Editors: Collins, Jannette; Stern, Eric J.
Title: Chest Radiology: The Essentials, 2nd Edition
> Table of Contents > Chapter 19 - Thoracic Aorta
Chapter 19
Thoracic Aorta
This chapter will focus on acquired aortic diseases, expanding on the content provided in Chapters 6 and 18. Chest computed tomography (CT) and magnetic resonance imaging (MRI) have replaced conventional angiography as the primary imaging modalities in the evaluation of thoracic aortic disease. In particular, multidetector CT is able to quickly and accurately provide imaging information regarding the diagnosis (e.g., dissection, aneurysm, intramural hematoma, penetrating ulcer), location, and extent of aortic disease, in addition to providing information regarding alternative diagnoses for the patient's symptomatology. Information provided by CT is also useful in presurgical planning and postsurgical follow-up.
Aortic Dissection
Acute aortic dissection is the most common cause of aortic emergency, exceeding that of thoracoabdominal aortic aneurysm rupture (1). Dissection is a life-threatening condition that requires immediate diagnosis and treatment. Intramural hematoma and penetrating atherosclerotic ulcer, discussed later in this chapter, are considered by some to represent atypical forms of dissection. All three entities can produce chest or back pain in a patient with hypertension. Thoracic aortic dissection is classified as acute if the symptoms last fewer than 2 weeks and chronic if the symptoms last longer (2).
Acute aortic dissection occurs most commonly in the sixth and seventh decades of life. However, it can also occur in patients under 40 years of age, especially those with Marfan syndrome (3). Risk factors for the development of aortic dissection are listed in Table 19-1. The initiating event is usually a tear in the intima of the aortic wall that allows blood to enter the media, resulting in separation of the intima from the adventitia. Dissection can also occur as a sequela of pre-existing intramural hematoma or penetrating atherosclerotic ulcer. The sites of intimal tear are most commonly within a few centimeters of the aortic valve (60%), at the origin of the descending aorta just distal to the left subclavian artery (30%), and in the aortic arch (10%) (2).
Two classification schemes are used to describe aortic dissection. Both define the descending aorta as distal to the left subclavian artery. The most widely used scheme is the Stanford classification, which includes two types, based on whether surgery is required: Type A (60%) involves the ascending aorta regardless of the site of intimal tear or distal extent (requires immediate repair), whereas type B (40%) does not involve the ascending aorta (treated medically for hypertension unless complications occur) (4). The DeBakey classification is as follows: Type I originates in the ascending aorta and extends distally throughout the aorta, type II is confined to the ascending aorta, and type III originates in the descending aorta and extends distally (5). Complications of type A dissection include rupture into the pericardium (producing cardiac tamponade) and left pleural space, occlusion of coronary artery and aortic arch branches, and severe aortic insufficiency with acute left heart failure. Rupture is less common in type B dissections, which usually progress to a chronic form. However, surgery is indicated for persistent pain or abdominal organ ischemia.
When acute aortic dissection is suspected, unenhanced CT should always precede contrast-enhanced scanning to detect intramural hematoma. The entire aorta must be imaged to assess the extent of disease. Typical aortic dissection is produced by an intimal tear that allows blood to enter the medial layer, giving rise to two lumina - one true and one false (see Fig. 6-28). The main finding on enhanced CT is the presence of an intimal flap separating the true lumen from the false lumen. If the false lumen is thrombosed, the intimal flap may not always be detected. The dissection flap is usually curved in an acute dissection and flat in a chronic dissection. Identification of the two lumens is critical for planning endovascular stent placement. The true lumen tends to lie close to the inner curvature of the aortic arch and anteromedially in the descending aorta, whereas the false lumen commonly lies in the outer portion of aorta (Fig. 19-1). The false lumen usually has a larger cross-sectional diameter than the true lumen and often has intraluminal thrombus, but there is great variability in appearance of the false lumen. Unenhanced CT may show internal displacement of intimal calcifications, if present. The "beak sign" is the cross-sectional imaging manifestation of the wedge of hematoma that cleaves a space for the propagation of the false lumen. Slender, linear areas of low attenuation occasionally appear in the false lumen, known as the "cobweb sign." This sign corresponds to residual ribbons of the media that have been incompletely sheared away by the dissection. Intimointimal intussusception is produced by circumferential dissection of the intimal layer, which subsequently invaginates like a windsock. On CT, this is seen as one lumen wrapped
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around the other in the aortic arch, with the inner lumen invariably being the true lumen. Other findings on enhanced CT include delayed enhancement of the false lumen and mediastinal and/or pericardial hematoma. Fluid around the aorta may be a sign of ongoing penetration or perforation.
TABLE 19-1 RISK FACTORS FOR DEVELOPMENT OF AORTIC DISSECTION
  • Hypertension (most common)
  • Connective tissue diseases
    • Marfan syndrome
    • Ehlers-Danlos syndrome
    • Turner syndrome
    • Familial aortic dissection
  • Cystic medial necrosis (most commonly associated with Marfan syndrome)
  • Congenital lesions
    • Aortic coarctation
    • Bicuspid and unicommissural aortic valve
  • Trauma
    • Cardiac surgery or catheterization
    • Blunt trama
  • Pregnancy
  • Aortitis
    • Aortic aneurysm
    • Aortic infection
  • Cocaine abuse
FIGURE 19-1. Acute ascending aortic dissection. A: CT of a 50-year-old man with chest pain, numbness of the left hand, and a history of hypertension shows a dissection involving the left subclavian artery (arrow). B: CT of the aortic arch shows dense enhancement of the true lumen (T), less dense enhancement of the false lumen more laterally (F), and medial hematoma (H). C: CT at the level of the aortic root shows periaortic hematoma (H).
The key information required for treatment is the extent of the dissection and whether branch vessels originate from the true lumen or the false lumen. When the dissection flap extends into the lumen of a branch vessel and narrows it, treatment is usually angioplasty, with or without deployment of an endovascular stent. Surgical treatment of type A dissection consists of replacement of the ascending aorta, aortic root, and aortic valve and reimplantation of the coronary arteries into the graft (Fig. 19-2).
Intramural Hematoma
Intramural hematoma (IMH) is caused by a spontaneous hemorrhage of the vasa vasorum of the medial layer. Unlike dissection, it is not associated with an intimal tear. The median age of patients with IMH is 68 years, and a common predisposing factor is hypertension (3). IMH, thought to account for approximately 13% of acute aortic dissections (6), is classified according to the Stanford system. It is generally considered to have a more favorable prognosis than classic aortic dissection.
On unenhanced CT, IMH appears as a crescent-shaped area of high attenuation in the aortic wall that corresponds to a hematoma in the medial layer. The hematoma may or may not compress the aortic lumen. Intimal calcifications may be displaced. It is important to perform unenhanced CT prior to
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enhanced CT, as IMH is usually more difficult or impossible to detect on enhanced scans. Unlike the false lumen in aortic dissection, IMH remains unenhanced after administration of contrast. Whereas dissection tends to spiral longitudinally around the aorta, IMH tends to maintain a circumferential relationship with the aortic wall. A type A IMH greater than 5 cm in diameter is at high risk for subsequent aortic dissection or aneurysm formation (3).
FIGURE 19-2. Acute ascending aortic dissection. A: Posteroanterior (PA) chest radiograph of a 31-year-old man with chest pain and shortness of breath shows a normal appearing aorta. Note that a normal appearing aorta on chest radiography does not exclude disease of the ascending aorta. B: CT shows a dilated aortic root (R). The origin of the left coronary artery is seen (solid arrow) and was noted to be involved at the time of surgery. The linear area of low attenuation near the left coronary artery is artifact (dashed arrow). C: CT at a level inferior to (B) shows an intimal flap in the ascending aorta and enhancement of the true (T) and false (F) lumens. D: CT after replacement of the ascending aorta, aortic root, and aortic valve and reimplantation of the left coronary artery shows a "ribbon" of high attenuation surrounding the repair (arrows). This is a normal postoperative appearance and should not be mistaken for a contrast leak. E: CT at the level of the aortic root, after repair, shows Teflon felt (Meadox Medical Inc., Oakland, NJ) (dashed arrows) around the reimplanted left coronary artery (solid arrow). A normal postoperative hematoma is seen (H).
Penetrating Atherosclerotic Ulcer
Penetrating atherosclerotic ulcer (PAU) is defined as an ulceration of atheromatous plaque that has eroded the inner, elastic layer of the aortic wall; reached the medial layer; and produced a hematoma in the media (7). Unlike typical aortic dissection, PAU most often occurs in elderly patients with severe underlying atherosclerosis. PAU may lead to aortic dissection, pseudoaneurysm formation if it penetrates through the media, or transmural aortic rupture if it extends through the adventitia (3). The most common location of PAU is the middle or distal third of the descending thoracic aorta, although any portion of the aorta can be involved. Surgical intervention with grafting of the affected area is indicated in patients with hemodynamic instability, persistent or recurrent pain, expanding hematoma, aortic rupture, distal embolization, and development of pseudoaneurysm, pericardial effusion, or bloody pleural effusion.
In patients with PAU, extensive atherosclerosis is usually seen on CT. On unenhanced CT, IMH and displacement of
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intimal calcification are commonly seen. Enhanced CT shows a collection of contrast material outside the aortic lumen, similar in appearance to a peptic ulcer, with adjacent subintimal hematoma. PAU lesions can be single or multiple. The aortic wall is often thickened. Care should be taken in making a diagnosis of PAU if the lesions are discovered incidentally in an asymptomatic patient and focal IMH is absent. Atheromatous ulcers that are confined to the intimal layer sometimes resemble PAU on enhanced CT. PAU is usually treated medically. Surgery is indicated when symptoms of chest or back pain persist, IMH expands, or there are other signs of impending rupture. Surgery involves local incision of the ulcerated portion of the aorta and replacement with an interposition graft. In nonsurgical candidates, an endovascular stent graft is placed or the PAU is percutaneously embolized.
Thoracic Aortic Aneurysm
Thoracic aortic aneurysm is defined as an aortic diameter greater than 4 cm and is classified as to location, morphology, integrity of the aortic wall, and etiology (Fig. 19-3). The most common etiology is atherosclerosis. The most common location is at the junction of the aortic arch and descending aorta (Fig. 19-4). Aneurysms that involve the ascending aorta are usually caused by cystic medial necrosis, connective tissue
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disorders such as Marfan and Ehlers-Danlos syndromes, and syphilis (now rare). Aneurysms involving the descending aorta are usually atherosclerotic, posttraumatic, infectious (mycotic), or inflammatory (rheumatoid arthritis and ankylosing spondylitis). Fusiform aneurysms are those with general enlargement of the entire aortic circumference (Fig. 19-5), whereas saccular aneurysms are sharply delineated and usually involve a localized segment of the aorta, which often appears as an eccentric outpouching. Regarding aortic wall integrity, aneurysms can be classified as true (having an intact aortic wall that is composed of intima, media, and adventitia) or false (also called pseudoaneurysm, characterized by a disrupted aortic wall contained by the adventitia, perivascular connective tissue, and organized blood clot). Atherosclerotic and connective tissue disorder–related aneurysms are true aneurysms. Posttraumatic and infectious (mycotic) aneurysms are usually false aneurysms.
FIGURE 19-3. Ascending aortic aneurysm. A: PA chest radiograph of a 54-year-old man with a heart murmur shows a tortuous-appearing aorta. B: Lateral view shows a markedly dilated ascending aorta. C: White-blood sagittal MRI shows fusiform dilation of the ascending aorta.
FIGURE 19-4. Thoracic aortic aneurysm. A: PA chest radiograph of a 77-year-old woman shows a left mediastinal mass contiguous with the contour of the aorta (arrow). B: CT shows an aneurysm of the proximal descending aorta with extensive mural thrombus (T). Adjacent rim of high attenuation represents atelectatic lung (arrow). C: Coronal CT shows a fusiform aneurysm involving the junction of the aortic arch and descending aorta; this is the most common location of atherosclerotic thoracic aortic aneurysms. D: CT after placement of endovascular stent graft shows the metallic stent, enhancing aortic lumen, and surrounding low-attenuation thrombus. There is no evidence of leak. E: Coronal CT shows overlapping stents. Note persistent thrombus (T). F: Sagittal CT shows normal appearance of overlapping stents.
FIGURE 19-5. Thoracic aortic aneurysm. PA (A) and lateral (B) chest radiographs of a 56-year-old woman with back pain show tortuosity and dilation of the thoracic aorta. C: CT shows fusiform dilation of the aortic arch and minimal low-attenuation mural thrombus. D: CT at a level inferior to (C) shows dilation of the descending aorta and mural thrombus. E: CT of the abdominal aorta shows extension of the aneurysm into the abdomen, atherosclerotic plaque, and mural thrombus.
Imaging assessment of aneurysms includes size, location, and relationship with branch vessels, as well as the morphological type of aneurysm and the presence or absence of findings that suggest impending rupture. The risk of rupture increases with size and with rapid expansion. Surgical repair should be considered when thoracic aneurysms reach a diameter of 5 to 6 cm (3). Characteristic CT findings include focal or diffuse aortic dilations and deformity, peripheral curvilinear and plaquelike intimal calcification at the edge of the aorta or near the aortic margin, thickened aortic wall, filling of the patent portion of lumen by contrast media, intraluminal thrombus that may be circumferential or crescentic, displacement of mediastinal structures, bone erosions, periaortic hematoma, or pleural fluid. Other complications include aortobronchial fistula, compression of the right pulmonary artery, aortoesophageal fistula, and distal embolization. The aorta may rupture into the mediastinum, pericardium, pleural sac, or extrapleural space. The presence of pleural or extrapleural blood on the left and contained aortic leak are signs of impending or actual rupture (see Fig. 6-27). A contained leak can be found when the aneurysm is in close contact with the spine, with lateral draping of the
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aneurysm around the vertebral body with a deficient posterior aortic wall.
Imaging the Repaired Aorta
Both CT and MRI can be used to evaluate the postprocedural aorta and monitor for complications. Numerous types of surgical repairs are performed, and the normal appearance on CT will depend on the type of repair made. Portions of the aorta may be resected, grafts may be sewn end to end or end to side, and branch vessels may be reimplanted or grafted using synthetic interposition grafts. A continuous suture, graft inclusion procedure involves aortotomy, graft inclusion, and enclosure of the graft within the native aorta. This procedure creates a space between the graft and native aorta that can fill with bland or infected fluid, blood/thrombus, or contrast material. A small amount of fluid and air in this space is normal immediately after surgery. Fluid seen 6 weeks after surgery and gas seen 2 weeks after surgery are reliable signs of infection.
Felt pledgets and strips are often used to reinforce sutures, which should not be mistaken for contrast material leaking from a graft. A small portion of the native aorta next to the coronary ostium is often implanted onto a coronary artery graft. This is called a coronary button and should not be mistaken for a pseudoaneurysm.
Endoluminal stent grafts are being used increasingly frequently to treat many aortic diseases. Imaging after stent graft deployment can be used to confirm complete exclusion of the aneurysm, assess patency of the stent graft and aortic branches, and evaluate sequential shrinkage of an aneurysm (Fig. 19-6) (3). An endoleak is defined as continued flow within an
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aneurysm sac after deployment of a stent. Type I endoleaks are leaks at the proximal or distal attachment sites of the stent and correlate with aneurysmal enlargement and late aneurysmal rupture. Type II endoleaks are caused by patent aortic side branches, including lumbar, inferior mesenteric, and accessory renal arteries.
FIGURE 19-6. Thoracic aortic aneurysm. A: PA chest radiograph of a 58-year-old man with hypertension shows a tortuous and dilated descending aorta. B: CT at the junction of the aortic arch and descending aorta shows atheromatous plaque and mural thrombus. C: CT at a level inferior to (B) shows atheromatous ulcers (arrow) confined to the intimal layer, which should not be mistaken for penetrating atherosclerotic ulcers. Note that there is no displacement of intimal calcifications. D: CT after placement of overlapping endovascular stent grafts shows a focal leak (arrow) and surrounding hematoma. E: CT at a level inferior to (D) shows that the hematoma (H) is compressing the posterior left atrium (LA). F: Delayed CT at the same level as (E) shows high-attenuation contrast leaking from the stent (arrows).
References
1. Castaner E, Andreu M, Gallardo X, et al. CT in nontraumatic acute thoracic aortic disease: typical and atypical features and complications. Radiographics. 2003;23:S93–S110.
2. Prete R, Von Segesser LK. Aortic dissection. Lancet. 1997;349:1461–1464.
3. Takahashi K, Stanford W. Multidetector CT of the thoracic aorta. Int J Cardiovasc Imaging. 2005;21:141–153.
4. Crawford ES, Svensson LG, Coselli JS, et al. Surgical treatment of aneurysm and/or dissection of the ascending aorta, transverse aortic arch, and ascending aorta and transverse aortic arch. Factors influencing survival in 717 patients. J Thorac Cardiovasc Surg. 1989;98:659–674.
5. DeBakey ME, Cooley DA, Creech O. Surgical treatment of dissecting aneurysm. JAMA. 1995;162:1654–1657.
6. Nienaber CA, von Kodolitsch Y, Peterson B, et al. Intramural hemorrhage of the thoracic aorta: diagnostic and therapeutic implications. Circulation. 1995;92:1465–1472.
7. Stanson AW, Kazmier FJ, Hollier LH, et al. Penetrating atherosclerotic ulcers of the thoracic aorta: natural history and clinicopathologic correlations. Ann Vasc Surg. 1986;1:15–23.