Chapter 22: Thoracic Aneurysms and Aortic Dissection

Scott A. LeMaire; Raja R. Gopaldas; Joseph S. Coselli

KEY POINTS

Assessing urgency of repair is essential to developing the appropriate management plan. Although emergent repair carries greater operative risk than does elective repair, any inappropriate delay of repair risks death.
The clinical progression of an aortic aneurysm is continued expansion and eventual rupture. Hence, regular noninvasive imaging studies, as part of a lifelong surveillance plan, are necessary to ensure long-term patient health. Even small asymptomatic aneurysms should be routinely imaged to assess overall growth and yearly rate of expansion.
Endovascular repair devices are approved for the treatment of descending thoracic aortic aneurysms, and some of the newer devices are also approved for the treatment of aortic trauma and penetrating aortic ulcer.
Practice guidelines were recently published that have helped to standardize the decision-making process and select an appropriate surgical intervention, as well as to standardize the use of imaging studies for patients with thoracic aortic disease.
Ascending aortic aneurysms that are symptomatic or >5.5 cm should be repaired. This threshold is lowered for patients with connective tissue disorders.
Surgical repair involves the development of a patient-tailored plan based on careful preoperative medical evaluation. When appropriate, optimizing a patient’s health status—to mitigate existing comorbidities—is important before surgical intervention.
The development and use of surgical adjuncts like antegrade selective cerebral perfusion and cerebrospinal fluid drainage have significantly reduced the morbidity rates traditionally associated with complex aortic repair.
Proximal aortic dissection is a life-threatening condition, and immediate operative repair is generally indicated, although definitive aortic repair may be delayed until after severe malperfusion has been treated.

The aorta consists of two major segments—the proximal aorta and the distal aorta—whose anatomic characteristics affect both the clinical manifestations of disease in these segments and the selection of treatment strategies for such disease (Fig. 22-1). The proximal aortic segment includes the ascending aorta and the transverse aortic arch. The ascending aorta begins at the aortic valve and ends at the origin of the innominate artery. The first portion of the ascending aorta is the aortic root, which includes the aortic valve annulus and the three sinuses of Valsalva; the coronary arteries originate from two of these sinuses. The aortic root joins the tubular portion of the ascending aorta at the sinotubular ridge. The transverse aortic arch is the area from which the brachiocephalic branches arise. The distal aortic segment includes the descending thoracic aorta and the abdominal aorta. The descending thoracic aorta begins distal to the origin of the left subclavian artery and extends to the diaphragmatic hiatus, where it joins the abdominal aorta. The descending thoracic aorta gives rise to multiple bronchial and esophageal branches, as well as to the segmental intercostal arteries, which provide circulation to the spinal cord.

Figure 22-1.

Illustration of normal thoracic aortic anatomy. The brachiocephalic vessels arise from the transverse aortic arch and are used as anatomic landmarks to define the aortic regions. The ascending aorta is proximal to the innominate artery, whereas the descending aorta is distal to the left subclavian artery.

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The volume of blood that flows through the thoracic aorta at high pressure is far greater than that found in any other vascular structure. For this reason, any condition that disrupts the integrity of the thoracic aorta, such as aortic dissection, aneurysm rupture, or traumatic injury, can have catastrophic consequences.

Historically, open surgical repair of such conditions has been an intimidating undertaking associated with significant morbidity and mortality. Strategies for protecting the brain and spinal cord during such repairs have become critical in preventing devastating complications. In recent years, endovascular therapy for thoracic aortic disease in selected patients has become accepted practice, producing fewer adverse outcomes than traditional approaches do.

THORACIC AORTIC ANEURYSMS

Listen

Aortic aneurysm is defined as a permanent, localized dilatation of the aorta to a diameter that is at least 50% greater than is normal at that anatomic level.¹ The annual incidence of thoracic aortic aneurysms is estimated to be 5.9 per 100,000 persons.² The clinical manifestations, methods of treatment, and treatment results in patients with aortic aneurysms vary according to the cause and the aortic segment involved. Causes of thoracic aortic aneurysms include degenerative disease of the aortic wall, aortic dissection, aortitis, infection, and trauma. Aneurysms can be localized to a single aortic segment, or they can involve multiple segments. Thoracoabdominal aortic aneurysms, for example, involve both the descending thoracic aorta and the abdominal aorta. In the most extreme cases, the entire aorta is aneurysmal; this condition is often called mega-aorta.

Aortic aneurysms can be either “true” or “false.” True aneurysms can take two forms: fusiform and saccular. Fusiform aneurysms are more common and can be described as symmetrical dilatations of the aorta. Saccular aneurysms are localized outpouchings of the aorta. False aneurysms, also called pseudoaneurysms, are leaks in the aortic wall that are contained by the outer layer of the aorta and/or the periaortic tissue; they are caused by disruption of the aortic wall and lead blood to collect in pouches of fibrotic tissue.

Aneurysms of the thoracic aorta consistently increase in size and eventually progress to cause serious complications. These include rupture, which is usually a fatal event. Therefore, aggressive treatment is indicated in all but the poorest surgical candidates. Small, asymptomatic thoracic aortic aneurysms can be followed, especially in high-surgical-risk patients, and can be treated surgically later if symptoms or complications develop, or if progressive enlargement occurs. Meticulous control of hypertension is the primary medical treatment for patients with small, asymptomatic aneurysms.

Elective resection with graft replacement is indicated in asymptomatic patients with an aortic diameter of at least twice normal in the involved segment (5–6 cm in most thoracic segments). Elective repair is contraindicated by extreme operative risk due to severe coexisting cardiac or pulmonary disease and by other conditions that limit life expectancy, such as malignancy. An emergency operation is performed for any patient in whom a ruptured aneurysm is suspected.

Patients with thoracic aortic aneurysm often have coexisting aneurysms of other aortic segments. A common cause of death after repair of a thoracic aortic aneurysm is rupture of a different aortic aneurysm. Therefore, staged repair of multiple aortic segments often is necessary. As with any major operation, careful preoperative evaluation for coexisting disease and subsequent medical optimization are important for successful surgical treatment.

An alternative to traditional open repair of a descending thoracic aortic aneurysm is endovascular stent grafting. Certain anatomic criteria need to be satisfied for this treatment option to be considered, including the presence of at least a 2-cm landing zone of healthy aortic tissue proximally and distally to the aneurysm to be excluded. Although data on long-term outcomes are still lacking, endovascular repair of a descending thoracic aortic aneurysm has become an accepted practice that produces excellent midterm results.

Causes and Pathogenesis

General Considerations

The normal aorta derives its elasticity and tensile strength from the medial layer, which contains approximately 45 to 55 lamellae of elastin, collagen, smooth muscle cells, and ground substance. Elastin content is highest within the ascending aorta, as would be expected because of its compliant nature, and decreases distally into the descending and abdominal aorta. Maintenance of the aortic matrix involves complex interactions among smooth muscle cells, macrophages, proteases, and protease inhibitors. Any alteration in this delicate balance can lead to aortic disease.

Thoracic aortic aneurysms have a variety of causes (Table 22-1). Although these disparate pathologic processes differ in biochemical and histologic terms, they share the final common pathway of progressive aortic expansion and eventual rupture.

Table 22-1Causes of thoracic aortic aneurysms

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Table 22-1 Causes of thoracic aortic aneurysms

Nonspecific medial degeneration

Aortic dissection

Genetic disorders

Marfan syndrome

Loeys-Dietz syndrome

Ehlers-Danlos syndrome

Familial aortic aneurysms

Aneurysms-Osteoarthritis syndrome

Congenital bicuspid aortic valve

Bovine aortic arch

Poststenotic dilatation

Infection

Aortitis

Takayasu arteritis

Giant cell arteritis

Rheumatoid aortitis

Trauma

Hemodynamic factors clearly contribute to the process of aortic dilatation. The vicious cycle of increasing diameter and increasing wall tension, as characterized by Laplace’s law (tension = pressure × radius), is well established. Turbulent blood flow is also recognized as a factor. Poststenotic aortic dilatation, for example, occurs in some patients with aortic valve stenosis or coarctation of the descending thoracic aorta. Hemodynamic derangements, however, are only one piece of a complex puzzle.

Atherosclerosis is commonly cited as a cause of thoracic aortic aneurysms. However, although atherosclerotic disease often is found in conjunction with aortic aneurysms, the notion that atherosclerosis is a distinct cause of aneurysm formation has been challenged. In most thoracic aortic aneurysms, atherosclerosis appears to be a coexisting process, rather than the underlying cause.

Research into the pathogenesis of abdominal aortic aneurysms has focused on the molecular mechanisms of aortic wall degeneration and dilatation. For example, imbalances between proteolytic enzymes (e.g., matrix metalloproteinases) and their inhibitors contribute to abdominal aortic aneurysm formation. Building on these advances, current investigations are attempting to determine whether similar inflammatory and proteolytic mechanisms are involved in thoracic aortic disease, in hope of identifying potential molecular targets for pharmacologic therapy.

Nonspecific Medial Degeneration

Nonspecific medial degeneration is the most common cause of thoracic aortic disease. Histologic findings of mild medial degeneration, including fragmentation of elastic fibers and loss of smooth muscle cells, are expected in the aging aorta. However, an advanced, accelerated form of medial degeneration leads to progressive weakening of the aortic wall, aneurysm formation, and eventual dissection, rupture, or both. The underlying causes of medial degenerative disease remain unknown.

Aortic Dissection

An aortic dissection usually begins as a tear in the inner aortic wall, which initiates a progressive separation of the medial layers and creates two channels within the aorta. This event profoundly weakens the outer wall. As the most common catastrophe involving the aorta, dissection represents a major, distinct cause of thoracic aortic aneurysms and is discussed in detail in the second half of this chapter.

Genetic Disorders

Marfan Syndrome

Marfan syndrome is an autosomal dominant genetic disorder characterized by a specific connective tissue defect that leads to aneurysm formation. The phenotype of patients with Marfan syndrome typically includes a tall stature, high palate, joint hypermobility, eye lens disorders, mitral valve prolapse, and aortic aneurysms. The aortic wall is weakened by fragmentation of elastic fibers and deposition of extensive amounts of mucopolysaccharides (a process previously called cystic medial degeneration or cystic medial necrosis). Patients with Marfan syndrome have a mutation in the fibrillin gene located on the long arm of chromosome 15. The traditionally held view is that abnormal fibrillin in the extracellular matrix decreases connective tissue strength in the aortic wall and produces abnormal elasticity, which predisposes the aorta to dilatation from wall tension caused by left ventricular ejection impulses.³ More recent evidence, however, shows that the abnormal fibrillin causes degeneration of the aortic wall matrix by increasing the activity of transforming growth factor beta (TGF-β).⁴ Between 75% and 85% of patients with Marfan syndrome have dilatation of the ascending aorta and annuloaortic ectasia (dilatation of the aortic sinuses and annulus).⁵ Such aortic abnormalities are the most common cause of death among patients with Marfan syndrome.⁶ Marfan syndrome also is frequently associated with aortic dissection.

Loeys-Dietz Syndrome

Loeys-Dietz syndrome is phenotypically distinct from Marfan syndrome. It is characterized as an aneurysmal syndrome with widespread systemic involvement. Loeys-Dietz syndrome is an aggressive, autosomal dominant condition that is distinguished by the triad of arterial tortuosity and aneurysms, hypertelorism (widely spaced eyes), and bifid uvula or cleft palate. It is caused by heterozygous mutations in the genes encoding TGF-β receptors.^7,8 Patients with Loeys-Dietz syndrome—including young children—are at increased risk of aortic rupture and aortic dissection; diameter-based thresholds of repair tend to be lower for patients with this syndrome than for patients with other connective tissue disorders.

Ehlers-Danlos Syndrome

Ehlers-Danlos syndrome includes a spectrum of inherited connective tissue disorders of collagen synthesis. The subtypes represent differing defective steps of collagen production. Vascular type Ehlers-Danlos syndrome is characterized by an autosomal dominant defect in type III collagen synthesis, which can have life-threatening cardiovascular manifestations. Spontaneous arterial rupture, usually involving the mesenteric vessels, is the most common cause of death in these patients. Thoracic aortic aneurysms and dissections are less commonly associated with Ehlers-Danlos syndrome, but when they do occur, they pose a particularly challenging surgical problem because of the reduced integrity of the aortic tissue.⁹ An Ehlers-Danlos variant of periventricular heterotopia associated with joint and skin hyperextensibility and aortic dilation has been described as being caused by mutations in the gene encoding filamin A (FLNA), an actin-binding protein that links the smooth muscle cell contractile unit to the cell surface.¹⁰

Familial Aortic Aneurysms

Families without the heritable connective tissue disorders described earlier also can be affected by genetic conditions that cause thoracic aortic aneurysms. In fact, it is estimated that at least 20% of patients with thoracic aortic aneurysms and dissections have a genetic predisposition to them. The involved mutations are characterized by autosomal dominant inheritance with decreased penetrance and variable expression. Thus far, mutations involving the genes for TGF-β receptors (TGFβR1 and TGFβR2), TGF-β2, β-myosin (MYH11 and MYLK), and α-smooth muscle cell actin (ACTA2)have been identified as causes of familial thoracic aortic aneurysms and dissection.^11,12,13ACTA2 mutations are present in approximately 14% of families with familial thoracic aortic aneurysms and dissections.

Aneurysms-Osteoarthritis Syndrome

Aneurysms-osteoarthritis syndrome is a recently identified autosomal dominant disorder. Patients with this syndrome suffer from aortic and arterial aneurysms, arterial tortuosity, aortic dissection, mild craniofacial abnormalities, and early onset osteoarthritis. Aneurysms-osteoarthritis syndrome is caused by mutations in the gene encoding SMAD3, a transcription factor for TGF-β. Affected patients have a high incidence of aortic dissection, which often occurs in a mildly dilated aorta (4–4.5 cm) and causes sudden death.¹⁴

Congenital Bicuspid Aortic Valve

Bicuspid aortic valve is the most common congenital malformation of the heart or great vessels, affecting up to 2% of Americans.¹⁵ Compared to patients with a normal, trileaflet aortic valve, patients with bicuspid aortic valve have an increased incidence of ascending aortic aneurysm formation and, often, a faster rate of aortic enlargement.¹⁶ The location of the fused leaflet, or raphe, may be predictive of aortic dilation and other abnormalities.¹⁷ About 50% to 70% of adults with bicuspid aortic valve, but without significant valve dysfunction, have echocardiographically detectable aortic dilatation.^18,19 This dilatation usually is limited to the ascending aorta and root.²⁰ Dilation occasionally is found in the arch and only rarely in the descending or abdominal aorta. In addition, aortic dissection occurs 10 times more often in patients with bicuspid valves than in the general population.²¹ Recent findings suggest that aneurysms associated with bicuspid aortic valve have a fundamentally different pathobiologic cause than aneurysms that occur in patients with trileaflet valves.²²

Although the exact mechanism responsible for aneurysm formation in patients with bicuspid aortic valve remains unclear, evidence suggests that these patients have a congenital connective tissue abnormality that predisposes the aorta to medial degeneration.^{22,23,24,25,26,27,28} For example, fibrillin 1 content is significantly lower and matrix metalloproteinase activity is significantly higher in the aortic media in patients with bicuspid aortic valve than in persons with a normal, tricuspid aortic valve.^22,23,24 Further, the process of medial degeneration in patients with bicuspid aortic valve may be exacerbated by the presence of chronic turbulent flow through the deformed valve.

Bovine aortic arch

Bovine aortic arch—a common origin of the innominate and left common carotid arteries—has been considered a normal anatomic variant. Recent studies from Yale University have identified a higher prevalence of bovine aortic arch in patients with thoracic aortic disease; an association was found between this anomaly and a generalized increase in aortic aneurysmal disease (without any predisposition to a particular aortic region). However, bovine aortic arch was not associated distinctly with bicuspid aortic valve or aortic dissection, but with a higher mean aortic growth rate: 0.29 cm/year in patients with bovine aortic arch, compared with 0.09 cm/year in controls. Therefore, bovine aortic arch may be better characterized as a precursor of aortic aneurysm than as a simple normal anatomic variant.²⁹ Further studies are needed to delineate the underlying mechanism for this association.

Infection

Primary infection of the aortic wall resulting in aneurysm formation is rare. Although these lesions are termed mycotic aneurysms, the responsible pathogens usually are bacteria rather than fungi. Bacterial invasion of the aortic wall may result from bacterial endocarditis, endothelial trauma caused by an aortic jet lesion, or extension from an infected laminar clot within a preexisting aneurysm. The most common causative organisms are Staphylococcus aureus, Staphylococcus epidermidis, Salmonella, and Streptococcus.^30,31 Unlike most other causes of thoracic aortic aneurysms, which generally produce fusiform aneurysms, infection often produces saccular aneurysms located in areas of aortic tissue destroyed by the infectious process.

Although syphilis was once the most common cause of ascending aortic aneurysms, the advent of effective antibiotic therapy has made syphilitic aneurysms a rarity in developed nations. In other parts of the world, however, syphilitic aneurysms remain a major cause of morbidity and mortality. The spirochete Treponema pallidum causes an obliterative endarteritis of the vasa vasorum that results in medial ischemia and loss of the elastic and muscular elements of the aortic wall. The ascending aorta and arch are the most commonly involved areas. The emergence of HIV infection in the 1980s was associated with a substantial increase in the incidence of syphilis in both HIV-positive and HIV-negative patients. Because syphilitic aortitis often presents 10 to 30 years after the primary infection, the incidence of associated aneurysms may increase in the near future.

Aortitis

In patients with preexisting degenerative thoracic aortic aneurysms, localized transmural inflammation and subsequent fibrosis can develop. The dense aortic infiltrate responsible for the fibrosis consists of lymphocytes, plasma cells, and giant cells. The cause of the intense inflammatory reaction is unknown. Although the severe inflammation is a superimposed problem rather than a primary cause, its onset within an aneurysm can further weaken the aortic wall and precipitate expansion.

Systemic autoimmune disorders also cause thoracic aortitis. Aortic Takayasu arteritis generally produces obstructive lesions related to severe intimal thickening, but associated medial necrosis can lead to aneurysm formation. In patients with giant cell arteritis (temporal arteritis), granulomatous inflammation may develop that involves the entire thickness of the aortic wall, causing intimal thickening and medial destruction. Rheumatoid aortitis is an uncommon systemic disease that is associated with rheumatoid arthritis and ankylosing spondylitis. The resulting medial inflammation and fibrosis can affect the aortic root, causing annular dilatation, aortic valve regurgitation, and ascending aortic aneurysm formation.

Pseudoaneurysms

Pseudoaneurysms of the thoracic aorta usually represent chronic leaks that are contained by surrounding tissue and fibrosis. By definition, the wall of a pseudoaneurysm is not formed by intact aortic tissue; rather, the wall develops from organized thrombus and associated fibrosis. Pseudoaneurysms can arise from primary defects in the aortic wall (e.g., after trauma or contained aneurysm rupture) or from anastomotic or cannulation site leaks that occur after cardiovascular surgery. Anastomotic pseudoaneurysms can be caused by technical problems or by deterioration of the native aortic tissue, graft material, or suture. Commonly, they occur in patients with Marfan syndrome.³² Tissue deterioration usually is related to either progressive degenerative disease or infection. Improvements in sutures, graft materials, and surgical techniques have decreased the incidence of thoracic aortic pseudoaneurysms. Should thoracic aortic pseudoaneurysms occur, they typically require expeditious surgical or other intervention because they are associated with a high incidence of morbidity and rupture.

Clinical History

Treatment decisions in cases of thoracic aortic aneurysm are guided by our current understanding of the clinical history of these aneurysms, which classically is characterized as progressive aortic dilatation and eventual dissection, rupture, or both. An analysis by Elefteriades of data from 1600 patients with thoracic aortic disease has helped quantify these well-recognized risks.³³ Average expansion rates were 0.07 cm/y in ascending aortic aneurysms and 0.19 cm/y in descending thoracic aortic aneurysms. As expected, aortic diameter was a strong predictor of rupture, dissection, and mortality. For thoracic aortic aneurysms >6 cm in diameter, annual rates of catastrophic complications were 3.6% for rupture, 3.7% for dissection, and 10.8% for death. Critical diameters, at which the incidence of expected complications significantly increased, were 6.0 cm for aneurysms of the ascending aorta and 7.0 cm for aneurysms of the descending thoracic aorta; the corresponding risks of rupture after reaching these diameters were 31% and 43%, respectively.³⁴

Certain types of aneurysms have an increased propensity for expansion and rupture. For example, aneurysms in patients with Marfan or Loeys-Dietz syndrome dilate at an accelerated rate and rupture or dissect at smaller diameters than non–connective tissue disorder-related aneurysms. Before the era of surgical treatment for aortic aneurysms, this aggressive form of aortic disease resulted in an average life expectancy of 32 years for Marfan patients; aortic root complications caused the majority of deaths.³⁵ Saccular aneurysms, which commonly are associated with aortic infection and typically affect only a discrete small section of the aorta, tend to grow more rapidly than fusiform aneurysms, which are associated with more widespread degenerative changes and generally affect a larger section of the aorta.

One common clinical scenario deserves special attention. A moderately dilated ascending aorta (i.e., 4–5 cm) often is encountered during aortic valve replacement or coronary artery bypass operations. The clinical history of these ectatic ascending aortas has been defined by several studies. Michel and colleagues³⁶ studied patients whose ascending aortic diameters were >4 cm at the time of aortic valve replacement; 25% of these patients required reoperation for ascending aortic replacement. Prenger and colleagues³⁷ reported that aortic dissection occurred in 27% of patients who had aortic diameters of >5 cm at the time of aortic valve replacement. Recently, attention has been directed toward whether or not a mildly dilated aortic root should be replaced in patients with bicuspid aortic valve who are undergoing isolated valve replacement, and at what threshold to intervene. Although this is a controversial issue, many surgeons believe that the tendency toward late aortic dilatation in these patients warrants aggressive treatment.^38,39 Current practice guidelines indicate that such early replacement should be considered in these patients when the ascending aorta is 4.0 to 4.5 cm.⁴⁰

Clinical Manifestations

In many patients with thoracic aortic aneurysms, the aneurysm is discovered incidentally when imaging studies are performed for unrelated reasons. Therefore, patients often are asymptomatic at the time of diagnosis. However, thoracic aortic aneurysms that initially go undetected eventually create symptoms and signs that correspond with the segment of aorta that is involved. These aneurysms have a wide variety of manifestations, including compression or erosion of adjacent structures, aortic valve regurgitation, distal embolism, and rupture.

Local Compression and Erosion

Initially, aneurysmal expansion and impingement on adjacent structures causes mild, chronic pain. The most common symptom in patients with ascending aortic aneurysms is anterior chest discomfort; the pain is frequently precordial in location but may radiate to the neck and jaw, mimicking angina. Aneurysms of the ascending aorta and transverse aortic arch can cause symptoms related to compression of the superior vena cava, the pulmonary artery, the airway, or the sternum. Rarely, these aneurysms erode into the superior vena cava or right atrium, causing acute high-output failure. Expansion of the distal aortic arch can stretch the recurrent laryngeal nerve, which results in left vocal cord paralysis and hoarseness. Descending thoracic and thoracoabdominal aneurysms frequently cause back pain localized between the scapulae. When the aneurysm is largest in the region of the aortic hiatus, it may cause middle back and epigastric pain. Thoracic or lumbar vertebral body erosion typically causes severe, chronic back pain; extreme cases can present with spinal instability and neurologic deficits from spinal cord compression. Although mycotic aneurysms have a peculiar propensity to destroy vertebral bodies, spinal erosion also occurs with degenerative aneurysms. Descending thoracic aortic aneurysms may cause various degrees of airway obstruction, manifesting as cough, wheezing, stridor, or pneumonitis. Pulmonary or airway erosion presents as hemoptysis. Compression and erosion of the esophagus cause dysphagia and hematemesis, respectively. Thoracoabdominal aortic aneurysms can cause duodenal obstruction or, if they erode through the bowel wall, gastrointestinal bleeding. Jaundice due to compression of the liver or porta hepatis is uncommon. Erosion into the inferior vena cava or iliac vein presents with an abdominal bruit, widened pulse pressure, edema, and heart failure.

Aortic Valve Regurgitation

Ascending aortic aneurysms can cause displacement of the aortic valve commissures and annular dilatation. The resulting deformation of the aortic valve leads to progressively worsening aortic valve regurgitation. In response to the volume overload, the heart remodels and becomes increasingly dilated. Patients with this condition may present with progressive heart failure, a widened pulse pressure, and a diastolic murmur.

Distal Embolization

Thoracic aortic aneurysms—particularly those involving the descending and thoracoabdominal aorta—are commonly lined with friable, atheromatous plaque and mural thrombus. This debris may embolize distally, causing occlusion and thrombosis of the visceral, renal, or lower-extremity branches.

Rupture

Patients with ruptured thoracic aortic aneurysms often experience sudden, severe pain in the anterior chest (ascending aorta), upper back or left chest (descending thoracic aorta), or left flank or abdomen (thoracoabdominal aorta). When ascending aortic aneurysms rupture, they usually bleed into the pericardial space, producing acute cardiac tamponade and death. Descending thoracic aortic aneurysms rupture into the pleural cavity, producing a combination of severe hemorrhagic shock and respiratory compromise. External rupture is extremely rare; saccular syphilitic aneurysms have been observed to rupture externally after eroding through the sternum.

Diagnostic Evaluation

Diagnosis and characterization of thoracic aneurysms require imaging studies, which also provide critical information that guides the selection of treatment options. Although the best choice of imaging technique for the thoracic and thoracoabdominal aorta is somewhat institution-specific, varying with the availability of imaging equipment and expertise, efforts have been made to standardize key elements of image acquisition and reporting. Recent practice guidelines⁴⁰ recommend that aortic imaging reports plainly state the location of aortic abnormalities (including calcification and the extent to which abnormalities extend into branch vessels), the maximum external aortic diameters (rather than internal, lumen-based diameters), internal filling defects, and any evidence of rupture. Whenever possible, all results should be compared to those of prior imaging studies.

Plain Radiography

Plain radiographs of the chest, abdomen, or spine often provide enough information to support the initial diagnosis of thoracic aortic aneurysm. Ascending aortic aneurysms produce a convex shadow to the right of the cardiac silhouette. The anterior projection of an ascending aneurysm results in the loss of the retrosternal space in the lateral view. An aneurysm may be indistinguishable from elongation and tortuosity.⁴¹ Above all, chest radiographs (CXRs) may appear normal in patients with thoracic aortic disease and, thus, cannot exclude the diagnosis of aortic aneurysm. Aortic root aneurysms, for example, often are hidden within the cardiac silhouette. Plain CXRs may reveal convexity in the right superior mediastinum, loss of the retrosternal space, or widening of the descending thoracic aortic shadow, which may be highlighted by a rim of calcification outlining the dilated aneurysmal aortic wall. Aortic calcification also may be seen in the upper abdomen on a standard radiograph made in the anteroposterior or lateral projection (Fig. 22-2). Once a thoracic aortic aneurysm is detected on plain radiographs, additional studies are required to define the extent of aortic involvement.

Figure 22-2.

Chest radiographs showing a calcified rim (arrows) in the aortic wall of a thoracoabdominal aortic aneurysm. A. Anteroposterior view. B. Lateral view.

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Echocardiography and Abdominal Ultrasonography

Ascending aortic aneurysms are commonly discovered during echocardiography in patients presenting with symptoms or signs of aortic valve regurgitation. Both transthoracic and transesophageal echocardiography provide excellent visualization of the ascending aorta, including the aortic root.⁴² Transesophageal echocardiography also allows visualization of the descending thoracic aorta but is not ideal for evaluating the transverse aortic arch (which is obscured by air in the tracheobronchial tree) or the upper abdominal aorta. Effective echocardiography requires considerable technical skill, both in obtaining adequate images and in interpreting them. This imaging modality has the added benefit of assessing cardiac function and revealing any other abnormalities that may be present. During ultrasound evaluation of a suspected infrarenal abdominal aortic aneurysm, if a definitive neck cannot be identified at the level of the renal arteries, the possibility of thoracoabdominal aortic involvement should be suspected and investigated by using other imaging modalities. Caution should be exercised while interpreting aneurysm dimensions from ultrasound imaging because intraluminal measurements are often reported, whereas external measurements are usually used in other imaging modalities.

Computed Tomography

Computed tomographic (CT) scanning is widely available, provides visualization of the entire thoracic and abdominal aorta, and permits multiplanar and 3-dimensional aortic reconstructions. Consequently, CT is the most common—and arguably the most useful—imaging modality for evaluating thoracic aortic aneurysms.⁴³ In addition to establishing the diagnosis, CT provides information about an aneurysm’s location, extent, anatomic anomalies, and relationship to major branch vessels. CT is particularly useful in determining the absolute diameter of the aorta, especially in the presence of a laminated clot, and also detects aortic calcification. Contrast-enhanced CT provides information about the aortic lumen and can detect mural thrombus, aortic dissection, inflammatory periaortic fibrosis, and mediastinal or retroperitoneal hematoma due to contained aortic rupture. To increase consistency and ensure uniform reporting, current practice guidelines suggest that measurements be taken perpendicular to blood flow and at standard anatomic locations⁴⁰ (Fig. 22-3); this should reduce the likelihood of erroneous measurements, especially during serial imaging surveillance.

Figure 22-3.

Current practice guidelines⁴⁰ seek to standardize the reporting of aortic diameters by indicating key locations of measurement. These include (1) the sinuses of Valsalva, (2) the sinotubular junction, (3) the mid-ascending aorta, (4) the proximal aortic arch at the origins of the innominate artery, (5) the mid-aortic arch, which is between the left common carotid and left subclavian arteries, (6) the proximal descending thoracic aorta, which begins at the isthmus (approximately 2 cm distal to the origins of the left subclavian artery), (7) the mid-descending thoracic artery, (8) the aorta at the diaphragm, and (9) the abdominal aorta at the origins of the celiac axis. (Used with permission of Baylor College of Medicine.)

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The major disadvantage of contrast-enhanced CT scanning is the possibility of contrast-induced acute renal failure in patients who are at risk (e.g., patients with preexisting renal disease or diabetes).⁴⁴ If possible, surgery is performed ≥1 day after contrast administration to allow time to observe renal function and to permit diuresis of the contrast agent. If renal insufficiency occurs or is worsened, elective surgery is postponed until renal function returns to normal or stabilizes.

Magnetic Resonance Angiography

Magnetic resonance angiography (MRA) is becoming widely available and can facilitate visualization of the entire aorta. This modality produces aortic images comparable to those produced by contrast-enhanced CT but does not necessitate exposure to ionizing radiation. In addition, MRA offers excellent visualization of branch vessel details, and it is useful in detecting branch vessel stenosis.⁴⁵ However, MRA is limited by high expense and a susceptibility to artifacts created by ferromagnetic materials, and gadolinium—the contrast agent for MRA—may be linked to nephrogenic systemic fibrosis and acute renal failure in patients with advanced renal insufficiency.⁴⁶ Furthermore, the MRA environment is not appropriate for many critically ill patients, and unlike CT imaging, MRA imaging is suboptimal in patients with extensive aortic calcification.

Invasive Aortography and Cardiac Catheterization

Although catheter-based contrast aortography was previously considered the gold standard for evaluating thoracic aortic disease, cross-sectional imaging (i.e., CT and MRA) has largely replaced this modality. Technologic improvements have enabled CT and MRA to provide excellent aortic imaging while causing less morbidity than catheter-based studies do, so CT and MRA are now the primary modes for evaluating thoracic aortic disease. Today, the use of invasive aortography in patients with thoracic aortic disease is generally limited to those undergoing endovascular therapies or when other types of studies are contraindicated or have not provided satisfactory results.

Unlike standard aortography, cardiac catheterization continues to play an important role in diagnosis and preoperative planning, especially in patients with ascending aortic involvement. Proximal aortography can reveal not only the status of the coronary arteries and left ventricular function but also the degree of aortic valve regurgitation, the extent of aortic root involvement, coronary ostial displacement, and the relationship of the aneurysm to the arch vessels.

The value of the information one can obtain from catheter-based diagnostic studies should be weighed against the established limitations and potential complications of such studies. A key limitation of aortography is that it images only the lumen and may therefore underrepresent the size of large aneurysms that contain laminated thrombus. Manipulation of intraluminal catheters can result in embolization of laminated thrombus or atheromatous debris. Proximal aortography carries a 0.6% to 1.2% risk of stroke. Other risks include allergic reaction to contrast agent, iatrogenic aortic dissection, and bleeding at the arterial access site. In addition, the volumes of contrast agent required to adequately fill large aneurysms can cause significant renal toxicity. To minimize the risk of contrast nephropathy, patients receive periprocedural intravenous (IV) fluids for hydration, mannitol for diuresis, and acetylcysteine.^47,48 As with contrast-enhanced CT, surgery is performed ≥1 day after angiography whenever possible to ensure that renal function has stabilized or returned to baseline.

Treatment

Selecting the Appropriate Treatment

Once a thoracic aortic aneurysm is detected, management begins with patient education, particularly if the patient is asymptomatic, because aortic disease may progress rapidly and unexpectedly in some patients. A detailed medical history is collected, a physical examination is performed, and a systematic review of medical records is carried out to clearly assess the presence or absence of pertinent symptoms and signs, despite any initial denial of symptoms by the patient. Signs of genetic diseases such as Marfan syndrome or Loeys-Dietz syndrome are thoroughly reviewed. If clinical criteria are met for such a genetic condition, confirmatory laboratory tests are conducted. Patients with such genetic diseases are best treated in a dedicated aortic clinic where they can be appropriately followed up. Surveillance imaging and aggressive blood pressure control are the mainstays of initial management for asymptomatic patients. When patients become symptomatic or their aneurysms grow to meet certain size criteria, the patients become surgical candidates.

Although long-term data are still lacking, endovascular therapy has become an accepted treatment for thoracic aortic aneurysms.⁴⁹ Its role in treating proximal aortic disease and thoracoabdominal aortic aneurysms remains experimental. Nonetheless, endoluminal stenting is approved by the U.S. Food and Drug Administration for the treatment of isolated descending thoracic aortic aneurysms, and some newer devices are approved for the treatment of blunt aortic injury and penetrating aortic ulcer. In practice, however, the off-label application of aortic stent grafts is widespread and accounts for well over half their use.⁵⁰ Endovascular approaches may be helpful in emergent aneurysm repair, such as for patients with aortic rupture.⁵¹ Recently, endovascular therapy has evolved to include hybrid repairs, which combine open “debranching” techniques (to reroute branching vessels) with endovascular aortic repair. Despite these advances, for the repair of aneurysms with proximal aortic involvement and of thoracoabdominal aortic aneurysms, open procedures remain the gold standard and preferred approach.

Determination of the Extent and Severity of Disease

Cross-sectional imaging with reconstruction is critical when one is evaluating a thoracic aneurysm, determining treatment strategy, and planning necessary procedures. Note that, commonly, patients with a thoracic aortic aneurysm also have a remote aneurysm.² In such cases, the more threatening lesion usually is addressed first. In many patients, staged operative procedures are necessary for complete repair of extensive aneurysms involving the ascending aorta, transverse arch, and descending thoracic or thoracoabdominal aorta.⁵² When the descending segment is not disproportionately large (compared with the proximal aorta) and is not causing symptoms, the proximal aortic repair is carried out first. An important benefit of this approach is that it allows treatment of valvular and coronary artery occlusive disease at the first operation.

Proximal aneurysms (proximal to the left subclavian artery) usually are addressed via a sternotomy approach. Aneurysms involving the descending thoracic aorta are evaluated in terms of criteria (described later) for potential endovascular repair; those unsuitable for an endovascular approach are repaired with open techniques through a left thoracotomy. A CT scan can reveal detailed information about aortic calcification and luminal thrombus. These details are important in preventing embolization during surgical manipulation.

Indications for Operation

Thoracic aortic aneurysms are repaired to prevent fatal rupture. Therefore, on the basis of the natural history studies and other data, practice guidelines for thoracic aortic disease⁴⁰ recommend elective operation in asymptomatic patients when the diameter of an ascending aortic aneurysm is >5.5 cm, when the diameter of a descending thoracic aortic aneurysm is >6.0 cm, or when the rate of dilatation is >0.5 cm/y. In patients with connective tissue disorders such as Marfan and Loeys-Dietz syndromes, the threshold for operation is based on a smaller aortic diameter (4.0–5.0 cm for the ascending aorta and 5.5 to 6.0 cm for the descending thoracic aorta). For women with connective tissue disorders who are considering pregnancy, prophylactic aortic root replacement is considered because the risk of aortic dissection or rupture increases at an aortic diameter of 4.0 cm or greater. For low-risk patients with chronic aortic dissection, descending thoracic repair is recommended at an aortic diameter of 5.5 cm or greater. For patients undergoing aortic valve replacement or repair, smaller ascending aortic aneurysms (>4.5 cm) are considered for concomitant repair.

The acuity of presentation is a major factor in decisions about the timing of surgical intervention. Many patients are asymptomatic at the time of presentation, so there is time for thorough preoperative evaluation and improvement of their current health status, such as through smoking cessation and other optimization programs. In contrast, patients who present with symptoms may need urgent operation. Symptomatic patients are at increased risk of rupture and warrant expeditious evaluation. The onset of new pain in patients with known aneurysms is especially concerning, because it may herald significant expansion, leakage, or impending rupture. Emergent intervention is reserved for patients who present with aneurysm rupture or superimposed acute dissection.⁵³

Open Repair vs. Endovascular Repair

As noted earlier, endovascular repair of thoracic aortic aneurysms has become an accepted treatment option in selected patients, particularly patients with isolated degenerative descending thoracic aortic aneurysms; in fact, practice guidelines recommend that endovascular repair be strongly considered for patients with descending thoracic aneurysm at an aortic diameter of 5.5 cm (which is slightly below the 6.0-cm threshold for open repair).⁴⁰ For endovascular repairs to produce optimal outcomes, several anatomic criteria must be met. For one, the proximal and distal neck diameters should fall within a range that will allow proper sealing. Also, the proximal and distal landing zones should ideally be at least 20 mm long so that an appropriate seal can be made. Note that the limiting structures proximally and distally are the brachiocephalic vessels and celiac axis, respectively. Another anatomic limitation for this therapy relates to vascular access: The femoral and iliac arteries have to be wide enough to accommodate the large sheaths necessary to deploy the stent grafts, although newer devices use a smaller sheath (or are “sheathless” self-deployed stent grafts) to accommodate smaller arteries. Tortuosity of the iliac vessels and abdominal aorta can make these procedures technically challenging. Occasionally, a “side graft” anastomosed to the iliac artery through a retroperitoneal incision is used because of poor distal access. When any of these anatomic criteria are not met, an open approach is preferable to an endovascular approach.

Of note, attempts have been made to extend the use of endovascular therapy to aortic arch aneurysms and thoracoabdominal aortic aneurysms. Although reports of purely endovascular repair of the aortic arch remain limited, Greenberg and colleagues⁵⁴ have reported their experience with a large series of purely endovascular thoracoabdominal aortic repairs. Additionally, there have been numerous reports of small series of off-label, experimental hybrid procedures that involve debranching the aortic arch or the visceral vessels of the abdominal aorta, followed by endovascular exclusion of the aneurysm. The majority of hybrid approaches involve repairing the aortic arch. In its simplest form, hybrid arch repair involves an open bypass from the left subclavian to the left common carotid artery, which is followed by deliberate coverage of the origins of the left subclavian artery by the stent graft. In its most complex form, hybrid arch repair involves rerouting all of the brachiocephalic vessels, followed by proximal placement of the stent graft in the ascending aorta and extending repair distally into the aortic arch and descending thoracic aorta.

The patients who theoretically may benefit more from an endovascular approach than from traditional open techniques are those who are of advanced age or have significant comorbidities. For example, the open repair of a descending thoracic aortic aneurysm can result in significant pulmonary morbidity. Therefore, patients with borderline pulmonary reserve may better tolerate an endovascular procedure than standard open repair. In contrast, patients with significant intraluminal atheroma may be better served by an open approach because of the risk of embolization and stroke posed by catheter manipulation. Similarly, patients with connective tissue disorders generally are not considered candidates for elective endovascular repair. Endovascular repair in patients with connective tissue disorders has produced poor results, which are mainly due to progressive dilatation, stent graft migration, and endoleak.⁵⁵

Preoperative Assessment and Preparation

Given the impact of comorbid conditions on perioperative complications, a careful preoperative assessment of physiologic reserve is critical in assessing operative risk. Therefore, most patients undergo a thorough evaluation—with emphasis on cardiac, pulmonary, and renal function—before undergoing elective surgery.^56,57

Cardiac Evaluation

Coronary artery disease is common in patients with thoracic aortic aneurysm and is responsible for a substantial proportion of early and late postoperative deaths in such patients. Similarly, valvular disease and myocardial dysfunction have important implications when one is planning anesthetic management and surgical approaches for aortic repair. Transthoracic echocardiography is a satisfactory noninvasive method for evaluating both valvular and biventricular function. Dipyridamole-thallium myocardial scanning identifies regions of myocardium that have reversible ischemia, and this test is more practical than exercise testing in older patients with concomitant lower-extremity peripheral vascular disease. Cardiac catheterization and coronary arteriography are performed in patients who have evidence of coronary disease—as indicated by either the patient’s history or the results of noninvasive studies—or who have a left ventricular ejection fraction of ≤30%. If significant valvular or coronary artery disease is identified before a proximal aortic operation, the disease can be addressed directly during the procedure. Patients who have asymptomatic distal aortic aneurysms and severe coronary occlusive disease undergo percutaneous transluminal angioplasty or surgical revascularization before the aneurysmal aortic segment is replaced.

Pulmonary Evaluation

Pulmonary function screening with arterial blood gas measurement and spirometry is routinely performed before thoracic aortic operations. Patients with a forced expiratory volume in 1 second of >1.0 L and a partial pressure of carbon dioxide of <45 mmHg are considered surgical candidates. In suitable patients, borderline pulmonary function can be improved by implementing a regimen that includes smoking cessation, weight loss, exercise, and treatment of bronchitis for a period of 1 to 3 months before surgery. Although surgery is not withheld from patients with symptomatic aortic aneurysms and poor pulmonary function, adjustments in operative technique should be made to maximize these patients’ chances of recovery. In such patients, preserving the left recurrent laryngeal nerve, the phrenic nerves, and diaphragmatic function is particularly important.

Renal Evaluation

Renal function is assessed preoperatively by measuring serum electrolyte, blood urea nitrogen, and creatinine levels. Information about kidney size and perfusion can be obtained from the imaging studies used to evaluate the aorta.

Obtaining accurate information about baseline renal function has important therapeutic and prognostic implications. For example, perfusion strategies and perioperative medications are adjusted according to renal function. Patients with severely impaired renal function frequently require at least temporary hemodialysis after surgery. These patients also have a mortality rate that is significantly higher than normal. Patients with thoracoabdominal aortic aneurysms and poor renal function secondary to severe proximal renal occlusive disease undergo renal artery endarterectomy, stenting, or bypass grafting during the aortic repair.

Operative Repair

Proximal Thoracic Aortic Aneurysms

Open Repair

Traditional open operations to repair proximal aortic aneurysms—which involve the ascending aorta, transverse aortic arch, or both—are performed through a midsternal incision and require cardiopulmonary bypass. The best choice of aortic replacement technique depends on the extent of the aneurysm and the condition of the aortic valve. The spectrum of operations (Fig. 22-4) ranges from simple graft replacement of the tubular portion of the ascending aorta (Fig. 22-4A) to graft replacement of the entire proximal aorta, including the aortic root, and reattachment of the coronary arteries and brachiocephalic branches. The options for treating aortic valve disease, repairing aortic aneurysms, and maintaining perfusion during repair procedures each deserve detailed consideration (Table 22-2).

Table 22-2Options for open surgical repair of proximal aortic aneurysms

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Table 22-2 Options for open surgical repair of proximal aortic aneurysms

Options for treating aortic valve disease

Aortic valve annuloplasty (annular plication)

Aortic valve replacement with mechanical or biologic prosthesis

Aortic root replacement

Composite valve graft

Aortic homograft

Stentless porcine root

Pulmonary autograft (Ross procedure)

Valve-sparing techniques

Options for graft repair of the aortic aneurysm

Patch aortoplasty

Ascending replacement only

Beveled hemiarch replacement

Total arch replacement with reattachment of brachiocephalic branches

Total arch replacement with bypass grafts to the brachiocephalic branches (Y-graft approaches)

Elephant trunk technique with island reattachment

Elephant trunk technique with Y-graft approach

Perfusion options

Standard cardiopulmonary bypass

Profound hypothermic circulatory arrest without adjuncts

Hypothermic circulatory arrest with adjuncts

Retrograde cerebral perfusion

Antegrade cerebral perfusion

Balloon perfusion catheters

Right axillary artery cannulation

Innominate artery cannulation

Combined antegrade and retrograde cerebral perfusion

Figure 22-4.

Illustrations of proximal aortic repairs in which the native aortic root is left intact. A. Graft replacement of the tubular portion of the ascending aorta with the aortic arch left intact. B. Hemiarch beveled graft replacement, in which the ascending aorta and a portion of the lesser curvature of the aortic arch are replaced. C. A modified hemiarch with additional graft replacement of the innominate artery. D. Patch repair of the aortic arch. E. Traditional total arch replacement using an island approach to reattach the brachiocephalic vessels. F. The branched graft approach, which replaces the brachiocephalic vessels by following their original anatomic location. G. The elephant trunk approach with a concomitant island brachiocephalic artery reattachment. Contemporary Y-graft arch repairs include H. the single Y-graft approach, I. the double Y-graft approach, J. the elephant trunk approach with a single Y-graft, and K. the elephant trunk approach with a double Y-graft. (Used with permission of Baylor College of Medicine.)

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Aortic Valve Disease and Root Aneurysms

Many patients undergoing proximal aortic operations have aortic valve disease that requires concomitant surgical correction. When such disease is present and the sinus segment is normal, separate repair or replacement of the aortic valve and graft replacement of the tubular segment of the ascending aorta are carried out. In such cases, mild to moderate valve regurgitation with annular dilatation can be addressed by plicating the annulus with mattress sutures placed below each commissure, thereby preserving the native valve. In patients with more severe valvular regurgitation or with valvular stenosis, the valve is replaced with a stented biologic or mechanical prosthesis. Mechanical prostheses necessitate following a lifelong anticoagulation regimen. Separate replacement of the aortic valve and ascending aorta is not performed in patients with Marfan syndrome, because progressive dilatation of the remaining sinus segment eventually leads to complications that necessitate reoperation. Therefore, patients with Marfan syndrome or those with annuloaortic ectasia require some form of aortic root replacement.⁵⁸

In many cases, the aortic root is replaced with a mechanical or biologic graft that has both a valve and an aortic conduit. Currently, three graft options are commercially available: composite valve grafts, which consist of a bileaflet mechanical valve attached to a polyester tube graft; aortic root homografts, which are harvested from cadavers and cryopreserved; and stentless porcine aortic root grafts.^59,60 Another option for surgeons is to construct a bioprosthetic composite valve graft during the operation by suturing a stented tissue valve to a polyester graft tube.

Although select patients may be offered the Ross procedure, in which the patient’s pulmonary artery root is excised and placed in the aortic position and then the right ventricular outflow tract is reconstructed by using a cryopreserved pulmonary homograft, this option is rarely used. This is largely because it is a technically demanding procedure, and there are concerns about the potential for autograft dilatation in patients with connective tissue disorders.⁶¹

An additional option is valve-sparing aortic root replacement, which has evolved substantially during the past decade.⁶² The valve-sparing technique that is currently favored is called aortic root reimplantation and involves excising the aortic sinuses, attaching a prosthetic graft to the patient’s annulus (Fig. 22-5), and resuspending the native aortic valve inside the graft. The superior hemodynamics of the native valve and the avoidance of anticoagulation are major advantages of the valve-sparing approach. Long-term results in carefully selected patients have been excellent.⁶³ Although the durability of this procedure in patients with either Marfan syndrome or bicuspid aortic valve has been questioned, reports suggest that long-term durability is possible for patients with Marfan syndrome who undergo the procedure at experienced centers.^64,65 Further, acceptable midterm outcomes have been reported for patients with bicuspid aortic valve.⁶⁶ Patients who have structural leaflet deterioration or excessive annular dilatation are typically deemed unsuitable for valve-sparing repair.

Figure 22-5.

Illustration of our current valve-sparing procedure for replacing the aortic root and ascending aorta for treatment of A. aortic root aneurysm. B. The ascending aorta is opened after cardiopulmonary bypass and cardioplegic arrest are established and the distal ascending aorta is clamped. The diseased aortic tissue (including the sinuses of Valsalva) is excised. Buttons of surrounding tissue are used to mobilize the origins of the coronary arteries. C. A synthetic graft is sewn to the distal ascending aorta with continuous suture. D. After the distal anastomosis is completed, six sutures reinforced with Teflon pledgets are placed in the plane immediately below the aortic valve annulus. E. The subannular sutures are placed through the base of a synthetic aortic root graft, which is then is parachuted down around the valve.F. After the root graft is cut to an appropriate length, the valve commissures and leaflets are positioned within the graft. The annular sutures are then tied. G. Each of the three commissures is then secured near the top of the graft. H. The supra-annular aortic tissue is sewn to the graft in continuous fashion. I. The button surrounding the origin of the left main coronary artery is sewn to an opening cut in the root graft. J. The two aortic grafts are sewn together with continuous suture. K. The button surrounding the origin of the right coronary artery is sewn to an opening cut in the root graft. L. The completed valve-sparing aortic root replacement and graft repair of the ascending aorta is shown. (Used with permission of Baylor College of Medicine.)

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Regardless of the type of conduit used, aortic root replacement requires reattaching the coronary arteries to openings in the graft. In the original procedure described by Bentall and De Bono,⁶⁷ this was accomplished by suturing the intact aortic wall surrounding each coronary artery to the openings in the graft. The aortic wall was then wrapped around the graft to establish hemostasis. However, this technique frequently produced leaks at the coronary reattachment sites that eventually led to pseudoaneurysm formation. The Cabrol modification, in which a separate, small tube graft is sutured to the coronary ostia and the main aortic graft, achieves tension-free coronary anastomoses and reduces the risk of pseudoaneurysm formation.⁶⁸ Kouchoukos’s button modification of the Bentall procedure is currently the most widely used technique.⁶⁹ The aneurysmal aorta is excised, and buttons of aortic wall are left surrounding both coronary arteries, which are then mobilized and sutured to the aortic graft (Fig. 22-6). The coronary suture lines may be reinforced with polytetrafluoroethylene felt or pericardium to enhance hemostasis. When the coronary arteries cannot be mobilized adequately because of extremely large aneurysms or scarring from previous surgery, the Cabrol technique or a related modification can be used. Another option, originally described by Zubiate and Kay,⁷⁰ is the construction of bypass grafts by using interposition saphenous vein or synthetic grafts.

Figure 22-6.

Illustration of a modified Bentall procedure for replacing the aortic root and ascending aorta. The aortic valve and entire ascending aorta, including the sinuses of Valsalva, have been replaced by a mechanical composite valve graft. The coronary arteries with buttons of surrounding aortic tissue have been mobilized and are being reattached to openings in the aortic graft.

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Aortic Arch Aneurysms

Several options are also available for handling aneurysms that extend into the transverse aortic arch (Fig. 22-4). The surgical approach depends on the extent of involvement and the need for cardiac and cerebral protection. Saccular aneurysms that arise from the lesser curvature of the distal transverse arch and that encompass <50% of the aortic circumference can be treated by patch graft aortoplasty. For fusiform aneurysms, when the distal portion of the arch is a reasonable size, a single, beveled replacement of the lower curvature (hemiarch) is performed. More extensive arch aneurysms require total replacement involving a distal anastomosis to the proximal descending thoracic aorta and separate reattachment of the brachiocephalic branches. The brachiocephalic vessels are reattached to one or more openings made in the graft, or if these vessels are aneurysmal, they are replaced with separate, smaller grafts. Recently, Y-graft approaches to aortic arch repair have been introduced⁷¹ that essentially debranch the brachiocephalic vessels and move them forward. This permits the distal anastomosis to be brought forward and aids in hemostasis. When the aneurysm involves the entire arch and extends into the descending thoracic aorta, it is approached by using Borst’s elephant trunk technique of staged total arch replacement.⁷² The distal anastomosis may be constructed by using a collared graft to accommodate any discrepancy in aortic diameter⁷³ and is performed such that a portion of the graft is left suspended within the proximal descending thoracic aorta (Fig. 22-7). During a subsequent operation, this “trunk” is used to facilitate repair of the descending thoracic aorta through a thoracotomy incision. This technique permits access to the distal portion of the graft during the second operation without the need for dissection around the distal transverse aortic arch; this reduces the risk of injuring the left recurrent laryngeal nerve, esophagus, and pulmonary artery if an open approach is used at the second stage. As described in the section on hybrid repair of arch aneurysms (see later), the elephant trunk can be completed by using a hybrid endovascular approach (Fig. 22-8) in certain settings.

Figure 22-7.

Illustration of a contemporary Y-graft approach to total arch replacement for aortic arch aneurysm. A. The proximal portions of the brachiocephalic arteries are exposed. B. The first two branches of the graft are sewn end-to-end to the transected left subclavian and left common carotid arteries. The proximal ends of the transected brachiocephalic arteries are ligated. C. A balloon-tipped perfusion cannula is placed inside the double Y-graft and used to deliver antegrade cerebral perfusion. After systemic circulatory arrest is initiated, the innominate artery is clamped, transected, and sewn to the distal end of the main graft. D. The proximal aspect of the Y-graft is clamped. This directs flow from the axillary artery to all three brachiocephalic arteries. The arch is then replaced with a collared elephant trunk graft. E. The distal anastomosis between the elephant trunk graft and the aorta is created between the innominate and left common carotid arteries. The collared graft accommodates any discrepancy in aortic diameter. F. The aortic graft is clamped, and a second limb from the arterial inflow tubing of the cardiopulmonary bypass circuit is used to deliver systemic perfusion through a side-branch of the arch graft while the proximal portion of the ascending aorta is replaced. Once the proximal aortic anastomosis is completed, the main trunk of the double Y-graft is cut to an appropriate length, and the beveled end is then sewn to an oval opening created in the right anterolateral aspect of the ascending aortic graft, which completes the repair G. (Adapted from LeMaire et al,⁷³ Fig. 2. Used with permission. Copyright The Society of Thoracic Surgeons.)

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Figure 22-8.

Illustration of Borst’s elephant trunk technique using a contemporary Y-graft approach. A. Stage 1: The proximal repair includes replacing the ascending aorta and entire arch, with Y-graft reattachment of the brachiocephalic vessels. The distal anastomosis is facilitated by using a collared elephant trunk graft to accommodate the larger diameter of the distal aorta. A section of the graft is left suspended within the proximal descending thoracic aorta. B. Stage 2: The distal repair uses the floating “trunk” for the proximal anastomosis. C. An alternate “hybrid” approach may be used in patients with less extensive distal aortic disease. Endovascular stent grafts are placed within the elephant trunk to complete the repair. (Used with permission of Baylor College of Medicine.)

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Cardiopulmonary Bypass Perfusion Strategies

Like the operations themselves, perfusion strategies used during proximal aortic surgery depend on the extent of the repair. Aneurysms that are isolated to the ascending segment can be replaced by using standard cardiopulmonary bypass and distal ascending aortic clamping. This provides constant perfusion of the brain and other vital organs during the repair. Aneurysms involving the transverse aortic arch, however, cannot be clamped during the repair, which necessitates the temporary withdrawal of cardiopulmonary bypass support; this is called circulatory arrest. To protect the brain and other vital organs during the circulatory arrest period, hypothermia must be initiated before pump flow is stopped. However, hypothermia is not without risk, and coagulopathy is associated with deep levels of hypothermia (below 20°C), which have been traditionally used in open arch repair. Recently, more moderate levels of hypothermia (often between 22°C and 24°C) have been introduced that appear to decrease risks associated with deep hypothermia while still providing sufficient brain protection. Nonetheless, although brief periods of circulatory arrest generally are well tolerated, even this recently modified technique continues to have substantial limitations; as the duration of circulatory arrest increases, the well-recognized risks of brain injury and death increase dramatically. Additionally, some authors have raised the concern that reducing the degree of hypothermia narrows the safety margin that deep hypothermia provides, because it increases the risk of ischemic complications involving the spinal cord, kidneys, and other organs that now receive less hypothermic protection.⁷⁴

Because of the inherent complexity of aortic arch repairs and their general tendency to require longer periods of hypothermic circulatory arrest, two cerebral perfusion strategies—retrograde cerebral perfusion (RCP) and antegrade cerebral perfusion (ACP)—were developed to supplement this process by delivering cold, oxygenated blood to the brain and further reduce the risks associated with repair. Retrograde cerebral perfusion involves directing blood from the cardiopulmonary bypass circuit into the brain through the superior vena cava.⁷⁵ However, RCP is thought to be less beneficial than ACP,⁷⁶ and although it may be helpful in the retrograde flushing of air and debris from the arch, most centers have stopped using RCP.

In contrast, ACP delivers blood directly into the brachiocephalic arteries to maintain cerebral flow. Although its use was cumbersome in the past, contemporary ACP techniques (Fig. 22-9) have been simplified and commonly involve cannulating either the right axillary artery or the innominate artery and subsequent connection to the cardiopulmonary bypass circuit.^77,78 Often, a small section of graft is used as a conduit to ease cannulation, but there remains a small procedure-related risk of brachial plexus or vascular injury. Upon initiation, cold blood is delivered into the brain via the right common carotid artery. Note that, with this technique, blood flow to the left side of the brain requires an intact circle of Willis.

Figure 22-9.

Illustration of a contemporary technique for delivering antegrade cerebral perfusion during aortic arch repair. A. A graft sewn to the right axillary artery is used to return oxygenated blood from the cardiopulmonary bypass circuit. B. After adequate hypothermia is established, the innominate artery is occluded with a tourniquet (inset) so that flow is diverted to the right common carotid artery, which maintains cerebral circulation. (Images adapted from Gravlee GP, Davis RF, Stammers AH, et al, eds. Cardiopulmonary Bypass: Principles and Practice, 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2008, Chap. 32, Fig. 1A,B. Copyright Wolters Kluwer Health.)

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Methods to help determine the adequacy of unilateral ACP to deliver cerebral cross-circulation include preoperative imaging and intraoperative monitoring. Our preferred method of intraoperative monitoring is brain near-infrared spectroscopy (NIRS), which measures cerebral oxygenation. If NIRS monitoring indicates inadequate perfusion, an additional perfusion catheter can be inserted into the left common carotid artery to provide blood flow to the left side of the brain. Because of the use of more moderate levels of hypothermia, some groups supplement ACP with additional perfusion strategies that provide flow to the descending aorta during arch repair.^79,80

Endovascular Repair

Experience with purely endovascular treatment of proximal aortic disease remains limited and only investigational. The unique anatomy of the aortic arch and the need for uninterrupted cerebral perfusion pose difficult challenges. There are reports of the use of “homemade” grafts to exclude arch aneurysms; however, these grafts are highly experimental at this time. For example, in 1999, Inoue and colleagues⁸¹ reported placing a triple-branched stent graft in a patient with an aneurysm of the aortic arch. The three brachiocephalic branches were positioned by placing percutaneous wires in the right brachial, left carotid, and left brachial arteries. The patient underwent two subsequent procedures: surgical repair of a right brachial pseudoaneurysm and placement of a distal stent graft extension to control a major perigraft leak. Since then, efforts to employ endovascular techniques in the treatment of the proximal aorta have been essentially limited to the use of approved devices for off-label indications, such as the exclusion of pseudoaneurysms in the ascending aorta.

Hybrid Repair

Unlike purely endovascular approaches, hybrid repairs of the aortic arch have entered the mainstream clinical arena, although they remain controversial. Hybrid arch repairs involve some form of “debranching” of the brachiocephalic vessels (which are not unlike Y-graft approaches), followed by endovascular exclusion of some or all of the aortic arch (Fig. 22-10). Although this technique has many variants, they often involve sewing a branched graft to the proximal ascending aorta with the use of a partial aortic clamp. The branches of the graft are then sewn to the arch vessels. Once the arch is “debranched,” the arch aneurysm can be excluded with an endograft. Commonly, a zone 0 approach (Fig. 22-11) is undertaken, in which the proximal end of the endograft lies between the ascending aorta and the origins of the innominate artery. Other hybrid approaches aim to extend repair into the distal arch and descending thoracic aorta (see later). The arguments for using a hybrid approach to treat aortic arch aneurysms include the elimination of cardiopulmonary bypass, circulatory arrest, and cardiac ischemia, although in practice, these adjuncts are frequently used during hybrid proximal aortic repairs.⁸²

Figure 22-10.

Illustration of a hybrid arch repair. A. A distal arch aneurysm, which extends into the proximal aspect of the descending thoracic aorta, is shown. B. The brachiocephalic vessels are debranched onto a double Y-graft, and a separate graft is used as a conduit for antegrade endovascular deployment of the stent-graft. C. The completed repair. The proximal landing zone of the endograft is within zone 0. (Used with permission from Baylor College of Medicine.)

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Figure 22-11.

Illustration of the Criado landing zones, which are used to describe aortic anatomy during thoracic endovascular repair. The arch is the short segment that includes the origins of the three brachiocephalic arteries—the innominate artery, the left common carotid artery, and the left subclavian artery. Zone 0 includes the ascending aorta and the origin of the innominate artery. Zone 1 includes the origin of the left common carotid artery. Zone 2 includes the left subclavian artery origin. Zone 3 is a short section of the aorta that comprises the 2 cm immediately distal to the origin of the left subclavian artery, and Zone 4 begins where Zone 3 ends. (Used with permission from Baylor College of Medicine.)

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It is not yet clear whether hybrid repairs are as durable as traditional ones because little mid- or long-term data have been published, and no large-scale studies have compared hybrid and traditional repairs. Procedure-related risks include the risk of embolization and stroke due to wire and device manipulation within the aortic arch (this risk appears to be greatest in zone 0 repairs⁸³), retrograde acute aortic dissection,⁸⁴ type I endoleak,⁸⁵ and paraplegia.²⁴ Some centers have begun to replace a small section of the ascending aorta such that the endograft does not land in native aortic tissue, because this may reduce the risk of iatrogenic dissection.⁸⁴ In a recent expert consensus document, the recommendation was to limit direct stenting of the aortic arch to patients who fall into the high surgical risk category. These are patients with significant comorbidities such as chronic pulmonary disease.⁸⁶

Distal Thoracic Aortic Aneurysms

Open Repair

In patients with descending thoracic or thoracoabdominal aortic aneurysms, several aspects of treatment—includingpreoperative risk assessment, anesthetic management, choice of incision, and use of protective adjuncts—are dictated by the overall extent of aortic involvement. By definition, descending thoracic aortic aneurysms involve the portion of the aorta between the left subclavian artery and the diaphragm. Thoracoabdominal aneurysms can involve the entire thoracoabdominal aorta, from the origin of the left subclavian artery to the aortic bifurcation. Surgical repair of thoracoabdominal aortic aneurysms is categorized by the extent of aortic replacement according to the Crawford classification scheme (Fig. 22-12). Extent I thoracoabdominal aortic aneurysm repairs involve most of the descending thoracic aorta, usually beginning near the left subclavian artery, and extend down into the suprarenal abdominal aorta. Extent II repairs also begin near the left subclavian artery but extend distally into the infrarenal abdominal aorta, and they often reach the aortic bifurcation. Extent III repairs extend from the lower descending thoracic aorta (below the sixth rib) and into the abdomen. Extent IV repairs begin at the diaphragmatic hiatus and often involve the entire abdominal aorta.

Figure 22-12.

Illustration of the Crawford classification of thoracoabdominal aortic aneurysm repair based on the extent of aortic replacement. (Reproduced with permission from Coselli et al,²³² Fig. 1. Copyright The Society of Thoracic Surgeons.)

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Descending thoracic aortic aneurysms are repaired through a left thoracotomy. In patients with thoracoabdominal aortic aneurysms, the thoracotomy is extended across the costal margin and into the abdomen. Use of a double-lumen endobronchial tube allows selective ventilation of the right lung and deflation of the left lung. Transperitoneal exposure of the thoracoabdominal aorta is achieved by performing medial visceral rotation and circumferential division of the diaphragm. During a period of aortic clamping, the diseased segment is replaced with a polyester tube graft. Important branch arteries—including intercostal arteries and the celiac, superior mesenteric, and renal arteries—are reattached to openings made in the side of the graft. Visceral and renal artery occlusive disease is commonly encountered during aneurysm repair; options for correcting branch vessel stenosis include endarterectomy, direct arterial stenting, and bypass grafting.

Clamping the descending thoracic aorta causes ischemia of the spinal cord and abdominal viscera. Clinically significant manifestations of hepatic, pancreatic, and bowel ischemia are relatively uncommon. However, both acute renal failure and spinal cord injury resulting in paraplegia or paraparesis remain major causes of morbidity and mortality after these operations. Therefore, several aspects of the operation are devoted to minimizing spinal and renal ischemia (Table 22-3). Our multimodal approach to spinal cord protection includes expeditious repair to minimize aortic clamping time, moderate systemic heparinization (1.0 mg/kg) to prevent small-vessel thrombosis, mild permissive hypothermia (32°C–34°C [89.6°–93.2°F] nasopharyngeal temperature), and reattachment of segmental intercostal and lumbar arteries. As the aorta is replaced from proximal to distal, the aortic clamp is moved sequentially to lower positions along the graft to restore perfusion to newly reattached branch vessels. During extensive thoracoabdominal aortic repairs (i.e., Crawford extent I and II repairs), cerebrospinal fluid drainage is used. The benefits of this adjunct, which improves spinal perfusion by reducing cerebrospinal fluid pressure, have been confirmed in a prospective, randomized trial performed by our group.⁸⁷ Motor evoked potentials are used by some groups to monitor the spinal cord throughout the operation.^88,89 Left heart bypass, which provides perfusion of the distal aorta and its branches during the clamping period, is also used during extensive thoracoabdominal aortic repairs.^90,91,92 Because left heart bypass unloads the heart, it is also useful in patients with poor cardiac reserve. Balloon perfusion cannulas connected to the left heart bypass circuit can be used to deliver blood directly to the celiac axis and superior mesenteric artery during their reattachment. The potential benefits of reducing hepatic and bowel ischemia include reduced risks of postoperative coagulopathy and bacterial translocation, respectively. Whenever possible, renal protection is achieved by perfusing the kidneys with cold (4°C [39.2°F]) crystalloid. In a randomized clinical trial, reduced kidney temperature was found to be associated with renal protection, and the use of cold crystalloid independently predicted preserved renal function.⁹³

Table 22-3Current strategy for spinal cord and visceral protection during repair of distal thoracic aortic aneurysms

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Table 22-3 Current strategy for spinal cord and visceral protection during repair of distal thoracic aortic aneurysms

All extents

• Permissive mild hypothermia (32°C–34°C, nasopharyngeal)

• Moderate heparinization (1 mg/kg)

• Aggressive reattachment of segmental arteries, especially between T8 and L1

• Sequential aortic clamping when possible

• Perfusion of renal arteries with 4°C crystalloid solution when possible

Crawford extent I and II thoracoabdominal repairs

• Cerebrospinal fluid drainage

• Left heart bypass during proximal anastomosis

• Selective perfusion of celiac axis and superior mesenteric artery during intercostal and visceral anastomoses

Hypothermic circulatory arrest can also be used during descending thoracic or thoracoabdominal aortic repairs.⁹⁴ At our center, the primary indication for this approach is the inability to clamp the aorta because of rupture, extremely large aneurysm size, or extension of the aneurysm into the distal transverse aortic arch, or because a prior endovascular repair hinders clamping.⁵⁵

As discussed previously, complete repair of extensive aneurysms involving the ascending aorta, transverse arch, and descending thoracic aorta generally requires staged operations. In such procedures, when the descending or thoracoabdominal component is symptomatic (e.g., causes back pain or has ruptured) or is disproportionately large (compared with the ascending aorta), the distal segment is treated during the initial operation, and repair of the ascending aorta and transverse aortic arch is performed as a second procedure. A reversed elephant trunk repair, in which a portion of the proximal end of the aortic graft is inverted down into the lumen, can be performed during the first operation; this technique facilitates the second-stage repair of the ascending aorta and transverse aortic arch (Fig. 22-13).⁹⁵

Figure 22-13.

Illustration of the reversed elephant trunk technique using a traditional “island” approach to total aortic arch replacement. A. Stage 1: The distal aorta is repaired through a left thoracoabdominal approach. The aneurysm is opened after the aorta is clamped between the left common carotid artery and the left subclavian artery, which is also clamped. Before the proximal anastomosis is performed, the end of the graft is partly invaginated to leave a “trunk” for the subsequent repair. Proximal intercostal arteries are oversewn. B. After the proximal suture line is completed, the clamps are repositioned to restore blood flow to the left subclavian artery. The repair is completed by reattaching patent intercostal arteries to an opening in the side of the graft and creating a beveled distal anastomosis at the level of the visceral branches. C. Stage 2: The proximal aorta is repaired through a median sternotomy. The aortic arch is opened under hypothermic circulatory arrest. The “trunk” is pulled out and used to replace the aortic arch and ascending aorta. This eliminates the need for a new distal anastomosis and simplifies the procedure. Circulatory arrest and operative time, along with their attendant risks, are reduced. D. The completed two-stage repair of the entire thoracic aorta. (Reproduced with permission from Coselli JS, LeMaire SA, Carter SA, et al: The reversed elephant trunk technique used for treatment of complex aneurysms of the entire thoracic aorta. Ann Thorac Surg 2005; 80:2166, Figs. 2, 3, 7,8. Copyright The Society of Thoracic Surgeons.)

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Although spinal cord ischemia and renal failure receive the most attention, several other complications warrant consideration. The most common complication of extensive repairs is pulmonary dysfunction. With aneurysms adjacent to the left subclavian artery, the vagus and left recurrent laryngeal nerves are often adherent to the aortic wall and thus are susceptible to injury. Vocal cord paralysis should be suspected in patients who have postoperative hoarseness, and the presence of nerve damage should be confirmed by endoscopic examination. Vocal cord paralysis can be treated effectively by direct cord medialization (type 1 thyroplasty). Injury to the esophagus during the proximal anastomosis can have catastrophic consequences. Carefully separating the proximal descending thoracic aorta from the underlying esophagus before performing the proximal anastomosis minimizes the risk of a secondary aortoesophageal fistula. In patients who have previously undergone coronary artery bypass with a left internal thoracic artery graft, clamping proximal to the left subclavian artery can precipitate severe myocardial ischemia and cardiac arrest. When the need to clamp at this location is anticipated in these patients, a left common carotid to subclavian bypass is performed to prevent cardiac complications (Fig. 22-14).⁹⁶

Figure 22-14.

Illustration of a thoracoabdominal aortic aneurysm repair in a patient with a patent left internal thoracic artery–to–left anterior descending coronary artery graft. The proximal anastomosis is being performed while the aorta is clamped between the left common carotid and subclavian arteries. Myocardial perfusion is maintained through the carotid-subclavian bypass graft. (Reproduced with permission from Jones et al,⁹⁶ Fig. 2. Copyright The Society of Thoracic Surgeons.)

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Endovascular Repair

Descending Thoracic Aortic Aneurysms

Stent graft repair of descending thoracic aortic aneurysms has become an accepted treatment option for selected patients.⁸⁶ Although aortic repair with a self-fixing endoprosthesis was reported by Volodos⁹⁷ in the mid-1980s, it was the report by Parodi and associates⁹⁸ of using endovascular stent grafting to repair abdominal aortic aneurysms that helped popularize this approach. Only 3 years after this seminal report was published, Dake and colleagues⁹⁹ reported performing endovascular descending thoracic aortic repair with “homemade” stent grafts in 13 patients.

Although endografting was initially approved to treat degenerative descending thoracic aortic aneurysms, recently some newer devices have been approved for use in blunt aortic injury, as well as for penetrating aortic ulcers (see Penetrating Aortic Ulcer discussed later). However, in practice, off-label use of stent-grafts is exceedingly common, and they are frequently used in patients with aortic dissection or ruptured aneurysm. Although the use of stent-grafts in cases of aortic infection is not ideal, patients with fistula or mycotic aneurysm may be treated endovascularly as a bridge to open repair. Reporting standards to uniformly describe the endovascular repair process have been recently introduced,¹⁰⁰ as have guidelines for the use of endovascular repair in thoracic aortic disease.⁴⁰

In elderly patients with severe comorbidity and patients who have undergone previous complex thoracic aortic procedures, endovascular repair is a particularly attractive alternative to standard surgical procedures. The patients tend to have a lower incidence of intraoperative complications, a shorter length of stay, and a higher likelihood of being discharged to home than those who undergo open repair.⁴⁹ As mentioned previously, appropriate patient selection depends on specific measurements taken from preoperative CT angiograms.

To protect patients against spinal cord ischemia during these endovascular repairs, many surgeons use cerebrospinal fluid drainage. The first step in the repair procedure is to obtain appropriate vascular access for the insertion of the thoracic stent graft. If the femoral artery will not accommodate the necessary sheath, then an iliac artery is exposed. A graft can be sewn to the iliac artery in an end-to-side fashion to facilitate the deployment of the endograft. After 5000 to 10,000 units of heparin are administered, a guidewire and the delivery sheath are typically inserted into the access artery under fluoroscopic guidance; recently, sheathless stent-grafts have been introduced, which are less bulky. The endograft is then advanced into the aorta and suitably positioned. Note that the best view of the distal arch and descending thoracic aorta is usually in the left anterior oblique position at an angle of approximately 40 to 50 degrees. The device is then deployed, and the proximal and distal ends are expanded by using a balloon catheter (“ballooned”), which optimizes the seal between the device and the aortic wall at this landing zone. An aortogram is then taken to rule out any endoleak, and protamine is administered.

Although it is not uncommon to cover the left subclavian artery with the endograft to lengthen the proximal landing zone,¹⁰¹ findings suggest that the risk of spinal cord complications is heightened when the subclavian artery is covered and not revascularized, presumably because of a loss of collateral circulation to the spinal cord.¹⁰² To prevent this complication, a carotid-to-subclavian bypass can be easily constructed to maintain vertebral artery blood flow and minimize neurologic injury (Fig. 22-15).^103,104 In addition, new generations of stent grafts are being designed with side branches that can be placed within the left subclavian artery. This feature is particularly attractive if the proximal neck is short or if the patient has a patent left internal thoracic artery–to–left anterior descending coronary artery bypass. Because a significant number of patients have coexisting coronary artery disease, care must be taken to avoid left subclavian artery occlusion in patients with previous coronary surgery unless a carotid-to-subclavian bypass has been performed.

Figure 22-15.

Illustration of a hybrid repair of the proximal descending thoracic aorta. A. The preoperative representation of the aneurysm shows that establishing a 2-cm proximal landing zone for a stent graft will require covering the origin of the left subclavian artery. B. Through a supraclavicular approach, a bypass from the left common carotid artery to the left subclavian artery is performed to reroute circulation and create a landing zone for the stent graft. After the bypass is completed, the left subclavian artery is ligated proximal to the graft. C. In the completed zone 2 hybrid repair, the aneurysm has been excluded successfully by a stent graft that covers the origin of the left subclavian artery, and blood flow to the left vertebral artery and arm is preserved by the bypass graft. (Reproduced with permission from Bozinovski et al,¹⁰³ Figs. 9, 10,11. Copyright The Society of Thoracic Surgeons.)

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Elephant Trunk Completion

In select patients, elephant trunk completion repairs may be done endovascularly (Fig. 22-8C), rather than by an open approach through a thoracotomy.¹⁰⁵ Recall that an elephant trunk is used when an aortic aneurysm extends from the distal arch to the descending thoracic aorta. An endograft can be deployed at the time of elephant trunk construction or during a separate, subsequent procedure.^84,106 When the stent is deployed in a retrograde manner in such a second-stage procedure, the procedure is facilitated by placing radiopaque markers at the end of the elephant trunk during the first-stage procedure. This allows the distal end of the trunk to be identified via fluoroscopy. A guidewire can then be manipulated into the trunk and advanced into the ascending aorta to stabilize it during stent deployment. Note that advancing a wire in retrograde fashion from the femoral artery into the elephant trunk can be challenging. Occasionally, the wire must be advanced in an antegrade fashion from a brachial artery. Variations of this approach include the frozen elephant trunk, but this technique is most commonly used in patients with extensive aortic dissection (see Acute Dissection discussed later).

Thoracoabdominal Aortic Aneurysms

Although endovascular thoracoabdominal aortic aneurysm repair remains experimental, it has been shown to be feasible in a few specialized centers. Endovascular thoracoabdominal aortic aneurysm repairs are quite complex, because at least one of the visceral arteries is incorporated into the repair. The number of visceral branches that need to be addressed varies with the extent of aortic coverage.¹⁰⁷ The types of stent grafts used include fenestrated grafts, reinforced fenestrated grafts, branched or cuffed grafts, modular combinations of grafts, and multilayer stents.¹⁰⁸ Graft fenestrations and branch vessels are typically aligned by using inflatable angioplasty balloons. Procedure time is not insignificant, nor is the amount of contrast medium required to obtain the highly detailed images needed to plan these procedures. In addition, some of the stent grafts used in endovascular thoracoabdominal aortic aneurysm repair are custom-made in advance and thus may take several weeks to obtain; therefore, their use is limited to cases of elective repair.⁸⁴ In efforts to hasten repair and utilize off-the-shelf devices, parallel graft approaches, which use a combination of large- and small-diameter stents, have been reported.¹⁰⁹ And, although some centers now propose distal coverage of the celiac axis¹¹⁰ for extent I thoracoabdominal aortic aneurysm repairs, this potentially risky approach is not widely used.

It should be noted that, like open thoracoabdominal aortic aneurysm repair, endovascular repair carries risks of paraplegia, renal failure, stroke, and death, despite the apparent benefits of its being a less invasive procedure. Notably, reports from centers experienced in endovascular thoracoabdominal aortic repair primarily describe limited extent IV repairs.⁵⁴ For the near future, endovascular thoracoabdominal aortic aneurysm repair should be considered investigational.

Hybrid Repair

As discussed previously, hybrid aortic repairs are extremely heterogeneous. For extensive distal aortic repairs, approaches such as the hybrid elephant trunk (described previously) are not feasible because the aneurysm extends beyond the visceral arteries. However, extensive hybrid thoracoabdominal aortic aneurysm repair^111,112 may be a life-saving option in patients at high surgical risk, such as those who have limited physiologic reserve, are of advanced age, or have significant comorbidities. Hybrid procedures use open surgical techniques to reroute blood supply to the visceral arteries so that their aortic origins can be covered by stent grafts without causing visceral ischemia (see Fig. 22-16). Endovascular methods are then used (either as part of the same procedure or at a later stage) to repair the aortic aneurysm, often with simple tube stent grafts; such devices are more readily available than the customized, modular stent grafts deployed in strictly endovascular repairs. Overall, results for hybrid thoracoabdominal aortic aneurysm repair have been somewhat disappointing.¹¹³ However, a few centers report acceptable outcomes in high-risk patients, particularly when a staged hybrid approach is used.¹¹⁴

Figure 22-16.

Illustration of a hybrid approach—which combines open and endovascular techniques—for repair of an extensive aortic aneurysm. Debranching the arch and thoracoabdominal segments allows the use of a series of endovascular stent grafts to exclude the entire aneurysm.

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Postoperative Considerations

Open Procedures

Aortic anastomoses are often extremely fragile during the early postoperative period. Even brief episodes of postoperative hypertension can disrupt suture lines and precipitate severe bleeding or pseudoaneurysm formation. Therefore, during the initial 24 to 48 hours, meticulous blood pressure control is maintained to protect the integrity of the anastomoses. Generally, we liberally use IV vasoactive agents to keep the mean arterial blood pressure between 80 and 90 mmHg. In patients with extremely friable aortic tissue, such as those with Marfan syndrome, we lower the target range to between 70 and 80 mmHg. It is a delicate balancing act, because one must be mindful of spinal cord perfusion and avoid periods of relative hypotension while maintaining these low pressures.

Endovascular Procedures

As experience with descending thoracic aortic stent grafts continues to accumulate, so too do reports of both early and late complications.^55,115,116 Many of these complications are directly related to manipulation of the delivery system within the iliac arteries and aorta.¹¹⁷ Patients with small, calcified, tortuous iliofemoral arteries are at particularly high risk for life-threatening iliac artery rupture. Although aortic rupture appears to be rare during thoracic stent graft procedures, acute iatrogenic retrograde dissection into the aortic arch and ascending aorta is a relatively common and life-threatening complication that requires emergency repair of the ascending aorta and aortic arch via sternotomy and cardiopulmonary bypass. There are many reports of this complication, and it appears most common in off-label applications⁵⁵ such as hybrid arch approaches⁸⁴ and the treatment of descending thoracic aortic dissection.¹¹⁸ Retrograde proximal dissection converts a localized descending thoracic aortic aneurysm into an acute problem involving the entire thoracic aorta. Of note, retrograde aortic dissection may also occur several months after initial repair.¹¹⁹

Another significant complication of descending thoracic aortic stent grafting is endoleak. An endoleak occurs when there is a persistent flow of blood (visible on radiologic imaging) into the aneurysm sac, and it may occur during the initial procedure or develop over time. Although endoleaks are a relatively common complication,¹²⁰ they are not benign, because they lead to continual pressurization of the sac, which can cause expansion or even rupture. These complications are categorized (Table 22-4) according to the site of the leak.¹⁰⁰ Although all endoleaks may progress such that they can be considered life-threatening, type I and type III endoleaks generally necessitate early and aggressive intervention. Recently published reporting guidelines aid standardized reporting.¹⁰⁰

Table 22-4Classification of and common treatment strategies for endoleak

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Table 22-4 Classification of and common treatment strategies for endoleak

Type I

• Incomplete seal between stent graft and aorta at the proximal landing site (Type Ia), the distal landing site (Type Ib), or branch module, fenestration, or plug (Type Ic)

• Early reintervention to improve seal or conversion to open surgery

Type II

• Retrograde perfusion of sac from excluded collateral arteries

• Surveillance; as-needed occlusion with percutaneous or other interventions

Type III

• Incomplete seal between overlapping stent graft or module (Type IIIa), or tear in graft fabric (Type IIIb)

• Early reintervention to cover gap or tear or conversion to open surgery

Type IV

• Perfusion of sac due to porosity of material

• Surveillance; as-needed reintervention to reline stent graft

Type V

• Expansion of sac with no identifiable source

• Surveillance; as-needed reintervention to reline stent graft

Other complications include stent graft misdeployment, device migration, endograft kinking, and stent-graft infection, including fistula. Although not all complications related to stent grafts are fatal, endovascular repairs should be performed by expert teams qualified to address the variety of problems that may arise; some patients may need to have these devices removed and replaced with polyester grafts.^55,115,116 Complications of endovascular repair are relatively common, so regularly scheduled radiologic imaging surveillance is of the utmost importance.

AORTIC DISSECTION

Listen

Pathology and Classification

Aortic dissection, the most common catastrophic event involving the aorta, is a progressive separation of the aortic wall layers that usually occurs after a tear forms in the intima and inner media. As the separation of the layers of the media propagates, at least two channels form (Fig. 22-17): the original lumen, which remains lined by the intima and which is called the true lumen, and the newly formed channel within the layers of the media, which is called the false lumen. The dissecting membrane separates the true and false lumens. Additional tears in the dissecting membrane that allow communication between the two channels are called reentry sites. Although the separation of layers primarily progresses distally along the length of the aorta, it can also proceed in a proximal direction; this process often is referred to as proximal extension or retrograde dissection.

Figure 22-17.

Illustration of longitudinal sections of the aortic wall and lumen. Blood flows freely downstream in normal aortic tissue. In classic aortic dissection, blood entering the media through a tear creates a false channel in the wall. Intramural hematomas arise when hemorrhage from the vasa vasorum causes blood to collect within the media; the intima is intact. Penetrating aortic ulcers are deep atherosclerotic lesions that burrow into the aortic wall and allow blood to enter the media. In each of these conditions, the outer aortic wall is severely weakened and prone to rupture.

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The extensive disruption of the aortic wall has severe anatomic consequences (Fig. 22-18). First, the outer wall of the false lumen is extremely thin, inflamed, and fragile, which makes it prone to expansion or rupture in the face of ongoing hemodynamic stress. Second, the expanding false lumen can compress the true lumen and cause malperfusion syndrome by interfering with blood flow in the aorta or any of its branch vessels, including the coronary, carotid, intercostal, visceral, renal, and iliac arteries. Finally, when the separation of layers occurs within the aortic root, the aortic valve commissures can become unhinged, which results in acute valvular regurgitation. The clinical consequences of each of these sequelae are addressed in detail in the section on clinical manifestations.

Figure 22-18.

Illustration of the potential anatomic consequences of aortic dissection, with a mapped diagram of affected regions (inset). A. Ascending aortic rupture and cardiac tamponade. B. Disruption of coronary blood flow. C. Injury to the aortic valve causing regurgitation. D, E, and F. Compromised blood flow to branch vessels, causing ischemic complications. (Images adapted from Creager MA, Dzau VS, Loscalzo J, eds. Vascular Medicine. Philadelphia: WB Saunders; 2006. Copyright © Saunders/Elsevier, 2006. Fig. 35-1.)

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Dissection vs. Aneurysm

The relationship between dissection and aneurysmal disease requires clarification. Dissection and aneurysm are separate entities, although they often coexist and are mutual risk factors. In most cases, dissection occurs in patients without aneurysms. The subsequent progressive dilatation of the weakened outer aortic wall results in an aneurysm. On the other hand, in patients with degenerative aneurysms, the ongoing deterioration of the aortic wall can lead to a superimposed dissection. The overused term dissecting aneurysm should be reserved for this specific situation.

Classification

For management purposes, aortic dissections are classified according to their location and chronicity. Improvements in imaging have increasingly revealed variants of aortic dissection that probably represent different forms along the spectrum of this condition.

Location

To guide treatment, dissections are categorized according to their anatomic location and extent. The two traditional classification schemes that remain in common use are the DeBakey and the Stanford classification systems (Fig. 22-19).^121,122 In their current forms, both of these schemes describe the segments of aorta that are involved in the dissection, rather than the site of the initial intimal tear. The main drawback of the Stanford classification system is that it does not distinguish between patients with isolated ascending aortic dissection and patients with dissection involving the entire aorta. Both types of patients would be classified as having type A dissections, despite the fact that their treatment, follow-up, and prognosis are substantially different.

Figure 22-19.

Illustration of the classification schemes for aortic dissection based on which portions of the aorta are involved. Dissection can be confined to the ascending aorta (left) or descending aorta (middle), or it can involve the entire aorta (right). (Reproduced with permission from Creager MA, Dzau VS, Loscalzo J, eds. Vascular Medicine. Philadelphia: WB Saunders; 2006. Copyright © Saunders/Elsevier, 2006, Fig. 35-2).

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Additional classification schemas include that by Borst and associates,¹²³ in which the ascending and descending aorta are considered independently; the recent modification of the DeBakey classification by Tsagakis et al,¹²⁴ which extends type II dissection into the aortic arch; and the Penn modification of the Stanford classification,^125,126 which expands the classification to include the presence of tissue and global malperfusion. These modifications may help to better streamline the primary surgical intervention; patients with isolated proximal aortic dissection usually undergo emergent operation, as do patients with both proximal and distal aortic dissection. Patients with isolated distal aortic dissection are typically treated medically, unless complications requiring surgery develop. Additionally, these changes are reflective of a shift in some aortic centers from the more traditional approach that is primarily focused on emergent surgical repair of the ascending aorta toward one that, in select patients, additionally treats distal dissection entry points with off-label endovascular therapy.¹²⁷

Chronicity

Aortic dissection also is categorized according to the time elapsed since the initial tear. Dissection is considered acute within the first 14 days after the initial tear; after 14 days, the dissection is considered chronic. Although arbitrary, the distinction between acute and chronic dissections has important implications, not only for decision-making about perioperative management strategies and operative techniques, but also for evaluating surgical results. Figure 22-20 provides an algorithm for the management of acute aortic dissection. In light of the importance of acuity, Borst and associates¹²³ have proposed a third phase—termed subacute—to describe the transition between the acute and chronic phases. The subacute period encompasses days 15 through 60 after the initial tear. Although this is past the traditional 14-day acute phase, patients with subacute dissection continue to have extremely fragile aortic tissue, which may complicate operative treatment and increase the risks associated with surgery.

Variants

As noted earlier, advancements in noninvasive imaging of the aorta have revealed variants of aortic dissection (see Fig. 22-17). The recently introduced term acute aortic syndrome encompasses classic aortic dissection and its variants. Other aortic syndromes, which were once thought to be rare, include intramural hematoma (IMH) and penetrating aortic ulcer (PAU). Although the issue is somewhat controversial, the current consensus is that, in most cases, these variants of dissection should be treated identically to classic dissection.

An IMH is a collection of blood within the aortic wall, without an intimal tear, that is believed to be due to rupture of the vasa vasorum within the media. The accumulation of blood can result in a secondary intimal tear that ultimately leads to a dissection.¹²⁸ Because IMH and aortic dissection represent a continuum, it is possible that IMH is seen less frequently than aortic dissection because IMH rapidly progresses to true dissection. The prevalence of IMH among patients with acute aortic syndromes is approximately 6%, and 16% progress to full dissection.¹²⁹ An IMH can be classified according to its location (i.e., ascending or descending) and should be treated analogously to classic dissection.¹³⁰

A PAU is essentially a disrupted atherosclerotic plaque that projects into the aortic wall and is associated with surrounding hematoma. Eventually, the ulcer can penetrate the aortic wall, which leads to dissection or rupture. The rate of disease progression is higher than that of IMH alone.¹³¹

Causes and Clinical History

Aortic dissection is a lethal condition with a reported incidence of 3.5 per 100,000 in the United States.¹³² Without appropriate modern medical or surgical treatment, most patients (approximately 90%) die within 3 months of dissection, mostly from rupture.^133,134

Although several risk factors for aortic dissection have been identified, the specific causes remain unknown. Ultimately, any condition that weakens the aortic wall increases the risk of aortic dissection. Common general cardiovascular risk factors, such as smoking, hypertension, atherosclerosis, and hypercholesterolemia, are associated with aortic dissection. Patients with connective tissue disorders, aortitis, bicuspid aortic valve, or preexisting medial degenerative disease are at risk for dissection, especially if they already have a thoracic aortic aneurysm.²¹ Aortic injury during cardiac catheterization, surgery, or endovascular aortic repair is a common cause of iatrogenic dissection. Other conditions that are associated with aortic dissection include cocaine and amphetamine abuse,¹³⁵ as well as severe emotional stress or extreme physical exertion such as during weightlifting.¹³⁶ Advances in the understanding of the molecular mechanisms behind abdominal aortic aneurysms have prompted similar investigations of thoracic aortic dissection.^137,138,139

Clinical Manifestations

The onset of dissection often is associated with severe chest or back pain, classically described as “tearing,” that migrates distally as the dissection progresses along the length of the aorta. The location of the pain often indicates which aortic segments are involved. Pain in the anterior chest suggests involvement of the ascending aorta, whereas pain in the back and abdomen generally indicates involvement of the descending and thoracoabdominal aorta. Additional clinical sequelae of acute aortic dissection vary substantially and are best considered in terms of the dissection’s potential anatomic manifestations at each level of the aorta (see Fig. 22-18 and Table 22-5). Thus, potential complications of dissection of the aorta (and involved secondary arteries) may include cardiac ischemia (coronary artery) or tamponade, stroke (brachiocephalic arteries), paraplegia or paraparesis (intercostal arteries), mesenteric ischemia (superior mesenteric artery), kidney failure (renal arteries), and limb ischemia or loss of motor function (brachial or femoral arteries).

Table 22-5Anatomic complications of aortic dissection and their associated symptoms and signs

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Table 22-5 Anatomic complications of aortic dissection and their associated symptoms and signs

ANATOMIC MANIFESTATION

SYMPTOMS AND SIGNS

Aortic valve insufficiency

Dyspnea

Murmur

Pulmonary rales

Shock

Coronary malperfusion

Chest pain with characteristics of angina

Nausea/vomiting

Shock

Ischemic changes on electrocardiogram

Elevated cardiac enzymes

Pericardial tamponade

Dyspnea

Jugular venous distension

Pulsus paradoxus

Muffled cardiac tones

Shock

Low-voltage electrocardiogram

Subclavian or iliofemoral artery malperfusion

Cold, painful extremity

Extremity sensory and motor deficits

Peripheral pulse deficit

Carotid artery malperfusion

Syncope

Focal neurologic deficit (transient or persistent)

Carotid pulse deficit

Coma

Spinal malperfusion

Paraplegia

Incontinence

Mesenteric malperfusion

Nausea/vomiting

Abdominal pain

Renal malperfusion

Oliguria or anuria

Hematuria

Ascending aortic dissection can directly injure the aortic valve, causing regurgitation. The severity of the regurgitation varies with the degree of commissural disruption, which ranges from partial separation of only one commissure, producing mild valvular regurgitation, to full separation of all three commissures and complete prolapse of the valve into the left ventricle, producing severe acute heart failure. Patients with acute aortic valve regurgitation may report worsening dyspnea.

Ascending dissections also can extend into the coronary arteries or shear the coronary ostia off of the true lumen, causing acute coronary occlusion; when this occurs, it most often involves the right coronary artery. The sudden disruption of coronary blood flow can cause a myocardial infarction. This presentation of acute myocardial ischemia can mask the presence of aortic dissection, which results in delayed diagnosis and treatment.¹⁴⁰

The thin and inflamed outer wall of a dissected ascending aorta often produces a serosanguineous pericardial effusion that can accumulate and cause tamponade. Suggestive signs include jugular venous distention, muffled heart tones, pulsus paradoxus, and low-voltage electrocardiogram (ECG) tracings. Free rupture into the pericardial space produces rapid tamponade and is generally fatal.

As the dissection progresses, any branch vessel from the aorta can become involved, which results in compromised blood flow and ischemic complications (i.e., malperfusion). Therefore, depending on which arteries are involved, the dissection can produce acute stroke, paraplegia, hepatic failure, bowel infarction, renal failure, or a threatened ischemic limb.

Diagnostic Evaluation

Because of the variations in severity and the wide variety of potential clinical manifestations, the diagnosis of acute aortic dissection can be challenging.^141,142,143 Only 3 out of every 100,000 patients who present to an emergency department with acute chest, back, or abdominal pain are eventually diagnosed with aortic dissection. Not surprisingly, diagnostic delays are common; delays beyond 24 hours after hospitalization occur in up to 39% of cases. Unfortunately, delays in diagnosis lead to delays in treatment, which can have disastrous consequences. The European Society of Cardiology Task Force on Aortic Dissection stated, “The main challenge in managing acute aortic dissection is to suspect and thus diagnose the disease as early as possible.”¹⁴¹ A recent study by the International Registry of Acute Aortic Dissection examined the reasons for delayed diagnosis and found that diagnosis lagged in women, as well as in patients with atypical symptoms, such as fever or mild pain (rather than severe pain).¹⁴⁰ A high index of suspicion is critical, particularly in younger, atypical patients, who may have connective tissue disorders or other, less common risk factors.

Most patients with acute aortic dissection (80%–90%) experience severe pain in the chest, back, or abdomen.^141,142,143 The pain usually occurs suddenly, has a sharp or tearing quality, and often migrates distally as the dissection progresses along the aorta. For classification purposes (acute vs. subacute vs. chronic), the onset of pain is generally considered to represent the beginning of the dissection process. Most of the other common symptoms either are nonspecific or are caused by the secondary manifestations of dissection.

A discrepancy between the extremities in pulse, blood pressure, or both is the classic physical finding in patients with aortic dissection. It often occurs because of changes in flow in the true and false lumens, and it does not necessarily indicate extension into an extremity branch vessel. Involvement of the aortic arch often creates differences between the right and left arms, whereas descending aortic dissection often causes differences between the upper and lower extremities. Like symptoms, most of the physical signs after dissection are related to the secondary manifestations and therefore vary considerably (Table 22-5). For example, signs of stroke or a threatened ischemic limb may dominate the physical findings in patients with carotid or iliac malperfusion, respectively.

Unfortunately, laboratory studies are of little help in diagnosing acute aortic dissection. There has been continued interest in using D-dimer level to aid in making this diagnosis.¹⁴⁴ Several reports indicate that D-dimer is an extremely sensitive indicator of acute aortic dissection; elevated levels are found in approximately 97% of affected patients.¹⁴⁵ Tests that are commonly used to detect acute coronary events—including ECG and tests for serum markers of myocardial injury—deserve special consideration and need to be interpreted carefully. Normal ECGs and serum marker levels in patients with acute chest pain should raise suspicion about the possibility of aortic dissection. It is important to remember that ECG changes and elevated serum marker levels associated with myocardial infarction do not exclude the diagnosis of aortic dissection, because dissection can cause coronary malperfusion. Of note, abnormal ECGs have recently been shown to delay the diagnosis of aortic dissection, and the possibility of aortic dissection should not be prematurely ruled out.^140,146 Similarly, although CXRs may show a widened mediastinum or abnormal aortic contour, up to 16% of patients with dissection have a normal-appearing CXR.¹⁴² The value of the CXR for detecting aortic dissection is limited, with a sensitivity of 67% and a specificity of 86%.¹⁴⁷

Once the diagnosis of dissection is considered, the thoracic aorta should be imaged with CT, MRA, or echocardiography. The accuracy of these noninvasive imaging tests has all but eliminated the need for diagnostic aortography in most patients with suspected aortic dissection. Currently, the diagnosis of aortic dissection is usually established with contrast-enhanced CT, which has a sensitivity of 98% and a specificity of 87%, and, acquires images swiftly.¹⁴⁸ The classic diagnostic feature is a double-lumen aorta (Fig. 22-21). In addition, CT scans provide essential information about the segments of the aorta involved; the acuity of the dissection; aortic dilatation, including the presence of preexisting degenerative aneurysms; and the development of threatening sequelae, including pericardial effusion, early aortic rupture, and branch vessel compromise. Although MRA also provides excellent imaging (with both a sensitivity and specificity of 98%), the MR suite is not well suited for critically ill patients. In patients who cannot undergo contrast-enhanced CT or MRA, transthoracic echocardiography can be used to establish the diagnosis.

Transesophageal echocardiography (TEE) is excellent for detecting dissection, aneurysm, and IMH in the ascending aorta. In appropriate hands, TEE has a demonstrated sensitivity and specificity as high as 98% and 95%, respectively.¹⁴⁹ Furthermore, TEE offers important information about ventricular function and aortic valve competency. Finally, TEE is the diagnostic modality of choice for hemodynamically unstable patients in whom the diagnosis of ascending dissection is suspected; ideally, these patients should be taken to the operating room, where the TEE can be performed and, if the TEE is confirmatory, surgery can be started immediately.

In selected patients with ascending aortic dissection (i.e., those who have evidence of preexisting coronary artery disease), coronary angiography can be considered before surgery. Specific relative indications in these patients include a history of angina or myocardial infarction, a recent myocardial perfusion study with abnormal results, previous coronary artery bypass or angioplasty, and acute ischemic changes on ECG. Contraindications include hemodynamic instability, aortic rupture, and pericardial effusion.¹⁵⁰ In our practice, patients with acute aortic dissections rarely undergo coronary angiography. However, all patients presenting for elective repair of chronic ascending dissections have diagnostic coronary angiograms taken.

Of note, when malperfusion of the renal, visceral, or lower extremity arteries develops, the patient is usually treated in an angiography suite or hybrid operating room.¹²⁷ Although the dissection usually is diagnosed on CT scan, these patients also undergo aortography, during which the mechanism of the malperfusion is ascertained and, if possible, corrected. Hence, catheter-based aortography may be obsolete as a diagnostic test for dissection, but it remains beneficial for patients with malperfusion.

Treatment

Initial Assessment and Management

Regardless of the location of the dissection, the initial treatment is the same for all patients with suspected or confirmed acute aortic dissection (see Fig. 22-20). Furthermore, because of the potential for rupture before the diagnosis is confirmed, aggressive pharmacologic management is started once there is clinical suspicion of dissection, and this treatment is continued during the diagnostic evaluation. The goals of pharmacologic treatment are to stabilize the dissection and prevent rupture.

Figure 22-20.

Algorithm used to facilitate decisions regarding treatment of acute aortic dissection. CT = computed tomography; MRA = magnetic resonance angiography; TEE = transesophageal echocardiography.

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Figure 22-21.

Computed tomographic scans showing that the aorta has been separated into two channels—the true (T) and false (F) lumens—in two patients with different phases of aortic dissection. A. An acute DeBakey type I aortic dissection. The dissecting membrane appears wavy (arrows) in the early phase of dissection. Here, the true lumen of the proximal aorta can be seen to be extensively compressed. This may lead to malperfusion of the heart. B. A chronic DeBakey type III aortic dissection. In the chronic phase, the membrane appears straighter and less mobile (arrow) because it has stabilized over time. (Used with permission of Baylor College of Medicine.)

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Patients are monitored closely in an intensive care unit. Indwelling radial arterial catheters are used to monitor blood pressure and optimize titration of antihypertensive agents. In cases of limb malperfusion, blood pressures in the affected limb can underrepresent the central aortic pressure; therefore, blood pressure is measured in the arm with the better pulse. Central venous catheters ensure reliable IV access for delivering vasoactive medications. Pulmonary artery catheters are reserved for patients with severe cardiopulmonary dysfunction.

In addition to confirming the diagnosis of dissection and defining its acuity and extent, the initial evaluation focuses on determining whether any of several life-threatening complications are present. Particular attention is paid to changes in neurologic status, peripheral pulses, and urine output. Serial laboratory studies—including arterial blood gas concentrations, complete blood cell count, prothrombin and partial thromboplastin times, and serum levels of electrolytes, creatinine, blood urea nitrogen, and liver enzymes—are useful for detecting organ ischemia and optimizing management.

The initial management strategy, commonly described as anti-impulse therapy or blood pressure control, focuses on reducing aortic wall stress, the force of left ventricular ejection, chronotropy, and the rate of change in blood pressure (dP/dT). Reductions in dP/dT are achieved by lowering both cardiac contractility and blood pressure. The drugs initially used to accomplish these goals include IV beta-adrenergic blockers, direct vasodilators, calcium channel blockers, and angiotensin-converting enzyme inhibitors. These agents are used to achieve a heart rate between 60 and 80 bpm, a systolic blood pressure between 100 and 110 mmHg, and a mean arterial blood pressure between 60 and 75 mmHg. These hemodynamic targets are maintained as long as urine output remains adequate and neurologic function is not impaired. Achieving adequate pain control with IV opiates, such as morphine and fentanyl, is important for maintaining acceptable blood pressure control.

Beta antagonists are administered to all patients with acute aortic dissections unless there are strong contraindications, such as severe heart failure, bradyarrhythmia, high-grade atrioventricular conduction block, or bronchospastic disease. Esmolol can be useful in patients with bronchospastic disease because it is a cardioselective, ultrafast-acting agent with a short half-life. Labetalol, which causes both nonselective beta blockade and postsynaptic alpha₁-blockade, reduces systemic vascular resistance without impairing cardiac output. Doses of beta antagonists are titrated to achieve a heart rate of 60 to 80 bpm. In patients who cannot receive beta antagonists, calcium channel blockers such as diltiazem are an effective alternative. Nitroprusside, a direct vasodilator, can be administered once beta blockade is adequate. When used alone, however, nitroprusside can cause reflex increases in heart rate and contractility, elevated dP/dT, and progression of aortic dissection. Enalapril and other angiotensin-converting enzyme inhibitors are useful in patients with renal malperfusion. These drugs inhibit renin release, which may improve renal blood flow.

Treatment of Ascending Aortic Dissection

Acute Dissection

Because of the risk of aortic rupture, acute ascending aortic dissection is usually considered an absolute indication for emergency surgical repair. However, specific patient groups may benefit from nonoperative management or delayed operation.¹⁵¹ Delayed repair should be considered for patients who (a) present with severe acute stroke or mesenteric ischemia, (b) are elderly and have substantial comorbidity, (c) are in stable condition and may benefit from transfer to specialized centers, or (d) have undergone a cardiac operation in the remote past. Regarding the last group, it is important that the previous operation not be too recent; dissections that occur during the first 3 weeks after cardiac surgery pose a high risk of rupture and tamponade, and such dissections warrant early operation.¹⁵²

In the absence of the circumstances listed earlier, most patients with acute ascending aortic dissection undergo emergent graft replacement of the ascending aorta. Operative repair is similar to that for aneurysm of the transverse aortic arch (described previously) because hypothermic circulatory arrest is commonly used regardless of the extent of repair. Immediately before the operation begins, intraoperative TEE is commonly performed to further assess baseline myocardial and valvular function and, if necessary, to confirm the diagnosis. The operation is performed via a median sternotomy with cardiopulmonary bypass and hypothermic circulatory arrest (Fig. 22-22). In preparation for circulatory arrest, cannulas are placed in the right axillary artery (to provide arterial inflow) and in the right atrium (to provide venous drainage).⁷⁷ After an appropriate level of cooling has been achieved (usually between 22°C and 24°C), cardiopulmonary bypass is stopped, and the ascending aorta is opened. The innominate artery is then occluded with a clamp or snare, and flow from the axillary artery cannula is used to provide ACP. A separate perfusion catheter can be placed in the left common carotid artery to ensure perfusion of the left side of the brain. This strategy of performing the distal anastomosis during a brief period of circulatory arrest, often termed open distal anastomosis, obviates the need to place a clamp across the fragile aorta, avoiding further aortic damage. Also, it allows the surgeon to carefully inspect the aortic arch for intimal tears. Traditionally, the entire arch is replaced only if a primary intimal tear is located in the arch or if the arch is aneurysmal; most commonly, repair is limited to replacement of the entire ascending aorta or to a beveled “hemiarch” repair.¹⁵³ Conservative repair has been shown to increase the likelihood of early survival.¹⁵⁴ The distal aortic cuff is prepared by tacking the inner and outer walls together and using surgical adhesive to obliterate the false lumen and strengthen the tissue. A polyester tube graft is sutured to the distal aortic cuff. The anastomosis between the graft and the aorta is fashioned so that blood flow will be directed into the true lumen; this often alleviates any distal malperfusion problems that were present preoperatively. After the distal anastomosis is reinforced with additional adhesive, the graft is de-aired and clamped, full cardiopulmonary bypass is resumed, rewarming is initiated, and the proximal portion of the repair is started. In the absence of annuloaortic ectasia or connective tissue disorders—which generally necessitate aortic root replacement—aortic valve regurgitation can be corrected by resuspending the commissures onto the outer aortic wall.¹⁵⁵ The proximal aortic cuff is prepared with tacking sutures and surgical adhesive before the proximal aortic anastomosis is performed.

Figure 22-22.

Illustration of proximal aortic repair for acute ascending aortic dissection. A. This repair requires a median sternotomy and cardiopulmonary bypass. The ascending aorta is opened during hypothermic circulatory arrest, while antegrade cerebral perfusion is delivered via an axillary artery graft (see Fig. 22-8). B. The dissecting membrane is removed to expose the true lumen. C. Surgical adhesive is used to obliterate the false lumen and strengthen the aorta for the distal anastomosis. A 30-mL balloon catheter is placed in the true lumen to compress the distal false lumen; this helps keep the adhesive (which strengthens the repair) within the proximal false lumen and prevents distal embolization of the adhesive through re-entry sites. A moist gauze sponge is placed in the true lumen to prevent the adhesive from running into the brachiocephalic vessels. D. An open distal anastomosis prevents clamp injury of the arch tissue and allows inspection of the arch lumen. A balloon perfusion catheter in the left common carotid artery ensures antegrade perfusion of the left cerebral circulation. If the origin of the dissection (i.e., intimal tear or disruption) does not extensively involve the greater curvature of the aortic arch, and if there is no evidence of a preexisting arch aneurysm, a beveled, hemi-arch repair is carried out, preserving most of the greater curvature of the arch. The aorta is transected, beginning at the greater curvature immediately proximal to the origin of the innominate artery and extending distally toward the lesser curvature to the level of the left subclavian artery. Consequently, most of the transverse aortic arch, except for the dorsal segment containing the brachiocephalic arteries, is removed. An appropriately sized, sealed (with collagen or gelatin) Dacron tube graft is selected, and the beveled distal anastomosis is made with continuous 3-0 or 4-0 monofilament suture. E. After the anastomosis is covered with additional adhesive and cardiopulmonary bypass is resumed, the aortic valve is assessed. Disrupted commissures are resuspended with pledgeted mattress sutures to restore valvular competence. F. The aorta is generally transected at the sinotubular junction, and adhesive is used to obliterate the false lumen within the proximal aortic stump. A moist gauze sponge is placed within the true lumen to prevent the adhesive from injuring the aortic valve leaflets or entering the coronary artery ostia. G. After the adhesive has set, the proximal anastomosis is carried out at the sinotubular junction, incorporating the distal margin of the commissures. (Reproduced with permission from Creager MA, Dzau VS, Loscalzo J, eds. Vascular Medicine. Philadelphia: WB Saunders; 2006. Copyright © Saunders/Elsevier, 2006, Fig. 35-3A–G.)

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In the majority of patients who undergo surgical repair of acute ascending dissection, the dissection persists distal to the site of the operative repair; the residually dissected aorta, which generally includes at least a portion of the transverse aortic arch as well as a large portion of the distal aorta, is susceptible to dilatation over time. Extensive dilatation of the arch or distal aorta develops in 25% to 40% of survivors^156,157 and often necessitates further aortic repair. Additionally, long-term survival after acute proximal aortic dissection is generally poor, and rupture of the dilated distal aorta is a common cause of late death in these patients.^{154,156,157,158}

The challenges that survivors of acute proximal aortic dissection commonly face over time have led to the development of alternate acute dissection strategies such as total arch replacement¹⁵⁹ and hybrid arch strategies to extend proximal aortic repair into the distal aorta. The goal of hybrid arch approaches in acute dissection is to thrombose the residual false lumen by compressing it with the radial force that is exerted by a stent-graft placed in the true lumen, thereby facilitating remodeling and preventing late aneurysm formation.¹⁶⁰ However, in such repairs, the compressed false lumen may continue to be perfused in a retrograde fashion.

In Europe, Japan, and elsewhere, one-piece hybrid prostheses are now available that incorporate a polyester graft for the proximal repair and a stent-graft component for the descending aorta. These devices are deployed in an antegrade fashion after the arch has been resected; this procedure is termed a “frozen elephant trunk” repair.¹⁶¹ In the United States, such devices are unavailable, so this repair is commonly done by concomitantly deploying a commercially available stent-graft in an antegrade fashion after fully or partly¹⁶² replacing the ascending aorta and aortic arch. In some variations of this off-label approach, the stent-graft is directly sutured to the distal aspect of the proximal open repair, whereas in others, there may be a gap of native tissue between the open and endovascular repair. Although this technique appears to be extensively used outside the United States, and with early and midterm success,^{160,163,164,165} only a few U.S. reports describe its use.^162,166,167 Emerging reports describe an enhanced risk of spinal cord ischemia, a risk that is not usually associated with open arch repair. This is probably due to the extensive coverage of the intercostal vessels by the stent-graft. Uncertainties in the frozen elephant trunk procedure need to be addressed before it becomes a standard recommendation for this subset of patients.¹⁶⁸

Chronic Dissection

Occasionally, patients with ascending aortic dissection present for repair in the chronic phase. In most respects, the operation is similar to that for acute dissection repair. One notable difference is that the tissue is stronger in chronic dissection than in acute dissection, which makes suturing safer. In addition, the false lumen is not obliterated at the distal anastomosis; instead, the dissecting membrane is fenestrated into the arch to ensure perfusion of both lumens and to prevent postoperative malperfusion complications. Unlike operations for acute dissection, operations for chronic dissection are often aggressive repairs that extend into the arch and root, because the tissues are much less fragile.

Treatment of Descending Aortic Dissection

Nonoperative Management

Nonoperative, pharmacologic management of acute descending aortic dissection results in lower morbidity and mortality rates than traditional surgical treatment does.¹⁴² The most common causes of death during nonoperative treatment are aortic rupture and end-organ malperfusion. Therefore, patients are continually reassessed for new complications. At least two serial CT scans—usually obtained on day 2 or 3 and on day 8 or 9 of treatment—are compared with the initial scan to rule out significant aortic expansion.

Once the patient’s condition has been stabilized, pharmacologic management is gradually shifted from IV to oral medications. Oral therapy, which usually includes a beta antagonist, is initiated when systolic pressure is consistently between 100 and 110 mmHg and the neurologic, renal, and cardiovascular systems are stable. Many patients can be discharged after their blood pressure is well controlled with oral agents and after serial CT scans confirm the absence of aortic expansion.

Long-term pharmacologic therapy is important for patients with chronic aortic dissection. Beta blockers remain the drugs of choice.¹⁶⁹ In a 20-year follow-up study, DeBakey and colleagues¹⁷⁰ found that inadequate blood pressure control was associated with late aneurysm formation. Aneurysms developed in only 17% of patients with “good” blood pressure control, compared with 45% of patients with “poor” control.

Aggressive imaging follow-up is recommended for all patients with chronic aortic dissection.¹⁷¹ Both contrast-enhanced CT and MRA scans provide excellent aortic imaging and facilitate serial comparisons to detect progressive aortic expansion. The first surveillance scan is obtained approximately 6 weeks after the onset of dissection. Subsequent scans are obtained at least every 3 months for the first year, every 6 months for the second year, and annually thereafter. Scans are obtained more frequently in high-risk patients, such as those with Marfan syndrome, and in those in whom significant aortic expansion is detected. For patients who have undergone graft repair of descending aortic dissection, annual CT or MRA scans are also obtained to detect false aneurysm formation or dilatation of unrepaired segments of aorta. Early detection of worrisome changes allows timely, elective intervention before rupture or other complications develop; rupture of the distal aorta is relatively common in patients with chronic aortic dissection and often results in death.¹⁵⁸

Indications for Surgery

In the acute phase, surgery has been traditionally reserved for patients who experience complications.¹⁷² In general terms, such intervention is intended to prevent or repair ruptures and relieve life-threatening ischemic manifestations.

During the acute phase of a dissection, the specific indications for operative intervention include aortic rupture, increasing periaortic or pleural fluid volume, rapidly expanding aortic diameter, uncontrolled hypertension, and persistent pain despite adequate medical therapy. Aortic rupture may be contained by nearby tissues (such as a localized periaortic hematoma detected on imaging studies) or it may be free and uncontained (presenting as a hemothorax, hemoperitoneum, or massive retroperitoneal hematoma accompanied by shock). Acute dissection superimposed on a preexisting aneurysm is considered a life-threatening condition and is therefore another indication for operation. Finally, patients who have a history of noncompliance with medical therapy may ultimately benefit more from surgical treatment if they are otherwise reasonable operative candidates.

Acute malperfusion syndromes also warrant intervention. In the recent past, visceral and renal malperfusion were considered indications for operation. Percutaneous interventions, however, have largely replaced open surgery for treatment of these complications. When the endovascular approach is unavailable or unsuccessful, surgical options can be used.

In the chronic phase, the indications for operative intervention for aortic dissections are similar to those for degenerative thoracic aortic aneurysms, although a slightly lower threshold of repair is now recommended. Guidelines for thoracic aortic disease⁴⁰ recommend elective operation in otherwise healthy patients when the affected segment has reached a diameter of 5.5 cm, especially in patients with connective tissue disorders. Rapid aortic enlargement (>1 cm per year) and other factors that increase the likelihood of aortic rupture may also be considered.

Endovascular Treatment

Malperfusion Syndrome

Endovascular therapy is routinely used in patients with descending aortic dissection complicated by visceral malperfusion.¹⁷³ Abdominal malperfusion syndrome often is fatal; prompt identification of visceral ischemia and expedited treatment to restore hepatic, gastrointestinal, and renal perfusion are imperative for a positive outcome. As described in a later section, several open surgical techniques can be used to re-establish blood flow to compromised organs. However, in acute cases, open surgery is associated with poor outcomes. Therefore, endovascular intervention is the preferred initial approach in such cases. In one endovascular technique known as endovascular fenestration, a balloon is used to create a tear in the dissection flap, which allows blood to flow in both the true and false lumens. This technique can be used when a visceral branch is being supplied by an underperfused true or false lumen. Placement of a stent graft in the true lumen of the aorta can resolve a “dynamic” malperfusion. Occasionally, a small stent must be placed directly in the lumen of a visceral or renal artery because the dissection has propagated into the branch, resulting in “static” malperfusion at the origin.

Iliofemoral malperfusion causing limb-threatening leg ischemia also can be treated via an endovascular approach. However, direct surgical revascularization—usually by placing a femoral-to-femoral arterial bypass graft—is a better option whenever the endovascular procedure cannot be performed expeditiously.

Acute Dissection

Although surgery has been traditionally recommended for patients with complicated acute descending aortic dissection, many centers have shifted toward using endovascular stent grafts as the preferred approach in these cases,¹⁷⁴ even though this is an off-label application of stent grafts. Evidence suggests that emergent endovascular repair in patients with true lumen collapse and complications such rupture or dynamic malperfusion may be lifesaving in these difficult-to-treat patients. However, these patients remain at risk of further complication or future reintervention. Although endovascular repair in patients with connective tissue disorder is generally not recommended, this technique may be used as a bridge to later definitive repair in such life-threatening circumstances.

Less convincing is the evidence in support of using endovascular stent grafts to treat uncomplicated acute descending dissection. The goal of this treatment strategy is to use the stent graft to cover the intimal tear, seal the entry site of the dissection, and eventually cause thrombosis of the false lumen to aid in aortic remodeling and reduce late aortic expansion. However, whether this approach is more effective than conventional nonoperative management remains controversial. Moreover, inadvertent retrograde perfusion or pressurization of the endovascularly repaired aortic section is still a risk; therefore, at this time, the use of endografts in patients with uncomplicated, classic dissection remains investigational.^175,176 Such procedures take place in a hybrid operating room, where access to the true lumen is gained through the femoral arteries. An aortogram is taken, and the intimal tear is identified. Note that the diameter of the true lumen is measured on both the aortogram and a preoperative contrast-enhanced CT scan. A stent graft approximately 10% wider in diameter than the true lumen is selected for these cases. Unlike stents deployed to treat most descending thoracic aortic aneurysms, stents deployed to treat descending aortic dissections must not be ballooned, because ballooning can cause a new intimal tear, retrograde dissection into the ascending aorta, or even aortic rupture.

Chronic Dissection

Endovascular treatment of chronic descending aortic dissection is also controversial and remains under investigation.^174,177 These dissections are particularly challenging because the relative rigidity of the dissecting membrane and the presence of multiple re-entry sites make it difficult to exclude the false lumen. Furthermore, interfering with false lumen perfusion may cause ischemic complications, such as bowel infarction or renal failure. Until the safety and effectiveness of endovascular repair for this condition have been demonstrated, patients with chronic descending aortic dissection should be treated with conventional nonoperative management until indications for open surgical repair develop.

Penetrating Aortic Ulcer

Unlike patients with classic descending aortic dissection, those with PAUs appear to be very well suited for endovascular intervention. Covering the focal ulceration with a stent graft has been shown to be an effective treatment.¹⁷⁸ In a recent study by Patel and colleagues,¹⁷⁹ endovascular repair of PAU was associated with better early outcomes than open repair. However, when PAU was associated with adjacent hematoma within the aortic wall, rates of subsequent reintervention were increased.

Open Repair

Acute Dissection

In patients with acute aortic dissection, surgical repair of the descending thoracic or thoracoabdominal aorta is traditionally associated with high morbidity and mortality.¹⁴² Therefore, the primary goals of surgery are to prevent fatal rupture and to restore branch vessel perfusion.¹⁷² A limited graft repair of the life-threatening aortic lesion achieves these goals while minimizing risks. Because the most common site of rupture in descending aortic dissection is in the proximal third of the descending thoracic aorta, the upper half of the descending thoracic aorta is usually repaired. The distal half also may be replaced if it exceeds 4 cm in diameter. Graft replacement of the entire thoracoabdominal aorta is not attempted in such cases unless a large coexisting aneurysm mandates this radical approach. Similarly, the repair is not extended into the aortic arch unless the arch is aneurysmal, even if the primary tear is located there. Patients with chronic dissection who require emergency repair because of acute pain or rupture also undergo limited graft replacement of the symptomatic segment.

Because repairing acute dissections entails an increased risk of paraplegia, adjuncts that provide spinal cord protection, such as cerebrospinal fluid drainage and left heart bypass, are used liberally during such repairs,¹⁸⁰ even if the repair is confined to the upper descending thoracic aorta. Proximal control usually is obtained between the left common carotid and left subclavian arteries; any mediastinal hematoma near the proximal descending thoracic aorta is avoided until proximal control is established. After the aorta is opened, the dissecting membrane is excised from the section undergoing graft replacement. The proximal and distal anastomoses use all layers of the aortic wall, thereby excluding the false lumen in the suture lines and directing all blood flow into the true lumen. Although the relative lack of mural thrombus ensures the presence of multiple patent intercostal arteries, extreme tissue fragility may preclude their reattachment.

Malperfusion Syndrome

Lower-extremity ischemia is commonly addressed with surgical extra-anatomic revascularization techniques, such as femoral-to-femoral bypass grafting. In patients with abdominal organ ischemia, flow to the compromised bed must be re-established swiftly. When an endovascular approach is unavailable or unsuccessful, open surgery is necessary. Although they are considered second-line therapies, multiple techniques are available, including graft replacement of the aorta (with flow redirected into the true lumen), open aortic fenestration, and visceral or renal artery bypass.

Chronic Dissection

A more aggressive replacement usually is performed during elective aortic repairs in patients with chronic dissection. In many regards, the operative approach used in these patients is identical to that used for descending thoracic and thoracoabdominal aortic aneurysms, as described in the first half of this chapter (Fig. 22-23). One key difference is the need to excise as much dissecting membrane as possible to clearly identify the true and false lumens and to locate all important branch vessels. When the dissection extends into the visceral or renal arteries, the membrane can be fenestrated, or the false lumen can be obliterated with sutures or intraluminal stents. Asymmetric expansion of the false lumen can create wide separation of the renal arteries. This problem is addressed by reattaching the mobilized left renal artery to a separate opening in the graft or by performing a left renal artery bypass with a side graft. Wedges of dissecting membrane also are excised from the aorta adjacent to the proximal and distal anastomoses, which allows blood to flow through both true and false lumens. When placing the proximal clamp is not technically feasible, hypothermic circulatory arrest can be used to facilitate the proximal portion of the repair.

Figure 22-23.

Illustration of distal aortic repair of a chronic dissection. A. Thoracoabdominal incision. B. Extent II thoracoabdominal aortic aneurysm resulting from chronic aortic dissection. The patient has previously undergone composite valve graft replacement of the aortic root and ascending aorta. After left heart bypass is initiated, the proximal portion of the aneurysm is isolated by placing clamps on the left subclavian artery, between the left common carotid and left subclavian arteries, and across the middle descending thoracic aorta. C. The isolated segment of aorta is opened by using electrocautery. D. The dissecting membrane is excised, and bleeding intercostal arteries are oversewn. The aorta is prepared for proximal anastomosis by transecting it distal to the proximal clamp and separating this portion from the esophagus (not shown). E. The proximal anastomosis between the aorta and an appropriately sized Dacron graft is completed with continuous polypropylene suture. F. After left heart bypass has been stopped and the distal aortic cannula has been removed, the proximal clamp is repositioned onto the graft, the other two clamps are removed, and the remainder of the aneurysm is opened. G. The rest of the dissecting membrane is excised, and the openings to the celiac, superior mesenteric, and renal arteries are identified. H. Selective visceral perfusion with oxygenated blood from the bypass circuit is delivered through balloon perfusion catheters placed in the celiac and superior mesenteric arterial ostia. Cold crystalloid is delivered to the renal arteries. The critical intercostal arteries are reattached to an opening cut in the graft. I. To minimize spinal cord ischemia, the proximal clamp is repositioned distal to the intercostal reattachment site. A second oval opening is fashioned in the graft adjacent to the visceral vessels. Selective perfusion of the visceral arteries continues during their reattachment to the graft. A separate anastomosis is often required to reattach the left renal artery. J. After the balloon perfusion catheters are removed and the visceral anastomosis is completed, the clamp is again moved distally, restoring blood flow to the celiac, renal, and superior mesenteric arteries. The final anastomosis is created between the graft and the distal aorta. (Reproduced with permission from Creager MA, Dzau VS, Loscalzo J, eds. Vascular Medicine. Philadelphia: WB Saunders; 2006. Copyright © Saunders/Elsevier, 2006, Fig. 35-8A–J.)

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OUTCOMES

Listen

Improvements in anesthesia, surgical techniques, and perioperative care have led to substantial improvements in outcome after thoracic aortic aneurysm repair. When performed in specialized centers, these operations are associated with excellent survival rates and acceptable morbidity rates. The interpretation of outcomes data is complicated by site-specific variables, such as the number of years reported and whether data are taken from single-practice centers or from pooled, multicenter, or national registries, and by patient-specific variables, such as type of enrollment, urgency and extent of repair, concomitant procedures performed, and the presence of preexisting risk factors such as advanced age, previous cardiovascular repair, disease of any system or organ, or connective tissue disorder.

Repair of Proximal Aortic Aneurysms

Risks associated with the open repair of the proximal aorta vary by extent of repair and are greatest for repairs involving total arch replacement. All varieties of aortic root replacement have shown acceptable early mortality rates and few complications. Two groups with 20 and 27 years’ experience with composite valve graft replacement reported early mortality rates of 5.6% and 1.9%, respectively; the more recent repairs had better outcomes.^181,182 Early mortality rates for stentless porcine tissue root replacements are also low, ranging from 3.6% to 6.0%.^{183,184,185,186,187} Early mortality rates for contemporary valve-sparing approaches to aortic root replacement are quite low (1%–2%) in experienced centers.^66,188,189 Late survival rates after valve-sparing root procedures range from 97% to 99% at 5 years^66,188,189 and approach 94% at 10 years.⁶⁶

Repairs incorporating the ascending aorta and aortic arch have acceptable outcomes; risk increases with patient-specific factors such as severe atherosclerosis¹⁹⁰ or as larger sections of the aortic arch are incorporated into the repair.^191,192 A revised surgical strategy—such as the use of hypothermic circulatory arrest—is often needed to avoid clamping atherosclerotic sections in the “porcelain” aorta. In Zingone and colleagues’ series¹⁹⁰ of 64 patients who underwent replacement of atherosclerotic ascending aorta, hypothermic circulatory arrest was used in 61 patients (95%). Even though these patients had substantial comorbidity and 83% underwent concomitant cardiac repairs, acceptable rates of early mortality (11%) and stroke (6%) were obtained. Other studies indicate that the enhanced risk of neurocognitive disturbances in ascending repairs using circulatory arrest are not offset by lower rates of early mortality.^193,194 Regarding extended proximal repair, reported early mortality rates after traditional stage 1 elephant trunk repairs (primarily using island reattachment strategies) range from 2.3% to 13.9%.^{195,196,197,198,199}

Contemporary mortality rates for extensive proximal aortic repair have improved as new strategies and modified adjuncts have been adopted. For example, by adopting contemporary approaches, we have reduced early mortality for stage 1 elephant trunk repairs from 12% to 2% in our patients.^73,196 Similarly, in a report by Kazui and colleagues²⁰⁰ covering 20 years of experience and 472 consecutive patients who underwent aortic arch repair with selective ACP, operative mortality was 16.0% for early repairs and 4.1% for more recent repairs. Other contemporary reports of the use of techniques such as moderate hypothermia and Y-graft approaches^{201,202,203,204} indicate similarly improved outcomes; early mortality ranges from 1% to 7%, stroke rates range from 1% to 6%, and no cases of paraplegia are reported. Although paraplegia has traditionally been an unusual and infrequent complication of aortic arch repair, it has been reported as a complication of “long” elephant trunk approaches²⁰⁵ and frozen elephant trunk approaches.²⁰⁶

Because of the heterogeneity of hybrid arch approaches and the tendency to use these approaches in high-risk patients, results of hybrid arch repair are difficult to interpret. A meta-analysis conducted by Koullias and Wheatley⁸² of data from 15 studies with 463 patients found an average 30-day mortality rate of 8.3%; stroke, 4.4%; paraplegia, 3.9%; and endoleak, 9.2%. Of note, relatively few repairs (30%) were performed “off-pump,” and the majority of repairs used cardiopulmonary bypass or hypothermic circulatory arrest. Additionally, several reports of small series (ranging from 33 to 66 patients) have documented a substantial risk of acute retrograde aortic dissection during hybrid arch repairs; rates range from 3.0% to 7.5%, and these patients face significant mortality risk (ranging from 33% to 100%) should this occur.^{85,207,208,209}

Treatment of Acute Ascending Aortic Dissection

The International Registry of Acute Aortic Dissection (IRAD) provides the most comprehensive data on contemporary outcomes in patients with acute aortic dissection. This registry was established in 1996 and has accumulated data from >3000 patients treated for acute aortic dissection at 30 centers in 11 countries. A recent IRAD analysis of data from 776 patients who underwent surgical repair of acute ascending aortic dissection revealed an in-hospital mortality rate of 23.8%.²¹⁰ The investigators identified several preoperative predictors of early mortality, including age >70 years, previous cardiac surgery, hypotension or shock at presentation, abrupt onset of symptoms, migrating pain, cardiac tamponade, preoperative renal failure, pulse deficit, and evidence of myocardial ischemia or infarction on ECG.^210,211 The German Registry for Acute Aortic Dissection (GERAADA) has collected data on more than 2500 patients from 52 centers since 2006. In a report of 1436 patients with acute proximal dissection that was surgically repaired using hypothermic circulatory arrest with or without unilateral and bilateral ACP, the early mortality rates ranged from 13.9% to 19.4%; the 628 patients with unilateral ACP had the lowest rate of early death.²¹²

Repair of Distal Aortic Aneurysms

Endovascular Repair of Descending Thoracic Aortic Aneurysms

In the earliest series of endovascular repairs of descending thoracic aortic aneurysms, mortality and morbidity were difficult to assess. Most of the reported series were small and included a large proportion of high-risk patients with substantial comorbidity. For example, in the Stanford experience with “first-generation” stent grafts in 103 patients with descending thoracic aortic aneurysms, the operative mortality rate was 9%, the stroke rate was 7%, the paraplegia/paraparesis rate was 3%, and actuarial survival was only 73 ± 5% at 2 years. However, 62 patients (60%) were not considered candidates for thoracotomy and open surgical repair; as expected, this group experienced the majority of the morbidity and mortality.²¹³ In a follow-up series, the Stanford group reported survival rates of 74% at 1 year and 31% at 5 years after stent grafting in patients who were deemed not to be surgical candidates; in contrast, survival rates were 93% at 1 year and 78% at 5 years (P<0.001) after stent grafting in patients who were deemed reasonable candidates for conventional open repair.²¹⁴ This study also found a 30% incidence of late aortic complications, which stresses the necessity for appropriate follow-up.

Evidence from pivotal, nonrandomized trials that compared patients who underwent endograft exclusion with historical or concurrent patients who underwent open repair^215,216,217 shows that the stent graft groups had significantly less morbidity and early mortality than the open repair groups, although in two of the trials, a nonsignificant between-group difference was observed in the rate of stroke.^215,217 Available 5-year comparative data show that the two groups differed significantly in their aneurysm-related mortality rates (2.8% for endovascular patients and 11.7% for open repair patients) but not in their rates of all-cause mortality (which were 32% and 31%, respectively).²¹⁸ Additional pivotal trial 5-year outcomes²¹⁹ indicate the growing disparity between aneurysm-related (96.1%) and all-cause survival (58.5%) in patients with endovascular repair, leading some to comment on the possible futility of repair in many patients.¹⁷⁴

Although the feasibility of endovascular treatment of chronic descending thoracic aortic dissection has been shown in small series,^148,220 the efficacy of such repairs has not been established. The eagerly anticipated initial outcomes of the INSTEAD trial (INvestigation of STEnt grafts in patients with type B Aortic Dissection), which involves 136 patients with uncomplicated chronic descending aortic dissection, show no survival benefit of stent grafting over standard medical antihypertensive therapy in the first 2 years after randomization.²²¹ However, it appears that the extended study may find a survival advantage at 5 years.¹⁷⁴ Likewise, the ADSORB (A Prospective Randomized Trial in Acute Uncomplicated Type B Dissections) trial²²² is currently underway, and once complete, it may help elucidate whether endovascular repair in patients with uncomplicated descending dissection provides an advantage over standard medical antihypertensive therapy as pertains to its study endpoints—thrombosis of the false lumen, aortic enlargement, and aortic rupture. Thus, at present, the use of stent grafts to treat chronic descending aortic dissection should be considered experimental.

Open Repair of Descending Thoracic and Thoracoabdominal Aortic Aneurysms

Contemporary results of open repairs of descending thoracic aortic aneurysms, including those performed in select patients with chronic dissection, indicate that early mortality rates range from 4.1% to 8.0%, renal failure rates range from to 4.2% to 7.5%, and paraplegia rates range from 2.3% to 5.7%; stroke rates are generally lower, ranging from 1.8% to 2.1%.^223,224,225 In our series, although the risk of paraplegia increased with the extent of repair, the risk of mortality was greatest for those undergoing repair of the proximal two thirds of the descending aorta.²²³ As expected, stroke rates after distal aortic repairs were highest when the clamp site was near the left subclavian artery.

Several studies have compared endovascular and surgical approaches to descending thoracic aortic repair. Some studies found no significant differences in rates of early death, stroke, and paraplegia,^217,226,227 whereas others found that surgical patients had higher rates of early mortality (27%)²²⁸ and paraplegia (14%).²¹⁵ However, a recent study of Medicare patients showed that the early survival advantage associated with stent grafts is soon lost in the majority of patients.²²⁹

Contemporary series of open thoracoabdominal aortic repairs show acceptable survival. Reported outcome rates range from 5% to 12% for early mortality, 3.8% to 9.5% for paraplegia, 1.7% to 5.2% for stroke, and 6% to 12% for renal complications.^{230,231,232,233,234} Many of these series summarize 10 to 20 years of surgical experience,^{231,232,233,234} although some present a shorter but more contemporary experience.²³⁰ Even for complex thoracoabdominal aortic repairs, such as stage 2 elephant trunk repairs, several centers report acceptable early mortality rates ranging from 0% to 10%.^{195,196,197,198,199} Worse outcomes are also documented, as in a statewide, nonfederal analysis of data from 1010 patients whose early mortality rate was 25%. Of note, 40% of these patients were treated at centers averaging only one thoracoabdominal aortic aneurysm repair per year.²³⁵ Cowan and colleagues,²³⁶ who examined the influence of familiarity with the procedure on rates of mortality and morbidity after thoracoabdominal aortic aneurysm repair, reported that patients treated at low-volume centers fared less well. Replacing the entire thoracoabdominal aorta (i.e., performing an extent II repair) carries the highest risk of death, bleeding, renal failure, and paraplegia.^92,231,232 Early survival has been estimated at 79% at 2 years,²³⁷ and midterm survival has been estimated at 63% at 5 years.²³⁴

Treatment of Acute Descending Aortic Dissection

Nonoperative Management

The in-hospital mortality rate is nearly 10% for patients with acute descending aortic dissection who receive nonoperative treatment¹⁴²; however, when IRAD stratified patients according to clinical presentation, the mortality rate for patients with uncomplicated dissection was less than 4%, whereas the mortality rate for patients with complicated dissection was more than 20%.^142,238 The primary causes of death during nonoperative management are rupture, malperfusion, and cardiac failure. Risk factors associated with treatment failure—defined as death or need for surgery—include an enlarged aorta, persistent hypertension despite maximal treatment, oliguria, and peripheral ischemia. Among patients who receive nonoperative treatment for descending aortic dissection and who survive the acute period, approximately 90% remain alive 1 year later, and approximately 76% are alive 3 years later.²³⁹

Endovascular Treatment

For malperfusion of the visceral or renal arteries, an endovascular approach is ideal. The Stanford group reported a 93% technical success rate for endovascular reperfusion of an ischemic bed.²⁴⁰ Their experience with the use of first-generation stents to treat acute complicated descending dissections was also encouraging: Complete thrombosis of the false lumen occurred in 79% of patients. The early mortality rate was 16%, comparable to that associated with open techniques.²⁴¹ A meta-analysis of observational studies of endovascular stenting, which included 248 patients with acute descending aortic dissection, found a 30-day mortality rate of 9.8%.²⁴² Compared with early mortality rates obtained from IRAD data,¹⁴² this rate is substantially lower than the rate associated with open surgical treatment but is similar to the rate achieved with nonoperative management. However, patients with complicated acute descending dissection remain susceptible to late events; at 1 year, survival is approximately 70%, and reintervention is needed in about 10% of survivors.²⁴³

Open Repair

We recently reported our contemporary experience with 32 patients with acute complicated descending aortic dissection, including 7 patients (22%) with aortic rupture. Complexities included dangerously large aneurysms in the majority of patients (69%), which implied either rapid expansion or an aneurysm superimposed on the dissection. Malperfusion was present in one patient; this patient had an open fenestration procedure. A substantial number of patients (n = 7, 22%) had connective tissue disorders. The operative mortality rate was 6% overall.²⁴⁴ There were 3 cases of permanent spinal cord complications (10%), 1 stroke (3%), and 2 cases of permanent renal failure (6%). In recent multicenter studies by IRAD, investigators found a 29% in-hospital mortality rate among 70 patients with acute dissection who underwent open surgical replacement of the descending thoracic aorta²³⁸ and a 22% in-hospital mortality rate among 18 patients who underwent open fenestration procedures. Another study found that, of patients who survived surgical treatment of acute descending aortic dissection, approximately 96% were alive at 1 year and approximately 83% were alive at 3 years after the procedure,²³⁹ which is substantially better than 1-year survival after endovascular repair in acute complicated distal dissection.^239,243

CONCLUSIONS

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Aortic aneurysm may present as localized or extensive disease. The availability and development of adjuncts and endovascular techniques have supported the constant evolution of surgical strategies to tackle these complex problems. Repair strategies range from isolated, totally endovascular aortic repair for descending thoracic aneurysms to extensive total aortic and staged replacements with a combination of both open and endovascular techniques. Regardless of the difficulty of accurately assessing the risks associated with aortic repair, surgical repair of the thoracoabdominal aorta clearly remains the most challenging aortic repair in terms of mortality and morbidity. Accordingly, replacing the entire thoracoabdominal aorta (i.e., performing an extent II repair) carries the highest risk of death, renal failure, and paraplegia.^89,221,226

ACKNOWLEDGMENTS

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The authors wish to thank Susan Y. Green, MPH, and Stephen N. Palmer, PhD, ELS, for editorial assistance; Scott A. Weldon, MA, CMI, and Carol P. Larson, CMI, for creating the illustrations; and Kapil Sharma, MD, for his substantial contributions to the chapter published in the 9th edition of the textbook, on which this updated chapter was based.

REFERENCES

Listen

Entries highlighted in bold are key references.

Johnston KW, Rutherford RB, Tilson MD et al. Suggested standards for reporting on arterial aneurysms. Subcommittee on Reporting Standards for Arterial Aneurysms, Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery and North American Chapter, International Society for Cardiovascular Surgery. J Vasc Surg. 1991;13(3):452–458. [PubMed: 1999868]

Bickerstaff LK, Pairolero PC, Hollier LH et al. Thoracic aortic aneurysms: a population-based study. Surgery. 1982;92(6):1103–1108. [PubMed: 7147188]

Segura AM, Luna RE, Horiba K et al. Immunohistochemistry of matrix metalloproteinases and their inhibitors in thoracic aortic aneurysms and aortic valves of patients with Marfan’s syndrome. Circulation. 1998;98(19 Suppl):II331-II337. [PubMed: 9852923]

Neptune ER, Frischmeyer PA, Arking DE et al. Dysregulation of TGF-β activation contributes to pathogenesis in Marfan syndrome. Nat Genet. 2003;33(3):407–411. [PubMed: 12598898]

Marsalese DL, Moodie DS, Vacante M et al. Marfan’s syndrome: natural history and long-term follow-up of cardiovascular involvement. J Am Coll Cardiol. 1989;14(2):422–428. [PubMed: 2526834]

Adams JN, Trent RJ. Aortic complications of Marfan’s syndrome. Lancet. 1998;352(9142):1722–1723. [PubMed: 9848345]

LeMaire SA, Pannu H, Tran-Fadulu V et al. Severe aortic and arterial aneurysms associated with a TGFBR2 mutation. Nat Clin Pract Cardiovasc Med. 2007;4(3):167–171. [PubMed: 17330129]

Loeys BL, Schwarze U, Holm T et al. Aneurysm syndromes caused by mutations in the TGF-β receptor. N Engl J Med. 2006;355(8):788–798. [PubMed: 16928994]

Oderich GS, Panneton JM, Bower TC et al. The spectrum, management and clinical outcome of Ehlers-Danlos syndrome type IV: a 30-year experience. J Vasc Surg. 2005;42(1):98–106. [PubMed: 16012458]

10.

Sheen VL, Jansen A, Chen MH et al. Filamin A mutations cause periventricular heterotopia with Ehlers-Danlos syndrome. Neurology. 2005;64(2):254–262. [PubMed: 15668422]

11.

Boileau C, Guo DC, Hanna N et al. TGFB2 mutations cause familial thoracic aortic aneurysms and dissections associated with mild systemic features of Marfan syndrome. Nat Genet. 2012;44(8):916–921. [PubMed: 22772371]

12.

Guo DC, Pannu H, Tran-Fadulu V et al. Mutations in smooth muscle alpha-actin (ACTA2) lead to thoracic aortic aneurysms and dissections. Nat Genet. 2007;39(12):1488–1493. [PubMed: 17994018]

13.

Pannu H, Tran-Fadulu V, Papke CL et al. MYH11 mutations result in a distinct vascular pathology driven by insulin-like growth factor 1 and angiotensin II. Hum Mol Genet. 2007;16(20):2453–2462. [PubMed: 17666408]

14.

van de Laar IM, Oldenburg RA, Pals G et al. Mutations in SMAD3 cause a syndromic form of aortic aneurysms and dissections with early-onset osteoarthritis. Nat Genet. 2011;43(2):121–126. [PubMed: 21217753]

15.

Hoffman JI, Kaplan S. The incidence of congenital heart disease. J Am Coll Cardiol. 2002;39(12):1890–1900. [PubMed: 12084585]

16.

Keane MG, Wiegers SE, Plappert T et al. Bicuspid aortic valves are associated with aortic dilatation out of proportion to coexistent valvular lesions. Circulation. 2000;102(19 Suppl 3):III35–III39. [PubMed: 11082359]

17.

Jassal DS, Bhagirath KM, Tam JW et al. Association of bicuspid aortic valve morphology and aortic root dimensions: a substudy of the aortic stenosis progression observation measuring effects of rosuvastatin (ASTRONOMER) study. Echocardiography. 2010;27(2):174–179. [PubMed: 19725842]

18.

Cecconi M, Manfrin M, Moraca A et al. Aortic dimensions in patients with bicuspid aortic valve without significant valve dysfunction. Am J Cardiol. 2005;95(2):292–294. [PubMed: 15642575]

19.

Nistri S, Sorbo MD, Marin M et al. Aortic root dilatation in young men with normally functioning bicuspid aortic valves. Heart. 1999;82(1):19–22. [PubMed: 10377302]

20.

Sabet HY, Edwards WD, Tazelaar HD, Daly RC. Congenitally bicuspid aortic valves: a surgical pathology study of 542 cases (1991 through 1996) and a literature review of 2,715 additional cases. Mayo Clin Proc. 1999;74(1):14–26. [PubMed: 9987528]

21.

Larson EW, Edwards WD. Risk factors for aortic dissection: a necropsy study of 161 cases. Am J Cardiol. 1984;53(6):849–855. [PubMed: 6702637]

22.

LeMaire SA, Wang X, Wilks JA et al. Matrix metalloproteinases in ascending aortic aneurysms: bicuspid versus trileaflet aortic valves. J Surg Res. 2005;123(1):40–48. [PubMed: 15652949]

23.

Fedak PW, de Sa MP, Verma S et al. Vascular matrix remodeling in patients with bicuspid aortic valve malformations: implications for aortic dilatation. J Thorac Cardiovasc Surg. 2003;126(3):797–806. [PubMed: 14502156]

24.

Koullias GJ, Korkolis DP, Ravichandran P et al. Tissue microarray detection of matrix metalloproteinases, in diseased tricuspid and bicuspid aortic valves with or without pathology of the ascending aorta. Eur J Cardiothorac Surg. 2004;26(6):1098–1103. [PubMed: 15541969]

25.

Martin LJ, Ramachandran V, Cripe LH et al. Evidence in favor of linkage to human chromosomal regions 18q, 5q, and 13q for bicuspid aortic valve and associated cardiovascular malformations. Hum Genet. 2007;121(2):275–284. [PubMed: 17203300]

26.

McKellar SH, Tester DJ, Yagubyan M et al. Novel NOTCH1 mutations in patients with bicuspid aortic valve disease and thoracic aortic aneurysms. J Thorac Cardiovasc Surg. 2007;134(2):290–296. [PubMed: 17662764]

27.

Wessels MW, Berger RM, Frohn-Mulder IM et al. Autosomal dominant inheritance of left ventricular outflow tract obstruction. Am J Med Genet. 2005;134A(2):171–179.

28.

Yasuda H, Nakatani S, Stugaard M et al. Failure to prevent progressive dilation of ascending aorta by aortic valve replacement in patients with bicuspid aortic valve: comparison with tricuspid aortic valve. Circulation. 2003;108 Suppl 1:II291–II294. [PubMed: 12970248]

29.

Hornick M, Moomiaie R, Mojibian H et al. ’Bovine’ aortic arch—a marker for thoracic aortic disease. Cardiology. 2012;123(2):116–124. [PubMed: 23037917]

30.

Brown SL, Busuttil RW, Baker JD et al. Bacteriologic and surgical determinants of survival in patients with mycotic aneurysms. J Vasc Surg. 1984;1(4):541–547. [PubMed: 6436514]

31.

Johnson JR, Ledgerwood AM, Lucas CE. Mycotic aneurysm: new concepts in therapy. Arch Surg.[Archives of Surgery Full Text] 1983;118(5):577–582. [PubMed: 6687676]

32.

Schwill S, LeMaire SA, Green SY, Bakaeen FG, Coselli JS. Endovascular repair of thoracic aortic pseudoaneurysms and patch aneurysms. J Vasc Surg. 2010;52(4):1034–1037. [PubMed: 20619593]

33.

Elefteriades JA. Natural history of thoracic aortic aneurysms: indications for surgery, and surgical versus nonsurgical risks. Ann Thorac Surg. 2002;74(5):S1877-1880

34.

Davies RR, Goldstein LJ, Coady MA et al. Yearly rupture or dissection rates for thoracic aortic aneurysms: simple prediction based on size. Ann Thorac Surg. 2002;73(1):17–27. [PubMed: 11834007]

35.

Murdoch JL, Walker BA, Halpern BL, Kuzma JW, McKusick VA. Life expectancy and causes of death in the Marfan syndrome. N Engl J Med. 1972;286(15):804–808. [PubMed: 5011789]

36.

Michel PL, Acar J, Chomette G, Iung B. Degenerative aortic regurgitation. Eur Heart J. 1991;12(8):875–882. [PubMed: 1915425]

37.

Prenger K, Pieters F, Cheriex E. Aortic dissection after aortic valve replacement: incidence and consequences for strategy. J Card Surg. 1994;9(5):495–498. [PubMed: 7994092]

38.

Bonow RO. Bicuspid aortic valves and dilated aortas: a critical review of the ACC/AHA practice guidelines recommendations. Am J Cardiol. 2008;102(1):111–114. [PubMed: 18572047]

39.

Girdauskas E, Disha K, Raisin HH et al. Risk of late aortic events after an isolated aortic valve replacement for bicuspid aortic valve stenosis with concomitant ascending aortic dilation. Eur J Cardiothorac Surg. 2012;42(5):832-837; –discussion 837-838. [PubMed: 22466700]

40.

Hiratzka LF, Bakris GL, Beckman JA et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. Circulation. 2010;121(13):e266–e369. [PubMed: 20233780]

41.

Isselbacher EM. Thoracic and abdominal aortic aneurysms. Circulation. 2005;111(6):816–828. [PubMed: 15710776]

42.

Wiet SP, Pearce WH, McCarthy WJ et al. Utility of transesophageal echocardiography in the diagnosis of disease of the thoracic aorta. J Vasc Surg. 1994;20(4):613–620. [PubMed: 7933263]

43.

Fillinger MF. Imaging of the thoracic and thoracoabdominal aorta. Semin Vasc Surg. 2000;13(4):247–263. [PubMed: 11156053]

44.

Weisbord SD, Palevsky PM. Radiocontrast-induced acute renal failure. J Intensive Care Med. 2005;20(2):63–75. [PubMed: 15855219]

45.

Danias P, Eldeman R, Manning W. Magnetic resonance angiography of the great vessels and the coronary arteries. In: Pohost GM, ed. Imaging in Cardiovascular Disease. Philadelphia: Lippincott Williams & Wilkins; 2000:449.

46.

Ergun I, Keven K, Uruc I et al. The safety of gadolinium in patients with stage 3 and 4 renal failure. Nephrol Dial Transplant. 2006;21(3):697–700. [PubMed: 16326736]

47.

Merten GJ, Burgess WP, Gray LV et al. Prevention of contrast-induced nephropathy with sodium bicarbonate: a randomized controlled trial. JAMA.[JAMA and JAMA Network Journals Full Text] 2004;291(19):2328–2334. [PubMed: 15150204]

48.

Tepel M, van der Giet M, Schwarzfeld C et al. Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine. N Engl J Med. 2000;343(3):180–184. [PubMed: 10900277]

49.

Gopaldas RR, Huh J, Dao TK et al. Superior nationwide outcomes of endovascular versus open repair for isolated descending thoracic aortic aneurysm in 11,669 patients. J Thorac Cardiovasc Surg. 2010;140(5):1001–1010. [PubMed: 20951252]

50.

Walker KL, Shuster JJ, Martin TD et al. Practice patterns for thoracic aneurysms in the stent graft era: health care system implications. Ann Thorac Surg. 2010;90(6):1833–1839. [PubMed: 21095320]

51.

Gopaldas RR, Dao TK, LeMaire SA, Huh J, Coselli JS. Endovascular versus open repair of ruptured descending thoracic aortic aneurysms: a nationwide risk-adjusted study of 923 patients. J Thorac Cardiovasc Surg. 2011;142(5):1010–1018. [PubMed: 21907356]

52.

Coselli JS, LeMaire SA, Buket S. Marfan syndrome: the variability and outcome of operative management. J Vasc Surg. 1995;21(3):432–443. [PubMed: 7877225]

53.

LeMaire SA, Rice DC, Schmittling ZC, Coselli JS. Emergency surgery for thoracoabdominal aortic aneurysms with acute presentation. J Vasc Surg. 2002;35(6):1171–1178. [PubMed: 12042727]

54.

Greenberg R, Eagleton M, Mastracci T. Branched endografts for thoracoabdominal aneurysms. J Thorac Cardiovasc Surg. 2010;140(6 Suppl):S171–S178. [PubMed: 21092788]

55.

LeMaire SA, Green SY, Kim JH et al. Thoracic or thoracoabdominal approaches to endovascular device removal and open aortic repair. Ann Thorac Surg. 2012;93(3):726-732; –discussion 733. [PubMed: 22364967]

56.

LeMaire SA, Miller CC III, Conklin LD, Schmittling ZC. Coselli JS. Estimating group mortality and paraplegia rates after thoracoabdominal aortic aneurysm repair. Ann Thorac Surg. 2003;75(2):508–513. [PubMed: 12607663]

57.

LeMaire SA, Miller CC III, Conklin LD et al. A new predictive model for adverse outcomes after elective thoracoabdominal aortic aneurysm repair. Ann Thorac Surg. 2001;71(4):1233–1238. [PubMed: 11308166]

58.

Gott VL, Cameron DE, Alejo DE et al. Aortic root replacement in 271 Marfan patients: a 24-year experience. Ann Thorac Surg. 2002;73(2):438–443. [PubMed: 11845856]

59.

Carrel TP, Berdat P, Englberger L et al. Aortic root replacement with a new stentless aortic valve xenograft conduit: preliminary hemodynamic and clinical results. J Heart Valve Dis. 2003;12(6):752–757. [PubMed: 14658817]

60.

Deleuze PH, Fromes Y, Khoury W et al. Eight-year results of Freestyle stentless bioprosthesis in the aortic position: a single-center study of 500 patients. J Heart Valve Dis. 2006;15(2):247–252. [PubMed: 16607908]

61.

Oury JH. Clinical aspects of the Ross procedure: indications and contraindications. Semin Thorac Cardiovasc Surg. 1996;8(4):328–335. [PubMed: 8899918]

62.

Fazel SS, David TE. Aortic valve-sparing operations for aortic root and ascending aortic aneurysms. Curr Opin Cardiol. 2007;22(6):497–503. [PubMed: 17921735]

63.

David TE, Ivanov J, Armstrong S, Feindel CM, Webb GD. Aortic valve-sparing operations in patients with aneurysms of the aortic root or ascending aorta. Ann Thorac Surg. 2002;74(5):S1758–S1761. [PubMed: 12440659]

64.

David TE, Armstrong S, Maganti M, Colman J, Bradley TJ. Long-term results of aortic valve-sparing operations in patients with Marfan syndrome. J Thorac Cardiovasc Surg. 2009;138(4):859-864; –discussion 863-864. [PubMed: 19769881]

65.

Kallenbach K, Baraki H, Khaladj N et al. Aortic valve-sparing operation in Marfan syndrome: what do we know after a decade? Ann Thorac Surg. 2007;83(2):S764-768.

66.

Kvitting JP, Kari FA, Fischbein MP et al. David valve-sparing aortic root replacement: equivalent mid-term outcome for different valve types with or without connective tissue disorder. J Thorac Cardiovasc Surg. 2013;145(1):117-126, 127.e1-127.e5; –discussion 126-127.

67.

Bentall H, De Bono A. A technique for complete replacement of the ascending aorta. Thorax. 1968;23(4):338–339. [PubMed: 5664694]

68.

Cabrol C, Pavie A, Gandjbakhch I et al. Complete replacement of the ascending aorta with reimplantation of the coronary arteries: new surgical approach. J Thorac Cardiovasc Surg. 1981;81(2):309–315. [PubMed: 7453242]

69.

Kouchoukos NT, Wareing TH, Murphy SF, Perrillo JB. Sixteen-year experience with aortic root replacement: results of 172 operations. Ann Surg. 1991;214(3):308–318. [PubMed: 1834031]

70.

Zubiate P, Kay JH. Surgical treatment of aneurysm of the ascending aorta with aortic insufficiency and marked displacement of the coronary ostia. J Thorac Cardiovasc Surg. 1976;71(3):415–421. [PubMed: 129589]

71.

Spielvogel D, Etz CD, Silovitz D, Lansman SL, Griepp RB. Aortic arch replacement with a trifurcated graft. Ann Thorac Surg. 2007;83(2):S791–S795. [PubMed: 17257928]

72.

Borst HG, Frank G, Schaps D. Treatment of extensive aortic aneurysms by a new multiple-stage approach. J Thorac Cardiovasc Surg. 1988;95(1):11–13. [PubMed: 3336224]

73.

LeMaire SA, Price MD, Parenti JL et al. Early outcomes after aortic arch replacement by using the Y-graft technique. Ann Thorac Surg. 2011;91(3):700-707; –discussion 707-708. [PubMed: 21352982]

74.

Svensson LG. Antegrade perfusion during suspended animation? J Thorac Cardiovasc Surg. 2002;124(6):1068–1070. [PubMed: 12447168]

75.

Ueda Y, Miki S, Kusuhara K et al. Surgical treatment of aneurysm or dissection involving the ascending aorta and aortic arch, utilizing circulatory arrest and retrograde cerebral perfusion. J Cardiovasc Surg (Torino). 1990;31(5):553–558. [PubMed: 2229147]

76.

Sundt TM III, Orszulak TA, Cook DJ, Schaff HV. Improving results of open arch replacement. Ann Thorac Surg. 2008;86(3):787-796; –discussion 796. [PubMed: 18721563]

77.

Wong DR, Coselli JS, Palmero L et al. Axillary artery cannulation in surgery for acute or subacute ascending aortic dissections. Ann Thorac Surg. 2010;90(3):731–737. [PubMed: 20732486]

78.

Preventza O, Bakaeen FG, Stephens EH et al. Innominate artery cannulation: An alternative to femoral or axillary cannulation for arterial inflow in proximal aortic surgery. J Thorac Cardiovasc Surg. 2013;145(3 Suppl):S191–S196. [PubMed: 23260457]

79.

Della Corte A, Scardone M, Romano G et al. Aortic arch surgery: Thoracoabdominal perfusion during antegrade cerebral perfusion may reduce postoperative morbidity. Ann Thorac Surg. 2006;81(4):1358–1364. [PubMed: 16564273]

80.

Panos A, Myers PO, Kalangos A. Novel technique for aortic arch surgery under mild hypothermia. Ann Thorac Surg. 2008;85(1):347–348. [PubMed: 18154850]

81.

Inoue K, Hosokawa H, Iwase T et al. Aortic arch reconstruction by transluminally placed endovascular branched stent graft. Circulation. 1999;100(19 Suppl):II316-321.

82.

Koullias GJ, Wheatley GH III. State-of-the-art of hybrid procedures for the aortic arch: a meta-analysis. Ann Thorac Surg. 2010;90(2):689–697. [PubMed: 20667392]

83.

Melissano G, Tshomba Y, Bertoglio L, Rinaldi E, Chiesa R. Analysis of stroke after TEVAR involving the aortic arch. Eur J Vasc Endovasc Surg. 2012;43(3):269–275. [PubMed: 22240331]

84.

Andersen ND, Williams JB, Hanna JM et al. Results with an algorithmic approach to hybrid repair of the aortic arch. J Vasc Surg. 2013;57(3):655–667. [PubMed: 23186868]

85.

Lotfi S, Clough RE, Ali T et al. Hybrid repair of complex thoracic aortic arch pathology: long-term outcomes of extra-anatomic bypass grafting of the supra-aortic trunk. Cardiovasc Intervent Radiol. 2013;36(1):46–55. [PubMed: 22526104]

86.

Svensson LG, Kouchoukos NT, Miller DC et al. Expert consensus document on the treatment of descending thoracic aortic disease using endovascular stent-grafts. Ann Thorac Surg. 2008;85(1 Suppl):S1–S41. [PubMed: 18083364]

87.

Coselli JS, LeMaire SA, Köksoy C, Schmittling ZC, Curling PE. Cerebrospinal fluid drainage reduces paraplegia after thoracoabdominal aortic aneurysm repair: results of a randomized clinical trial. J Vasc Surg. 2002;35(4):631–639. [PubMed: 11932655]

88.

Jacobs MJ, Mess W, Mochtar B et al. The value of motor evoked potentials in reducing paraplegia during thoracoabdominal aneurysm repair. J Vasc Surg. 2006;43(2):239–246. [PubMed: 16476594]

89.

van Dongen EP, Schepens MA, Morshuis WJ et al. Thoracic and thoracoabdominal aortic aneurysm repair: use of evoked potential monitoring in 118 patients. J Vasc Surg. 2001;34(6):1035–1040. [PubMed: 11743557]

90.

Coselli JS. The use of left heart bypass in the repair of thoracoabdominal aortic aneurysms: current techniques and results. Semin Thorac Cardiovasc Surg. 2003;15(4):326–332. [PubMed: 14710373]

91.

Coselli JS, LeMaire SA. Left heart bypass reduces paraplegia rates after thoracoabdominal aortic aneurysm repair. Ann Thorac Surg. 1999;67(6):1931–1934. [PubMed: 10391341]

92.

Safi HJ, Miller CC III, Huynh TT et al. Distal aortic perfusion and cerebrospinal fluid drainage for thoracoabdominal and descending thoracic aortic repair: ten years of organ protection. Ann Surg. 2003;238(3):372–380. [PubMed: 14501503]

93.

Köksoy C, LeMaire SA, Curling PE et al. Renal perfusion during thoracoabdominal aortic operations: cold crystalloid is superior to normothermic blood. Ann Thorac Surg. 2002;73(3):730–738. [PubMed: 11899174]

94.

Kouchoukos NT, Masetti P, Rokkas CK, Murphy SF. Hypothermic cardiopulmonary bypass and circulatory arrest for operations on the descending thoracic and thoracoabdominal aorta. Ann Thorac Surg. 2002;74(5):S1885–S1887. [PubMed: 12440687]

95.

Coselli JS, Oberwalder P. Successful repair of mega aorta using reversed elephant trunk procedure. J Vasc Surg. 1998;27(1):183–188. [PubMed: 9474099]

96.

Jones MM, Akay M, Murariu D, LeMaire SA, Coselli JS. Safe aortic arch clamping in patients with patent internal thoracic artery grafts. Ann Thorac Surg. 2010;89(4):e31–e32. [PubMed: 20338300]

97.

Volodos NL, Shekhanin VE, Karpovich IP, Troian VI, Gur’ev Iu A. [A self-fixing synthetic blood vessel endoprosthesis]. Vestn Khir Im I I Grek. 1986;137(11):123–125. [PubMed: 3824776]

98.

Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg. 1991;5(6):491–499. [PubMed: 1837729]

99.

Dake MD, Miller DC, Semba CP et al. Transluminal placement of endovascular stent-grafts for the treatment of descending thoracic aortic aneurysms. N Engl J Med. 1994;331(26):1729–1734. [PubMed: 7984192]

100.

Fillinger MF, Greenberg RK, McKinsey JF, Chaikof EL, Society for Vascular Surgery Ad Hoc Committee on TEVAR Reporting Standards. Reporting standards for thoracic endovascular aortic repair (TEVAR). J Vasc Surg. 2010;52(4):1022-1033, 11033e.1–1033e.5.

101.

Riesenman PJ, Farber MA, Mendes RR et al. Coverage of the left subclavian artery during thoracic endovascular aortic repair. J Vasc Surg. 2007;45(1):90–94. [PubMed: 17210389]

102.

Buth J, Harris PL, Hobo R et al. Neurologic complications associated with endovascular repair of thoracic aortic pathology: incidence and risk factors. A study from the European Collaborators on Stent/Graft Techniques for Aortic Aneurysm Repair (EUROSTAR) registry. J Vasc Surg. 2007;46(6):1103–1110. [PubMed: 18154984]

103.

Bozinovski J, LeMaire SA, Weldon SA, Coselli JS. Hybrid repairs of the distal aortic arch and proximal descending thoracic aorta. Op Tech Thorac Cardiovasc Surg. 2007;12(3):167–177.

104.

Woo EY, Bavaria JE, Pochettino A et al. Techniques for preserving vertebral artery perfusion during thoracic aortic stent grafting requiring aortic arch landing. Vasc Endovascular Surg. 2006;40(5):367–373. [PubMed: 17038570]

105.

Fann JI, Dake MD, Semba CP et al. Endovascular stent-grafting after arch aneurysm repair using the “elephant trunk”. Ann Thorac Surg. 1995;60(4):1102–1105. [PubMed: 7574959]

106.

Lin PH, Dardik A, Coselli JS. A simple technique to facilitate antegrade thoracic endograft deployment using a hybrid elephant trunk procedure under hypothermic circulatory arrest. J Endovasc Ther. 2007;14(5):669–671. [PubMed: 17924732]

107.

Greenberg RK, West K, Pfaff K et al. Beyond the aortic bifurcation: branched endovascular grafts for thoracoabdominal and aortoiliac aneurysms. J Vasc Surg. 2006;43(5):879–886. [PubMed: 16678676]

108.

Greenberg RK, Qureshi M. Fenestrated and branched devices in the pipeline. J Vasc Surg. 2010;52(4 Suppl):15S-21S. [PubMed: 20800422]

109.

Moulakakis KG, Mylonas SN, Avgerinos E et al. The chimney graft technique for preserving visceral vessels during endovascular treatment of aortic pathologies. J Vasc Surg. 2012;55(5):1497–1503. [PubMed: 22236883]

110.

Mehta M, Darling RC III, Taggert JB et al. Outcomes of planned celiac artery coverage during TEVAR. J Vasc Surg. 2010;52(5):1153–1158. [PubMed: 20709480]

111.

Black SA, Wolfe JH, Clark M et al. Complex thoracoabdominal aortic aneurysms: endovascular exclusion with visceral revascularization. J Vasc Surg. 2006;43(6):1081–1089. [PubMed: 16765218]

112.

Zhou W, Reardon M, Peden EK, Lin PH, Lumsden AB. Hybrid approach to complex thoracic aortic aneurysms in high-risk patients: surgical challenges and clinical outcomes. J Vasc Surg. 2006;44(4):688–693. [PubMed: 16926086]

113.

Patel R, Conrad MF, Paruchuri V et al. Thoracoabdominal aneurysm repair: hybrid versus open repair. J Vasc Surg. 2009;50(1):15–22. [PubMed: 19563950]

114.

Hughes GC, Barfield ME, Shah AA et al. Staged total abdominal debranching and thoracic endovascular aortic repair for thoracoabdominal aneurysm. J Vasc Surg. 2012;56(3):621–629. [PubMed: 22575483]

115.

Geisbusch P, Hoffmann S, Kotelis D et al. Reinterventions during midterm follow-up after endovascular treatment of thoracic aortic disease. J Vasc Surg. 2011;53(6):1528–1533. [PubMed: 21609796]

116.

Dumfarth J, Michel M, Schmidli J et al. Mechanisms of failure and outcome of secondary surgical interventions after thoracic endovascular aortic repair (TEVAR). Ann Thorac Surg. 2011;91(4):1141–1146. [PubMed: 21440134]

117.

Modine T, Lions C, Destrieux-Garnier L et al. Iatrogenic iliac artery rupture and type A dissection after endovascular repair of type B aortic dissection. Ann Thorac Surg. 2004;77(1):317–319. [PubMed: 14726088]

118.

Dong Z, Fu W, Wang Y et al. Stent graft-induced new entry after endovascular repair for Stanford type B aortic dissection. J Vasc Surg. 2010;52(6):1450–1457. [PubMed: 20800417]

119.

Tshomba Y, Bertoglio L, Marone EM et al. Retrograde type A dissection after endovascular repair of a “zone 0” nondissecting aortic arch aneurysm. Ann Vasc Surg. 2010;24(7):952 .e1–952.e7

120.

Desai ND, Pochettino A, Szeto WY et al. Thoracic endovascular aortic repair: evolution of therapy, patterns of use, and results in a 10-year experience. J Thorac Cardiovasc Surg. 2011;142(3):587–594. [PubMed: 21767852]

121.

Daily PO, Trueblood HW, Stinson EB, Wuerflein RD, Shumway NE. Management of acute aortic dissections. Ann Thorac Surg. 1970;10(3):237–247. [PubMed: 5458238]

122.

DeBakey ME, Henly WS, Cooley DA et al. Surgical management of dissecting aneurysms of the aorta. J Thorac Cardiovasc Surg. 1965;49:130–149. [PubMed: 14261867]

123.

Borst HG, Heinemann MK, Stone CD. Surgical Treatment of Aortic Dissection. New York: Churchill Livingstone; 1996.

124.

Tsagakis K, Tossios P, Kamler M et al. The DeBakey classification exactly reflects late outcome and re-intervention probability in acute aortic dissection with a slightly modified type II definition. Eur J Cardiothorac Surg. 2011;40(5):1078–1084. [PubMed: 21570858]

125.

Augoustides JG, Geirsson A, Szeto WY et al. Observational study of mortality risk stratification by ischemic presentation in patients with acute type A aortic dissection: the Penn classification. Nat Clin Pract Cardiovasc Med. 2009;6(2):140–146. [PubMed: 19065126]

126.

Augoustides JG, Szeto WY, Woo EY et al. The complications of uncomplicated acute type-B dissection: the introduction of the Penn classification. J Cardiothorac Vasc Anesth. 2012;26(6):1139–1144. [PubMed: 22920842]

127.

Tsagakis K, Konorza T, Dohle DS et al. Hybrid operating room concept for combined diagnostics, intervention and surgery in acute type A dissection. Eur J Cardiothorac Surg. 2013;43(2):397–404. [PubMed: 22743082]

128.

Nienaber CA, Sievers HH. Intramural hematoma in acute aortic syndrome: more than one variant of dissection? Circulation. 2002;106(3):284–285. [PubMed: 12119238]

129.

Evangelista A, Mukherjee D, Mehta RH et al. Acute intramural hematoma of the aorta: a mystery in evolution. Circulation. 2005;111(8):1063–1070. [PubMed: 15710757]

130.

Maraj R, Rerkpattanapipat P, Jacobs LE, Makornwattana P, Kotler MN. Meta-analysis of 143 reported cases of aortic intramural hematoma. Am J Cardiol. 2000;86(6):664–668. [PubMed: 10980220]

131.

Ganaha F, Miller DC, Sugimoto K et al. Prognosis of aortic intramural hematoma with and without penetrating atherosclerotic ulcer: a clinical and radiological analysis. Circulation. 2002;106(3):342–348. [PubMed: 12119251]

132.

Clouse WD, Hallett JW Jr., Schaff HV et al. Acute aortic dissection: population-based incidence compared with degenerative aortic aneurysm rupture. Mayo Clin Proc. 2004;79(2):176–180. [PubMed: 14959911]

133.

Anagnostopoulos CE, Prabhakar MJ, Kittle CF. Aortic dissections and dissecting aneurysms. Am J Cardiol. 1972;30(3):263–273. [PubMed: 4557973]

134.

Hirst AE Jr, Johns VJ Jr, Kime SW Jr. Dissecting aneurysm of the aorta: a review of 505 cases. Medicine (Baltimore). 1958;37(3):217–279. [PubMed: 13577293]

135.

Daniel JC, Huynh TT, Zhou W et al. Acute aortic dissection associated with use of cocaine. J Vasc Surg. 2007;46(3):427–433. [PubMed: 17826227]

136.

Hatzaras IS, Bible JE, Koullias GJ et al. Role of exertion or emotion as inciting events for acute aortic dissection. Am J Cardiol. 2007;100(9):1470–1472. [PubMed: 17950810]

137.

Wang X, LeMaire SA, Chen L et al. Decreased expression of fibulin-5 correlates with reduced elastin in thoracic aortic dissection. Surgery. 2005;138(2):352–359. [PubMed: 16153447]

138.

Wang X, LeMaire SA, Chen L et al. Increased collagen deposition and elevated expression of connective tissue growth factor in human thoracic aortic dissection. Circulation. 2006;114(1 Suppl):I200–205. [PubMed: 16820572]

139.

Shen YH, Zhang L, Ren P et al. AKT2 confers protection against aortic aneurysms and dissections. Circ Res. 2013;112(4):618–632. [PubMed: 23250987]

140.

Harris KM, Strauss CE, Eagle KA et al. Correlates of delayed recognition and treatment of acute type A aortic dissection: the International Registry of Acute Aortic Dissection (IRAD). Circulation. 2011;124(18):1911–1918. [PubMed: 21969019]

141.

Erbel R, Alfonso F, Boileau C et al. Diagnosis and management of aortic dissection. Eur Heart J. 2001;22(18):1642–1681. [PubMed: 11511117]

142.

Hagan PG, Nienaber CA, Isselbacher EM et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA.[JAMA and JAMA Network Journals Full Text] 2000;283(7):897–903. [PubMed: 10685714]

143.

Klompas M. Does this patient have an acute thoracic aortic dissection? JAMA.[JAMA and JAMA Network Journals Full Text] 2002;287(17):2262–2272. [PubMed: 11980527]

144.

Shimony A, Filion KB, Mottillo S, Dourian T, Eisenberg MJ. Meta-analysis of usefulness of D-dimer to diagnose acute aortic dissection. Am J Cardiol. 2011;107(8):1227–1234. [PubMed: 21296332]

145.

Sodeck G, Domanovits H, Schillinger M et al. D-dimer in ruling out acute aortic dissection: a systematic review and prospective cohort study. Eur Heart J. 2007;28(24):3067–3075. [PubMed: 17986466]

146.

Rapezzi C, Longhi S, Graziosi M et al. Risk factors for diagnostic delay in acute aortic dissection. Am J Cardiol. 2008;102(10):1399–1406. [PubMed: 18993163]

147.

von Kodolitsch Y, Nienaber CA, Dieckmann C et al. Chest radiography for the diagnosis of acute aortic syndrome. Am J Med. 2004;116(2):73–77. [PubMed: 14715319]

148.

Nienaber CA, von Kodolitsch Y, Nicolas V et al. The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med. 1993;328(1):1–9. [PubMed: 8416265]

149.

Keren A, Kim CB, Hu BS et al. Accuracy of biplane and multiplane transesophageal echocardiography in diagnosis of typical acute aortic dissection and intramural hematoma. J Am Coll Cardiol. 1996;28(3):627–636. [PubMed: 8772749]

150.

Miller JS, LeMaire SA, Coselli JS. Evaluating aortic dissection: when is coronary angiography indicated? Heart. 2000;83(6):615–616. [PubMed: 10814612]

151.

Scholl FG, Coady MA, Davies R et al. Interval or permanent nonoperative management of acute type A aortic dissection. Arch Surg.[Archives of Surgery Full Text] 1999;134(4):402–405. [PubMed: 10199313]

152.

Gillinov AM, Lytle BW, Kaplon RJ et al. Dissection of the ascending aorta after previous cardiac surgery: differences in presentation and management. J Thorac Cardiovasc Surg. 1999;117(2):252–260. [PubMed: 9918965]

153.

Kirsch M, Soustelle C, Houel R, Hillion ML, Loisance D. Risk factor analysis for proximal and distal reoperations after surgery for acute type A aortic dissection. J Thorac Cardiovasc Surg. 2002;123(2):318–325. [PubMed: 11828292]

154.

Crawford ES, Kirklin JW, Naftel DC et al. Surgery for acute dissection of ascending aorta. Should the arch be included? J Thorac Cardiovasc Surg. 1992;104(1):46–59. [PubMed: 1614214]

155.

Westaby S, Saito S, Katsumata T. Acute type A dissection: conservative methods provide consistently low mortality. Ann Thorac Surg. 2002;73(3):707–713. [PubMed: 11899170]

156.

Geirsson A, Bavaria JE, Swarr D et al. Fate of the residual distal and proximal aorta after acute type A dissection repair using a contemporary surgical reconstruction algorithm. Ann Thorac Surg. 2007;84(6):1955–1964. [PubMed: 18036916]

157.

Malvindi PG, van Putte BP, Sonker U et al. Reoperation after acute type A aortic dissection repair: a series of 104 patients. Ann Thorac Surg. 2013;95(3):922–927. [PubMed: 23369349]

158.

Glower DD, Speier RH, White WD et al. Management and long-term outcome of aortic dissection. Ann Surg. 1991;214(1):31–41. [PubMed: 2064469]

159.

Kazui T, Washiyama N, Muhammad BA et al. Extended total arch replacement for acute type A aortic dissection: experience with seventy patients. J Thorac Cardiovasc Surg. 2000;119(3):558–565. [PubMed: 10694617]

160.

Hoffman A, Damberg AL, Schalte G et al. Thoracic stent graft sizing for frozen elephant trunk repair in acute type A dissection. J Thorac Cardiovasc Surg. 2013;145(4):964–969. [PubMed: 22507842]

161.

Karck M, Chavan A, Khaladj N et al. The frozen elephant trunk technique for the treatment of extensive thoracic aortic aneurysms: operative results and follow-up. Eur J Cardiothorac Surg. 2005;28(2):286-290; –discussion 290. [PubMed: 15922612]

162.

Roselli EE, Rafael A, Soltesz EG, Canale L, Lytle BW. Simplified frozen elephant trunk repair for acute DeBakey type I dissection. J Thorac Cardiovasc Surg. 2013;145(3 Suppl):S197–S201. [PubMed: 23260435]

163.

Gorlitzer M, Weiss G, Meinhart J et al. Fate of the false lumen after combined surgical and endovascular repair treating Stanford type A aortic dissections. Ann Thorac Surg. 2010;89(3):794–799. [PubMed: 20172130]

164.

Di Bartolomeo R, Di Marc L, Armaro A et al. Treatment of complex disease of the thoracic aorta: the frozen elephant trunk technique with the E-vita open prosthesis. Eur J Cardiothorac Surg. 2009;35(4):671-675; –discussion 675-676. [PubMed: 19233674]

165.

Uchida N, Katayama A, Tamura K et al. Long-term results of the frozen elephant trunk technique for extended aortic arch disease. Eur J Cardiothorac Surg. 2010;37(6):1338–1345. [PubMed: 20303777]

166.

Lima B, Roselli EE, Soltesz EG et al. Modified and “reverse” frozen elephant trunk repairs for extensive disease and complications after stent grafting. Ann Thorac Surg. 2012;93(1):103-109; –discussion 109. [PubMed: 22088418]

167.

Roselli EE, Soltesz EG, Mastracci T, Svensson LG, Lytle BW. Antegrade delivery of stent grafts to treat complex thoracic aortic disease. Ann Thorac Surg. 2010;90(2):539–546. [PubMed: 20667347]

168.

Kouchoukos NT. Frozen elephant trunk technique for extensive chronic thoracic aortic dissection: is it the final answer? Ann Thorac Surg. 2011;92(5):1557–1558. [PubMed: 22051249]

169.

Genoni M, Paul M, Jenni R et al. Chronic beta-blocker therapy improves outcome and reduces treatment costs in chronic type B aortic dissection. Eur J Cardiothorac Surg. 2001;19(5):606–610. [PubMed: 11343940]

170.

DeBakey ME, McCollum CH, Crawford ES et al. Dissection and dissecting aneurysms of the aorta: twenty-year follow-up of five hundred twenty-seven patients treated surgically. Surgery. 1982;92(6):1118–1134. [PubMed: 7147190]

171.

Fann JI, Smith JA, Miller DC et al. Surgical management of aortic dissection during a 30-year period. Circulation. 1995;92(9 Suppl):II113–II121. [PubMed: 7586393]

172.

Elefteriades JA, Hartleroad J, Gusberg RJ et al. Long-term experience with descending aortic dissection: the complication-specific approach. Ann Thorac Surg. 1992;53(1):11–20. [PubMed: 1728218]

173.

Barnes DM, Williams DM, Dasika NL et al. A single-center experience treating renal malperfusion after aortic dissection with central aortic fenestration and renal artery stenting. J Vasc Surg. 2008;47(5):903–910. [PubMed: 18455638]

174.

Miller DC. Through the looking glass: The first 20 years of thoracic aortic stent-grafting. J Thorac Cardiovasc Surg. 2013;145(3 Suppl):S142–S148. [PubMed: 23410771]

175.

Hughes GC, Andersen ND, McCann RL. Management of acute type B aortic dissection. J Thorac Cardiovasc Surg. 2013;145(3 Suppl):S202–S207. [PubMed: 23267526]

176.

Kusagawa H, Shimono T, Ishida M et al. Changes in false lumen after transluminal stent-graft placement in aortic dissections: six years’ experience. Circulation. 2005;111(22):2951–2957. [PubMed: 15927978]

177.

Nienaber CA, Rousseau H, Eggebrecht H et al. Randomized comparison of strategies for type B aortic dissection: the INvestigation of STEnt Grafts in Aortic Dissection (INSTEAD) trial. Circulation. 2009;120(25):2519–2528. [PubMed: 19996018]

178.

Demers P, Miller DC, Mitchell RS et al. Stent-graft repair of penetrating atherosclerotic ulcers in the descending thoracic aorta: mid-term results. Ann Thorac Surg. 2004;77(1):81–86. [PubMed: 14726040]

179.

Patel HJ, Sood V, Williams DM et al. Late outcomes with repair of penetrating thoracic aortic ulcers: the merits of an endovascular approach. Ann Thorac Surg. 2012;94(2):516-522; –discussion 522-523. [PubMed: 22621877]

180.

Coselli JS, LeMaire SA, de Figueiredo LP, Kirby RP. Paraplegia after thoracoabdominal aortic aneurysm repair: is dissection a risk factor? Ann Thorac Surg. 1997;63(1):28–35. [PubMed: 8993237]

181.

Aomi S, Nakajima M, Nonoyama M et al. Aortic root replacement using composite valve graft in patients with aortic valve disease and aneurysm of the ascending aorta: twenty years’ experience of late results. Artif Organs. 2002;26(5):467–473. [PubMed: 12000445]

182.

Kindo M, Billaud P, Gerelli S et al. Twenty-seven-year experience with composite valve graft replacement of the aortic root. J Heart Valve Dis. 2007;16(4):370–377. [PubMed: 17702361]

183.

David TE, Mohr FW, Bavaria JE et al. Initial experience with the Toronto Root bioprosthesis. J Heart Valve Dis. 2004;13(2):248–251. [PubMed: 15086264]

184.

Gleason TG, David TE, Coselli JS, Hammon JW Jr., Bavaria JE. St. Jude Medical Toronto biologic aortic root prosthesis: early FDA phase II IDE study results. Ann Thorac Surg. 2004;78(3):786–793. [PubMed: 15336992]

185.

Kincaid EH, Cordell AR, Hammon JW, Adair SM, Kon ND. Coronary insufficiency after stentless aortic root replacement: risk factors and solutions. Ann Thorac Surg. 2007;83(3):964–968. [PubMed: 17307442]

186.

Kon ND, Cordell AR, Adair SM, Dobbins JE, Kitzman DW. Aortic root replacement with the freestyle stentless porcine aortic root bioprosthesis. Ann Thorac Surg. 1999;67(6):1609–1615. [PubMed: 10391263]

187.

Melina G, De Robertis F, Gaer JA et al. Mid-term pattern of survival, hemodynamic performance and rate of complications after Medtronic Freestyle versus homograft full aortic root replacement: results from a prospective randomized trial. J Heart Valve Dis. 2004;13(6):972–975. [PubMed: 15597592]

188.

Badiu CC, Eichinger W, Bleiziffer S et al. Should root replacement with aortic valve-sparing be offered to patients with bicuspid valves or severe aortic regurgitation? Eur J Cardiothorac Surg. 2010;38(5):515–522. [PubMed: 20400326]

189.

David TE, Maganti M, Armstrong S. Aortic root aneurysm: principles of repair and long-term follow-up. J Thorac Cardiovasc Surg. 2010;140(6 Suppl):S14-S19; discussion S45-S51.

190.

Zingone B, Gatti G, Spina A et al. Current role and outcomes of ascending aortic replacement for severe nonaneurysmal aortic atherosclerosis. Ann Thorac Surg. 2010;89(2):429–434. [PubMed: 20103316]

191.

Achneck HE, Rizzo JA, Tranquilli M, Elefteriades JA. Safety of thoracic aortic surgery in the present era. Ann Thorac Surg. 2007;84(4):1180–1185. [PubMed: 17888967]

192.

Estrera AL, Miller CC III, Madisetty J et al. Ascending and transverse aortic arch repair: the impact of glomerular filtration rate on mortality. Ann Surg. 2008;247(3):524–529. [PubMed: 18376199]

193.

Fleck TM, Czerny M, Hutschala D et al. The incidence of transient neurologic dysfunction after ascending aortic replacement with circulatory arrest. Ann Thorac Surg. 2003;76(4):1198–1202. [PubMed: 14530011]

194.

Immer FF, Barmettler H, Berdat PA et al. Effects of deep hypothermic circulatory arrest on outcome after resection of ascending aortic aneurysm. Ann Thorac Surg. 2002;74(2):422–425. [PubMed: 12173823]

195.

Heinemann MK, Buehner B, Jurmann MJ, Borst HG. Use of the “elephant trunk technique” in aortic surgery. Ann Thorac Surg. 1995;60(1):2–6. [PubMed: 7598596]

196.

LeMaire SA, Carter SA, Coselli JS. The elephant trunk technique for staged repair of complex aneurysms of the entire thoracic aorta. Ann Thorac Surg. 2006;81(5):1561–1569. [PubMed: 16631635]

197.

Safi HJ, Miller CC III, Estrera AL et al. Staged repair of extensive aortic aneurysms: long-term experience with the elephant trunk technique. Ann Surg. 2004;240(4):677–684. [PubMed: 15383795]

198.

Sundt TM, Moon MR, DeOliviera N et al. Contemporary results of total aortic arch replacement. J Card Surg. 2004;19(3):235–239. [PubMed: 15151651]

199.

Svensson LG, Kim KH, Blackstone EH et al. Elephant trunk procedure: newer indications and uses. Ann Thorac Surg. 2004;78(1):109–116. [PubMed: 15223413]

200.

Kazui T, Yamashita K, Washiyama N et al. Aortic arch replacement using selective cerebral perfusion. Ann Thorac Surg. 2007;83(2):S796-S798; discussion S824-S831.

201.

Bischoff MS, Brenner RM, Scheumann J et al. Long-term outcome after aortic arch replacement with a trifurcated graft. J Thorac Cardiovasc Surg. 2010;140(6 Suppl):S71-76; –discussion S86-S91.

202.

Iba Y, Minatoya K, Matsuda H et al. Contemporary open aortic arch repair with selective cerebral perfusion in the era of endovascular aortic repair. J Thorac Cardiovasc Surg. 2013;145(3 Suppl):S72–S77. [PubMed: 23260455]

203.

Thomas M, Li Z, Cook DJ, Greason KL, Sundt TM. Contemporary results of open aortic arch surgery. J Thorac Cardiovasc Surg. 2012;144(4):838–844. [PubMed: 22177097]

204.

Urbanski PP, Lenos A, Bougioukakis P et al. Mild-to-moderate hypothermia in aortic arch surgery using circulatory arrest: a change of paradigm? Eur J Cardiothorac Surg. 2012;41(1):185–191. [PubMed: 21616675]

205.

Kondoh H, Taniguchi K, Funatsu T et al. Total arch replacement with long elephant trunk anastomosed at the base of the innominate artery: a single-centre longitudinal experience. Eur J Cardiothorac Surg. 2012;42(5):840-848; –discussion 848. [PubMed: 22518042]

206.

Flores J, Kunihara T, Shiiya N et al. Extensive deployment of the stented elephant trunk is associated with an increased risk of spinal cord injury. J Thorac Cardiovasc Surg. 2006;131(2):336–342. [PubMed: 16434262]

207.

Antoniou GA, Mireskandari M, Bicknell CD et al. Hybrid repair of the aortic arch in patients with extensive aortic disease. Eur J Vasc Endovasc Surg. 2010;40(6):715–721. [PubMed: 20920861]

208.

Geisbusch P, Kotelis D, Muller-Eschner M, Hyhlik-Durr A, Bockler D. Complications after aortic arch hybrid repair. J Vasc Surg. 2011;53(4):935–941. [PubMed: 21215585]

209.

Czerny M, Weigang E, Sodeck G et al. Targeting landing zone 0 by total arch rerouting and TEVAR: midterm results of a transcontinental registry. Ann Thorac Surg. 2012;94(1):84–89. [PubMed: 22595468]

210.

Trimarchi S, Eagle KA, Nienaber CA et al. Role of age in acute type A aortic dissection outcome: report from the International Registry of Acute Aortic Dissection (IRAD). J Thorac Cardiovasc Surg. 2010;140(4):784–789. [PubMed: 20176372]

211.

Rampoldi V, Trimarchi S, Eagle KA et al. Simple risk models to predict surgical mortality in acute type A aortic dissection: the International Registry of Acute Aortic Dissection score. Ann Thorac Surg. 2007;83(1):55–61. [PubMed: 17184630]

212.

Kruger T, Weigang E, Hoffmann I et al. Cerebral protection during surgery for acute aortic dissection type A: results of the German Registry for Acute Aortic Dissection Type A (GERAADA). Circulation. 2011;124(4):434–443. [PubMed: 21747050]

213.

Dake MD, Miller DC, Mitchell RS et al. The “first generation” of endovascular stent-grafts for patients with aneurysms of the descending thoracic aorta. J Thorac Cardiovasc Surg. 1998;116(5):689–703. [PubMed: 9806376]

214.

Demers P, Miller DC, Mitchell RS et al. Midterm results of endovascular repair of descending thoracic aortic aneurysms with first-generation stent grafts. J Thorac Cardiovasc Surg. 2004;127(3):664–673. [PubMed: 15001894]

215.

Bavaria JE, Appoo JJ, Makaroun MS et al. Endovascular stent grafting versus open surgical repair of descending thoracic aortic aneurysms in low-risk patients: a multicenter comparative trial. J Thorac Cardiovasc Surg. 2007;133(2):369–377. [PubMed: 17258566]

216.

Fairman RM, Criado F, Farber M et al. Pivotal results of the Medtronic Vascular Talent Thoracic Stent Graft System: the VALOR trial. J Vasc Surg. 2008;48(3):546–554. [PubMed: 18572352]

217.

Matsumura JS, Cambria RP, Dake MD et al. International controlled clinical trial of thoracic endovascular aneurysm repair with the Zenith TX2 endovascular graft: 1-year results. J Vasc Surg. 2008;47(2):247–257. [PubMed: 18241743]

218.

Makaroun MS, Dillavou ED, Wheatley GH, Cambria RP. Five-year results of endovascular treatment with the Gore TAG device compared with open repair of thoracic aortic aneurysms. J Vasc Surg. 2008;47(5):912–918. [PubMed: 18353605]

219.

Foley PJ, Criado FJ, Farber MA et al. Results with the Talent thoracic stent graft in the VALOR trial. J Vasc Surg. 2012;56(5):1214–1221 1221.e1. [PubMed: 22925732]

220.

Czerny M, Zimpfer D, Rodler S et al. Endovascular stent-graft placement of aneurysms involving the descending aorta originating from chronic type B dissections. Ann Thorac Surg. 2007;83(5):1635–1639. [PubMed: 17462371]

221.

Nienaber CA. Results from the INSTEAD trial. Paper presented at: Sixth Annual International Symposium on Advances in Understanding Aortic Diseases; Sept 30-Oct 1, 2005; Berlin, Germany.

222.

Brunkwall J, Lammer J, Verhoeven E, Taylor P. ADSORB: a study on the efficacy of endovascular grafting in uncomplicated acute dissection of the descending aorta. Eur J Vasc Endovasc Surg. 2012;44(1):31–36. [PubMed: 22575291]

223.

Coselli JS, LeMaire SA, Conklin LD, Adams GJ. Left heart bypass during descending thoracic aortic aneurysm repair does not reduce the incidence of paraplegia. Ann Thorac Surg. 2004;77(4):1298–1303. [PubMed: 15063255]

224.

Chiesa R, Tshomba Y, Civilini E et al. Open repair of descending thoracic aneurysms. HSR Proc Intensive Care Cardiovasc Anesth. 2010;2(3):177–190. [PubMed: 23440685]

225.

Estrera AL, Miller CC III, Chen EP et al. Descending thoracic aortic aneurysm repair: 12-year experience using distal aortic perfusion and cerebrospinal fluid drainage. Ann Thorac Surg. 2005;80(4):1290–1296. [PubMed: 16181856]

226.

Dick F, Hinder D, Immer FF et al. Outcome and quality of life after surgical and endovascular treatment of descending aortic lesions. Ann Thorac Surg. 2008;85(5):1605–1612. [PubMed: 18442547]

227.

Stone DH, Brewster DC, Kwolek CJ et al. Stent-graft versus open-surgical repair of the thoracic aorta: mid-term results. J Vasc Surg. 2006;44(6):1188–1197. [PubMed: 17145420]

228.

Brandt M, Hussel K, Walluscheck KP et al. Stent-graft repair versus open surgery for the descending aorta: a case-control study. J Endovasc Ther. 2004;11(5):535–538. [PubMed: 15482026]

229.

Goodney PP, Travis L, Lucas FL et al. Survival after open versus endovascular thoracic aortic aneurysm repair in an observational study of the Medicare population. Circulation. 2011;124(24):2661–2669. [PubMed: 22104552]

230.

LeMaire SA, Price MD, Green SY, Zarda S, Coselli JS. Results of open thoracoabdominal aortic aneurysm repair. Ann Cardiothorac Surg. 2012;1(3):286–292. [PubMed: 23977510]

231.

Chiesa R, Melissano G, Civilini E et al. Ten years experience of thoracic and thoracoabdominal aortic aneurysm surgical repair: lessons learned. Ann Vasc Surg. 2004;18(5):514–520. [PubMed: 15534729]

232.

Coselli JS, Bozinovski J, LeMaire SA. Open surgical repair of 2286 thoracoabdominal aortic aneurysms. Ann Thorac Surg. 2007;83(2):S862–S864. [PubMed: 17257942]

233.

Conrad MF, Crawford RS, Davison JK, Cambria RP. Thoracoabdominal aneurysm repair: a 20-year perspective. Ann Thorac Surg. 2007;83(2):S856–S861. [PubMed: 17257941]

234.

Schepens MA, Kelder JC, Morshuis WJ et al. Long-term follow-up after thoracoabdominal aortic aneurysm repair. Ann Thorac Surg. 2007;83(2):S851–S855. [PubMed: 17257940]

235.

Rigberg DA, McGory ML, Zingmond DS et al. Thirty-day mortality statistics underestimate the risk of repair of thoracoabdominal aortic aneurysms: a statewide experience. J Vasc Surg. 2006;43(2):217–222. [PubMed: 16476589]

236.

Cowan JA Jr, Dimick JB, Henke PK et al. Surgical treatment of intact thoracoabdominal aortic aneurysms in the United States: hospital and surgeon volume-related outcomes. J Vasc Surg. 2003;37(6):1169–1174. [PubMed: 12764260]

237.

Wong DR, Parenti JL, Green SY et al. Open repair of thoracoabdominal aortic aneurysm in the modern surgical era: contemporary outcomes in 509 patients. J Am Coll Surg. 2011;212(4):569-579; –discussion 579-581. [PubMed: 21463791]

238.

Trimarchi S, Tolenaar JL, Tsai TT et al. Influence of clinical presentation on the outcome of acute B aortic dissection: evidences from IRAD. J Cardiovasc Surg (Torino). 2012;53(2):161–168. [PubMed: 22456637]

239.

Tsai TT, Fattori R, Trimarchi S et al. Long-term survival in patients presenting with type B acute aortic dissection: insights from the International Registry of Acute Aortic Dissection. Circulation. 2006;114(21):2226–2231. [PubMed: 17101856]

240.

Slonim SM, Miller DC, Mitchell RS et al. Percutaneous balloon fenestration and stenting for life-threatening ischemic complications in patients with acute aortic dissection. J Thorac Cardiovasc Surg. 1999;117(6):1118–1126. [PubMed: 10343260]

241.

Dake MD, Kato N, Mitchell RS et al. Endovascular stent-graft placement for the treatment of acute aortic dissection. N Engl J Med. 1999;340(20):1546–1552. [PubMed: 10332016]

242.

Eggebrecht H, Nienaber CA, Neuhauser M et al. Endovascular stent-graft placement in aortic dissection: a meta-analysis. Eur Heart J. 2006;27(4):489–498. [PubMed: 16227309]

243.

White RA, Miller DC, Criado FJ et al. Report on the results of thoracic endovascular aortic repair for acute, complicated, type B aortic dissection at 30 days and 1 year from a multidisciplinary subcommittee of the Society for Vascular Surgery Outcomes Committee. J Vasc Surg. 2011;53(4):1082–1090. [PubMed: 21334174]

244.

Coselli JS, LeMaire SA. Acute type B dissections: open surgical options. In: Eskandari MK, Pearce WH, Yao JST, eds. Current Vascular Surgery 2012. Shelton: People’s Medical Publishing House-USA; 2013:351–362.

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Figure 22-1.

Causes and Pathogenesis

General Considerations

Nonspecific Medial Degeneration

Aortic Dissection

Genetic Disorders

Marfan Syndrome

Loeys-Dietz Syndrome

Ehlers-Danlos Syndrome

Familial Aortic Aneurysms

Aneurysms-Osteoarthritis Syndrome

Congenital Bicuspid Aortic Valve

Bovine aortic arch

Infection

Aortitis

Pseudoaneurysms

Clinical History

Clinical Manifestations

Local Compression and Erosion

Aortic Valve Regurgitation

Distal Embolization

Rupture

Diagnostic Evaluation

Plain Radiography

Figure 22-2.

Echocardiography and Abdominal Ultrasonography

Computed Tomography

Figure 22-3.

Magnetic Resonance Angiography

Invasive Aortography and Cardiac Catheterization

Treatment

Selecting the Appropriate Treatment

Determination of the Extent and Severity of Disease

Indications for Operation

Open Repair vs. Endovascular Repair

Preoperative Assessment and Preparation

Cardiac Evaluation

Pulmonary Evaluation

Renal Evaluation

Operative Repair

Proximal Thoracic Aortic Aneurysms

Open Repair

Figure 22-4.

Figure 22-5.

Figure 22-6.

Figure 22-7.

Figure 22-8.

Figure 22-9.

Endovascular Repair

Hybrid Repair

Figure 22-10.

Figure 22-11.

Distal Thoracic Aortic Aneurysms

Open Repair

Figure 22-12.

Figure 22-13.

Figure 22-14.

Endovascular Repair

Figure 22-15.

Hybrid Repair

Figure 22-16.

Postoperative Considerations

Open Procedures

Endovascular Procedures

Pathology and Classification

Figure 22-17.

Figure 22-18.

Dissection vs. Aneurysm

Classification

Location

Figure 22-19.

Chronicity

Variants

Causes and Clinical History

Clinical Manifestations

Diagnostic Evaluation

Treatment

Initial Assessment and Management