The Core Curriculum: Cardiopulmonary Imaging, 1st Edition (2004)

Chapter 18. The Thoracic Aorta

Many articles and books have been written about the aorta. However, there is still confusion regarding the aorta and aortic diseases among radiologists. Specifically, confusion exists regarding the various terms used to describe acquired aortic diseases, progression of disease, and the postoperative aortic imaging features. In this chapter we discuss the congenital aorta, coarctation, and pseudocoarctation. Acquired aortic diseases are discussed, such as aortic dissection, intramural hematoma, penetrating ulcers, aneurysms, and rare tumors. Finally, the imaging features of the aorta after surgical intervention are described. The goal of this chapter is to clarify the terminology and provide a better understanding of the aorta and the diseases that affect it.

Aortic Dissection

Acute aortic dissection is the most dramatic and common thoracic aortic emergency. Untreated dissections have a mortality of 36% to 72% within the first 48 hours and 62% to 91% within the first week. Dissections are classified as acute if the diagnosis occurs within 2 weeks or less of the first symptoms. Dissections detected after 2 weeks are classified as chronic. Acute aortic dissection usually occurs in patients between the ages of 30 and 85 years, with a peak incidence in the sixth and seventh decades of life. It is more common in men than women, at a ratio of 3:1 (1,2).

There are many conditions that increase a patient’s risk of aortic dissection, as described in Table 18.1. These include systemic hypertension (90%) and connective tissue disorders such as Marfan syndrome, cystic medial necrosis, Ehlers-Danlos syndrome, and Turner syndrome. Aortic dissection noted in women younger than 40 years old is often associated with pregnancy. Congenital cardiovascular diseases, such as aortic stenosis, bicuspid aortic valve, and aortic isthmic coarctation, are all risk factors. Aortic dissection can also be induced by trauma, either blunt or iatrogenic during aortic cannulation or bypass surgery. A history of aortic surgery also increases the risk of subsequent dissection.

Presenting Symptoms

The classic clinical presentation of aortic dissection is the acute onset of severe tearing or ripping substernal chest pain with radiation to the back. This occurs in up to 70% of patients. Aortic valvular murmur due to creation of aortic valve insufficiency occurs in up to 65% of patients. Asymmetric pulses, as well as absent femoral pulses (25%), may occur in the upper extremities if the aortic arch is involved. Unfortunately, 15% to 20% of patients have no chest pain, making the diagnosis difficult. These patients usually present with symptoms related to secondary involvement of aortic branch vessels. Such presentations include myocardial infarction and congestive heart failure, abdominal pain due to mesenteric ischemia, stroke, confusion, coma, or syncope with involvement of the cranial or spinal arteries (25%) (1).

The classic presentation of aortic dissection is acute tearing substernal pain radiating to the back. However, atypical presentations are common and often result in delayed diagnosis.

Table 18.1: Risk Factors for Aortic Dissection

Hypertension
Marfan syndrome
Ehlers-Danlos syndrome
Cystic medial necrosis
Pregnancy
Turner syndrome

Aortic stenosis
Bicuspid aortic valve
Aortic coarctation
Trauma
Prior aortic surgery

Pathogenesis

Aortic dissection is a tear of the aortic wall intima, followed by separation of the tunica media, thereby creating two channels for passage of blood. The true lumen is surrounded by intima, and the false lumen is surrounded by media. This is seen in approximately 70% of cases. The tear in the intima allows blood to enter the aortic wall and extend longitudinally along the wall, thus separating the media and forming true and false lumens. The entry point most commonly arises in the ascending aorta within several centimeters of the aortic root or in the descending aorta between the origin of the left subclavian artery and ligamentum arteriosum. Iatrogenically induced aortic dissections arise at sites of aortic cannulation, bypass grafting and cross-clamping, or during catheterization.

All aortic dissections have blood (hematoma) within the media of the aortic wall.

Classification

There are two widely used systems for the classification of aortic dissections: the Stanford classification and the DeBakey classification.

The exact etiology of dissection is still debated. The entry tear may come first, leading to hematoma in the aortic wall, or may arise after the hematoma has already developed. In some cases a tear is never found.

Stanford Classification

Stanford A dissections involve the ascending aorta, regardless of the site of tear or distal extent. These dissections usually begin approximately 2 cm cephalad to the sinotubular junction. These comprise approximately 60% of all aortic dissections. Stanford B dissections involve only the descending aorta distal to the left subclavian artery and comprise approximately 40% of all dissections (3).

Stanford type A dissections involve the ascending aorta. Stanford type B do not.

DeBakey Classification

A DeBakey I dissection involves both the ascending and descending aorta. DeBakey II involves only the ascending aorta, and DeBakey III involves only the descending aorta distal to the left subclavian artery. These occur as 30%, 20%, and 50% of dissections, respectively (4).

DeBakey type I dissections involve ascending and descending thoracic aorta. Type II involves only the ascending aorta and type III, only the descending aorta.

Dissections involving the ascending aorta are treated emergently and surgically because of the high mortality if not treated. Complications if untreated include acute aortic insufficiency in approximately 90% of patients due to destruction of aortic valve, acute heart failure, occlusion of coronary or supraortic branch vessels, rupture into the pleural space, or rupture into the pericardium with acute cardiac tamponade (1). Dissections involving only the descending aorta are associated with a lower complication rate and are treated medically when possible. However, risk of descending thoracic aorta ruptures increases at a greater than 6 cm diameter. This is accompanied by altered branch vessel perfusion or occlusion or pseudocoarctation syndrome with uncontrollable hypertension; surgical intervention or therapeutic percutaneous stent grafting is required (1,5). Branch vessel occlusions, such as hepatic, mesenteric, or renal artery involvement, are associated with increased morbidity and mortality.

Ascending aortic dissection is a surgical emergency, because rupture into the pericardium, aortic valve failure, and coronary artery involvement are causes of mortality.

Imaging

The methods used for the diagnosis of aortic dissection include catheter aortography (the traditional gold standard) and bedside transesophageal echocardiography. More commonly, noninvasive techniques, such as computed tomography (CT) and magnetic resonance imaging (MRI), are used both to establish the diagnosis of dissection and to evaluate the extent of dissection in the aorta and branch vessels.

Chest radiographs are the most commonly used radiologic examination in all acute thoracic conditions. Although findings can indicate the presence of aortic dissection (Table 18.2), a normal chest radiograph does not exclude the presence of an aortic dissection (Fig. 18.1).

A normal chest radiograph does not exclude the diagnosis of aortic dissection.

CT is probably the most commonly used radiologic examination to diagnose and evaluate aortic dissection. Often, the extent is sufficiently well presented as to avert the need for catheter angiography before surgery and to plan for aortic stent grafting. Fast helical CT scanners accurately and consistently display the aorta and branch vessels (Fig. 18.1), and advanced multiplanar and three-dimensional reconstructions are important to do this. The CT findings of aortic dissection are listed in Table 18.3. The most characteristic finding is the intimal flap. The typical configuration of the flap is a linear filling defect within the aorta. The intimal flap may also have an atypical configuration: dissection of the entire intima creates a circumferential intimal flap, filiform (extremely narrow) true lumen, a three-channel aorta (Mercedes-Benz sign), and several false channels (Fig. 18.2). The dissection flap is more likely to be curved in an acute dissection and flat in a chronic dissection. CT findings that indicate a ruptured type B dissection include irregularity of the aortic wall, extravasation of vascular contrast material, mediastinal or pericardial hematoma, and hemothorax (1) (Fig. 18.3).

Helical CT with multiplanar reconstructions and magnetic resonance angiography are used for both diagnosis of dissection and surgical or stent-graft planning.

Once the diagnosis of aortic dissection is made, the key information needed by the surgeon is the extent of the dissection and whether branch vessels originate from the true lumen or false lumen. Key features that can be used to distinguish between the true and false lumens are listed in Table 18.4 (Fig. 18.4) (6,7).

The false lumen is often larger than the true lumen, contains cobwebs (strands of media), and is filled with blood that may have slow flow or be thrombosed.

A limitation of CT is the use of intravenous contrast, for which some patients are known to be allergic and which must be avoided in other patients with acute renal failure secondary to dissection or preexisting renal insufficiency. In such settings, MRI is recommended (Table 18.5).

The true lumen gives rise to the coronary arteries and aortic valve and may be surrounded by intimal calcification.

MRI features are similar to those seen on CT. The intensity of signaling of the false lumen is variable and dependent on the blood flow, as well as the age and composition of thrombus. Standard MRI techniques demonstrate pleural and pericardial effusions, mediastinal hemorrhage, and aortic wall thickening (Fig. 18.5).

Table 18.2: Chest Radiograph Findings of Aortic Dissection

Widening of the mediastinum
Diffuse enlargement of aorta ± irregular contour
Progressive aortic enlargement on serial examinations
Change in arch configuration on serial examinations
Inward displacement of intimal classification by ≥ 6 mm
Double aortic contour
Tracheal displacement to the right
Pleural effusion (especially on the left)
Pericardial effusion

Figure 18.1 Stanford type A aortic dissection. A. Chest radiograph demonstrates abnormal aortic contour. B–D. Axial computed tomographies demonstrate perfusion of the true and false lumens with slower flow in the false lumen. B. Extension of dissection into right brachiocephalic artery (arrowhead) and into the aortic arch (C) (arrow). D. Dissection flap in ascending aorta. Dissection flap in descending aorta (long arrow).

Table 18.3: Computed Tomographic Findings of Aortic Dissection

Intimal flap (approximately 70%)
Inward displacement of intimal calcifications
Hyperattenuating intima
Increased aortic diameter
Delayed enhancement of false lumen
Increased attenuation of acutely thrombosed false lumen (noncontrast computed tomography)
Mediastinal, pleural, or pericardial hematoma
Enlargement of the false lumen with compression of true lumen

Figure 18.2 Aortic dissection flaps on contrast enhanced computed tomography. A. Multiple false lumens (asterisks). B. Circumferential intimal flap in the ascending thoracic aorta. TL, true lumen.

Figure 18.3 Stanford type B aortic dissection with ruptured false lumen. A. Contrast enhanced axial computed tomography demonstrates intimal flap (arrow) within the descending aorta. Note extensive hemomediastinum and bilateral pleural effusions. B.Oblique sagittal reconstruction demonstrates intimal flap (arrows) and false lumen (asterisk).

Table 18.4: Features to Distinguish True and False Lumens on Computed Tomography

Acute Dissection

·   True lumen
   –Surrounded by intimal calcification
   –Eccentric flap calcification
   –Continuous with undissected portion of aorta
   –In cases in the aortic arch with one lumen wrapping around the other, the inner lumen is the true lumen

·   False lumen
   –Presence of cobwebs that are band or cords of media that bridge the junction of the dissection flap with the outer wall of the false lumen
   –Larger cross-sectional area than the true lumen
   –Presence of the break sign, which is an acute angle between the dissection flap and outer wall
   –Filled with contrast-enhanced slowly flowing blood or hematoma

Chronic dissection

·   True lumen
   –Eccentric flap calcification

·   False lumen
   –Outer wall calcification
   –Intraluminal thrombus within false lumen (Fig. 18.4)

Table 18.5: MR Imaging Findings of Aortic Dissection

Intimal flap.
Variable false lumen signal.
Intimal calcification is usually not seen. However, at times an intimal flap is seen as an intervening stripe of soft tissue signal intensity.
Signal flow voids in true lumen and false lumen depending on luminal flow rate (spin-echo MR).

MR, magnetic resonance.

Figure 18.4 Chronic Stanford type B aortic dissection on axial computed tomography with calcification along the peripheral (outer wall) of the thrombosed false lumen.

Figure 18.5 Stanford type B acute aortic dissection. A. Axial T1-weighted inversion recovery, (B) axial reconstruction three-dimensional gadolinium-enhanced magnetic resonance imaging, (C) coronal reconstruction from subvolume MIP gadolinium-enhanced magnetic resonance imaging of the aortic arch, and (D) sagittal three-dimensional gadolinium magnetic resonance imaging. Aortic dissection with intimal flap in descending aorta (arrow) and thrombosed false lumen. Asterisk, false lumen.

 

Aortography

At aortography dissection appears as an intimal flap or multiple lumens, with opacification of double channels. Linear radial lucency may be seen secondary to the torn or separated intima, with entry and reentry points. Additional findings include a true lumen compressed by the false lumen, a thick aortic wall greater than 5 mm, ulcer-like contrast projections beyond the true lumen, abnormal catheter position away from the lateral aortic border, and arterial branch occlusion.

A thin thrombosed false lumen can result in a normal-appearing aortogram.

Transesophageal Echocardiography

This method can image the entire thoracic aorta, with the exception of the distal transverse arch that is partially obscured by the trachea. Transesophageal echocardiography has the advantage of being performed at the bedside in acutely ill or unstable patients. At transesophageal echocardiography, dissection appears as a mobile linear echo within the aortic lumen. Transesophageal echocardiography also provides information regarding ventricular and aortic valve function, both important in surgical decision making.

Acutely, transesophageal echocardiography can be used for diagnosis at the bedside but is insufficient for surgical planning.

Management

Aortic dissection that involves branch vessels and compromises blood flow is treated based on the mechanism of occlusion. When the dissection flap extends into the lumen of the branch vessel and statically narrows it, treatment is usually angioplasty, with or without the deployment of an intravascular stent. When the dissection flap does not enter the branch vessel but dynamically occludes the vessel by prolapse of the intimal flap into the vessel origin, this obstructs the true lumen above the branch vessel origin and is usually treated with balloon fenestration of the dissection flap, intraaortic endoluminal stent in the true lumen, or both. Additionally, the compressed true lumen may be enlarged, by using an uncovered intraaortic stent (5,8).

Surgical treatment of type A dissection consist of replacing the ascending aorta, aortic root, and aortic valve, reconstructing the aortic root to restore aortic valve competence, and directing blood flow to the true lumen. The coronary arteries are reimplanted into the graft. Mortality rates for surgical treatment range from 10% to 35% (9). Type B dissections are usually treated medically with aggressive antihypertensive control and pain control. For type B dissections treated surgically, a graft is usually placed in the proximal descending thoracic aorta. Early postoperative complications of dissection include myocardial infarction, stroke, respiratory insufficiency, pulmonary embolism, aortic rupture, pseudoaneurysm, and graft infection. Late complications are noted 10 years or more after surgery in 15% to 30% of patients and require reoperation for dilatation of the dissected region to avoid rupture. Reoperation may be required for progressive reduction of myocardial perfusion due to aortic insufficiency (1).

Aortic Dissection Follow-Up

After the diagnosis or repair of an aortic dissection, follow-up imaging is usually performed annually. Complications that may be noted include an aneurysm of the false lumen, with continuous dilatation of the aorta that may result in aortic rupture. An aneurysm of the true lumen may develop, particularly in older hypertensive patients with advanced atherosclerosis. Obstruction or aneurysm of aortic branch vessels may also occur. Postoperatively, pseudoaneurysms may develop at the anastomosis of the graft to the native aorta, further weakening the aorta and usually requiring additional surgery.

Intramural Hematoma

Intramural hematoma was first described by Krutenberg in 1920 as bleeding into the outer layers of the aortic media due to rupture of the vasa vasorum without primary intimal tear, leading to subintimal hemorrhage (10). Intramural hematoma is a variant of aortic dissection, characterized by the absence of both the intimal tear and the direct flow communication between the true and false lumens. It has been postulated that a proximal intramural hematoma may be a precursor or early stage of classic aortic dissection. Acute intramural hematoma has a mortality of 21% (10). Intramural hematoma may progress to a classic aortic dissection, with rupture rates ranging from 32% to 40% for intramural hematoma confined to the descending aorta and 50% to 100% when it involves the ascending aorta. Hence, emergent surgical repair is usually recommended for intramural hematoma involving the ascending aorta.

Successful patient outcome with medical therapy has been shown similar to the treatment of type B classic aortic dissection. These patients can be frequently followed with annual noninvasive imaging studies, either CT or MRI. Surgery is performed if a classic aortic dissection or aortic rupture develops (11,12).

Clinical Presentation

Initial presenting symptoms include chest pain (50% to 74%), intrascapular back pain (44% to 84%), and neurologic or vascular complications such as syncope, transient ischemic attack, hoarse voice, paraplegia, mesenteric ischemia, and acute renal failure (13). Patients are usually older than those with classic aortic dissection, with a mean age of 66 years versus 55 years for classic aortic dissection. There is an equal male-to-female ratio for intramural hematoma, compared with the 3:1 ratio for classic aortic dissection. Risk factors for intramural hematoma include hypertension or previous trauma.

Imaging

Intramural hematoma can be diagnosed by CT, MRI, and transesophageal echocardiography. At aortography, it may not be detected due to the inability to opacify a false lumen with contrast in the absence of an entrance tear. This often occurs when the intramural hematoma is thin and does not deform the true lumen.

On nonintravenous contrast-enhanced CT, a continuous high attenuation crescent along the aortic wall representing hematoma is usually found without mass effect on the true lumen (Fig. 18.6). As in classic dissection, internally displaced intimal calcification may be seen. At intravenous contrast-enhanced CT, the crescentic area along the aortic wall appears as low attenuation thrombus. There is no intimal flap. The intramural hematoma usually maintains a constant circumferential relationship with the aortic wall. Associated features include pericardial effusion, hemothorax, pleural effusion, and hemomediastinum. Distinguishing an intramural hematoma from classic aortic dissection with a thrombosed false lumen is still problematic.

Acute intramural hematoma is a aortic dissection with no entry tear and appears as a thrombosed false lumen.

At MRI, focal crescentic wall thickening, without mass effect on the aortic lumen and an absence of intimal flap, is seen. In reference to true spin echo (SE) sequences, the signal characteristics of the intramural hematoma depend on the age of the hematoma. If acute, it appears high signal on T2-weighted images and isointense or hypointense to muscle on T1-weighted images due to oxyhemoglobin. When subacute, it is high signal on both T1- and T2-weighted images due to methemoglobin. When chronic, it appears low signal on T1- and T2-weighted images due to organization of the blood (14). At transesophageal echocardiography, intramural hematoma appears as localized circular or crescentic thickening of the aortic wall, greater than or equal to 5 mm, and again, no intimal tear is seen.

Management

Treatment consists of intensive care unit monitoring, aggressive medical treatment with antihypertensive therapy, and frequent serial follow-up noninvasive imaging studies. Surgery is performed in patients with coexistent aneurysmal dilatation or when the intramural hematoma progresses on serial studies. Evaluation of intramural hematoma on serial noninvasive imaging has shown that intramural hematomas may decrease in size and partially or completely resolve, particularly if the aortic diameter is less than 5 cm (12,15). Sometimes ulcer-like projections into the intramural hematoma develop, which can progress to saccular aneurysm. Fusiform aneurysms without ulcer-like projections and even overt aortic dissection can develop (12). Risk factors for overt aortic dissection include intramural hematoma involving the ascending aorta that had a maximum thickness of 16 mm, compression of the true lumen, and the presence of pericardial or pleural effusion (16).

Figure 18.6 Acute intramural hematoma. A–C. Axial nonenhanced computed tomography images demonstrate a crescent of high attenuation blood (arrows) involving the arch and descending thoracic aorta. D–F. Contrast enhanced helical computed tomography images at the same three levels depict hypodense hematoma (arrows) when compared with the contrast enhanced true lumen. There is a left pleural effusion (asterisk).

Penetrating Atherosclerotic Ulcer

Penetrating atherosclerotic ulcer is characterized by ulcerating atherosclerotic plaque that penetrates into the internal elastic lamina and media, resulting in hematoma formation within the media of the aortic wall (17,18). Penetrating atherosclerotic ulcer is most often seen in hypertensive elderly patients with a mean age of 70 years. There is a high prevalence of diffuse systemic atherosclerosis and hyperlipidemia. Clinical presentation includes chest or back pain. Less frequently, embolization of atheromatous debris or overlying thrombus results in ischemia and infarction of downstream tissues.

Pathophysiology

Atheromatous ulcers develop in patients with advanced atherosclerosis. At this stage, lesions are usually asymptomatic and confined to the intimal layer. As the lesion progresses and a deep atheromatous ulcer penetrates through the elastic lamina into the media, an intramural hematoma is formed. The hematoma can extend through the adventitia, forming a false aneurysm. Rarely, it may progress to complete transmural aortic rupture (19).

In penetrating atherosclerotic ulcer, an ulcerated plaque erodes into the media, allowing the entry of blood into the aortic wall.

Natural History

Penetrating atherosclerotic ulcers can heal spontaneously. The aorta and penetrating atherosclerotic ulcer may remain stable. The intramural hematoma associated with the ulcer may become smaller or it can enlarge. In 25% to 30% of patients the ulcer extends through the media but not yet through the adventitia, resulting in saccular or fusiform false aneurysm or pseudoaneurysm. Transmural penetration or aortic wall rupture rarely occurs, approximately 8%. The aortic diameter itself may enlarge, sometimes as the result of incorporation of the ulcer crater (20).

In contrast to “classic” dissection, penetrating ulcers are associated with atherosclerotic disease in older individuals and are usually focal.

Chest Radiography and Photography

Chest radiographic findings include diffuse or focal enlargement of descending thoracic aorta, widening of the mediastinum indicative of hematoma, pleural fluid, left apical mass adjacent to the aortic arch, and deviation of the trachea. At aortography, findings include presence of an aortic ulcer similar in appearance to gastric ulcers on barium examinations. The ulcer is only seen if it projects tangentially from the aortic wall. Depression of aortic wall due to adjacent intramural hematoma and aortic wall thickening may also be seen (21).

Computed Tomography

A focal contrast material–filled outpouching or focal ulcer is seen in the setting of extensive atherosclerosis, surrounding by localized subintimal hematoma. It most commonly occurs in the middle or distal thirds of the descending thoracic aorta, although any portion of the thoracic or abdominal aorta may be involved. Other findings include displacement of the calcified intima, pleural, extrapleural, and/or mediastinal fluid; a thick aortic wall associated with or without enhancement; contained perforation; or pseudoaneurysm (Fig. 18.7) (19).

On imaging tests, a penetrating ulcer extends beyond the expected location of the aortic wall.

Figure 18.7 Penetrating atherosclerotic ulcer. Axial computed tomography depicts a penetrating ulcer of the left lateral wall of the descending aorta (arrow) (A) and intramural thrombus (asterisk) (B).

Magnetic Resonance

MRI demonstrates localized areas of high signal intensity on T1- and T2-weighting in the aortic wall representing localized subacute intramural hematoma. Signals are due to presence of methemoglobin. Ectasia, atherosclerotic disease, and focal aortic wall ulceration are found similar to CT (22,23).

Management

Critical complications of penetrating atherosclerotic ulcers may not be identified on initial imaging studies. Careful noninvasive follow-up with CT and MRI is mandatory to monitor the status of the ulcer and both the lumen diameter and wall thickness. Penetrating atherosclerotic ulcers are initially treated medically, with emphasis on aggressive hypertension control. If symptoms such as chest or back pain persist after medical therapy or signs of intramural hematoma expansion or impending rupture develop, surgical intervention is undertaken. Surgery entails local incision of the ulcerated portion of the aorta and replacement with an interposition graft. For patients who are not surgical candidates, endovascular stent graft placement or percutaneous embolization of the ulcer and associated pseudoaneurysm are used (24).

Coarctation

A coarctation is a congenital narrowing of the thoracic aortic lumen, characterized by eccentric narrowing of the proximal descending thoracic aorta, usually in the region of the ligamentum arteriosum. Coarctation is more common in males than females, with a ratio of 4:1. Manifestations of the anomaly range from minimal narrowing to complete luminal atresia. Coarctation is associated with complex obstructive lesions, such as tubular hypoplasia of the aortic arch, left ventricular outflow tract obstruction, and hypoplastic left heart syndrome. It is also associated with congenital intracardiac defects, such as ventricular septal defect, patent ductus arteriosus, aortic stenosis, and mitral stenosis (Table 18.6). Approximately 80% of patients have a bicuspid aortic valve, with or without aortic stenosis. Patients with Turner syndrome have an increased incidence of coarctation. Intracranial berry aneurysms involving the circle of Willis may be observed in patients with coarctation.

Most patients with coarctation have a bicuspid aortic valve.

Table 18.6: Coarctation Associations

Ventricular septal defect
Patent ductus arteriosus
Aortic stenosis
Mitral stenosis
Bicuspid aortic valve
Turner syndrome
Vasculitis
Intracranial aneurysms

Pathogenesis

Congenital coarctation is a developmental anomaly of the paired primitive dorsal aorta. In contrast, an acquired coarctation may be idiopathic or may occur because of an inflammatory condition or postradiation vasculitis.

The older child or adult type is the more common than the infantile type. It is characterized by a localized, short, juxtaductal narrowing, creating an abrupt stenosis produced by a diaphragm-like ridge extending into the aortic lumen. This narrowing occurs near the ligamentum arteriosum, usually distal to the left subclavian artery. In addition to thoracic aortic coarctation, rarely is the abdominal aorta involved (0.5% to 2%). This may present as smooth diffuse or segmental narrowing of the abdominal aorta extending anywhere from the celiac axis to below the renal arteries (25). Patients present with severe hypertension caused by increased renin levels secondary to renal artery stenosis or decreased blood flow to renal arteries.

Coarctation of the aorta has a distinct appearance depending on the patient’s age at the time of detection. The infantile type is characterized by a long segment of hypoplastic narrowing involving the aorta distal to origin of the innominate artery. It is associated with tubular hypoplasia of the aortic arch or descending thoracic aorta and has a high incidence of intracardiac abnormalities, especially bicuspid valve (Fig. 18.8).

Infantile coarctation usually involves a long segment of the aorta and presents with heart failure early in life.

Figure 18.8 Coarctation of the aorta. Sagittal three-dimensional time-of-flight magnetic resonance image depicts bovine aortic arch and “diffuse” type coarctation distal to the innominate artery (white arrows).

Clinical Presentation

Infants with aortic coarctation are usually symptomatic, presenting with congestive heart failure in the neonatal period. Lower extremity cyanosis, left ventricular failure, cardiomegaly, increased pulmonary vascularity (left-to-right shunt through patent ductus arteriosus/ventricular septal defect), and pulmonary venous hypertension may be seen. In contrast, most adults are asymptomatic. Physical examination demonstrates higher systolic blood pressure in the arms than in the legs, with similar diastolic pressures, thereby creating widened pulse pressure in the arms. This may be associated with weak and delayed femoral arterial pulses. Left ventricular enlargement and systolic ejection click occur. When symptomatic, patients usually suffer from hypertension, headache, epistaxis, dizziness, palpitations, and possibly claudication. The complications of aortic coarctation include aortic dissection, aneurysm, cerebrovascular accidents caused by rupture of berry aneurysm, and infective endocarditis.

Most coarctations are focal and may be asymptomatic, until hypertension or abnormal pulses prompt diagnosis.

Chest Radiograph

Symmetric, smooth, bilateral, inferior surface rib notching of the third to ninth posterior ribs is classic. Rib notching is caused by tortuous and dilated intercostal arteries that occur as collateral blood flow. On occasion, unilateral rib notching may occur. Left-sided rib notching occurs if the coarctation is located between the normal left subclavian artery and an aberrant right subclavian artery or if there is atresia or stenosis at the origin of the right subclavian artery. Right-sided rib notching occurs when the coarctation is located proximal to the left subclavian artery or if the origin of the left subclavian artery is stenotic or atretic (Fig. 18.9).

Unilateral notching may occur if the coarctation is located between the right-sided circulation (innominate artery) and the left-sided circulation (left subclavian artery).

A “figure 3” sign is formed on the chest radiograph by the indentation in the contour of the descending aorta, with poststenotic dilatation. A “reverse 3” sign is seen on esophagram, creating an indentation on the esophagus at the level of the aortic arch at the site of poststenotic dilatation of the descending thoracic aorta. Additional findings include left ventricular hypertrophy, prestenotic ascending aorta dilatation if there is an associated stenotic bicuspid aortic valve, linear retrosternal aortic soft tissue opacity created by enlarged internal mammary arteries, and dilated brachiocephalic vessels (4).

Bilateral rib notching and a “figure 3” aortic knob are the chest radiographic hallmarks of coarctation.

Figure 18.9 Coarctation of aorta. A. Frontal chest radiograph reveals inferior rib notching (straight arrows) and (B) “figure 3” sign(curved arrow).

Angiography

In neonates, a discrete area of narrowing adjacent to ductus or ligamentum arteriosum is seen. In infants, a focal narrowing of the aorta is seen with or without aortic arch hypoplasia. In adults, the maximum stenosis is usually short and often resembles a diaphragm. The left subclavian artery may be stenotic at its origin or dilated. This dilatation accounts for the soft tissue widening seen in the left superior mediastinum on radiographs. Poststenotic dilatation, ascending aorta dilatation, and collateral vessels are seen (26).

Computed Tomography and Magnetic Resonance

Noninvasive imaging assessment of the aorta with CT or MRI can detect the coarctation, postoperative residual coarctation, or recurrent coarctation, as well as complications such as aneurysms and dissections (26,27).

Currently, MRI is the imaging modality of choice. MRI techniques performed in the axial and sagittal oblique plane can evaluate the entire ascending and descending aorta, defining the site and extent of stenosis and the concurrent collateral vessels (Fig. 18.10) (28). Cine MR and phase contrast imaging estimate hemodynamic information such as flow and pressure gradient measurements, thereby precluding the need for angiography (29). MRI is also used to noninvasively evaluate the postoperative aorta and potential complications.

MRI is the test of choice for evaluating coarctation providing both anatomic and hemodynamic information.

Management

Surgical repair of coarctation entails resection and end-to-end anastomosis, patch angioplasty, subclavian flap aortoplasty (Waldhausen technique), Dacron patch, or Dacron bypass conduit. Balloon dilatation angioplasty has been successful with discrete juxtaductal type coarctation, for neonatal coarctation, and persistent pressure gradients after surgery. (30) Postoperative complications of aortic coarctation include restenosis at site of repair, pseudoaneurysm formation, intramural hematoma, dissection, and systolic paradoxical hypertension (31) (Fig. 18.11).

Figure 18.10 Coarctation of aorta. A. Sagittal three-dimensional time-of-flight magnetic resonance image demonstrates coarctation (arrowheads). Note internal mammary and thoracic intercostal collaterals (arrows)B. Subvolume maximum intensity projection along long axis aortic arch from three-dimensional gadolinium magnetic resonance imaging depicts coarctation (arrows) and collateral vessels. (From 

Gaba R, Carlos R, Weadock W, et al. Cardiac magnetic resonance imaging: technique, optimization and detection in pathology in clinical practice. Accepted pending revision to Radiographics

, with permission.)

Figure 18.11 Pseudoaneurysm after repair. Oblique sag maximum intensity projection of three-dimensional gadolinium enhanced magnetic resonance imaging reveals pseudoaneurysm at site of Gore-Tex graft repair. (From 

Gaba R, Carlos R, Weadock W, et al. Cardiac magnetic resonance imaging: technique, optimization and detection in pathology in clinical practice. Accepted pending revision to Radiographics

, with permission.)

Pseudocoarctation

Pseudocoarctation is a congenital anomaly of the aorta characterized by redundancy and kinking of the descending aortic arch, just distal to the left subclavian artery at the ligamentum arteriosum (32). This kink usually creates little or no blood flow obstruction; therefore, there is usually no significant pressure gradient across the kink, and no collateral blood flow through collateral vessels is seen. Pseudocoarctation is associated with bicuspid aortic valve, patent ductus arteriosus, ventricular septal defect, aortic and subaortic stenosis, and anomalies of aortic arch branches.

Pseudocoarctation is a redundant kinked aortic arch, usually with no pressure gradient across the “kink.”

Pathogenesis and Clinical Features

Pseudocoarctation develops because of the failure of the third to seventh dorsal aortic segments to properly condense and form a normal aortic arch. Patients are usually asymptomatic. Hypertension may be seen, particularly in middle-aged men. A systolic ejection murmur near the cardiac base may be detected on physical examination (33). In contrast to coarctation, the femoral pulses are present and either a small (less than 25 mm Hg) or absent arterial pressure gradient exists between the arms and legs.

Chest Radiography

A smooth round to ovoid left superior mediastinal mass is seen, deforming the mediastinal contour. Below the mass, a denser round opacity is seen in the usual position of the aortic knob. The opacity represents the superimposed buckled aortic arch and descending aortic segments. The widened mediastinum is secondary to elongation of the ascending aorta and aortic arch, with a high-riding or cervical aortic arch (Fig. 18.12) (33).

Figure 18.12 Pseudocoarctation of the aorta. Chest radiograph depicts a left superior mediastinal mass manifested by a bulge (arrows)above what appears to be the aortic knob (asterisk). No rib notching is apparent.

Computed Tomography, Magnetic Resonance Imaging, and Angiography

CT delineates the solid mass identified on chest radiograph as vascular, with its continuity to the aorta. The ascending aorta is normal in caliber. The narrowed segment of the descending aorta distal to the kink is often dilated and then gradually narrows to normal caliber. The aortic arch is abnormally high in position. An aneurysm or dissection below the kink rarely occurs. There is an increased distance between the left common carotid and left subclavian artery, anterior displacement of the esophagus, and anteromedial descending aorta (Fig. 18.13). CT cannot assess whether there is a pressure gradient across the kink, unless collateral vessels are seen, in which case a gradient is by definition present, but the severity of the gradient remains unmeasured. At angiography the pressure gradient is measured; however, this generally has been relatively replaced by the use of MRI for the diagnosis of pseudocoarctation, allowing both anatomic definition and measurement of any pressure gradient by MRI.

Figure 18.13 Pseudocoarctation of the aorta. A. Axial computed tomography depicts the arch of the pseudocoarcted aorta high in the mediastinum. B. Sagittal three dimensional shaded surface display computed tomography of reconstruction.

The angiographic findings of a high position of the aortic arch, presence of a kink without stenosis, and collateral vessels or impediment of blood flow can be evaluated noninvasively with MRI. Cine phase contrast MRI can estimate physiologic flow information, such as flow or pressure gradient measurements (29). Although pseudocoarctation is not treated surgically, close attention with noninvasive imaging may be performed for the early detection of aneurysm or dissection. Monitoring and early surgical intervention is undertaken to prevent the increase risk of aortic rupture (34).

Aortic Aneurysm

Thoracic aortic aneurysm is defined as abnormal irreversible dilatation of the aortic lumen, generally greater than 4 cm in diameter. It is degeneration of the aortic media, specifically weakening and destruction of the elastic fibers that results in aneurysm formation (35). The aortic aneurysm may be classified according to location, morphology, integrity of aortic wall, and etiology. Causes of aortic aneurysm are listed in Table 18.7.

Classification According to Location

Aneurysm locations may be summarized as follows:

1. Ascending thoracic aorta, between aortic annulus and origin innominate artery;

2. Transverse aortic arch, in conjunction with brachiocephalic vessels;

3. Descending aorta, originating distal to origin of the left subclavian artery;

4. Thoracoabdominal, which originates in the descending thoracic aortic and extends below the diaphragm to involve a variable extent of the abdominal aorta.

Aneurysms that classically involve the ascending aorta are due to cystic medial necrosis, connective tissue disorders such as Marfan and Ehlers-Danlos syndromes, and syphilis, the latter now rare. Aneurysms involving the descending aorta are usually atherosclerotic, posttraumatic, infectious (mycotic), or inflammatory (rheumatoid arthritis and ankylosing spondylitis) (36).

Classification According to Morphology

Morphology may be characterized as either fusiform or saccular. Fusiform aneurysms involve the entire aortic circumference, thus appearing cylindrical or spindle-shaped. Saccular aneurysms are sharply delineated and usually involve a localized segment of the aorta. They can present as an eccentric outpouching from one side of the aortic wall.

Table 18.7: Etiologies of Aortic Aneurysms

Atherosclerosis
Infection (mycotic)
Cystic medial necrosis
Connective tissue disorders (Marfan and Ehlers-Danlos syndromes)
Syphilis
Trauma
Inflammatory (rheumatoid arthritis, ankylosing spondylitis)

Classification According to Aortic Wall Integrity

Aneurysms can be classified as true aneurysms or false aneurysms depending on the integrity of aortic wall. True aneurysms are characterized by an intact aortic wall, composed of all three layers: intima, media, adventitia. Atherosclerotic and connective tissue disorder–related aneurysms are true aneurysms. False aneurysms or pseudoaneurysms are characterized by a disrupted aortic wall contained by the adventitia, perivascular connective tissue, and organized blood clot (37). Posttraumatic and infectious (mycotic) aneurysms are usually false aneurysms.

Classification According to Etiology

Atherosclerosis

Thoracic aortic aneurysms are most commonly caused by atherosclerosis. These occur in elderly hypertensive patients with a mean age of 69 years (range, 42 to 94 years) (38). Three-fourths of atherosclerotic aneurysms occur in men, and smokers are at increased risk. There is a high incidence of other cardiovascular diseases in patients with thoracic aortic aneurysms, including coronary artery disease, cerebrovascular disease, and aneurysms of abdominal aorta and iliac arteries (39). The basis for aneurysm formation is degeneration and fibrous replacement of the media underlying the atherosclerotic intimal lesions. Once dilatation occurs, the aneurysm wall is exposed to increased mechanical stress; poor nutrition leads to further degeneration and progressive enlargement of the aneurysm. Atherosclerotic aneurysms are usually fusiform because of the long segments of the aorta they affect. However, they can be saccular in up to 20% of patients. They most commonly involve the aortic arch and descending thoracic aorta, usually distal to the left subclavian artery. They are relatively uncommon in the ascending aorta (37).

Most thoracic aortic aneurysms are fusiform in morphology and secondary to atherosclerosis.

Cystic Medial Degeneration

Cystic medial degeneration is the most common cause of an ascending aorta aneurysm (37). It may be associated with disorders such as Marfan or Ehlers-Danlos syndromes or acquired weakness or a defect in the aortic media. The cause of cystic medial degeneration is unknown. It is postulated to be the result of ongoing repetitive aortic injury and repair that occurs in the aging aorta. This process eventually leads to aortic wall weakening and dilatation.

The most common case of an ascending aortic aneurysm is cystic medial degeneration.

Marfan Syndrome

Marfan syndrome is characterized by musculoskeletal deformities, ocular abnormalities, generalized defect of connective tissue, and cardiovascular lesions. Cardiovascular manifestations are present in 98% of patients and may cause death in more than 90%. Manifestations include aortic root dilatation complicated by aortic dissection or rupture, usually extending into sinuses of Valsalva, and valve regurgitation. Aortic regurgitation is present in up to 81% of patients with an aortic root diameter greater than 5 cm and in 100% of patients with an aortic diameter greater than 6 cm. Aneurysmal dilatation generally diminishes higher up in the ascending aorta, and the aortic arch is usually normal. Aortic lesions in patients with Marfan syndrome are identical to idiopathic medial cystic degeneration; however, the onset of degeneration occurs earlier in life and progresses more rapidly. Because of the risk of aortic emergency, patients with Marfan syndrome are usually followed with serial annual imaging, such as CT, MRI, and/or echocardiography (Fig. 18.14).

Because of the high risk of aortic abnormality, patients with Marfan syndrome usually undergo regular surveillance with echocardiography and CT or MRI.

Annuloaortic Ectasia

Annuloaortic ectasia is a pathoanatomic description for the combined lesions of aortic root aneurysm and aortic valve regurgitation due to dilatation of the aortic annulus. This is associated with degenerative changes in the aortic media even in the absence of Marfan syndrome. Aortic rupture and to lesser extent aortic dissection are frequent complications.

Figure 18.14 Marfan syndrome. A. Axial computed tomography image and sagittal (B) reconstruction of ascending aortic aneurysm (asterisk). Compressed superior vena cavas.

Posttraumatic Aneurysms

Posttraumatic aneurysms are usually the result of rapid deceleration injury and most commonly secondary to motor vehicle accident injury. They may also result from penetrating trauma. The two most common sites of aortic tears are at points of relative aortic fixation, the aortic knob and at the level of the ligamentum arteriosum just distal to the origin of the left subclavian artery. The proximal tears usually result in sudden death. The proximal descending tears arise from a circumferential tear of the intima and media and are often contained by the adventitia. Posttraumatic aneurysms are classified as false aneurysms and are an acute surgical emergency. A focal aneurysm presenting in the proximal descending aorta distant from the time of surgery should raise suspicion for delayed pseudoaneurysm (Fig. 12.1).

Saccular aneurysms should raise suspicion of a posttraumatic aneurysm (especially if at the ligamentum arteriosum) or mycotic aneurysm.

Syphilis

Syphilis, once the most common cause of a thoracic aneurysm, is rare today. Approximately 12% of patients with untreated syphilis develop cardiovascular disease. Symptoms usually occur 10 to 30 years after primary infection and are usually confined to the thoracic aorta, with the ascending aorta and transverse arch as the most common sites. Manifestations include aortic aneurysm, aortic insufficiency, and asymmetric enlargement of the sinuses of Valsalva. Most of the aneurysms are saccular, with about one-fourth fusiform. The prognosis for untreated syphilitics (luetic) aneurysm is poor, with death occurring within months of symptom onset. In 40% of cases, death is due to aortic rupture.

Mycotic Aneurysm

The term was first used by William Osler in 1885 to describe aneurysms from septic emboli in patients with bacterial endocarditis. Today this term is used for any infected aneurysm. Predisposing factors include immunocompetent states such as malignancy, alcoholism, steroid use or chemotherapy, drug abuse, and aortic trauma caused by accidents, surgical manipulation, or arterial catheterization (37).

The pathogenesis of mycotic aneurysm includes the embolization of infected material directly to diseased intima or vasa vasorum; direct extension from inflammatory process (such as osteomyelitis or abscess); and invasion of the aortic wall from intravascular sources or lymphangitic spread. Infectious agents usually responsible for these aneurysms include Staphylococcus aureusSalmonella species,Pneumococcus, and nonhemolytic Streptococcus. These are classified as false aneurysms (pseudoaneurysms) and are typically saccular (Fig. 18.15). Unlike noninfected aneurysms, mycotic aneurysms are usually symptomatic. Patients present with thoracic or back pain, fever, and laboratory changes indicating infection.

Figure 18.15 Mycotic aneurysm. A. Axial computed tomography when the patient was first seen with contrast material–filled ulcer (asterisk) in descending thoracic aorta (ao), intramural hematoma, and bilateral pleural fluid collections. B and C. Six weeks later, images at same level and at the level of the descending right pulmonary artery demonstrate interval growth of the pseudoaneurysm (asterisk). D. Angiogram depicts the pseudoaneurysm.

Clinical Manifestations

Most patients with atherosclerotic aneurysms are asymptomatic and are first diagnosed by routine chest radiograph or during evaluation for some other disease (40). Symptoms are produced by the enlarging space-occupying nature of the aneurysm, which compresses adjacent mediastinal structures. Symptoms include chest pain, hoarseness due to compression of recurrent laryngeal nerve, postobstructive atelectasis due to compression of bronchus, and dysphagia secondary to esophageal compression. Physical signs are rare; on occasion a large aneurysm can be palpated in the suprasternal notch. Additional physical signs include venous distension due to obstruction of the superior vena cava or innominate vein, vocal cord paralysis, abnormal pulsations in the upper anterior chest wall, tracheal deviation or “tug,” and Horner syndrome (36). Patients with impending or actual rupture and aneurysm larger than 5 cm experience severe chest pain.

Chest Radiographs

A mediastinal mass immediately adjacent to and indistinguishable from the aortic contours should raise the suspicion of aortic aneurysm. Other findings include mediastinal widening, particularly of the aorta; aortopulmonary window and left paraspinal stripe; and displacement and/or compression of the trachea and esophagus. Leaking or ruptured aneurysms are associated with hemothorax and mediastinal widening. Ascending aortic aneurysms produce abnormal convex opacity of the right superior mediastinum and fill the retrosternal clear space on the lateral view. Aortic arch aneurysms produce diffuse aortic enlargement or superimposed localized mass (Fig. 18.16).

Many thoracic aneurysms are detected as an incidental finding on a chest radiograph performed for another purpose, because they are clinically silent.

Computed Tomography

CT is an extremely valuable noninvasive modality to confirm the diagnosis and delineate the extent of thoracic aortic aneurysms. The findings of aortic aneurysm on CT are listed in Table 18.8. It allows detection of not just the contrast-filled lumen as seen in aortograms, but also the intraluminal thrombus. Characteristic CT findings include focal or diffuse aortic dilatation and deformity, peripheral curvilinear and plaque-like 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, and intraluminal thrombus that may be circumferential or crescentic. The intraluminal thrombus may have internal calcification with linear or curvilinear pattern when longstanding (41). Displacement of mediastinal structures, bone erosions, and presence of periaortic hematoma or pleural fluid collections may be seen (36,42). CT may also detect impending or actual aortic rupture and dissection, particularly when the aneurysm is greater than 5 cm in diameter. Other complications include aortobronchial fistula, compression of the right pulmonary artery, aortoesophageal fistula, and distal embolization, the latter leading to ischemia or infarction of bowel and abdominal organs. The aorta may rupture into the mediastinum, pericardium, pleural sac, or extrapleural space (Fig. 18.17). The presence of pleural or extrapleural blood on the left, and rarely across the posterior mediastinum into the right side of the chest, and contained aortic leak “draped aorta” are all signs of impending or actual rupture. A contained leak can be found when the aneurysm is in close contact with the spine, with lateral draping of the aneurysm around the vertebral body with a deficient posterior aortic wall (43,44).

Figure 18.16 Ruptured aneurysm. Anteroposterior chest radiograph reveals a widened mediastinum.

Table 18.8: Computed Tomographic Imaging Findings of Aortic Aneurysm

Focal or diffuse aortic dilatation
Peripheral curvilinear intimal calcification
Thickened aortic wall
Intraluminal thrombus
Displacement of mediastinal structures
Periaortic hematoma
Pleural fluid collections

Hemoptysis in a patient with an aortic aneurysm or prior aortic graft should raise the suspicion of an aortobronchial fistula.

Previous authors have advocated the use of angiography for the evaluation of aneurysms involving the aortic arch. As CT has evolved with angiographic features and multiplanar reconstruction, it has become the first line of imaging, even when the aneurysm involves the aortic arch (45). Quint et al. (45) showed that CT can accurately determine the need for intraoperative hypothermic circulatory arrest during repair.

Magnetic Resonance Imaging

MRI can accurately detect and assess aortic aneurysms. Multiplanar capability allows for precise measurement of ascending aortic aneurysm. MRI can accurately identify effacement of the sinotubular junction by aortic root aneurysm.

Figure 18.17 Computed tomography depicts a ruptured aortic arch aneurysm, hemomediastinum (high attenuation material indicative of blood), and small bilateral pleural effusions.

The Repaired Aorta

Thoracic surgery and endoscopic procedures of the aorta change its normal appearance. Evaluation of the postprocedural aorta with noninvasive imaging provides monitoring and early detection of complications, allowing intervention before aortic rupture occurs. Knowledge of the postoperative appearance enables one to distinguish the postoperative structures that may mimic pathology from complications that require prompt surgical intervention.

Figure 18.18 Diagram of different surgical procedures performed. A. Root replacement with distal anastomosis at the level of the brachiocephalic (innominate) artery (I). Arrows, coronary artery anastomoses; C, left common carotid artery; S, left subclavian artery.B. Root, ascending aorta, and partial arch replacement. C. Complete arch replacement with reimplantation of the arch vessels as a single island. D. Complete root and arch replacement with the elephant trunk technique used as a staged procedure for complete replacement of the aorta. E. Same as D except each arch vessel is implanted separately. F. Descending aortic graft. G. Descending aortic graft with complete arch replacement and reimplantation of the arch vessels as a single island. Coronary arteries are anastomosed to the root graft in parts A, B, D, and E (frontal view); heart removed in F and G. (A-E from 

Deeb GM, Jenkins E, Bolling SF, et al. Retrograde cerebral perfusion during hypothermic circulatory arrest reduces neurologic morbidity. J Thorac Cardiovasc Surg1995;109:259–268

Quint LE, Francis IR, Williams DM, et al. Synthetic interposition grafts of the thoracic aorta: postoperative appearance on serial CT studies. Radiology 1999;211:317–324

, with permission.)

Surgical procedures are complex. Portions of the aorta may be resected or opened, grafts may be sewn end to end or end to side, branch vessels may be reimplanted or grafted using synthetic interposition grafts (Fig. 18.18), or an inclusion graft technique may be used (46). The continuous suture graft inclusion technique (Fig. 18.19) entails aortotomy, graft inclusion, and enclosure of the graft within the native aorta. This technique creates a potential space between the graft and native aorta that may contain fluid, blood, thrombus, or contrast media in the setting of partial suture dehiscence. The potential space between the graft and native aorta may contain small amount of blood and gas normally in the immediate postoperative period. Blood may leak into the space if the suture dehiscences, either proximally or distally. This is evident on CT with contrast material in the space (Fig. 18.20). Aortic enlargement or pseudoaneurysm formation may occur. In chronic cases, thrombus may occupy the space. Although rare, aortic graft infection may occur. Fluid between the graft and native aorta 6 weeks after surgery is highly suspicious. The presence of gas in the space 2 weeks after surgery is virtually pathognomonic of infection (37). Other complications include perigraft blood flow and perigraft thickening (47).

It is important to be familiar with the normal postoperative appearance of the aorta, because many of the normal findings can be confused for pseudoaneurysm or aortic leak.

When repaired using synthetic interposition grafts, the aorta has a characteristic appearance on CT. Early postoperative findings include pleural or pericardial effusion, mediastinal lymph node enlargement, and/or left lower lobe atelectasis.

During aortic reconstruction felt pledgets and strips are used to reinforce sutures. On CT, these present as high-attenuation material bordering the aortic wall or graft. The felt pledgets are also used to repair bypass cannulation sites in the native aorta or air evacuation needle sites in the graft. Felt strips are used to reinforce the graft to aorta anastomosis (Figs. 18.21 and 18.22). The felt may be mistaken for contrast material secondary to a leaking graft (Fig. 18.23). There is often circumferential low attenuation and/or soft tissue attenuation material surrounding or adjacent to the aortic graft. This may diminish over time or remain unchanged. This can be mistaken for an infected surgical site or a leaking aorta. The normal appearance of the reconstructed aorta should not be mistaken for pathology. These include a collapsed native aorta adjacent to the graft (Fig. 18.24), reinforcement of the graft with bovine pericardium (Fig. 18.25), and the presence of a coronary button. In the latter, a small portion of the native aorta around the coronary artery ostium (coronary button) is implanted onto the graft. On occasion, a button may be mistaken for a pseudoaneurysm (Fig. 18.26) (48). At times, surgical intervention is not undertaken because of the poor condition of the patient. In such cases, percutaneous endovascular stent grafts are the procedure of choice (Fig. 18.27).

Figure 18.19 Diagrams illustrate (left and center) continuous suture graft inclusion technique. After aortotomy, graft material is placed within the native aorta. The distal anastomosis is created first, followed by the proximal anastomosis, both with continuous-suture technique. In these illustration, the hemiarch technique is shown, with a tongue of graft material extending along the inferior surface of the aortic arch, beyond the origins of the great vessels (straight arrow in left). The superior edge of the graft material does not extend beyond the origin of the brachiocephalic artery (curved arrow in left)Right. The native aortic sac is wrapped around the prothesis, and its cut edges are sutured together. (From 

Rofsky NM, Weinreb JC, Grossi EA, et al. Aortic aneurysm and dissection: normal MR imaging and CT findings after surgical repair with the continuous-suture graft-inclusion technique. Radiology 1993;186:195–201

, with permission.)

Figure 18.20 Large pseudoaneurysm and contained leak 4 months after composite root grafting. A. Axial computed tomography and (B) parasagittal reconstruction demonstrate low attenuation material, hematoma (H) and extravasated contrast material (C) adjacent to the distal anastomosis (white arrow in B). Black arrow in A, dissection flap in descending aorta.

Figure 18.21 Felt reinforcing ring. Axial computed tomography depicts felt reinforcing ring (white arrows) at anastomosis of an ascending aortic interposition graft. Black arrow, dissection flap in descending aorta.

Figure 18.22 Normal synthetic interposition graft of ascending aorta 14 months after surgery. Computed tomographic image demonstrates circumferential high attenuation felt reinforcing ring (arrows) around the ascending aortic graft.

Figure 18.23 Synthetic interposition graft demonstrates felt (arrow) reinforcing ring at distal anastomosis, which can mimic a pseudoaneurysm

Figure 18.24 Collapsed native aorta. Axial computed tomography 27 months after reconstruction of descending thoracic aorta demonstrates the collapsed native aorta (A) medial to graft (G).

Figure 18.25 Bovine pericardial wrap. Axial computed tomography 29 months after reconstruction of the descending thoracic aorta demonstrates low attenuation material along the left of the aorta (arrow) representing the bovine pericardial wrap.

Figure 18.26 Left coronary artery button simulating a pseudoaneurysm. Computed tomographic image demonstrates an outpouching from the ascending thoracic aortic graft. L, left coronary artery button. This may simulate a pseudoaneurysm.

Figure 18.27 Percutaneous endovascular stent. Frontal chest radiograph reveals an endovascular stent in the descending thoracic aorta after traumatic injury.

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