上期回顧：

本綜述介紹了CT血管造影術的起源與發展。

本期内容：

CT血管造影術對于臨床的貢獻：急性主動脈綜合症（AAS）——新的知(zhī)識重新定義疾病分(fēn)類。

AAS（急性主動脈綜合症）是指一(yī)系列急性的、危及生(shēng)命的主動脈異常病變，它以突然出現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，而當心電(diàn)門控技術廣泛應用于CTA掃描時，則從根本上更易理解AAS的症狀，它正成為對AAS進行診斷、定性、制定治療計劃的一(yī)項優越技術。

CTA對于臨床應用的貢獻

Contributions of CT Angiography to Clinical Practice 

由于技術的巨大(dà)進步，CTA已經發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的應用改變了臨床診療的标準并且值得不斷的精細化，但我(wǒ)(wǒ)們還是選擇特别關注的三個方面，CTA拓寬我(wǒ)(wǒ)們對人類血管性疾病（急性主動脈綜合征（AAS）和外(wài)周動脈疾病）的理解，其中(zhōng)有指導疾病治療方面引導（主動脈内支架置入和經皮主動脈瓣膜置換）的新策略，以及這新技術提供進一(yī)步優化（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(zhī)識重新定義疾病分(fēn)類

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

AAS是指一(yī)系列急性的，威及生(shēng)命的主動脈異常，以突然出現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），而且當掃描采集與心電(diàn)圖（ECG）同步時，就從根本上更易理解AAS的症狀（30），它正成為對AAS進行診斷、定性、制定治療計劃的一(yī)項優越技術。除了克服因升主動脈搏動所導緻誤診與虛假的病理結果（30，31），心電(diàn)圖的同步能對主動脈根部及相關的冠狀動脈窦進行正确評價。

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.

無運動僞影幹擾的圖像能夠可靠的識别原發性内膜撕裂的位置，夾層的位置和程度，以及所累及的分(fēn)支動脈，這對指導治療非常重要（圖2，3）。在病理學上一(yī)些常見但至今無法可視化的征象（例如，壁間血腫【IMH】内的血池與側支血管（32））與在活體(tǐ)診斷圖像上以前認為無法探測的細微病變能力（即，局限性夾層（30，33））等已由CT血管造影（CTA）技術引導并發展出了急性主動脈病變新的分(fēn)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則線樣陰影（箭頭）

（B）升主動脈中(zhōng)段沒有夾層皮瓣

（C）升主動脈遠端可見夾在真、假腔之間的夾層皮瓣（細箭）

（D）VR重建展示夾層，近端夾層撕裂皮瓣下(xià)垂向下(xià)通過主動脈瓣膜（箭頭）。細箭所指遠端升主動脈的夾層皮瓣。在無ECG門控的時候，這些細微的發現并不可見。（轉載、許可、引用30）

圖3  升主動脈局限性内膜撕裂

（A）上方：無心電(diàn)門控的CTA顯示升主動脈運動僞影，模糊；下(xià)方：12小(xiǎo)時後，心電(diàn)門控 CTA示：升主動脈近端内膜皮瓣(箭頭)，伴随一(yī)個侵蝕邊緣的局限性内膜撕裂。局限性内膜撕裂的邊緣（大(dà)箭頭）和主動脈壁破壞形成的突起（小(xiǎo)箭頭）清晰可見。這些微妙細節如果沒有使用心電(diàn)門控是不可見的。

（B）VR重建顯示腔内一(yī)側6cm長的損傷。一(yī)個小(xiǎo)的破損皮瓣（細箭）代表撕裂的起始端，并一(yī)直延伸到主動脈弓的近端。虛線，代表撕裂的邊緣。（轉載，許可，引用24。）

傳統的AAS分(fēn)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），現在可通過CTA分(fēn)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技術帶來的最重要的見解之一(yī)是，IMH除了發生(shēng)在多種典型的主動脈夾層外(wài)，還可以發生(shēng)在任何急性主動脈異常中(zhōng)，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、相關的連接組織、黴菌、甚至創傷後、醫源性以及非醫源性因素）（圖4）導緻的主動脈瘤破裂。

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(fēn)展示6cm的降主動脈瘤（A）。IMH（開(kāi)放(fàng)箭頭）在動脈瘤的下(xià)緣，伴有内膜鈣化（細箭頭）與中(zhōng)縱膈内持續出血（粗箭頭）。

（B）斜位薄層MIP的CTA成像顯示IMH（開(kāi)放(fàng)箭頭）在動脈瘤（A）下(xià)緣，長條狀的血液（實心箭頭）貫穿縱膈擴展到胸膜腔，一(yī)個大(dà)的血腫（H）占據了右半胸廓的近一(yī)半位置，與低密度的胸腔積液和強化的右肺膨脹不全有明顯的區别。（轉載、許可、引用24）

因此，IMH可以被認為是伴随急症如主動脈夾層，PAU，和主動脈瘤破裂的影像征象，而非目前通常所認為的IMH隻是AAS一(yī)個獨特“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伴随征象也引出了這樣一(yī)個問題：為什麼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(yī)個完全不同的概念，它認為AAS是一(yī)系列疾病的表現，由三個主要的病理過程引起：第一(yī)組，血管中(zhōng)層病變導緻的主動脈夾層和其變異；第二組，PAU，是動脈粥樣硬化進展的表現，然後是内膜病變；第三組，主動脈瘤破裂，其臨床表現與主動脈夾層和PAU明顯不同（表）（30）。注意，IMH并不是這個分(fēn)類的一(yī)部分(fēn)，因為它可以伴随以上三個病理過程，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.

由于有着共同的病理改變，代表主動脈夾層及其變異的第一(yī)組病變都是動脈壁中(zhōng)層病變。典型夾層的征象是主動脈壁内形成一(yī)個通道或者假腔，後者通過撕裂的内膜與真腔分(fēn)離(lí)（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内膜流向假腔，然後再通過一(yī)個或多個撕裂破口流回真腔。無論有無明确的撕裂内膜片，當假腔内新鮮血液凝固時，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.

少數有中(zhōng)層病變的患者，出現表淺或者部分(fēn)撕裂（相當于原發性内膜撕裂），但并沒有形成一(yī)個單獨的流出道，或者造成壁内血液的存留。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(zhōng)層病變的患者，其病變進展迅速，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（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）正常心髒外(wài)周胸主動脈壁的分(fēn)層結構：内膜、中(zhōng)膜、外(wài)膜。大(dà)部分(fēn)主動脈壁的結構是中(zhōng)層（灰色）。内膜和外(wài)膜（如圖，黑色主動脈壁的内外(wài)輪廓）在CT上是不可見的。所有主動脈夾層變異都發生(shēng)在主動脈壁的中(zhōng)層。

（B）經典的主動脈夾層發生(shēng)在中(zhōng)層結構的外(wài)三分(fēn)之一(yī)，将血流分(fēn)成兩個通道。注意，分(fēn)隔真、假腔的組織實際是中(zhōng)層結構，應稱之為内中(zhōng)膜皮瓣。

（C）當分(fēn)離(lí)的中(zhōng)層結構中(zhōng)充滿靜止血液而非流動血液時，稱為IMH。

（D）局限性内膜撕裂實際指部分(fēn)撕裂（箭頭）穿透内膜和中(zhōng)膜内層，殘餘的中(zhōng)膜/外(wài)膜暴露，這導緻動脈壁圓周局限性“膨脹”（箭頭）。（轉載、許可、引用30）

第二組病變代表PAU，其特點是在增厚的病變内膜上，潰瘍穿透了内膜的彈性層到達了主動脈壁的深層，這可能與IMH相關。伴有PAU的IMH病變通常比合并中(zhōng)層病變（夾層變異）的單純IMH預後更差（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，最常發生(shēng)在腹主動脈（圖4）。不穩定動脈瘤的特征是一(yī)層慢(màn)性的血栓包裹新鮮血液（新月征），壁内出現血液和瘤周滞留。

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以及并發症的結構特征可以由現代CTA進行評估。這種綜合形态學評估的普及為AAS自然病程提供了獨特見解，可以精确分(fēn)類，并有利于外(wài)科手術的實施和血管内治療。

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.