所有計(jì)量數(shù)據(jù)均經(jīng)Shapiro-Wilk進(jìn)行正態(tài)性檢驗(yàn),符合正態(tài)分布的以均數(shù)±標(biāo)準(zhǔn)差表示,不符合正態(tài)分布的以中位數(shù)(四分位數(shù)間距)表示。數(shù)據(jù)符合正態(tài)分布且方差齊性,組間比較采用獨(dú)立樣本t檢驗(yàn),否則采用Mann-Whitney U檢驗(yàn)。以Plt;0.05為差異有統(tǒng)計(jì)學(xué)意義。
2" 結(jié)果
2.1" 患者的臨床資料
ICAO患者的基本特征(表1)。
2.2" 有癥狀和無(wú)癥狀I(lǐng)CAO患者區(qū)域CBF差異
有癥狀和無(wú)癥狀I(lǐng)CAO患者全腦CBF在PLD 1.5 s[23.312±4.803 vs 26.000±3.555 mL/(min·100 g),P=0.285]和PLD 2.5 s[28.457±5.338 vs 29.888±2.264 mL/(min·100 g),P=0.579]的差異無(wú)統(tǒng)計(jì)學(xué)意義。
在閉塞側(cè)半球,PLD 1.5 s時(shí),癥狀性ICAO患者M(jìn)5區(qū)域CBF較無(wú)癥狀者降低[13.586±6.930 vs 22.176±4.929 mL/(min·100 g), P=0.026],內(nèi)囊CBF較無(wú)癥狀者升高[25.861±3.122 vs 21.392±2.791 mL/(min·100 g),P=0.016],其它14個(gè)腦區(qū)的差異無(wú)統(tǒng)計(jì)學(xué)意義(Pgt;0.05);在PLD 2.5 s時(shí),癥狀性和無(wú)癥狀I(lǐng)CAO患者16個(gè)區(qū)域CBF的差異無(wú)統(tǒng)計(jì)學(xué)意義(Pgt;0.05)。
在非閉塞側(cè)半球,有癥狀和無(wú)癥狀I(lǐng)CAO患者在PLD=1.5 s和PLD=2.5 s時(shí)各區(qū)域CBF的差異無(wú)統(tǒng)計(jì)學(xué)意義(Pgt;0.05)。
2.3" 急性和慢性ICA閉塞區(qū)域CBF差異
急性和慢性ICAO患者在PLD 1.5 s[22.945±5.344 vs 25.359±3.440 mL/(min·100 g),P=0.301)]和PLD 2.5 s[27.411±6.003 vs 30.398±1.871 mL/(min·100 g),P=0.115]全腦CBF的差異無(wú)統(tǒng)計(jì)學(xué)意義。
在閉塞側(cè)半球,當(dāng)PLD 1.5 s時(shí),急性ICAO患者在MCA、M1、M5及額葉的區(qū)域CBF較慢性ICAO者降低(Plt;0.05,表2),但在其它12個(gè)腦區(qū)CBF的差異無(wú)統(tǒng)計(jì)學(xué)意義(Pgt;0.05);當(dāng)PLD 2.5 s時(shí),急性ICAO患者在MCA、M1、M5、M6及額葉的區(qū)域CBF較慢性ICAO者降低(Plt;0.05,表3),而在其它11個(gè)腦區(qū)CBF的差異無(wú)統(tǒng)計(jì)學(xué)意義(Pgt;0.05)。
在非閉塞側(cè)半球,急性和慢性ICAO患者在PLD 1.5 s和PLD 2.5 s時(shí)各區(qū)域CBF的差異無(wú)統(tǒng)計(jì)學(xué)意義(Pgt;0.05)。
2.4" 頸內(nèi)動(dòng)脈起始部和顱內(nèi)段閉塞區(qū)域CBF差異
起始部ICAO患者和顱內(nèi)段ICAO患者全腦CBF在PLD 1.5 s[24.068±3.872 vs 23.676±5.287 mL/(min·100 g),P=0.943]和PLD 2.5 s[29.868±4.337 vs 27.941±4.868 mL/(min·100 g),P=0.417]的差異均無(wú)統(tǒng)計(jì)學(xué)意義。起始部和顱內(nèi)段閉塞患者在PLD 1.5 s和PLD 2.5 s時(shí),兩側(cè)半球所有腦區(qū)CBF的差異均無(wú)統(tǒng)計(jì)學(xué)意義(Pgt;0.05)。
3" 討論
ICAO基于側(cè)支血流的差異可以有不同的臨床過(guò)程,從無(wú)癥狀到嚴(yán)重的神經(jīng)功能不足[16] 。癥狀性ICAO的年發(fā)病率在一般人群中約為6/100 000人[17] 。本研究納入ICAO患者中,68.75%(11/16)表現(xiàn)為有癥狀,31.25%(5/16)表現(xiàn)為無(wú)癥狀。癥狀性ICAO患者長(zhǎng)期預(yù)后較差[13] ,卒中年復(fù)發(fā)率為5%~6%[13] ,腦血流動(dòng)力學(xué)受損及側(cè)支流嚴(yán)重的患者復(fù)發(fā)率為9%~18%[18-20] 。無(wú)癥狀性ICAO腦卒中復(fù)發(fā)率小于2%[19, 21] 。既往研究表明,無(wú)癥狀和有癥狀I(lǐng)CAO患者與對(duì)照組相比,閉塞側(cè)ACA和MCA基線CBF均顯著降低[22] 。然而,目前國(guó)內(nèi)外尚無(wú)關(guān)于有/無(wú)癥狀I(lǐng)CAO患者腦血流量差異的對(duì)比研究。國(guó)內(nèi)一項(xiàng)研究顯示前循環(huán)大血管嚴(yán)重狹窄/閉塞患者,在PLD 1.5 s和PLD 2.5 s,有癥狀患者雙側(cè)半球腦CBF均低于無(wú)癥狀患者[23] 。本研究結(jié)果顯示,在PLD 1.5 s時(shí),有癥狀I(lǐng)CAO者較無(wú)癥狀者閉塞側(cè)M5區(qū)CBF降低,非閉塞側(cè)有/無(wú)癥狀患者CBF在雙PLD時(shí)均無(wú)差異,提示ICA閉塞導(dǎo)致閉塞側(cè)灌注行為異常,閉塞側(cè)區(qū)域性腦灌注減低及延遲可能是患者癥狀出現(xiàn)的原因,但由于本文樣本量有限,需要進(jìn)一步的大樣本研究來(lái)明確ICAO患者癥狀與腦區(qū)灌注不足關(guān)系。
急性ICAO與嚴(yán)重和持續(xù)的神經(jīng)功能缺陷有關(guān),對(duì)靜脈溶栓無(wú)效,并預(yù)示著更可怕的臨床結(jié)果[7, 24] 。慢性ICAO患者通常沒(méi)有明顯的臨床癥狀,很多時(shí)候是常規(guī)影像學(xué)檢查時(shí)偶然發(fā)現(xiàn)。本研究中,87.5%(7/8)的急性ICAO患者表現(xiàn)為缺血性卒中,12.5%(1/8)表現(xiàn)為TIA;62.5%(5/8)的慢性ICAO患者表現(xiàn)為頭痛或頭暈,25%(2/8)表現(xiàn)為卒中,12.5%(1/8)表現(xiàn)為TIA。當(dāng)前的分析結(jié)果顯示,在閉塞側(cè)半球PLD 1.5 s和PLD 2.5 s時(shí),急性ICAO患者部分MCA和ASPECTS皮質(zhì)區(qū)域CBF明顯低于慢性ICAO者,提示急性ICAO腦灌注受損更加嚴(yán)重,更低灌注是急性ICAO者腦缺血事件更高發(fā)病率的原因。這可能與急性ICA閉塞阻止了閉塞血管的側(cè)支循環(huán)建立、調(diào)節(jié)和限制腦損傷的進(jìn)展,慢性閉塞進(jìn)展可能允許遠(yuǎn)端側(cè)支血管的發(fā)育以避免嚴(yán)重的缺血事件發(fā)生有關(guān)[7] 。目前國(guó)內(nèi)外尚無(wú)關(guān)于急性/慢性ICAO患者腦血流量差異的對(duì)比研究,本研究結(jié)果明確了急慢性期ICAO對(duì)腦灌注影響,認(rèn)為判斷ICA急慢性期閉塞對(duì)臨床決策至關(guān)重要,隨著ICA閉塞時(shí)間的延長(zhǎng),血栓逐漸纖維化,阻礙微導(dǎo)絲通過(guò)閉塞動(dòng)脈,使其難以再通,增加并發(fā)癥的風(fēng)險(xiǎn)[25] 。除了結(jié)合臨床特征,高分辨MR血管壁成像在評(píng)估閉塞時(shí)期、閉塞位置及范圍方面也有重要臨床價(jià)值。
根據(jù)Bouthillier分類,頸內(nèi)動(dòng)脈的顱內(nèi)外部分可分為7個(gè)節(jié)段[26]。由于近端血流動(dòng)力學(xué)復(fù)雜,低剪切應(yīng)力、血流停滯和血流分離,ICA閉塞在近端更常見[27] 。有研究注意到ICAO患者神經(jīng)系統(tǒng)的嚴(yán)重程度和梗死面積從近端到遠(yuǎn)端不斷增加[28] 。本研究結(jié)果顯示,ICA起始部和顱內(nèi)段閉塞患者的全腦CBF以及雙側(cè)半球區(qū)域CBF在PLD 1.5 s和PLD 2.5 s的差異均無(wú)統(tǒng)計(jì)學(xué)意義,提示頸內(nèi)動(dòng)脈的不同閉塞位置其腦灌注本質(zhì)無(wú)明顯差異。目前國(guó)內(nèi)外尚無(wú)關(guān)于不同ICAO閉塞位置腦血流量差異的研究,本文小樣本量也可能是導(dǎo)致其差異無(wú)統(tǒng)計(jì)學(xué)意義的原因。但I(xiàn)CA的閉塞位置對(duì)于血管內(nèi)治療至關(guān)重要,它可以幫助醫(yī)生為患者選擇合適的再通技術(shù)、支架或介入裝置的大小[8] 。既往研究表明,ICA閉塞部位越低,再通成功率越高[29] 。此外,既往研究顯示再通的維持基本依賴于閉塞位置,以頸內(nèi)動(dòng)脈床突段為界,其遠(yuǎn)端和近端再閉塞的年發(fā)生率分別為91%和0%[30] 。所以,閉塞位置評(píng)估對(duì)臨床決策仍然具有重要意義。
綜上所述,急性ICAO較慢性ICAO患者閉塞側(cè)大腦中動(dòng)脈供血區(qū)和部分ASPECTS皮質(zhì)區(qū)域腦灌注受損更加嚴(yán)重;癥狀性ICAO與閉塞側(cè)ASPECTS部分區(qū)域灌注進(jìn)一步受損可能有關(guān);頸內(nèi)動(dòng)脈不同閉塞位置的腦灌注無(wú)明顯差異。本研究創(chuàng)新性地使用新技術(shù)實(shí)現(xiàn)更快速、細(xì)致全腦和區(qū)域CBF評(píng)估,首次評(píng)估了ICAO患者ASPECTS區(qū)域腦灌注,解決了臨床實(shí)際問(wèn)題,為后續(xù)的研究和臨床治療決策提供了理論基礎(chǔ)。但本研究由于樣本量有限,在將現(xiàn)有結(jié)果解釋應(yīng)用至其它人群時(shí)應(yīng)謹(jǐn)慎,后續(xù)研究將繼續(xù)擴(kuò)大樣本量。
參考文獻(xiàn):
[1]" "Rodda RA. The arterial patterns associated with internal carotid disease and cerebral infarcts[J]. Stroke, 1986, 17(1): 69-75.
[2]" "Saini H, Cerejo R, Williamson R, et al. Internal Carotid Artery Occlusion: Management[J]. Curr Neurol Neurosci Rep, 2022, 22(7): 383-8.
[3]" "Bhatia R, Hill MD, Shobha N, et al. Low rates of acute recanalization with intravenous recombinant tissue plasminogen activator in ischemic stroke: real?world experience and a call for action[J]. Stroke, 2010, 41(10): 2254-8.
[4]" "Paciaroni M, Inzitari D, Agnelli G, et al. Intravenous thrombolysis or endovascular therapy for acute ischemic stroke associated with cervical internal carotid artery occlusion: the ICARO-3 study[J]. J Neurol, 2015, 262(2): 459-68.
[5]" "Faught WE, van Bemmelen PS, Mattos MA, et al. Presentation and natural history of internal carotid artery occlusion[J]. J Vasc Surg, 1993, 18(3): 512-24.
[6]" "Powers WJ, Derdeyn CP, Fritsch SM, et al. Benign prognosis of never-symptomatic carotid occlusion[J]. Neurology, 2000, 54(4): 878-82.
[7]" "Malhotra K, Goyal N, Tsivgoulis G. Internal carotid artery occlusion: pathophysiology, diagnosis, and management[J]. Curr Atheroscler Rep, 2017, 19(10): 41.
[8]" "Morofuji Y, Horie N, Tateishi Y, et al. Arterial spin labeling magnetic resonance imaging can identify the occlusion site and collateral perfusion in patients with acute ischemic stroke: comparison with digital subtraction angiography[J]. Cerebrovasc Dis, 2019, 48(1/2): 70-6.
[9]" "Barber PA, Demchuk AM, Zhang J, et al. Validity and reliability of a quantitative computed tomography score in predicting outcome of hyperacute stroke before thrombolytic therapy. ASPECTS Study Group. Alberta Stroke Programme Early CT Score[J]. Lancet, 2000, 355(9216): 1670-4.
[10] Goyal M, Demchuk AM, Menon BK, et al. Randomized assessment of rapid endovascular treatment of ischemic stroke[J]. N Engl J Med, 2015, 372(11): 1019-30.
[11] Lloyd M. A randomized trial of intraarterial treatment for acute ischemic stroke[J]. J Emerg Med, 2015, 48(4): 521.
[12] Saver JL, Goyal M, Bonafe A, et al. Stent-retriever thrombectomy after intravenous t-PA vs. t-PA alone in stroke[J]. N Engl J Med, 2015, 372(24): 2285-95.
[13] Klijn CJ, Kappelle LJ, Algra A, et al. Outcome in patients with symptomatic occlusion of the internal carotid artery or intracranial arterial lesions: a meta?analysis of the role of baseline characteristics and type of antithrombotic treatment[J]. Cerebrovasc Dis, 2001, 12(3): 228-34.
[14] Michel P, Ntaios G, Delgado MG, et al. CT angiography helps to differentiate acute from chronic carotid occlusion: the \"carotid ring sign\"[J]. Neuroradiology, 2012, 54(2): 139-46.
[15] Iwata T, Mori T, Tajiri H, et al. Long-term angiographic and clinical outcome following stenting by flow reversal technique for chronic occlusions older than 3 months of the cervical carotid or vertebral artery[J]. Neurosurgery, 2012, 70(1): 82-90.
[16]" Liebeskind DS, Flint AC, Budzik RF, et al. Carotid I’s, L’s and T’s: collaterals shape the outcome of intracranial carotid occlusion in acute ischemic stroke[J]. J Neurointerv Surg, 2015, 7(6): 402-7.
[17] Flaherty ML, Flemming KD, McClelland R, et al. Population-based study of symptomatic internal carotid artery occlusion: incidence and long-term follow-up[J]. Stroke, 2004, 35(8): e349-52.
[18]Grubb RL, Derdeyn CP, Fritsch SM, et al. Importance of hemodynamic factors in the prognosis of symptomatic carotid occlusion[J]." JAMA, 1998, 280(12): 1055-60.
[19] Vernieri F, Pasqualetti P, Passarelli F, et al. Outcome of carotid artery occlusion is predicted by cerebrovascular reactivity[J]. Stroke, 1999, 30(3): 593-8.
[20] Klijn CJ, Kappelle LJ, van Huffelen AC, et al. Recurrent ischemia in symptomatic carotid occlusion: prognostic value of hemodynamic factors[J]. Neurology, 2000, 55(12): 1806-12.
[21]" Bornstein NM, Norris JW. Benign outcome of carotid occlusion[J]. Neurology, 1989, 39(1): 6-8.
[22] Hartkamp NS, Petersen ET, Chappell MA, et al. Relationship between haemodynamic impairment and collateral blood flow in carotid artery disease[J]. J Cereb Blood Flow Metab, 2018, 38(11): 2021-32.
[23]" 谷家美, 王" 雁. 動(dòng)脈自旋標(biāo)記技術(shù)在前循環(huán)大血管嚴(yán)重狹窄/閉塞患者中的應(yīng)用價(jià)值[J]. 臨床醫(yī)學(xué)進(jìn)展, 2020, 6(7): 1269-76.
[24] Kwak JH, Zhao L, Kim JK, et al. The outcome and efficacy of recanalization in patients with acute internal carotid artery occlusion[J]. AJNR Am J Neuroradiol, 2014, 35(4): 747-53.
[25]" Xu BF, Liu R, Jiao LQ, et al. Carotid endarterectomy for in-stent restenosis: a case report and literature review[J]. Biomed Rep, 2017, 7(2): 128-32.
[26] Alain B, Van LHR, Keller JT. Segments of the internal carotid artery: a new classification[J]. Neurosurgery, 1996, 38(3): 425-32.
[27]Harrison MJ, Marshall J. The finding of thrombus at carotid endarterectomy and its relationship to the timing of surgery[J]. Br J Surg, 1977, 64(7): 511-2.
[28]Hong JM, Lee SE, Lee SJ, et al. Distinctive patterns on CT angiography characterize acute internal carotid artery occlusion subtypes[J]. Medicine, 2017, 96(5): e5722.
[29] Chen YH, Leong WS, Lin MS, et al. Predictors for successful endovascular intervention in chronic carotid artery total occlusion[J]. JACC Cardiovasc Interv, 2016, 9(17): 1825-32.
[30]" Lee CW, Lin YH, Liu HM, et al. Predicting procedure successful rate and 1?year patency after endovascular recanalization for chronic carotid artery occlusion by CT angiography[J]. Int J Cardiol, 2016, 221: 772-6.
(編輯:林" 萍)