Atherosclerosis

Atherosclerosis affects the aortic wall in many ways, such as through erosion of the internal elastic lamina and subsequent exposure of the medial layer of the aortic wall to the pulse pressure or through ischemia of the media from reduced blood supply due to disease in the vasa vasorum. Another mechanism of aneurysm formation is through progression of atherosclerotic plaque ulceration to a penetrating atherosclerotic ulcer with breakage of the intimal layer. Penetrating atherosclerotic ulcer may result in a saccular aneurysm (Fig. 92-2). Atherosclerotic aneurysms are associated with hypertension, coronary artery disease, and abdominal aortic aneurysms.⁴

FIGURE 92-2 Ulceration of the atherosclerotic plaque leads to a penetrating atherosclerotic ulcer, which can cause dilation of the aorta (arrows). Sagittal oblique maximum intensity projection CT angiographic image (A) demonstrates extensive atherosclerotic plaque in the descending thoracic aorta. Plaque ulceration eventually breaks through the intimal layer, causing a penetrating atherosclerotic ulcer, which can result in an aneurysm with a focal bulge or saccular configuration (B).

Cystic Medial Necrosis

As the name implies, cystic medial necrosis affects the medial layer of the arterial wall; degeneration of the smooth muscle creates “cystic spaces,” resulting in a fusiform aneurysm.⁴ This is the most common cause of aneurysms of the ascending aorta. The pathophysiologic process involves the aortic root, resulting in dilation of the annulus of the aortic valve. Associated aortic regurgitation may require concomitant replacement of the aortic valve.⁶ Cystic medial necrosis is the hallmark of the pathologic changes in Marfan syndrome (Figs. 92-3 to 92-6). Other connective tissue disorders, such as Ehlers-Danlos and Loeys-Dietz (Fig. 92-7) syndromes, also affect the medial layer of the aorta.⁴ These entities are both familial and have an identifiable gene leading to the abnormal biochemistry.

FIGURE 92-3 Oblique coronal reformatted contrast-enhanced CT image shows dilation of the aortic root (arrow) and typical effacement of the sinotubular junction in Marfan syndrome.

FIGURE 92-4 Associated cardiac abnormalities are common in Marfan syndrome. Oblique axial reformatted contrast-enhanced CT images show a dilated aortic root and mitral valve ring (arrow, B). The mitral valve was dysfunctional because of associated mitral valve prolapse.

FIGURE 92-5 In Marfan syndrome, the proximal aorta is affected, with the disease commencing at the aortic root. The descending aorta and abdominal aorta are rarely affected. The sinotubular junction can be effaced, resulting in a “spring onion” appearance to the aortic root and ascending aorta. Oblique coronal multiplanar reformatted image before (A) and 2 years after (B) uncomplicated repair of dilated aortic root. Note the typical appearance of a repaired aorta with kinking at the anastomosis (arrow).

FIGURE 92-6 The dilated root and effaced sinotubular junction (A) in Marfan syndrome is of a distinctive configuration. Note the difference in appearance of an ascending aortic aneurysm that spares the root (B).

FIGURE 92-7 In Loeys-Dietz syndrome, the dilated aortic root is repaired much earlier than in other connective tissue diseases. Oblique coronal reformatted contrast-enhanced CT image shows a mildly dilated aortic root (arrow, A), which resulted in a valve-sparing aortic root repair with coronary artery reimplantation (arrow, B), the modified David procedure (B and C).

Marfan syndrome is the most common of the connective tissue processes, with an incidence of 1:10,000.⁷ Marfan syndrome is an autosomal dominant condition that results in a mutation in the gene encoding fibrillin 1,⁸ an essential protein for elastic properties, causing cardiovascular and musculoskeletal abnormalities. The elastin-depleted aorta is stiffer and more prone to dilation as it incurs higher pulse pressure than the normally distensible aorta does. The dilation starts in the root and extends to the mid-ascending aorta.⁹ Aortic rupture and dissection are the leading causes of death in patients with Marfan syndrome.⁷ Repair in patients with Marfan syndrome is recommended in the asymptomatic patient when the aortic root or ascending aorta exceeds 5 cm in diameter because of the high risk of aortic rupture and aortic dissection.¹⁰ Associated cardiovascular abnormalities include aortic insufficiency and mitral valve prolapse, which frequently necessitate valve repair, and pulmonary artery aneurysms.⁹

Loeys-Dietz syndrome has only recently been characterized as a distinct phenotype that is caused by mutations in genes encoding type 1 or type 2 transforming growth factor β.¹¹ Aneurysms form at an earlier age than in other connective tissue disorders and tend to rupture at a smaller size, with a greater propensity for dissection. The arteriopathy tends to be more systemic than in Marfan syndrome, and the postoperative surveillance must factor both the repaired artery and the remote arteries including the intracranial circulation.

Vascular Ehlers-Danlos syndrome is an autosomal dominant disorder caused by heterozygous mutations of the COL3A1 gene. The syndrome is characterized by fragile arterial tissue that not only is prone to aneurysm, dissection, and rupture but can also make surgical repair difficult. Noninvasive imaging, such as computed tomographic angiography (CTA) and magnetic resonance angiography (MRA), is preferred because of the risk of dissection and rupture with arterial access. Unlike Marfan and Loeys-Dietz syndromes, which have a predilection for the aortic root, Ehlers-Danlos syndrome more often affects the visceral arteries.¹²

Dissection

Aortic dissection is different enough in pathogenesis and management to be considered separately from thoracic aortic aneurysms. The term dissecting aneurysm is discouraged. Nonetheless, a dissected aorta may become aneurysmal (Fig. 92-8), and an aneurysm may dissect; both scenarios alter the management and approach. Of note, any cause of an acute aortic syndrome can result in aneurysm formation.

FIGURE 92-8 Sagittal reformatted (A) and axial (B) contrast-enhanced CT images show a type B dissection (arrow) and aneurysm of the descending aorta.

Trauma

Blunt thoracic trauma with a sudden deceleration mechanism injures the aorta at its points of relative fixation (due to shear), which includes the aortic isthmus (in the region of the ligamentum arteriosum), the hiatus, and the aortic root, in descending frequency. Injury may cause transection or intimal disruption and, if unrecognized, may be manifested as a saccular aneurysm that may involve disruption of the intima and media (pseudoaneurysm or false aneurysm).¹³

Mild bulging of the proximal descending aorta at the attachment of the ligamentum arteriosum (ductus bump) is a common normal finding and should not be confused with aneurysms in that region, particularly those due to trauma (Fig. 92-9).

FIGURE 92-9 A, Sagittal oblique maximum intensity projection from contrast-enhanced MRA shows mild dilation of the inferior wall of the proximal descending aorta (arrow), a common finding known as the ductus bump. B, In another patient, an aneurysm (arrow) of the proximal descending aorta is shown for comparison.

Inflammation and Infection

Infection may primarily involve the artery and secondarily lead to aneurysm, or an aneurysm may become infected. The most common site of infection is the ascending aorta near the sinus of Valsalva (Fig. 92-10).¹⁴ Infected aortic aneurysms, despite the pseudonym mycotic aneurysms, are rarely due to fungal agents and mostly caused by bacteria in an acute or chronic setting, classically due to syphilis.

FIGURE 92-10 A, Sagittal reformatted contrast-enhanced CT image shows a tubular outpouching (arrow) inferior to the aortic arch with a thick rind of surrounding soft tissue. This is an infected aneurysm. B, Axial contrast-enhanced CT image shows infarcts (arrow) in the spleen due to emboli from the infected complex.

Infected aortitis leading to aneurysms may occur by direct extension from endocarditis or seeding of the vasa vasorum with infected complexes from remote septic foci. These remote foci may not be clinically evident, and Salmonella and Staphylococcus are the most common etiologic agents in this situation. Predisposing factors include intravenous drug abuse and immunocompromised state.¹⁵

Vasculitides such as Takayasu arteritis and giant cell arteritis may lead to aneurysmal dilation, but mural thickening is the predominant finding in such inflammatory conditions. The mural thickening may lead to reduction in luminal caliber even if the adventitia-adventitia measurement indicates arterial enlargement.¹⁶

Post-stenotic Dilation

Aortic stenosis can cause dilation of the ascending aorta, usually the right lateral and posterior wall, from the post-stenotic jet. This is commonly seen in those with a bicuspid aortic valve (Fig. 92-11), although the dilation may be partly due to a systemic arteriopathy because this condition is also associated with coarctation of the aorta.¹⁷ Coarctation can also lead to post-stenotic dilation.

FIGURE 92-11 Sagittal oblique (A) and oblique axial (B) maximum intensity projection images from contrast-enhanced CT show post-stenotic dilation (arrow) of the ascending aorta enlarging the right lateral and posterior wall from bicuspid aortic valve.

Increased Aortic Flow

The increased stroke volume from aortic regurgitation or from a patent ductus arteriosus can dilate the ascending aorta. Treatment is aimed at treating these entities.

Asymptomatic

Nearly half of thoracoabdominal aortic aneurysms are discovered incidentally, some in the context of vascular disease elsewhere and others on chest radiography or echocardiography. Patients with known phenotype or family history of connective tissue disease should have routine work-up to search for aneurysm.

Local Mass Effect

Symptoms depend on the structure being compressed, such as the airway (breathing difficulty, recurrent pneumonia, and cough), esophagus (dysphagia), pulmonary vein (focal pulmonary edema, varix), systemic veins (limb and facial swelling), and vertebral body (backache). In the event of fistula formation, the patient may present with hemoptysis (airway) or hematemesis (esophagus).

Systemic Symptoms

Inflammatory and infected aneurysms or prosthetic grafts may present with constitutional symptoms such as fever and weight loss.

Embolism of the atherosclerotic plaque or thrombus will cause clinical signs of distal ischemia, such as blue toe syndrome.

Rupture

Chest pain in the context of a known aneurysm signifies increase in size, development of a dissection, or rupture. With rupture, chest pain is accompanied by diaphoresis and hypotension, and the patient may be in extremis. The signs and symptoms may point to end-organ ischemia, such as abdominal pain disproportionate to physical examination findings (mesenteric ischemia), paraplegia (spinal cord ischemia), and angina pectoris (myocardial ischemia).

The strongest predictor of rupture is the initial size of the aneurysm. Also, the etiology of the aneurysm must be taken into consideration as certain connective tissue disorders are associated with rupture at a smaller aneurysm size. For thoracoabdominal aortic aneurysms due to atherosclerosis, the rupture rate is 18% at 2 years for aneurysms greater than 5 cm. Another risk factor for rupture is aneurysm growth of more than 5 mm in 6 months. Aneurysm growth correlates with smoking, forced expiratory volume in 1 second (FEV₁) of less than 1.5 L/ min, female sex, and advancing age.²⁰ The diameter at which elective surgery on the ascending aorta is recommended is considered to be 5.5 cm.¹⁰ Ascending aortic aneurysms grow faster in association with a bicuspid aortic valve (0.19 cm/yr) than with a non–bicuspid valve (0.13 cm/yr).²¹

Aneurysm and Its Extent

The questions that need to be answered are

The following information concerning the aneurysm and vascular tree needs to be determined:

FIGURE 92-14 Color-coded oblique sagittal volume rendered image of the aorta. There are extensive calcifications in the aorta. The calcifications have a green shade. Stent graft placement for the aneurysmal descending thoracic aorta will be difficult because of the severe angulation and tortuosity of the aorta.

(Image courtesy of Dr. Ron Fairman, Chief, Division of Vascular Surgery and Endovascular Therapy, Hospital of the University of Pennsylvania.)

The state of the axillary and iliofemoral arteries is important to note for many reasons. The iliofemoral arteries provide stent graft access and must be of a certain minimal diameter to allow the sheath to enter without complication. Bypass may use the axillary arteries. In addition, an axillary-femoral bypass may achieve distal aortic perfusion that is critical to reducing visceral ischemia during the cross-clamp period.¹

Associated Abnormalities

Postoperative Surveillance

Surveillance in the postoperative period is performed to detect complications that are inherent to the procedure (e.g., endoleaks for stent grafts), to observe for complications due to the hemodynamic alteration consequent to the procedure (e.g., dissection), and to monitor the effects of the causative arteriopathy on the nontreated vasculature.

Radiography

Chest radiography can suggest the presence of an aneurysm and its complications. Aneurysms often present incidentally on chest radiography. Findings on chest radiography include dilation of the aortic contour (Fig. 92-15) and calcification. Associated cardiac abnormalities will lead to an abnormal cardiac size and configuration.²³

FIGURE 92-15 In two different patients, aneurysms of the ascending (A) and descending (B) aorta can be seen on plain radiography as enlargement of the aortic contour.

Dilation of the aortic contour may be focal, segmental, or diffuse. Ascending aortic dilation can be inferred by a right convex contour above the right atrial border. Dilation of the proximal descending aorta, the aortic knob, will cause an indentation on the trachea.

Long-standing aneurysms due to atherosclerosis or syphilis are likely to calcify. Calcification is usually of the intimal layer. Less commonly, the medial layer calcifies, and the calcification has a “railroad” configuration. Diabetes and renal impairment are known causes of medial calcification. Displacement of the intimal calcification, meaning that the calcification is no longer peripheral in location, suggests a dissection or intramural hematoma. Calcification of the mural thrombus or plaque, also known as neointimal calcification, can simulate the displaced calcifications.

Aneurysms of the sinus of Valsalva may mimic a mass on chest radiography. Sinus of Valsalva aneurysms are symmetric or asymmetric. Connective tissue disease typically causes symmetric dilation of the sinuses. The location of the contour abnormality or “mass” on chest radiography can predict the involved sinus. Aneurysms of the right sinus project anteriorly (best seen on the lateral view) and can erode the sternum. Aneurysms from the anterior portion of the noncoronary sinus project over the right atrium, and those from the posterior portion of this sinus project over the left atrium.²⁴

Rupture of an aneurysm and the presence of a mediastinal hematoma are suggested by the following¹: displacement of the esophagus, obscuration of the aortic contour, pleural effusion (left), and apical cap (left).

Ultrasonography

Two-dimensional echocardiography (either transthoracic or transesophageal) is not primarily used for the characterization of the aneurysm or the arterial tree. However, the transesophageal approach can provide useful information about the presence of plaque and a dissection flap. The one area not usually visualized by the more invasive but more sensitive transesophageal approach is that part of the ascending aorta overlapped by the trachea because of loss of the acoustic window.²⁵

Echocardiography is performed for assessment of valvular function, particularly that of the aortic valve. As mentioned, aortic regurgitation may influence the decision to operate on the aortic valve concurrently. Also, in the presence of aortic regurgitation, cross-clamping should be done with caution, possibly with bypass of the left side of the heart.¹ The intra-aortic balloon pump, a frequent intensive care unit support device, is contraindicated in patients with significant aortic regurgitation.

Carotid duplex ultrasonography is helpful in detecting concomitant carotid artery stenosis and assessing the risk of postoperative complications, such as stroke and subclavian steal phenomenon.

Computed Tomography

With the advent of multidetector CTA and novel contrast injection mechanisms and protocols, CTA has become the most accessible, used, and important modality for the assessment of patients with thoracic aortic aneurysms. Although the risk of radiation exposure and the nephrotoxicity of iodinated contrast medium cannot be discounted, CTA gives excellent spatial and vascular information enabling improved computer postprocessing, such as multiplanar reformation, maximum intensity projection, and volume rendering. Postprocessed viewing of data provides a surgeon or interventionalist with a valuable three-dimensional perspective of the aneurysm, its location, and its position relative to its branch vessels and adjacent structures. The combination of fast acquisition and spatial resolution enables evaluation of the arch to the femoral arteries (and even the toes, if necessary) with the administration of one contrast media bolus (“run”) and with only one breath-hold requirement. In addition, ECG-gated cardiac CT can provide information on cardiac function and the coronary arteries. CT of the aortic valve, however, does not provide direct measurement of blood flow, as can be achieved with MRI. Nonetheless, planimetry of CT data can detect and to some extent quantify aortic stenosis (e.g., aortic valve area) or aortic regurgitation (e.g., comparison of right and left ventricular volumes). CTA will assess nonvascular organs, notably the lungs, and may direct the need for pulmonary function tests.²⁶

Pre-contrast and arterial phase images are obtained routinely. Delayed (venous phase) images are often beneficial. Venous phase images help in the assessment of solid organs and in the characterization of masses that are incidentally found. Very large aneurysms may not uniformly opacify in the arterial phase, thereby overestimating the size of the thrombus, and only in the venous phase may the true luminal diameter be reflected. Venous phase imaging is routinely obtained in surveillance CT after stent graft placement to detect endoleaks.

Images should be inspected before the administration of contrast material for signs of aortic rupture and for intramural hematoma (Fig. 92-16). Signs of aortic rupture (Fig. 92-17) include irregular aortic wall with broken intimal calcifications, periaortic and mediastinal hematoma, hemothorax (left sided for rupture of aneurysms of the descending aorta), hemopericardium (rupture of ascending aortic aneurysms), and soft tissue “stranding” in the mediastinal fat. Intramural hematoma is indicated by a crescentic high attenuation (50 to 80 HU) along the aortic wall. High attenuation within the mural thrombus is important to identify because this sign is associated with instability and subsequent rupture of aneurysms. Adjacent atelectatic lung should be distinguished from periaortic hematoma.

FIGURE 92-16 Intramural hematoma (arrow) before (A) and after (B) contrast-enhanced CT. Subacute blood products are of high attenuation. Note that the intramural hematoma is peripheral to the intimal calcifications. On MRI, the T1-weighted image (C) displays the high signal from subacute blood. The intramural hematoma does not enhance (B).

FIGURE 92-17 Non–contrast-enhanced images are crucial in detecting aortic rupture on CT. This patient with a ruptured intramural hematoma (A, arrow) has hemopericardium (B, arrow) and bilateral pleural effusions.

A distinction must be made between high attenuation within a mural thrombus and an intramural hematoma. Intramural hematoma is due to bleeding within the medial layer of the aorta and has a smooth margin and a partially circumferential and somewhat helical configuration. Intimal calcifications, if present, are displaced by the intramural hematoma toward the lumen, that is, the hematoma is peripheral to the calcification. Mural thrombus is usually chronic and adherent to the arterial wall. This has an irregular border. The intima is at the periphery of the mural thrombus, that is, the thrombus is internal to the wall of the aorta. Thrombus may calcify, giving the appearance of a displaced intima. However, the distinction can be made by the irregular edge of the thrombus.²⁷

Wall thickening of the aorta may be due to an intramural hematoma, a mural thrombus, or an inflammatory process such as vasculitis. Inflammatory wall thickening is distinguishable by the presence of peri-inflammatory fibrosis and wall enhancement.

The aneurysm is best defined on the arterial phase images. A sense of the degree of mural thrombus and atherosclerotic plaque is obtained with the high contrast between lumen and wall. In the setting of an acute rupture, extravasation of contrast material indicates active bleeding and is a sign that must be communicated urgently to the surgeon. However, the absence of extravasated contrast material into the periaortic tissue is not reassuring. To emphasize, the definitive sign of rupture is the periaortic hematoma.

It is critical to ensure that the periaortic process thought to be a hematoma from acute rupture does not enhance in either the arterial or venous phase; mediastinal soft tissue processes such as lymphoma and extramedullary hematopoiesis may have similar imaging features. Similarly, any area questioned in the arterial or venous phase to represent contrast should be correlated with the images obtained before the administration of contrast medium. Calcium and surgical material may not be distinguishable from iodinated contrast media.

Infected aneurysms present as a saccular structure eccentrically from the aortic wall with rapid enlargement, periaortic gas, and erosion of the adjacent osseous structures such as the vertebral body or sternum. Associated reactive adenopathy is frequent.¹⁵

Magnetic Resonance

MRI can provide much of the same information that CT can, with no radiation and without the complications of iodinated contrast media.²⁸ However, the use of gadolinium-based contrast agents in patients with severe renal impairment may be a problem secondary to their increased risk for nephrogenic systemic fibrosis.²⁹ MRI is not as readily available, takes longer to perform than CTA, and may be demanding for the unstable patient. Importantly, MRI does not assess the lungs and cannot detect calcium reliably.

MRI provides flow information and quantifies valvular heart disease with hemodynamic as well as planimetric parameters. MRI also can provide a complete evaluation of the heart, including function, viability, and contractile or perfusion reserve. Assessment of the coronary arteries by MRI remains an evolving indication.

Multiplanar single-shot fast spin-echo may be used for localizers and overview of anatomy. At least one T1-weighted pulse sequence (e.g., T1-weighted gradient-echo, dual-echo, or fast spin-echo) should be obtained in the axial plane to assess for the presence of hemorrhage in the aortic wall (i.e., intramural hematoma). The post-gadolinium sequence is a three-dimensional spoiled gradient-echo with acquisition parameters optimized for an acquisition that is within the breath-hold capacity of the patient. An axial delayed two-dimensional post-gadolinium pulse sequence, preferably with fat suppression, completes the evaluation. Subtraction images are obtained with use of the pre-gadolinium three-dimensional acquisition as the mask. The angiographic part of MRI is much more amenable to three-dimensional postprocessing, such as maximum intensity projection and volume rendering, than are angiographic images in CT. This is because the nonarterial structures have little contribution to signal, particularly after accurate subtraction.

Although, in general, MRA does not typically require ECG synchronization, the use of prospectively triggered double inversion recovery fast spin-echo black blood imaging allows a better distinction between the aortic wall and lumen, especially near the base of the heart. The addition of inversion recovery fat suppression picks up mural edema, a feature of inflammatory aneurysms.

Cine bright blood images through the thoracic aorta can be useful. In patients with connective tissue disease such as Marfan syndrome, the reduced distensibility of the aorta can be picked up by measuring the change in aortic diameter between end-diastole and end-systole in relation to the pulse pressure.

The morphologic findings of aneurysms are similar to those described with CTA. Subacute blood is of high signal on T1-weighted images, and the signal of the aortic wall and pleural and pericardial effusions should be assessed on this sequence. In the absence of fat suppression, mediastinal hematoma can be difficult to distinguish from fat. Active extravasation of contrast material may be picked up on the multiphase three-dimensional acquisitions or on the delayed venous images.

MRI is more sensitive than is CT in detecting marrow changes due to osteomyelitis that may be associated with infected aortic aneurysms.

Nuclear Medicine/Positron Emission Tomography

Inflammatory aneurysms, infected aneurysms, and infected grafts take up radiotracers indicative of inflammation. Nuclear medicine has a clear role in the evaluation of patients with suspected prosthetic graft infection and equivocal CTA or MRA findings. Leukocytes labeled with technetium Tc 99m exametazime offer the highest sensitivity, although cross-labeling of platelets reduces its usefulness in the early postoperative period. Leukocytes may be labeled with indium 111. The use of gallium requires delayed as well as early imaging. Nuclear medicine lacks spatial sensitivity, and more accurate localization of infection may require CT/PET or CT/SPECT.

Angiography

The use of angiography is declining with the availability of CTA and MRA. Certain indications remain, notably the evaluation of the coronary arteries. Aortography will show the dilated aorta, although it is only a luminogram and does not provide information about the aortic wall, thus underestimating aneurysm size.³⁰

In connective tissue disease such as Marfan syndrome, there is effacement of the sinotubular junction, which provides a “spring onion” appearance to the aortic root. Furthermore, aortic root dilation may be symmetric or asymmetric; symmetry is a feature of cystic medial necrosis.

Aneurysms involving the sinus of Valsalva typically have a windsock morphology. A regurgitant jet in diastole signifies aortic incompetence. The sequence of chamber opacification is important to note. For example, early opacification of the right-sided chamber points to a rupture of a sinus of Valsalva aneurysm and fistula or the concomitant presence of aortic insufficiency and a ventricular septal defect.

Stent Graft

Stent grafts can be used for aneurysms in the descending thoracic aorta in both the emergent and elective scenario.³¹ Not all aneurysms are suitable for treatment by stents. The proximal and distal neck of the aneurysm must be long enough to provide a suitable cuff for proper deployment of a stent. The neck should not exceed 36 mm in diameter, be relatively free of plaque or thrombus, and not be excessively angulated or calcified. The proximal landing zone should be at least 15 mm and may be defined from the origin of either the left subclavian artery or left common carotid artery; if the latter is chosen, the left subclavian artery is necessarily occluded. In that situation, an ipsilateral carotid-subclavian bypass graft is performed to avoid the steal phenomenon and vertebrobasilar insufficiency. Saccular aneurysms due to trauma (including iatrogenic trauma) or penetrating ulcer, because of their focality and relative absence of disease in the proximal and distal landing zones, have the best response rate to stent graft treatment.

The stent is composed of a metallic framework and fabric and is usually self-expanding. The proximal and distal parts of the stent are composed of the metal strut only and not the fabric. The uncovered part of the stent results in better fixation with the arterial wall and allows one to cross an arterial origin without occlusion of flow.

Cross-sectional imaging plays an important role in the pre–stent graft evaluation for accurate sizing of the stent graft. If desired, CTA can also provide comprehensive angiographic information to include the iliac arteries if the surgeon or interventionalist desires evaluation for suitability of the iliac arteries for access. The least tortuous and widest iliac artery is used for access by a femoral arterial surgical cutdown. Alternatively, the iliac arteries can be reached through an extraperitoneal approach, or the stent graft apparatus can be manipulated through a combination of upper extremity and lower extremity vascular access.

Complications of stent grafts include endoleak, stent kinking, migration and fracture, and graft thrombosis and occlusion. Detection of complications warrants surveillance with CTA and MRA.

The stent material determines MR compatibility. Ferromagnetic stents distort the local magnetic field, causing T2* susceptibility artifacts that may render images nondiagnostic, and safety issues have been raised with one stainless steel stent used for abdominal aortic aneurysms. Nitinol and Elgiloy stents cause relatively little artifact at MRA, with good visualization of the lumen and aneurysm sac. The likely stent choice may be operator specific and, if known prospectively, should influence the baseline imaging test.

Stent migration is more likely to occur in those with atherosclerotic aneurysms whose aorta is more tortuous. Strategies to reduce the chances for or complications of stent migration include a longer proximal landing zone (20 mm) and the use of overlapping stents.³¹

An endoleak is diagnosed by the identification of contrast agent opacification of the excluded aneurysms (Fig. 92-18). Endoleaks due to failure of proximal and distal attachment (type 1) may occur immediately in the period after intervention or after a delay. Delayed type 1 endoleaks suggest graft migration. A proximal landing zone that is short, wide, angulated, ulcerated, or of reverse tapering or trapezoidal morphology predisposes to type 1 endoleak. Retrograde flow through a collateral artery such as the intercostal artery is a type 2 endoleak, which is less common after stent placement in the thoracic aorta than in the abdominal aorta. Type 3 and type 4 endoleaks (due to graft disruption or separation of components in a modular stent graft or porosity, respectively) are less common than type 1 and type 2. In the absence of a visualized endoleak, the continued expansion of the sac is classified as a type 5 endoleak or endotension.

FIGURE 92-18 Oblique maximum intensity projection (A) and axial (B) contrast-enhanced CT images show a stent in the descending thoracic aorta and an endoleak (arrow). The endoleak, located peripherally, appears to connect to an intercostal artery and was presumed to be type 2.

Visualization of the direction of flow characterizes the type of endoleak definitively. This may be possible in high temporal resolution MRA (time-resolved MRA) but usually requires catheter angiography. In the absence of information of the directionality of flow, the type of endoleak can be inferred by the location, configuration, and timing of the appearance of the endoleak. For example, type 1 endoleaks are closer to the stent than the periphery of the sac and tend to be visible in the arterial phase of imaging. Type 2 endoleaks have a peripheral location closest to the feeding artery, have a tubular configuration, and may be visible only in the venous phase.

The CTA protocol for surveillance includes images obtained before the administration of contrast medium and acquisition in both the arterial and venous phases of the examination. The MRA protocol involves the T1-weighted spin-echo sequence to look for subacute blood products and a three-dimensional dynamic arterial phase acquisition, usually with two phases. Delayed two-dimensional gradient-echo acquisitions complete the assessment.

Prosthetic Graft

A description of open surgery for thoracic aortic aneurysms is beyond the scope of this chapter. A brief description is made of the surgical principles. Imagers must be familiar with the surgery to detect complications and to avoid the misinterpretation of expected surgical findings for pathologic changes (Fig. 92-19).

FIGURE 92-19 Sagittal oblique reformatted image from contrast-enhanced CT shows the appearance of an ascending aortic prosthetic graft.

The placement of a prosthetic graft may be without disruption of vascular continuity (interposition graft) or with disruption of vascular continuity (extra-anatomic bypass graft). Interposition grafts may be placed within the native artery (inclusion repair), that is, the aneurysm sac is not repaired and is peripheral to the graft. Alternatively, the aneurysm sac is resected (total repair). Repair of the ascending aorta is accompanied by root repair if the root exceeds 4.5 cm. Surgery of the aortic root may be accompanied by valve repair or coronary artery reimplantation. Surgery may involve the arch in a partial or complete manner, with or without reimplantation of the great arteries. In those with aneurysms of both the ascending and descending aorta, one strategy is a prosthetic graft repair of the ascending aorta and a stent graft repair of the descending aorta.³²

Complications of Prosthetic Grafts

Imaging has a role to play in the diagnosis or prediction and prevention of complications. These include infection, anastomotic aneurysms and dehiscence, rupture, and paraplegia.

Infection of the graft can have serious consequences locally and systemically, with a high mortality. Local complications can involve the repaired aorta (anastomotic dehiscence, pseudoaneurysm, and rupture) and neighboring nonvascular structures (osteomyelitis). The clinical presentation can be remarkably nonspecific, requiring a high index of suspicion.

CTA and MRA offer effective assessment for graft infection; CTA is more often used. The key to suspicion of infection is the timing of surgery as many of the signs of infection are also expected findings in the early postsurgical period.

CTA signs of infection of prosthetic grafts in the thoracic aorta are perigraft soft tissue rind; fluid in the operative bed (persistence of fluid beyond 3 months of surgery should not be considered normal); air in the vicinity of the graft (this may be normal in the first 10 postoperative days); anastomotic dehiscence and rupture; pseudoaneurysm—2% of patients with graft infection develop pseudoaneurysm, whereas the majority of those with a pseudoaneurysm do not have graft infection; fistula; unexplained sternal wound infection or mediastinitis; and tethering of the esophagus.

On MRI, the low signal of air can be difficult to distinguish from calcium, which may also have low signal on all pulse sequences. Nuclear medicine studies help in equivocal cases.

Aneurysms in the repaired aorta may be due to infection or occur at the surgical anastomosis or sites of cannulation for bypass.

The most devastating postoperative complication is paraplegia. Despite progress in perioperative care, the incidence of paraplegia has not been reduced to acceptable levels. Risk factors include cross-clamp time of more than 30 minutes, hypotension, and mesenteric ischemia. Operative maneuvers such as sequential reperfusion of the intercostal arteries could be of benefit (Fig. 92-20). Preoperative localization of the artery of Adamkiewicz may be of value, and both CTA and MRA have been used for this purpose (Fig. 92-21). This artery arises from the anterior branch of the radiculomedullary artery, which is a branch of the left posterior intercostal artery (usually 9th to 12th). The diameter of the artery is 0.8 to 1.3 mm, and it has a characteristic hairpin course. Owing to its small diameter and tortuous course, high spatial resolution acquisition with the ability to render three-dimensional reformations is critical.³³

FIGURE 92-20 Volume rendered sagittal oblique image from contrast-enhanced CT shows prosthetic repair of a descending thoracic aortic aneurysm. There is an aorto-aortic extra-anatomic bypass graft (arrow) created intraoperatively to ensure perfusion of the intercostal arteries, a mechanism to reduce the risk of paraplegia.

FIGURE 92-21 Volume rendered (A) and maximum intensity projection (B) images from CE CT show the artery of Adamkiewicz with its characteristic hairpin turn as it enters the spinal cord.

(Images courtesy of Scott Steingall, Chief Technologist, 3 D Lab, University of Pennsylvania.)