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上期回顧：

本綜述介紹了CT血管造影術(shù)的起源與發(fā)展。

本期內(nèi)容：

CT血管造影術(shù)對于臨床的貢獻(xiàn)：急性主動脈綜合癥（AAS）——新的知識重新定義疾病分類。

AAS（急性主動脈綜合癥）是指一系列急性的、危及生命的主動脈異常病變，它以突然出現(xiàn)的劇烈胸部或背部疼痛為主要特征。CT血管造影（CTA）不僅徹底改變了對AAS的診斷與治療，而當(dāng)心電門控技術(shù)廣泛應(yīng)用于CTA掃描時(shí)，則從根本上更易理解AAS的癥狀，它正成為對AAS進(jìn)行診斷、定性、制定治療計(jì)劃的一項(xiàng)優(yōu)越技術(shù)。

CTA對于臨床應(yīng)用的貢獻(xiàn)

Contributions of CT Angiography to Clinical Practice 

由于技術(shù)的巨大進(jìn)步，CTA已經(jīng)發(fā)展到可以為心血管疾病的診斷與治療方面提供非常重要的見解。雖然許多CTA的應(yīng)用改變了臨床診療的標(biāo)準(zhǔn)并且值得不斷的精細(xì)化，但我們還是選擇特別關(guān)注的三個(gè)方面，CTA拓寬我們對人類血管性疾病（急性主動脈綜合征（AAS）和外周動脈疾?。┑睦斫?，其中有指導(dǎo)疾病治療方面引導(dǎo)（主動脈內(nèi)支架置入和經(jīng)皮主動脈瓣膜置換）的新策略，以及這新技術(shù)提供進(jìn)一步優(yōu)化（對冠心病的診療）的承諾。

As a result of tremendous technologic developments, CT angiography has evolved to provide important insights into cardiovascular disease diagnosis and management. While there are many applications of CT angiography that have transformed the standard for clinical care and are worthy of detailed elaboration, we have chosen to focus specifically on three areas in which CTangiography has expanded our under- standing of human vascular disease (AAS and peripheral arterial disease), in which it has guided new strategies in disease management (aortic endograft deployment and transaortic valve implantation),and in which new CT techniques offer promise for further refinements (coronary heart disease). 

急性主動脈綜合征（AAS）：新知識重新定義疾病分類

Acute AorticSyndromes: New Knowledge Redefining Disease Acute Acute Aortic Syndromes: New Knowledge Redefining Disease Classification

AAS是指一系列急性的，威及生命的主動脈異常，以突然出現(xiàn)的劇烈胸部或背部疼痛為特征(28)。

AAS refers to a spectrum of acute, life-threatening abnormalities of theaorta characterized by an abrupt onset of in- tense chest or back pain(28).

CT血管造影（CTA）不僅徹底改變了對AAS的診斷與治療（29），而且當(dāng)掃描采集與心電圖（ECG）同步時(shí)，就從根本上更易理解AAS的癥狀（30），它正成為對AAS進(jìn)行診斷、定性、制定治療計(jì)劃的一項(xiàng)優(yōu)越技術(shù)。除了克服因升主動脈搏動所導(dǎo)致誤診與虛假的病理結(jié)果（30，31），心電圖的同步能對主動脈根部及相關(guān)的冠狀動脈竇進(jìn)行正確評價(jià)。

CT angiography has not only revolutionized the diagnosis and management of cases of AAS(29), but when acquired with electrocardiographic (ECG) synchronization has fundamentally advanced our understanding of these conditions(30), becoming the preeminent technique for the diagnosis,characterization, and treatment planning of AAS. In addition to overcoming ascending aortic pulsation artifacts that have resulted in both missed andspurious pathologic findings (30,31), ECG synchronization enables assessment of aortic root and coronary ostial involvement.

無運(yùn)動偽影干擾的圖像能夠可靠的識別原發(fā)性內(nèi)膜撕裂的位置，夾層的位置和程度，以及所累及的分支動脈，這對指導(dǎo)治療非常重要（圖2，3）。在病理學(xué)上一些常見但至今無法可視化的征象（例如，壁間血腫【IMH】內(nèi)的血池與側(cè)支血管（32））與在活體診斷圖像上以前認(rèn)為無法探測的細(xì)微病變能力（即，局限性夾層（30，33））等已由CT血管造影（CTA）技術(shù)引導(dǎo)并發(fā)展出了急性主動脈病變新的分類方法（34）。

Motion-free images enable reliable identification of the site of the primary intimal tear, location and extent of dissection flaps, and branch-artery involvement— features important in guiding therapy (Figs 2, 3). Visualization of hitherto unknown but common pathologic features（eg, blood pools and side branch communications within an intramural hematoma [IMH]（32））and theability to detect subtle lesions previously deemed inaccessible to in vivodiagnostic imaging（ie, limited dissection（30,33））have allowed CT angiography to lead the way to new classifications of acute aortic lesions.

圖2  45歲，男，A型急性主動脈夾層

（A-C）CT橫斷位圖像：

（A）主動脈根部水平不規(guī)則線樣陰影（箭頭）

（B）升主動脈中段沒有夾層皮瓣

（C）升主動脈遠(yuǎn)端可見夾在真、假腔之間的夾層皮瓣（細(xì)箭）

（D）VR重建展示夾層，近端夾層撕裂皮瓣下垂向下通過主動脈瓣膜（箭頭）。細(xì)箭所指遠(yuǎn)端升主動脈的夾層皮瓣。在無ECG門控的時(shí)候，這些細(xì)微的發(fā)現(xiàn)并不可見。（轉(zhuǎn)載、許可、引用30）

圖3  升主動脈局限性內(nèi)膜撕裂

（A）上方：無心電門控的CTA顯示升主動脈運(yùn)動偽影，模糊；下方：12小時(shí)后，心電門控 CTA示：升主動脈近端內(nèi)膜皮瓣(箭頭)，伴隨一個(gè)侵蝕邊緣的局限性內(nèi)膜撕裂。局限性內(nèi)膜撕裂的邊緣（大箭頭）和主動脈壁破壞形成的突起（小箭頭）清晰可見。這些微妙細(xì)節(jié)如果沒有使用心電門控是不可見的。

（B）VR重建顯示腔內(nèi)一側(cè)6cm長的損傷。一個(gè)小的破損皮瓣（細(xì)箭）代表撕裂的起始端，并一直延伸到主動脈弓的近端。虛線，代表撕裂的邊緣。（轉(zhuǎn)載，許可，引用24。）

傳統(tǒng)的AAS分為主動脈夾層、IMH與穿透樣動脈粥樣硬化性潰瘍（penetrating atherosclerotic ulcer，PAU）（34，35），現(xiàn)在可通過CTA分析重新定義。

The traditional "classification" of AAS into aortic dissection, IMH, and penetrating atherosclerotic ulcer (PAU) (34,35) can be refined through analysis of CT angiography.

CTA技術(shù)帶來的最重要的見解之一是，IMH除了發(fā)生在多種典型的主動脈夾層外，還可以發(fā)生在任何急性主動脈異常中，包括全部各種夾層，穿透樣動脈粥樣硬化性潰瘍，以及任何病因（動脈粥樣硬化、相關(guān)的連接組織、霉菌、甚至創(chuàng)傷后、醫(yī)源性以及非醫(yī)源性因素）（圖4）導(dǎo)致的主動脈瘤破裂。

Perhaps one of the most important insights gleaned from CT angiography is that in addition toits classic description as a variant of aortic dissection, IMH may be seen in association with virtually any acute aortic abnormality, including the entirespectrum of dissection variants, PAUs, and rupturing aortic aneurysms of anyetiology (atherosclerotic, connective tissue-related, mycotic, and even posttraumatic, iatrogenic or noniatrogenic) (Fig4).

圖4：合并IMH的動脈瘤破裂

（A）橫斷位CT部分展示6cm的降主動脈瘤（A）。IMH（開放箭頭）在動脈瘤的下緣，伴有內(nèi)膜鈣化（細(xì)箭頭）與中縱膈內(nèi)持續(xù)出血（粗箭頭）。

（B）斜位薄層MIP的CTA成像顯示IMH（開放箭頭）在動脈瘤（A）下緣，長條狀的血液（實(shí)心箭頭）貫穿縱膈擴(kuò)展到胸膜腔，一個(gè)大的血腫（H）占據(jù)了右半胸廓的近一半位置，與低密度的胸腔積液和強(qiáng)化的右肺膨脹不全有明顯的區(qū)別。（轉(zhuǎn)載、許可、引用24）

因此，IMH可以被認(rèn)為是伴隨急癥如主動脈夾層，PAU，和主動脈瘤破裂的影像征象，而非目前通常所認(rèn)為的IMH只是AAS一個(gè)獨(dú)特“條件”的征象（34，35）。而且，主動脈夾層和PAU，與主動脈瘤破裂的IMH伴隨征象也引出了這樣一個(gè)問題：為什么AAS不包括主動脈瘤破裂（30）。

Thus, IMH might be more appropriately classified as an imaging marker of acuity associated with aortic dissection, PAU, and rupturing aneurysm rather than thecurrently in vogue characterization of IMH as a distinct "condition" of AAS(34,35). Moreover, the association of IMH with both the classic AAS conditions of aortic dissection and PAU and with rupturing aortic aneurysm introduces the question as to why rupturing aortic aneurysms are not included as AAS (30).

由ECG門控的CTA揭示了另一個(gè)完全不同的概念，它認(rèn)為AAS是一系列疾病的表現(xiàn)，由三個(gè)主要的病理過程引起：第一組，血管中層病變導(dǎo)致的主動脈夾層和其變異；第二組，PAU，是動脈粥樣硬化進(jìn)展的表現(xiàn)，然后是內(nèi)膜病變；第三組，主動脈瘤破裂，其臨床表現(xiàn)與主動脈夾層和PAU明顯不同（表）（30）。注意，IMH并不是這個(gè)分類的一部分，因?yàn)樗梢园殡S以上三個(gè)病理過程，是急性過程的指征。

An alternative concept informed by observations from ECG-gated CT angiography regards AAS as a spectrum of disease manifestations caused by three main pathologic processes: group 1, aorticdissection and its variants resulting from a diseased media; group 2, PAU,which is a manifestation of advanced atherosclerosis and thus a disease of the intima; and group 3, rupturing aortic aneurysms, as the clinical presentationis indistinguishable from aortic dissection and PAU (Table)（30）. Note that IMH is not part of this classification as it may be associated with any of the three main categories asan indicator of an acute process.

由于有著共同的病理改變，代表主動脈夾層及其變異的第一組病變都是動脈壁中層病變。典型夾層的征象是主動脈壁內(nèi)形成一個(gè)通道或者假腔，后者通過撕裂的內(nèi)膜與真腔分離（圖2）。

Group 1 lesions representing aortic dissection and its variants share a diseased aorticmedia as their common pathologic lesion. Classic dissection is characterized by the development of a flow channel or false lumen within the aortic wall, which is separated from the true lumen by a dissection membrane (Fig2).

血液常常通過撕裂的內(nèi)膜流向假腔，然后再通過一個(gè)或多個(gè)撕裂破口流回真腔。無論有無明確的撕裂內(nèi)膜片，當(dāng)假腔內(nèi)新鮮血液凝固時(shí)，就可以稱之為IMH或者撕裂變異。

Blood most commonly flows into the false lumen through a primary intimal tear, and re-entersthe true lumen through one or more exit tears. Regardless of the presence of an identifiable primary intimal tear, when fresh blood coagulates within a falselumen space, we refer to it as an IMH or dissection variant.

少數(shù)有中層病變的患者，出現(xiàn)表淺或者部分撕裂（相當(dāng)于原發(fā)性內(nèi)膜撕裂），但并沒有形成一個(gè)單獨(dú)的流出道，或者造成壁內(nèi)血液的存留。這些少見的病變稱之為局限撕裂或者局限性夾層，與典型夾層對比往往具有細(xì)微的影像改變（30，33，36）（圖3）。

In a small number of patients with medial disease, a superficial/partial thickness tear develops (the equivalent of a primary intimal tear) without the development ofa separate flow channel or accumulation of intramural blood. These rare lesionsare referred to as limited tears or limited dissection and tend to have subtle imaging findings when compared with classic dissection (30,33,36)(Fig 3).

具有中層病變的患者，其病變進(jìn)展迅速，以主動脈夾層，IMH和局限撕裂為特征，這些特征常常重疊出現(xiàn)（圖5）。

In patientswith medial disease, lesions can evolve rapidly, and features of aortic dissection, IMH, and limited tears can and often do overlap (Fig 5).

圖5：主動脈夾層變異的示意圖

（A）正常心臟外周胸主動脈壁的分層結(jié)構(gòu)：內(nèi)膜、中膜、外膜。大部分主動脈壁的結(jié)構(gòu)是中層（灰色）。內(nèi)膜和外膜（如圖，黑色主動脈壁的內(nèi)外輪廓）在CT上是不可見的。所有主動脈夾層變異都發(fā)生在主動脈壁的中層。

（B）經(jīng)典的主動脈夾層發(fā)生在中層結(jié)構(gòu)的外三分之一，將血流分成兩個(gè)通道。注意，分隔真、假腔的組織實(shí)際是中層結(jié)構(gòu)，應(yīng)稱之為內(nèi)中膜皮瓣。

（C）當(dāng)分離的中層結(jié)構(gòu)中充滿靜止血液而非流動血液時(shí)，稱為IMH。

（D）局限性內(nèi)膜撕裂實(shí)際指部分撕裂（箭頭）穿透內(nèi)膜和中膜內(nèi)層，殘余的中膜/外膜暴露，這導(dǎo)致動脈壁圓周局限性“膨脹”（箭頭）。（轉(zhuǎn)載、許可、引用30）

第二組病變代表PAU，其特點(diǎn)是在增厚的病變內(nèi)膜上，潰瘍穿透了內(nèi)膜的彈性層到達(dá)了主動脈壁的深層，這可能與IMH相關(guān)。伴有PAU的IMH病變通常比合并中層病變（夾層變異）的單純IMH預(yù)后更差（37）。

Group 2 lesions representing PAUs are characterized by defects in the thickened and diseased intima that penetrate through the internal elastic lamina into deeperlayers of the aortic wall, which may be associated with IMH. When associatedwith PAU, IMH generally has a worse prognosis than uncomplicated IMH associated with medial disease (dissection variant) (37).

第三組病變是主動脈瘤破裂，最常發(fā)生在腹主動脈（圖4）。不穩(wěn)定動脈瘤的特征是一層慢性的血栓包裹新鮮血液（新月征），壁內(nèi)出現(xiàn)血液和瘤周滯留。

Group 3 lesions are rupturing aortic aneurysms, occurring most frequently in the abdominal aorta (Fig 4). Signs of unstable aneurysms are fresh blood within a layerof chronic thrombus (crescent sign), intramural blood, and perianeurysmal stranding.  

幾乎所有AAS以及并發(fā)癥的結(jié)構(gòu)特征可以由現(xiàn)代CTA進(jìn)行評估。這種綜合形態(tài)學(xué)評估的普及為AAS自然病程提供了獨(dú)特見解，可以精確分類，并有利于外科手術(shù)的實(shí)施和血管內(nèi)治療。

Virtually all structural features associated with AAS and their complications can be reliably assessed with modern CT angiography.The widespread availability of this comprehensive morphologic assessment is providing unique in- sights into the natural history of AAS, allowing refined classification schemes and better implementation of surgical and endovascular treatments.