CT Artifacts and Aortic Diseases

Although CT is the principal diagnostic test for diseases of the aorta, CT artifacts may confound assessment of aortic diseases. The older the CT scanner, the greater the number of artifacts (at least half of CT studies on scanners from 1999 or earlier have significant artifacts over the ascending aorta).

Potentially problematic artifacts include:

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  Streak artifacts off the brachiocephalic vein (from contrast), confounding assessment of the aortic arch behind it

  
  
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  Streak artifacts off the superior vena cava (from contrast or pacer wires), confounding assessment of the ascending aorta beside it

  
  
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  Streak artifacts off the spine, confounding assessment of the descending aorta beside it

  
  
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  Older scanners (slow, or without cardiac gating) may generate “pulsation” artifacts of superimposed images of the aorta in different positions due to translation from cardiac motion, conferring the impression of an intimal flap. There is almost 1 cm of translational motion of the ascending aorta through the cardiac cycle.

  
  
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  Motion artifacts

  
  
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  See Figure 26-1 .

  
  

  
  

  
  

  

  
  

  
  

  The systolic motion (translation and pulsation) of the aorta on non–ECG-gated imaging may render a superimposition image artifact to suggest an intimal flap.

  
  

Atherosclerotic Calcification

Atherosclerotic plaques in the aorta are extremely common. The two sites most often involved are the abdominal aorta and the distal floor of the arch. Although there is general correlation between the extent of aortic and coronary atherosclerosis, many patients will have small flecks of aortic calcification without having significant coronary disease.

Intimal calcification is a marker of intimal position. “Intimal displacement” (into the lumen) is a convenient sign of mural thickening due to either occurrence of a false lumen within the wall of the aorta or development of intramural hematoma. If there is thickening over (i.e., on the luminal side of) intimal calcification, it usually is from thrombus, particularly if the aorta is dilated at that site.

For images of calcification of the aorta, see Figures 26-2 and 26-3 .

Porcelain aorta—unclampable in the ascending segment. A, Three-dimensional volume-rendered image of the aortic root and ascending aorta reveals extensive contiguous and circumferential calcification of the aorta well into the ascending portion. Above that, the calcification is spotty. B, Calcification at the ostium of the left main stem coronary artery and in a plaque in the left anterior descending artery. All the coronary arteries had extensive “hard” plaques. C and D, Non–contrast-enhanced axial CT images reveal nearly circumferential calcification of the aortic root and calcification down the proximal left coronary artery ( C ) and down the proximal right coronary artery ( D ). E and F , Extensive aortic valve and annular calcification ( E ) and mitral annular calcification ( F ).

Cardiac CT images of a 78-year-old man being assessed for a redo coronary artery bypass graft (CABG). A, The precontrast image demonstrates extensive—almost circumferential—calcification around the ascending aorta. This configuration can be termed a porcelain aorta. B, Administration of intravenous contrast somewhat decreases the conspicuity of the underlying extensive aortic calcification. An evaluation of the extent of calcification and atherosclerotic disease of the ascending aorta is available to the cardiothoracic surgeon in the planning of the patient’s redo CABG by noncontrast CT scanning.

Aortic Dissection

CT is the principal modality used to diagnose acute aortic dissection (AAD). CCT has emerged as the initial diagnostic modality to identify or exclude AAD by virtue of:

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  Imaging both the thoracic and abdominal aorta (vs. echocardiography), which has far more limited field-of-view

  
  
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  Its speed (vs. MRI)

  
  
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  Its very high degree of accuracy (vs. angiography)

  
  
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  Its ability to image the majority of side branches (vs. echocardiography)

  
  
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  Its ability to image important variants of dissection such as intramural hematoma (vs. angiography)

  
  
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  The fact that most referring physicians are comfortably familiar with it

Studies comparing CT to other modalities were numerous 12 to 15 years ago; however, few studies have been done involving the current generation of CT equipment. Studies from a decade ago cannot depict the relative accuracy of any test that has developed as much as CCT has in the past 5 years. To further complicate comparisons, TEE and MRI also have evolved over the last decade.

Findings of aortic dissection that CCT is able to image include:

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  Intimal flap

  
  
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  False lumen. The false lumen generally arises off the outer curvature of the aorta (as the tear is usually located on the outside curvature).

  
  
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  Thrombosis within the false lumen (suggests/consistent with chronicity or healing)

  
  
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  Entry tear. The two most common sites of entry tears are 2 cm above the aortic valve and 1 cm distal to the left subclavian artery.

  
  
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  Exit (re-entry) tear

  
  
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  Pleural effusion

  
  
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  Pericardial effusion

  
  
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  Mediastinal hematoma

  
  
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  Branch vessel involvement. The finding that a branch vessel arises from the false lumen does not establish that its vascular bed is underperfused, only that it is jeopardized. One of the few signs of vascular bed hypoperfusion that is clinically supported is that of pallor of the kidneys during a contrast-enhanced scan.

  
  
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  Coronary artery involvement, especially if ECG gating is employed

The diagnosis of a dissection is made when an intimal flap is identified. Lack of thrombosis within the false lumen supports acuity of the dissection, while thrombosis supports chronicity.

Potential false positives that may occur include streak artifact from residual contrast in the SVC across the ascending aorta appearing as linear artifact masquerading as an intimal flap. The linearity of the line artifact across the ascending aorta, the presence of multiple lines, the presence of nearby bright lines, and the traversing of tissue planes by the lines indicate that these are artifact. Intimal flaps are not straight in their entirety.

CCT is the most commonly used modality for following aortic diameter in patients with aortic dissection in the chronic phase and is able to identify progressive enlargement as well as persistence of flow in the false lumen. Aortic diameter of type B (distal) dissection cases increases in 37% of cases with a thrombosed false lumen and in 90% of cases with a persistent false lumen. Growth rate has been noted to be 4 ± 7 mm/year in the ascending aorta, 2 ± 9 mm/year in the arch, and 1 ± 6 mm/year in the descending aorta.

For images of acute aortic dissection, see Figures 26-4 through 26-13 andVideo 26-1.

Composite images from a cardiac CT study in a patient with Marfan syndrome demonstrate a type A dissection with an associated ascending aortic aneurysm. No extension of this flap into either coronary artery was present.

A, The left sagittal view displays an intimal tear immediately distal to the left subclavian artery, and a flap extending distally. There are sternal wires from a recent aortocoronary bypass grafting operation. B, The right coronal abdominal view reveals gross distention with air, due to mesenteric ischemia malperfusion from the dissection flap.

Acute type B aortic dissection with protracted hypertensive crisis. The intimal flap can be seen to the right renal ostium and may continue past the calcified plaque into the proximal renal artery. The right kidney enhances less than the left one. The diagnosis was renal ischemia and refractory hypertension.

Aneurysm of the ascending aorta in chronic type B/distal dissection of the aorta. Note the extensive calcification of the free wall of the false lumen of the type B dissection, which is perfectly seen on the noncontrast images ( C , D ) and poorly seen on the contrast-enhanced images ( A ).

Triple lumen: a “triple-barreled” aorta due to recurrent dissection of the aorta. Note the pleural effusion, which was hemorrhagic.

A 44-year-old man with severe aortic stenosis. This study was done preoperatively prior to aortic valve surgery to rule out any underlying significant coronary artery disease. A, Moderate aortic valve thickening, calcification, and restriction of the aortic valve leaflets. Curved multiplanar reformations through the right coronary artery ( B ), left anterior descending artery ( C ), and circumflex/OM1 ( D ) are normal.

An abdominal level–only type B dissection, in a patient with a family history of the same.

Contrast-enhanced CT aortography images of a patient with a chronic type B aortic dissection. The intimal flap is well visualized because it has become stiff and immobile.

Non-contrast and contrast-enhanced CT scan images of a patient with a chronic type B aortic dissection. A, Non-contrast axial image reveals intimal displacement by the false lumen, marked by the inward displacement of calcified intimal plaques, and indicating either aortic dissection or intramural hematoma. B, Contrast-enhanced axial image at the lower arch level reveals intimal displacement, an intimal flap, an entry intimal tear in the proximal descending aorta, as well as partial thrombosis of the false lumen. C and D, Three-dimensional volume-rendered images of the irregularities of the distal false lumen. SeeVideo 26-1.

Chronic dissection of the ascending aorta in a patient with a previously inserted bioprosthetic aortic valve, whose three wire struts are apparent, as is the ring. The intimal flap is straight and clear, as is often seen with chronic dissection. There is a fair volume of thrombus within the false lumen, also consistent with chronicity. The ascending aorta is aneurysmal, and the aortic diameter normalizes only by the distal aortic arch.

Intramural Hematoma

An important variant of aortic dissection is acute intramural hematoma (IMH; Figs. 26-14 through 26-17 ). Approximately 10% of suspected dissection cases are IMH. Merely ruling out dissection does not achieve the diagnosis of this equally important, underrecognized pathology. There are fewer data delineating the natural history, prognostic features, and outcomes of management strategies on IMH than on AAD. To summarize what is known:

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  Outcomes parallel those of AAD.

  
  
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  Description of the anatomic site of involvement using “Type A/Ascending” and “Type B/Descending/Non-Ascending”) as per AAD classification is suitable. The only location of IMH and AAD that does not lend itself to description by this classification is that of isolated arch involvement.

  
  
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  Both non–contrast- and contrast-enhanced views are useful to depict the mural thickening of IMH.

  
  
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  The appearance usually is of a crescentic thickening of the wall. Occasionally the mural thickening is circumferential (“annular”).

  
  
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  The longitudinal extent of involvement is generally much less than that of AAD (8–12 cm only). Unlike AAD, most IMH do not involve the entire aorta.

  
  
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  Risk appears related to:

  
  
  
  
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    Proximal location

    
    
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    Leakage

    
    
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    Greater anatomic extent of involvement

    
    
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    Association with atherosclerotic penetrating ulcer

  
  
  
  
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  There is no intimal tear or connection of the false lumen to the true lumen.

  
  
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  The differential is of aortic dissection with a thrombosed false lumen.

  
  
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  About 5% to 10% of cases will, in time, become frank dissection with an intimal tear connecting the true and false lumens.

  
  
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  Management is undertaken according to the paradigm of AAD management:

  
  
  
  
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    Surgery for proximal involvement

    
    
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    Medical management for uncomplicated distal involvement

  
  

Non–contrast-enhanced ( A ) and contrast-enhanced ( B ) CT scans, at approximately the same level in a patient with intramural hematoma of the distal aorta. The noncontrast view shows posterior intimal calcification with displacement and the faint appearance of posterior crescentic wall thickening, with higher attenuation. The contrast-enhanced view effectively defines the lumen and reveals the crescentic wall thickening of the posterior aorta, but the contrast obscures visualization of the calcium.

Contrast-enhanced views of the mid-thoracic ( A ) and abdominal aorta ( B ). Contrast dye within a recess in a thickened wall ( A ). The wall thickening has a uniform and non-atherosclerotic appearance and suggests intramural hematoma by its crescentic shape and even texture. This may be either a penetrating ulcer or a tear complicating the intramural hematoma.

A 45-year-old woman was admitted for severe chest pain associated with sinus tachycardia. Echocardiography showed normal left ventricular function, without wall motion abnormalities, a mild aortic regurgitation, and ascending aorta dilation. Dual-source system CT showed a moderate aneurysm of the ascending aorta (46 mm) and bicuspid aortic valve. A and B, A 6-mm smooth-shaped wall thickening on the noncoronary sinus was detected, suggesting intramural aortic hematoma, without evidence of an intimal tear. C and D, MRI was performed, and the thickened aortic wall T2-weighted dark blood hypersignal confirmed the presence of fluid within the aortic wall. The patient underwent replacement of the ascending aorta and noncoronary sinus, with aortic valve sparing. E and F, Histologic examination revealed an intact intimal layer and a slender, cleftlike lesion within the outer part of the tunica media in continuous association in a larger adventitial hematoma.

(Reprinted with permission from Cavarretta E, Ramadan R, Dorfmuller P, Raoux F, Paul JF. Intramural aortic hematoma definitive diagnosis combining computed tomography and magnetic resonance imaging. J Am Coll Cardiol. 2011;58(16):e30.)

Sagittal contrast-enhanced chest CT scans of a patient with a type A intramural hematoma at presentation ( A ) and at 48 hours ( B ) with progression into a type A dissection with hemopericardium.

CT is highly accurate (100%) at identifying IMH.

The aspect of surgery that is theoretically less well suited to address IMH pathology is aortic root replacement for AAD, which has a high chance of eliminating the entry tear, thus depressurizing the false lumen distal to the root replacement and facilitating its thrombosis. In IMH, there is no entry tear to eliminate. Root replacement in the context of IMH provides protection to the aortic valve and coronary artery ostia, as well as to the pericardial space.

Identification of a penetrating ulcer responsible for IMH establishes a significantly worse prognosis. Sustained or recurrent pain, increasing left pleural effusion, increasing maximal aortic diameter, and increasing penetrating ulcer depth reliably predict progression and risk. Development of an “ulcer-like” projection of the ascending aorta or arch is a sign of progression to overt dissection.

Ulcers, Penetrating Ulcers, and Overlying Aortic Thrombus of the Aorta

The least common acute aortic syndrome is penetrating ulcer of the aorta. Atherosclerotic plaques in the aorta, as elsewhere (e.g., carotid and coronary trees), may ulcerate. Atherosclerotic plaques may eventually extend to variable depths (i.e., penetrate) within the wall of the aorta. The deeper the extent into the wall, the greater the chance of disruption of the integrity of the wall.

Weakening of the plaque that allows for communication of the lumen with deeper sections of the wall may result in propagation of blood into the wall and formation of an intramural hematoma within the wall. It also may result in leakage of blood out of the aorta (with or without an intramural hematoma), and, rarely, rupture of the aorta may occur.

CT is able to image aortic ulcers and penetrating ulcers. The challenge for all imaging modalities, including CT, is to distinguish between the two. Ulcers are common; penetrating ulcers are not. Ulcers will not lead to disruption of the aorta, whereas penetrating ulcers may do so. Ideally, imaging modalities would have sufficient resolution to depict the layers of the wall of the aorta distinct from the plaque itself. However, this is not always the case. Depiction of a deep “button-shaped” ulcer is usually convincing evidence of penetration.

Thrombi of variable size usually form on atheromatous plaques and may embolize. They commonly coexist.

Thrombosis and thromboembolism are other complications of atherosclerotic plaques of the aorta. Thrombosis is evident only on contrast-enhanced views as contrast void. A prominent plaque usually underlies the thrombus.

For images of atherosclerosis of the aorta, see Figures 26-18 and 26-19 .

Atheromatous disease of the aorta with plaque involving the ostia to the right renal artery ( A ) and the superior mesenteric artery ( B ). Calcified plaque at the ostia to both renal arteries ( C and D ) and the tight stenosis of the superior mesenteric artery seen by three-dimensional reconstruction ( E ) and by “vessel extraction” ( F ).

A 77-year-old woman underwent coronary artery bypass grafting in 2002. The surgeon noted a mass on the ascending aorta, adjacent to the innominate artery. He performed an off-pump coronary artery bypass grafting procedure to avoid manipulation of the aorta. The patient subsequently experienced two documented cerebral embolic events. The most recent resulted in a permanent bilateral visual field defect. Serial CT studies demonstrated progressive enlargement of a penetrating atherosclerotic ulcer of the ascending aorta adjacent to the origin of the innominate artery ( A, arrow ). The patient underwent excision of the penetrating ulcer ( B, arrow ), the ascending aorta, and the aortic arch to the level between the origins of the left carotid and innominate arteries. The ascending aorta and innominate artery were replaced with prosthetic grafts. Penetrating atherosclerotic ulcers are commonly found in the descending but rarely in the ascending thoracic aorta. Embolization from the ulcer crater was the likely cause of the cerebral embolic events.

(Reprinted with permission from Stamou SC, Kouchoukos NT. Penetrating ulcer of the ascending aorta. J Am Coll Cardiol 2011;57(11):1327.)

For images of atherothrombosis of the aorta, see Figures 26-20 and 26-21 .

Atheromatous aorta with a penetrating ulcer of the floor of the distal arch. The upper coronal views ( A and B ) reveal the partially thrombus-laden penetrating ulcer extending from the floor of the distal arch. C and D, The extensive burden of protruding thrombus, and the topographically complex surface of the lumen. E, Three-dimensional reconstruction does provide a representation of the irregularity of the surface of the aorta, but largely fails to capture the nature of the disease as effectively as the planar views. F, A large abdominal aortic aneurysm in the same patient, with a large amount of mural thrombus.

A 52-year-old man presented with strokes in dispersed territories. Diffusion-weighted MRI images ( C, D ). Chest CT ( C ) revealed a soft tissue mass in the ascending aorta, which was better imaged on an ECG-gated cardiac CT ( B ) to minimize motion artifact. The lesion was believed to be thrombus.

Occlusion of the Aorta

Occlusion of the aorta may be acute, resulting from either LV apical or left atrial thromboembolism, from local thrombosis often seen in low flow-shock states, from intra-aortic balloon counterpulsation, or, rarely, from more proximal aortic embolization of thrombus. Occlusion will only be apparent on contrast enhancement. Chronic occlusion usually is associated with extensive collaterals, which depend on the level of occlusion and may be caused by atherosclerosis or aortitis.

For images of occlusion of the aorta, see Figure 26-22 .

Contrast-enhanced volume intensity projection image. The complete occlusion of the aorta is evident, as are extensive collaterals and reconstitution of the femoral arteries.

Middle Aortic Syndrome

“Middle aortic syndrome” is isolated abdominal level stenosis, which has many clinical similarities with coarctation of the thoracic aorta. It may be caused by aortitis.

For images of the middle aortic syndrome, see Figure 26-23 .

A 46-year-old woman was admitted with signs of lower limb ischemia. Her examination demonstrated a nonpalpable distal pulse. CT angiography revealed an anomalous origin of both renal arteries ( A and B ) and severe aortic narrowing between the renal arteries, confirmed by the angiogram ( C ). The diagnosis was middle aortic syndrome. Endovascular treatment was decided on, and a balloon-expandable covered stent (Jomed, Abbott Laboratories, Abbott Park, IL) was placed, with good stent expansion ( D ). Physical examination revealed distal pulse recovery. At 5 months, the patient remains asymptomatic. E and F, CT angiography showed stent patency. Middle aortic syndrome refers to an isolated disease of the thoracoabdominal aorta causing segmental narrowing. It often is associated with hypertension in childhood. This is a rare case of middle aortic syndrome with lower limb ischemia successfully resolved with endovascular treatment.

(Reprinted with permission from Rabellino M, Garcia-Nielsen L, Gonzalez G, Baldi S, Zander T, Maynar M. Middle aortic syndrome: percutaneous treatment with a balloon-expandable covered stent. J Am Coll Cardiol. 2010;56(6):521.)

Aortic Aneurysm

CT scanning is extremely well suited to diagnosing and assessing aneurysmal disease of the aorta: thoracic, abdominal and thoracoabdominal ( Figs. 26-24 through 26-30 ). CT scanning is able to:

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  Identify aneurysms

  
  
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  Establish anatomic extent

  
  
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  Establish (accurately) aneurysm diameter

  
  
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  Distinguish aneurysms from dissection and false aneurysm

  
  
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  Identify mural thrombus within aneurysms

  
  
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  Identify leakage

  
  
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  Identify the relation of the aneurysm to branch vessels

  
  
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  Establish interventional suitability and planning

  
  
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  Establish the relation of aneurysms of the aortic root and sinuses to coronary arteries

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