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Z. Hartley-Blossom et al.

Normal Aortic Anatomy

Familiarity with aortic anatomy is important to understanding the pathophysiology and in turn the imaging appearances of AAS.There are three discrete layers of the aortic wall: the tunica intima (or intima), tunica media (or media), and the adventitia (Fig.1a). The intima is the luminal layer of the aorta and is in direct contact with the blood pool by which it is nourished. It is the thinnest of the three layers, consisting of only a single layer of endothelial cells, supporting connective tissue, and a very thin internal elastic lamina that separates it from the media. The media (middle layer) is the thickest of the three layers and consists of smooth muscle, collagen, and elastic tissue, and is responsible for the vascular tone of the aorta. Consisting chiey of connective tissue, the outermost layer, the adventitia, provides additional structural support [3, 8]. The blood supply to the mid and outer aortic wall comes by way of the vasa vasorum which is a network of small arteries that enter through the adventitia before terminating in the media [8–10]. Coronary and brachiocephalic arteries supply the vasa vasorum of the ascending aorta and intercostal arteries supply those of the descending thoracic aorta. Lumbar and mesenteric arteries supply the vasa vasorum of the abdominal aorta [3, 11]. Normal aortic wall thickness is <3mm [8]. The cross-sectional imaging methods described in this chapter and routinely used in clinical imaging are not typically able to resolve these layers in the normal aorta.

For descriptive purposes, the aorta is typically divided into longitudinal segments (Fig.2). The ascending segment extends from the aortic annulus to the origin of the brachiocephalic artery. The aortic root is the most proximal portion of the ascending segment and spans from the annulus through the sinuses of Valsalva to

ab c

Fig. 1 Diagram of the aortic wall in cross-section. (a) Normal. The innermost layer—the thin tunica intima (light blue)—is nourished directly from luminal blood (L).The middle layer—or tunica media (light brown)—is the thickest of the 3 layers, contains smooth muscle cells, and provides vasomotor tone to the wall. The outer adventitial layer (dark blue) consists chiey of connective tissue and provides structural support. Vasa vasorum (branching black lines) are small blood vessels that provide blood ow to the mid and outer wall. These small vessels penetrate through the adventitia and terminate in the media. (b) Intramural hematoma (IMH). A proposed mechanism of IMH is rupture of the vasa vasorum with the formation of crescentic or circumferential hematoma (burgundy crescent). Typically, both the lumen and the outer wall of the aorta remain smooth at imaging. (c) Penetrating atherosclerotic ulcer (PAU). Rupture through an atheromatous plaque (yellow) leads to a focal outpouching through the intima and into the media of the aortic wall. This results in focal outward bulging of the outer wall, often with surrounding periaortic edema and inammation. IMH and PAU may coexist

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desc

arch

asc

root

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Fig. 2 Oblique views of the heart and aorta using reconstructed data from computed tomography. Segments of the thoracic aorta are delineated as follows: The root extends from the virtual basal ring of the aortic valve (1) to the sinotubular junction (2). The ascending aorta (asc) extends above this to the origin of the brachiocephalic artery (*) (3). The aortic arch consists of the short segment between the brachiocephalic artery and left subclavian (#) arteries. The remainder of the aorta— the descending (desc) aorta—extends to the iliac bifurcation and is divided by the diaphragm into thoracic and abdominal components. The coronary arteries (arrows) arise from the aortic root. This patient has an ectactic ascending aorta measuring 44cm in diameter

the sinotubular junction just distal to the coronary artery origins. The aortic arch is a short segment that gives rise to the vessels of the head, neck, and upper extremities and extends from the brachiocephalic artery to the left subclavian artery. The descending aorta continues from the left subclavian artery to the iliac bifurcation and is further subdivided by the diaphragm into thoracic and abdominal components.

Pathophysiology ofIMH andPAU

Aortic intramural hematoma was rst described in 1920 as “dissection without an intimal tear” [12], yet a century later our understanding of its pathophysiology continues to evolve. It has historically been attributed to the spontaneous rupture of the vascular supply to the aorta itself, the vasa-vasorum (Fig.1b). This in turn has been felt to result from a combination of factors including hypertension, chronic

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inammation, wall stress, and connective tissue weakening [2, 13]. While in some cases this may be an accurate representation of the underlying pathophysiology, there is an emerging body of literature suggesting that micro-intimal tears may represent a sentinel event for these lesions, and rupture of the vaso-vasorum a secondary process [14–17]. In any case, a common denominator across a broad range of non-traumatic aortic injuries seems to include medial degeneration (formerly ‘cystic medial necrosis’), characterized by fragmentation of elastic bers, increased deposition of proteoglycans, and loss of smooth muscles cells in the media [18–20].

Penetrating atherosclerotic (or aortic) ulceration is caused by a rupture of an atheromatous plaque that compromises the intima, probably through local inammatory factors, and creates a focal communication between the lumen and the media (Fig.1c). This resulting outpouching or ulceration into the weakened wall causes a focal outward bulge of the aorta, often with surrounding periaortic edema and inammation. The injury to the media may propagate locally or distally in the form of an IMH or a frank dissection. In fact, all three lesions may coexist and PAU often has at least a small associated IMH. Conversely, IMH may be seen in the absence of signicant atherosclerosis—a prerequisite of PAU—and may demonstrate small luminal outpouchings that protrude into the media. These lesions are referred to as intramural blood pools (IBP) and ulcer-like projections (ULP). The former are pseudoaneurysms of intercostal, bronchial, or lumbar artery origins within the aortic wall. Although a ULP demonstrates a clear communication with the lumen owing to a frank intimal disruption, direct continuity of the lumen with IBPs, which are usually small, are typically not evident at imaging. ULPs may also be referred to as focal intimal disruptions (FIDs). These IMH-associated microlesions are mimickers of PAU but are not related to atheroma.

The typical patient risk factors, demographics, aortic location, and basic imaging characteristics of IMH and PAU are presented in Table1. In addition to characterizing the primary lesion, the imaging description of acute aortic syndromes is based on the layer(s) and segment(s) involved (including the presence and size of intimal tears and intramural blood sacs such as ULPs and IBPs), the aortic diameter and wall thickness, and associated complications.

Z. Hartley-Blossom et al.

Stanford Classication

All acute aortic syndromes are classied according to the Stanford classication scheme. This system is based on lesion location and helps guide management decisions. According to the original description, any lesion involving the ascending aorta was recognized as Stanford Type A, and any lesion limited to the descending aorta was classied as Stanford Type B [21]. This description left unclassied those lesions conned to or originating in the aortic arch. The surgical repair of Type A lesions involves interposition graft replacement of the ascending aorta to prevent complications related to coronary artery and aortic valve involvement or rupture

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• Rupture

thickening

• Crescentic or circumferential

Descending >

Ascending > Arch

syndrome

• Irregular surface • IMH

Descending >>> Arch

>> Ascending

syndrome

• Rupture

• Trauma • No intimal ap • Dissection

• Iatrogenic • No false lumen • Aneurysm

Lesion Layer Affected Demo. Risk Factors Presentation Location Appearance Complications

IMH Medial 65 y + Males • HTN Acute aortic

sources [1–7].

Table 1 Pertinent features and associations of aortic intramural hematoma (IMH) and penetrating atherosclerotic ulcer (PAU) gleaned from multiple

PAU Intimal 70 y + Males • HTN Acute aortic

• Tobacco • Focal luminal outpouching • Aneurysm

• COPD • No intimal ap • Embolization

• CAD • Dissection

Demo Demographics; HTN Hypertension; COPD Chronic Obstructive Pulmonary Disease; CAD Coronary artery disease

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into the pericardium. In this context, a lesion beginning in the arch has come to be recognized as a Type B lesion since surgery is not usually warranted. Despite this, the controversy has lingered with many manuscripts, book chapters, and textbooks adhering to the original classication description. Offering recognition of this controversy and a descriptive remedy, some authors have suggested an additional classication of “type B with arch involvement” [22]. In general, the simplest distinction is ‘Type A’ or ‘not Type A’. The majority of IMH lesions are type B (up to 63%) and similarly for PAU [3, 4, 19, 23].

Z. Hartley-Blossom et al.

CT andMRI forAAS: Imaging Techniques andFindings

Imaging for AAS needs to be fast, readily available, and straightforward to perform and interpret. Imaging these lesions is critical for prompt, accurate diagnosis, identication of associated complications, risk stratication, and ultimately formulating a management plan. While there are several imaging modalities available for imaging the aorta, CT and MRI are the primary tools used for the initial diagnosis, risk-stratication, and subsequent follow-up of AAS.Initial diagnosis of AAS by CT and MRI have sensitivities and specicities ranging from 90% to 100% [6, 24–26]. Owing to their 3-dimensional nature these modalities permit multi-planar reconstruction, and as warranted a more complete assessment of the entire aorta and surrounding structures.

Computed Tomography: Techniques

Although CT and MRI are generally complementary techniques, CT is usually preferred over MRI for the initial evaluation of suspected AAS in the acute setting as it is faster, more straightforward to perform, and more widely available, usually within or a short distance from an emergency department. Radiation is an inevitable concern associated with any CT scan, especially in young patients, but widely available and ever-improving dose reduction strategies are usually implemented to minimize patient risk. As an additional concern, a small percentage of patients are allergic to iodinated contrast, with an incidence of approximately 0.2–0.7% [27]. The administration of intravenous contrast to patients with impaired renal function has historically been controversial owing to a possible contrast-associated exacerbation. However, according to the most recent literature and joint statements from the American College of Radiology (ACR) and National Kidney Foundation (NKF) intravenous iodinated contrast is not felt to cause nephrotoxicity, and this should not be a principle consideration in the imaging of AAS [28]. This is particularly true given the necessity of a timely and accurate diagnosis. The sensitivity and negative predictive value of CT for the diagnosis of AAS are very high, both approaching 100% in optimal settings [29–31]. As will be discussed, in some cases subtle

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abnormalities may be missed and normal ndings may be misinterpreted due to a variety of patient and technical factors (such as motion artifact and poor contrast opacication). These constitute diagnostic pitfalls of which an interpreting physician must be aware.

A CT protocol for suspected AAS virtually always includes a contrast enhanced CT angiography (CTA) acquisition. This is typically obtained as a standard helical (or ‘spiral’) acquisition conducted without ECG-gating and with exogenous intravenous iodinated contrast injected at a relatively high rate (~4–5cc/s) to densely opacify vascular structures of interest. Contrast opacication will ultimately be determined by a host of imaging and injection parameters that are typically preset in the protocol and include X-ray tube current (mA) and voltage (kVp), scanner table speed, contrast injection rate and timing strategy (e.g. bolus tracking, bolus trigger, or xed delay), as well as by patient-related parameters such as body-mass index, cardiac output, and breath-holding capability. Imaging data are then reconstructed in multiple imaging planes for improved diagnostic clarity. Additional reconstructions methods, such as maximum intensity projection and volumerendering, can be implemented as needed. A comprehensive CT protocol may benet from an initial noncontrast scan, but it comes at the cost of additional radiation. Importantly, the specic diagnosis of intramural hematoma can commonly be made on noncontrast CT imaging (as will be discussed), and the lesion can often be seen to better advantage on the noncontrast series than on the post-contrast series. Therefore, in the setting of suspected AAS, a noncontrast series is usually advised [32].

Since the imaging acquisition of standard helical CT is not synchronized to the ECG, some degree of cardiac-related motion will be present around the heart and the aortic root, potentially reducing the accuracy for detecting short or subtle lesions in the ascending aorta. If the initial CT study is inconclusive or demonstrates spurious ndings, a repeat CT with ECG-gating or an MRI with ECG-gating may be performed. (ECG-gating is not typically performed at the outset because of slightly increased technical complexity and increased radiation dose relative to a non-gated helical acquisition.)

An ECG-gated CT can be performed using a non-helical, prospective acquisition—also colloquially referred to as ‘step-and-shoot’—during which the x-ray tube is active for only a short period of the cardiac cycle and sequential sections have no or minimal irradiation overlap, or a helical, retrospective acquisition during which the X-ray tube output peaks during a predetermined phase of the cardiac cycle, but is active at a nominal output throughout the remainder of the acquisition. In retrospective mode, scanners usually use low pitch meaning that there is substantial overlap of sequential acquisition volumes. Broadly, this means that the radiation dose of the former method is considerably less than that of the latter, but the latter permits image reconstruction at multiple cardiac phases throughout the cardiac cycle. Multiphase availability enables cine imaging if desired or simply evaluation of different regions of the aorta at different points in the cardiac cycle, potentially conrming pathology or reducing artifact. Moreover, unlike non- or even prospectively ECG-gated CT, retrospectively gated CT can provide limited functional

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information regarding the ventricles and valves, like echocardiography and MRI, but with poorer temporal resolution—akin to a slower camera shutter speed. Typically, patients with tachycardia or high normal heart rates are better served with retrospective gating (versus prospective gating) to reduce motion- related artifacts. Newer scanner technology, such as that offered by dual-source scanners employing ultra-high pitch acquisition, overcomes some of these motion and radiation dose related issues.

Z. Hartley-Blossom et al.

Magnetic Resonance Imaging: Techniques

For reasons stated above, CT is preferred for suspected AAS in the acute setting. However, for stable patients, patients with iodinated contrast allergy, those with questionable imaging ndings on initial CT, or patients requiring follow-up, MRI is often the modality of choice. MRI offers improved soft tissue contrast compared to CT, does not involve ionizing radiation, and has sensitivity and negative predictive values comparable to that of CT [13, 30, 31]. Unfortunately, MRI is not as widely available, takes longer, and is more technically challenging than CT, usually requiring patient cooperation for compliance with breath-holding and staying-still. Furthermore, monitoring unstable to marginally stable patients or those with MRI compatible instruments/hardware can be cumbersome and challenging. An additional consideration is that gadolinium based contrast agents have been linked to cases of nephrogenic systemic brosis (NSF). It is important to recognize that for the newer contrast agents there have been no reported cases of NSF across patients with a wide range of renal function [33]. Nevertheless, it remains a consideration and the ACR guidelines advise caution and thoughtful risk-benet analysis for patients with impaired renal function (GFR<30) [34]. Finally, there is also a risk of MRI contrast allergy, but this risk is very low, occurring in approximately 0.08% of administrations [35]. Importantly, it is even possible to diagnose AAS by MRI with- out contrast using standard imaging methods as described below.

While the specics of MRI methodology are beyond the scope of this text, there are important imaging techniques that when utilized appropriately can substantially assist in the diagnosis and management of AAS.MRI uses ‘bright-blood’ and ‘darkblood’ pulse sequences with ECG-gating (and with and without fat-suppression) in combination with 3-D MR angiography (MRA) to optimally visualize the aorta and branch vessels. Often patients have been imaged by other modalities prior to MRI, allowing the MRI to focus on a specic area of interest. As with CTA, MRA requires a high contrast injection rate and specically timed data acquisition to best visualize the vascular region in question. MRA is performed over several seconds without ECG-gating. (ECG-gating cannot be employed with MRA because of the necessity for acquiring a large volume of 3-D data during a single breath-hold as the contrast bolus transits the vascular system.) As a consequence, motion artifacts in the aortic root are again a common problem. However, although MRA with its high spatial resolution is preferred for detailing branch vessel pathology and identifying

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intramural outpouchings/ulcerations, AAS can frequently be diagnosed and accurately characterized using noncontrast MR techniques. ECG-gated MRI can reveal intramural aortic injuries such as hematomas, ulcerations, and intimomedial aps with high accuracy. Importantly, bright-blood cine MR imaging, like that used in cardiac imaging and generically referred to as ‘steady-state free precision’ (SSFP), can be readily implemented for visualization of the aorta and adjacent structures throughout the cardiac cycle. If present a dissection ap can be identied and distinguished from common artifacts that are typically associated with cardiac pulsation or blood ow. There is a limited, possibly benecial role for cine imaging in the detection of IMH and PAU.These particular lesions are frequently best visualized using dark-blood pulse sequences (“T1-” and “T2-weighted fast spin- echo”) that are sensitive to intramural blood, and by virtue of the changing magnetization states of hemoglobin over time may even assist in IMH dating. As with CT, ECG-gated MRI provides more optimal visualization of the aortic root.

Imaging Findings

Both noncontrast and postcontrast CT images can be helpful when diagnosing IMH and distinguishing it from other acute aortic pathologies. Noncontrast images demonstrate smooth crescentic or circumferential thickening of the aortic wall with increased mural attenuation relative to the vessel lumen (Fig.3). The thickened hyperdense wall is virtually diagnostic of IMH.Visualization of this hyperdense crescent may be aided through the use of thicker slice reconstruction (e.g. 5mm)— due to reduced image noise—and a narrow display window (e.g. width 100–200 HU, level 40 HU). Although the wall density is the same on pre- and postcontrast imaging, increased lumen density on postcontrast images may visually obscure the intramural hyperattenuation rendering it less conspicuous, especially in subtle cases

MPA

Fig. 3 Noncontrast (a-b) and postcontrast contrast (c-d) coronal (a, c) and axial (b, d) CT images demonstrate a large type A IMH in a 97-year old woman with chest pain. Noncontrast images show the high-density crescent of IMH (arrows) that is even evident, but subtle, in the anteromedial descending aorta (DA) (b, d). As noted in the text section ‘Predictors of Outcome’, the maximal wall thickness of 17mm and maximum ascending aortic diameters of 56mm seen in this case would generally be considered high risk features of IMH. AA ascending aorta; DA descending aorta; MPA main pulmonary artery

MPA

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ab cd

MPA

Fig. 4 Noncontrast (a, b) and postcontrast (c, d) axial (a, c) and coronal (b, d) CT images demonstrate a type A IMH in a 76-year old man with chest pain. Noncontrast images show a subtle, thin high-density crescent of IMH (white arrows) that is even evident in the posterolateral descending aorta (DA) (a, c). Addition ndings of hemopericardium (yellow arrow) and blood in the mediastinum around the main pulmonary artery (MPA) (dotted arrows) are consistent with rupture. AA Ascending aorta

Fig. 5 Sequential transaxial CTA images (a–d) demonstrate a ruptured type A IMH (arrows) in an 88-year old woman with chest pain. Mediastinal hemorrhage (dotted arrow) tracks into the shared adventitia between the aorta and pulmonary arteries causing severe narrowing of the main pulmonary artery (MPA) and occlusion of the right PA (RPA). The left PA (*) is narrowed but patent. Poor cardiac output results in diminished contrast in the descending aorta (DA). Note the ulcerlike projection arising from the posterior ascending aorta (AA)(arrowhead) and the displaced intimal calcication in the DA (yellow arrow) (a). LSPV Left superior pulmonary vein

bc d

MPA

LSPV

MPA

(Fig. 4). In addition, the postcontrast appearance of IMH may appear similar to mural atheroma, though the latter is usually irregular and demonstrates a lower density. Attenuation in the aortic wall of >45 HU on postcontrast CTA images has been proposed as an accurate threshold for IMH diagnosis [36]. Medial displacement of intimal atheromatous calcication in IMH may aid in this distinction (Figs. 5a and 6e).

Although intimal injuries have not classically been a hallmark of IMH, improvements in imaging techniques—especially spatial resolution—combined with careful scrutiny at surgery have revealed micro-intimal tears in up to 80% of IMH cases. These small injuries may in some cases represent a sentinel insult [14, 17, 23, 37]. There has been a growing consideration in fact that IMH may represent a subset of aortic dissection, with little or no ow within the false lumen, rather than a discretely separate entity [14, 37–39]. On the other hand, intimal defects not apparent on initial imaging may develop and become evident at follow-up. Noting the

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Fig. 6 Noncontrast (d) and postcontrast (a-c, e) axial (a-d) and sagittal (e) CT images demonstrate a type A IMH in a 79-year old woman with chest pain. The noncontrast image shows a thin high- density crescent of IMH (white arrows) in both the ascending aorta (AA) and the descending aorta (DA). An ascending aneurysm is evident (52mm). A large ulcer-like projection (ULP) arises from the anterior AA (arrowheads). Note the displaced intimal calcication in the DA (dotted arrow). Mild hemopericardium (yellow arrows) is present. MPA Main pulmonary artery

presence and size of these defects may be important for prognosis (Figs.5, 6, and

7). ULPs (or FIDs) occurring in the rst two weeks of diagnosis in type B IMH and

a broad neck >3mm are associated with a higher risk of pseudoaneurysm formation and rupture than those lesions with tiny intimal defects (TIDs)<3mm, no defects at all, or larger defects occurring after two weeks [40, 41]. Moreover, the likelihood for progression to aneurysm, dissection, and rupture increases with lesion size, and lesions having a diameter of >20mm and a depth of >10mm, as well as those in the ascending aorta and arch, are particularly ominous [42, 43]. ULPs can resemble PAUs but can usually be distinguished by the appearance of the surrounding aorta. Unlike the latter, ULPs commonly protrude through a smooth intima and are not specically associated with ulceration through an atheromatous plaque (Fig.7).

As mentioned earlier, intramural blood pools (IBPs) are small, blood containing sacs that represent pseudoaneurysms of intercostal, bronchial, and lumbar arteries at their origins within the aortic wall (43,44) (Figs.8, 9, and 10). Curiously, they frequently do not appear to communicate with the aortic lumen, probably due to their small size, local mechanical effects, and the spatial resolution of imaging [14,

44]. Occasionally, a series of IBPs will be present in the descending aorta generating

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