Treating aneurysms that arise from the aortic segments distal to the left subclavian artery poses challenges that are distinct from those presented by aneurysms of the more proximal ascending and arch segments. The distal aortic segments comprise the descending thoracic aorta, which extends from the left subclavian artery to the diaphragm within the chest, and the abdominal segment that extends from the diaphragm to the iliac bifurcation. The diaphragm divides the thoracic aorta from the abdominal aorta.

An aortic aneurysm that is limited to the chest (distal to the left subclavian artery) is classified as a descending thoracic aortic aneurysm (DTAA). An aortic aneurysm that traverses the diaphragm and extends into both the chest and the abdomen to any degree is considered a thoracoabdominal aortic aneurysm (TAAA) (Fig. 49-1). Aneurysms in these locations can be extensive and can involve many or all of the aortic branch vessels. In the last decade there have been substantial changes regarding the treatment of distal aortic aneurysms because of the emergence of thoracic endovascular aortic repair (TEVAR) and its near dominance in DTAA repair. Although open repair remains the standard of care for TAAAs, it is now selectively used for DTAAs. Modern critical care and continually refined surgical adjuncts for organ protection have made the outcomes of surgical repair better than they were in previous decades, but operative treatment of DTAA and TAAA continues to represent a significant clinical challenge to the cardiovascular surgeon.

The etiology of DTAA and TAAA has changed over time. Whereas tertiary syphilis was the most common cause of thoracic aneurysms in the early 1900s, other causes are more prevalent today. Well-established causes of DTAA and TAAA include medial degeneration, atherosclerosis, aortic dissection, connective tissue disorders, aortitis (eg, Takayasu arteritis), aortic coarctation, infection, and trauma. As our understanding of genetics increases, and as more advanced genetic testing becomes available, classification systems are likely to evolve to include more molecular factors. Perhaps partly because of improved screening for aneurysmal disease and the increasing age of the population, it is certain that the incidence and prevalence of thoracic aortic aneurysms are increasing over time.¹

The most common types of aneurysms of the descending and thoracoabdominal aorta today are grouped into the category of atherosclerotic aneurysms. Unfortunately, although this term may be descriptive, it may not accurately describe the mechanism of aneurysmal changes. Although atherosclerosis and aortic aneurysms share common risk factors and frequently coexist, thoracic aortic aneurysms are primarily the result of age-related medial degeneration, which is characterized by changes in elastin and collagen that reduce aortic integrity and tensile strength. Subsequent aortic enlargement and aneurysm formation provide fertile ground for superimposed intimal atherosclerosis and further degeneration of the aortic wall. The usual histologic changes in the aging aorta include elastin fragmentation, fibrosis with increased collagen deposition, and medial degeneration.² As with most aneurysmogenic processes, medial degeneration usually causes diffuse, fusiform aortic dilatation. In some cases, medial degeneration produces discrete saccular aneurysms along the descending thoracic aorta; however, saccular aneurysms are more commonly associated with aortic infection (see below). Additionally, saccular aneurysms may be superimposed on or coexist with more generalized, fusiform aneurysmal disease of the thoracoabdominal aorta.

Risk factors for aortic dissection and aortic aneurysm overlap to a great extent, but once an aorta becomes dissected, the dissection itself becomes an independent risk factor for subsequent dilation and aneurysmal changes. Two of the DeBakey types of aortic dissection involve the distal aorta: type I, in which nearly the entire length of the aorta is dissected, and type III, in which the dissection is limited to varying portions of the distal aorta, and the proximal aorta is unaffected. Aortic dissections occur in the medial layer separating the intima from the adventitia; blood flows through the true aortic lumen and through one or more false lumen channels that can form at various points along the aorta. This process weakens the outer aortic wall, making it prone to progressive aneurysmal dilatation (Fig. 49-2).

In survivors of DeBakey type I dissection, the persistence of a pressurized false lumen has been associated with subsequent distal aneurysm formation, need for intervention, and increased mortality.³ In an attempt to thrombose the false channel and thereby decrease the risk of late aneurysm formation, endovascular strategies have been developed to exclude segments of the false lumen in both acute (≤2 weeks since onset)⁴ and chronic⁵ aortic dissection. Such approaches are dependent on a variety of factors, including the extent of aortic dissection; downstream portions of the false lumen—those without endovascular obliteration—continue to be pressurized and may perfuse upstream portions in a retrograde fashion.

Penetrating aortic ulcers and intramural hematomas are two variants of aortic dissection that can occur in the descending and abdominal aortic segments. Penetrating aortic ulcers are disrupted atherosclerotic plaques that can penetrate the aortic wall, leading to classic dissection or rupture. Intramural hematomas are collections of blood within the aortic wall that occur without an intimal tear; growth of the hematoma can result in classic dissection.

Genetic mutations or defects can give rise to defective components of the aortic extracellular matrix, leading to aortic aneurysm and dissection. Aortic aneurysms that occur in patients with these genetic disorders can be a part of a named syndrome, accompanied by a constellation of extra-aortic symptoms, or they may be part of a heterogeneous group of familial thoracic aortic aneurysms and dissections that occur in isolation. In a national registry of genetically triggered thoracic aortic aneurysms, Marfan syndrome is the most common genetic cause of aortic aneurysms (36%).⁶ Marfan syndrome is a connective tissue disorder that results from a fibrillin-1 (FBN1) gene mutation; the altered fibrillin leads to aberrant signaling of transforming growth factor beta (TGF-β) and other events that lead to the deposition of extensive amounts of mucopolysaccharides in the aortic extracellular matrix and fragmentation of elastic fibers. The aorta in Marfan syndrome patients is prone to dissection, which is the most common cause of DTAAs and TAAAs in these patients.^7,8 Other syndromes that are infrequently encountered during DTAA and TAAA repairs include vascular Ehlers-Danlos, aneurysms-osteoarthritis, and Loeys-Dietz. Like Marfan syndrome, Loeys-Dietz syndrome is an autosomal dominant disorder that is linked to an alteration in TGF-β signaling. First described in 2005, Loeys-Dietz is a particularly aggressive aortic disorder, characterized by vascular tortuosity, and a greater propensity for rupture at smaller aortic diameters than in patients with Marfan syndrome. Recently, four types of Loeys-Dietz have been identified, each associated with a mutation in a particular gene: transforming growth factor (TGF)-beta receptor I (TGFBR1), TGF-beta receptor II (TGFBR2), decapentaplegic homolog 3 (SMAD3), and transforming growth factor beta 2 ligand (TGFB2).⁹

Both chronic, nonspecific aortitis and systemic autoimmune disorders—such as Takayasu arteritis, giant cell arteritis (temporal arteritis), and rheumatoid aortitis—can cause destruction of the aortic media and progressive aneurysm formation. Although Takayasu arteritis usually causes obstructive lesions related to severe intimal thickening, the associated medial destruction can result in aneurysmal dilatation.

Aneurysms involving the upper descending thoracic aorta can develop in patients with congenital aortic coarctation. These aneurysms may occur concomitantly with unrepaired native coarctation or years after any manner of coarctation repair, including endovascular repair.^10,11 The postrepair aneurysms appear to be more common in patients who have had balloon angioplasty than in those who underwent surgery; this is speculated to be due to the rupture of elastic fibers during dilatation.¹¹

Infection can produce a saccular “mycotic” aneurysm in a localized area of the aortic wall that has been damaged by the infectious process. For unknown reasons, such mycotic aneurysms tend to occur along the lesser curvature of the transverse aortic arch or in the upper abdominal aorta adjacent to the origins of the visceral branches. In such cases, only a portion of the aortic circumference is affected; consequently, localized weakening causes a diverticular or saccular outpouching. Common causative organisms include Staphylococcus aureus, Staphylococcus epidermidis, Salmonella, and Streptococcus,¹² and more than one pathogen may be present. Although uncommon, when a distal mycotic aneurysm is suspected, urgent evaluation is warranted; mycotic saccular aneurysms tend to be unpredictable, often have periods of rapid growth, and rupture more readily than fusiform aneurysms caused by medial degeneration.¹³

Each of the disease processes described above causes aneurysms through progressive degeneration and dilatation of the aortic wall. In contrast, pseudoaneurysms of the thoracic aorta form as the result of chronic leaks through discrete defects in the aortic wall. These leaks are initially contained by surrounding tissue; the accumulation of organized thrombus and the associated fibrosis forms the wall of the pseudoaneurysm. Pseudoaneurysms can develop after aortic surgery, endovascular aortic repair, invasive imaging, or from primary defects in the aortic wall. Unrepaired blunt and penetrating injuries are the other common cause of aortic pseudoaneurysms. Chronic traumatic pseudoaneurysms typically develop in the proximal descending thoracic aorta after blunt aortic injuries; the management of these lesions is covered in detail in a subsequent chapter.

An untreated aneurysm in the thoracic and thoracoabdominal aorta can progress to dissection, rupture, or both if given enough time. A dissected aorta that was originally of normal caliber will tend to dilate and become aneurysmal. The causes and genetics of these aneurysms vary, but there are commonalities in the mechanical and pathophysiologic aspects of their formation and development. Understanding these processes will help surgeons determine the timing and the nature of the operative intervention needed.

An aneurysm is defined as a permanent dilation of an artery to at least 1.5 times its normal diameter at a given location.¹⁴ However, the normal aortic diameter is perhaps more difficult to define because it varies by the patient’s age, gender, and body size. Even when adjusted for age and body surface area, mean aortic size is significantly smaller in women than in men; on average, aortic diameter is 2 to 3 mm greater in men than in women. In the community-based Framingham Heart Study, computed tomography studies from 3431 adults, at least 35 years old, were analyzed by age, gender, and body surface area. At the descending thoracic aorta, the average aortic diameter was 25.8 mm for men and 23.1 mm for women; at the infrarenal abdominal aorta, it was 19.3 mm for men and 16.7 mm for women; and at the lower abdominal aorta, it was 18.7 mm for men and 16.0 mm for women.¹⁵ In this study, aortic enlargement was strongly correlated with male gender, advancing age, and increased body surface area—for men ≥ 65 years old and with a large body surface area (≥2.1), the mean descending thoracic aortic diameter increased by 4.5 to 30.3 mm; and for women ≥ 65 years and with a large body surface area (≥1.9), this increased by 4.0 to 27.1 mm. Notably, body surface area is a better predictor of aortic size than height or weight, particularly in patients less than 50 years of age.¹⁶

The descending thoracic aorta has a slightly higher rate of expansion over time than the ascending aorta and is noted to average 1 to 4 mm/year.¹⁷ The rate is not constant, and it increases as the diameter increases. A dissection in an otherwise small aneurysm can lead to a sudden increase in the rate of growth; likewise, a chronically dissected aorta tends to dilate at a faster rate than a nondissected one. The relationship among pressure, vessel diameter, and vessel wall tension is described by Laplace’s law. As the luminal diameter increases, there is increasing wall tension, which in turn contributes to the cycle of progressive dilatation. Unfortunately, as the dilation progresses, the wall tension eventually becomes too great for the maximally stretched aortic wall. A tear can occur within the intimal and medial layers, resulting in a dissection that propagates down the length of the aorta, or a tear can penetrate the full thickness of the aortic wall, resulting in contained or free rupture. The aortic size at which this event occurs is determined by several factors, including the presence or absence of a connective tissue disorder, the presence and severity of hypertension, and the patient’s body size. In a large series of patients, Elefteriades and colleagues¹⁸ have shown that in the thoracic aorta, there is a sharp increase in the incidence of aortic complications at aneurysmal diameters greater than 6 cm, with a 14% combined risk of rupture, dissection, and death. In a population-based study, the 5-year risk of rupture doubled from 16% for aneurysms 4 to 5.9 cm in diameter to 31% in aneurysms 6 cm or more in diameter.¹⁹

At the time of diagnosis, patients with DTAAs and TAAAs are commonly asymptomatic. For example, Panneton and Hollier²⁰ reported that degenerative TAAAs are asymptomatic in roughly 43% of patients. In asymptomatic patients, DTAAs and TAAAs are often discovered when imaging studies are performed to evaluate unrelated problems. For example, computed tomography scans may indicate aortic dilatation, and chest radiographs may show widening of the descending thoracic aortic shadow, which may be outlined by a rim of calcification outlining the dilated aneurysmal aortic wall (Fig. 49-3). Aneurysmal calcium may also be seen in the upper abdomen on standard radiograms.

Although DTAAs and TAAAs remain asymptomatic for long periods of time, most ultimately produce a variety of symptoms before they rupture. Degenerative TAAAs produce symptoms in approximately 57% of patients; 9% of patients present with rupture.²⁰ The most frequent symptom is back pain between the scapulae. When the aneurysm is large in the region of the aortic hiatus, pressure on adjacent structures may cause mid-back and epigastric pain. Other potential signs and symptoms related to compression or erosion of adjacent organs include stridor, wheezing, cough, hemoptysis, dysphagia, and gastrointestinal obstruction or bleeding. Hoarseness results from traction on the vagus nerve as the distal aortic arch expands and causes recurrent laryngeal nerve paralysis. Thoracic or lumbar vertebral body erosion (Fig. 49-4) causes back pain, spinal instability, and neurologic deficits from spinal cord compression; mycotic aneurysms have a peculiar propensity to destroy vertebral bodies. Additionally, neurologic symptoms, including paraplegia, paraparesis, or both, may result from thrombosis of intercostal and lumbar arteries. This is most frequently seen with acute aortic dissection, which may occur primarily or be superimposed on medial degenerative fusiform aneurysmal disease. Thoracic aortic aneurysms, like aneurysms in other locations, may produce distal emboli of clot or atheromatous debris that gradually obliterate and thrombose visceral, renal, or lower-extremity branches.

Imaging technology is critical in diagnosis and determining anatomic details for operative planning. Computed tomography (CT) scanning and magnetic resonance angiography (MRA) enable clinicians to obtain excellent images without the potential morbidity or cost associated with angiography. CT scanning is widely available and can image the entire thoracic and abdominal aorta, major branch vessels, and virtually all adjacent organs. Computer programs can construct sagittal, coronal, and oblique images, as well as three-dimensional reconstructions, from CT data. Contrast-enhanced CT scanning (Figs. 49-2, 49-4, and 49-5) also provides information about the aortic lumen, intraluminal thrombus, presence of aortic dissection, intramural hematoma, mediastinal or retroperitoneal hematoma, aortic rupture, and periaortic fibrosis associated with inflammatory aneurysms.²¹ CT angiography with multiplanar reconstruction is especially useful for planning endovascular procedures. Advantages of CT include being less expensive and somewhat quicker to perform than MRA and, at present, the wider availability of CT expertise. Also, CT can be used with patients who have implanted ferromagnetic prostheses or other devices, which can cause injury in patients undergoing MRA. The chief advantages of MRA are that it does not expose the patient to ionizing radiation and that it reveals disease within the aortic wall, including intramural hemorrhage. The gadolinium-based contrast agents used in MRA were once considered to be safer for patients with renal insufficiency than CT contrast media. Ironically, reports have associated the use of certain gadolinium-based contrast agents with nephrogenic systemic fibrosis (NSF)—a scleroderma-like fibrotic process that can affect not only the skin but also internal organs—in patients with renal insufficiency.²² The current recommendation is to avoid using such agents in patients with advanced renal failure (ie, with a glomerular filtration rate < 30 mL/min) or in patients who are dialysis-dependent.²³

Ongoing improvements in noninvasive imaging modalities have substantially reduced the role of catheter aortography in assessing thoracic aortic aneurysms. However, catheter aortography remains useful in situations where noninvasive methods are not feasible—for example, when artifact or heavy calcification obscures the area of interest. Anterior, posterior, oblique, and lateral views provide detailed information about branch vessels. The risks posed by aortography include renal toxicity from the large volumes of contrast material required to adequately fill large aneurysms. There is also a risk of embolization from laminated thrombus secondary to manipulation of intraluminal catheters. Furthermore, angiography underestimates the size of an aneurysm in areas of laminated thrombus. Nonetheless, angiography can be helpful in patients with suspected renal or visceral ischemia, aortoiliac occlusive disease, horseshoe kidney, or peripheral aneurysms.

Whenever possible, patients with known aortic disease (ie, patients with previous aortic dissection, prior aortic repair, or abnormal aortic diameter) are regularly followed by an imaging surveillance protocol to monitor the possible development of distal aortic aneurysm. For this and other incidental findings, once an aneurysm involving the descending thoracic or thoracoabdominal aorta has been discovered, precise determination of the extent and severity of disease is the critical next step toward clarifying the specific diagnosis, determining the appropriate treatment, and, when repair is indicated, planning the appropriate intervention.

Indications for Operation

In asymptomatic patients, the decision to consider surgical repair is based primarily on the diameter of the aneurysm. To prevent fatal rupture, current guidelines recommend elective operation when the aortic diameter exceeds 5.5 cm in cases of chronic dissection and 6 cm in cases of degenerative aneurysm. In patients with connective tissue disorders, such as Marfan syndrome and related disorders, the diameter-based threshold for operation is lowered. Although guidelines specify a rapid dilatation rate for only the proximal aorta, indicating repair when expansion exceeds 0.5 cm/year, it is not unreasonable to apply this threshold to the distal aorta as well.²⁴ Nonoperative management—which consists of strict blood pressure control, cessation of smoking, and at least yearly surveillance with imaging studies—is appropriate for asymptomatic patients who have small aneurysms. Symptomatic patients, however, are at increased risk of rupture and warrant expeditious evaluation and urgent aneurysm repair, even when the abovementioned threshold diameters have not been reached. The onset of new pain in a patient with a known aneurysm is particularly concerning and often heralds significant expansion, leakage, or impending rupture. Malperfusion caused by chronic dissection is also an indication for TAAA repair. Degenerative DTAAs and TAAAs with superimposed acute dissection are especially prone to rupture and are therefore treated with emergent repair.

Endovascular Considerations

Since 2005, when a TEVAR device was approved by the US Food and Drug Administration (FDA) to treat DTAA, indications for TEVAR have expanded, and TEVAR devices are now approved for treating all lesions of the descending thoracic aorta—acute or chronic aortic dissection, penetrating aortic ulcer, and blunt trauma—with suitable anatomy. In contrast, custom-manufactured fenestrated or branched endovascular repair of TAAA remains experimental in the United States with ongoing clinical trials.²⁵ Although endovascular repairs are covered in detail in a subsequent chapter, all patients in our practice are evaluated for possible endovascular intervention, and an individualized surgical option best suited for the patient is selected. Appropriate anatomy is also critical for successful endovascular repair. Landing zones that have inadequate length, excessive angulation, extensive intraluminal thrombus, dissection in the proximal landing zone, or severe vessel calcification will not allow secure endograft fixation, precluding endovascular repair. Two important factors to consider when deciding between open and endovascular aneurysm repair are the patient’s physiologic reserve and vascular anatomy.²⁶ Open repairs have well-documented outcomes and excellent long-term durability, and they allow repair of aneurysms with complex anatomy. However, the patients must have considerable physiologic reserve to undergo and recover from these procedures.

Hybrid, off-label approaches that combine open and endovascular repair have been selectively used to repair DTAAs and TAAAs. A common type of hybrid DTAA repair involves extending the proximal landing zone by rerouting the left subclavian artery such that the endograft may cover the ostia of the left subclavian artery; this has been done in fairly large numbers of patients and is thought to add little risk and protect against the risk of stroke.²⁷ Additionally, a traditional open “elephant trunk” repair—which leaves a small section of replacement graft floating in the descending thoracic aorta after replacing the aortic arch—can be subsequently combined with TEVAR, either as part of the initial repair or in a subsequent procedure (see following section). Hybrid “elephant trunk” procedures involve landing the proximal portion of the endograft in the trunk, but this approach is not widely used. In contrast, “frozen elephant trunk” procedures (performed in a single stage) are now commonly performed in Europe, especially for the treatment of acute DeBakey type I dissections, with the use of several readily available hybrid devices. The ultimate goal of this approach is to thrombose the false lumen to prevent additional late aortic complications.²⁸ In the United States, there are several versions of this approach, including the antegrade placement of the endograft in the proximal descending thoracic aorta after proximal hemiarch repair.²⁹

Hybrid TAAA approaches typically involve open visceral bypass grafting, which is performed to secure organ perfusion, and followed by stent-graft coverage of the entire aneurysm, including visceral and other branch-vessel ostia. However, a recent approach to hybrid TAAA repair involves replacing the visceral portion of aorta with a multibranched graft in an open fashion (such as in an extent III or IV repair) and repairing the more proximal section of the descending thoracic aorta with a stent graft that is then secured to the proximal section of the multibranched graft.³⁰ Although hybrid TAAA procedures are somewhat less invasive than open TAAA repair, they have not yet yielded a substantial decrease in morbidity and mortality rates, and patient fitness must again be considered in order to obtain an optimal outcome.³¹

Other off-label approaches to TAAA repair include the use of parallel grafts (also called “chimney,” “sandwich,” or “snorkel” approaches); a large diameter endograft is used to cover the aneurysm, and a small diameter stent is run parallel to the main endograft and into branching arteries so that they are perfused. In select patients with substantial comorbidities, parallel endovascular repair remains an option; however, because published reports describe only small patient series,²⁵ it is difficult to judge the utility of this approach. The same is true for the multilayer modulator stent, which is now being used for TAAA repair outside the United States, because only short-term data are available.³²

Endovascular descending thoracic aortic repair is widespread, and its use to treat degenerative aneurysm should be strongly considered when feasible per current US guidelines.²⁴ Furthermore, recent 5-year evidence from the INSTEAD-XL randomized trial of 140 patients with uncomplicated chronic aortic dissection who underwent either optimal medical therapy or TEVAR with optimal medical therapy suggests that TEVAR substantially improves late aortic-specific survival and delays disease progression.⁵ Data suggest that, in general, endovascular repair of the descending thoracic aorta is associated with less early mortality and morbidity than open repair,^33,34 and TEVAR is less likely to be affected by whether the repair is performed at a high-volume or low-volume center,³⁵ even in cases of rupture.³⁶ However, the early survival benefit may be lost within a few years after repair, because 5-year survival is similar between those with open and endovascular Medicare cohorts³⁷ or is worse after endovascular repair.^38,39 There also appears to be a greater need for reintervention after TEVAR than after open DTAA repair.^39-41 Of interest, emerging evidence suggests that different aortic pathologies (degenerative aneurysm vs chronic dissection vs acute dissection) are associated with different modes of repair failure after TEVAR.^42,43

Because endovascular aortic repair has become substantially more common in recent years and the indications for its use have evolved, these devices are increasingly encountered in subsequent open operations. Complications after endovascular repair may result from progression of the aneurysmal process to an adjacent portion of the aorta that is not amenable to further endovascular treatment, progressive dilation of the treated segment owing to persistent endoleak, infection of the endovascular device, or device migration. In certain cases, endovascular devices do not incorporate into the aneurysm thrombus and aortic intima in the way that conventional Dacron grafts incorporate into the periadventitial tissue. Explantation of the endovascular device and open graft replacement of the thoracic aorta can be accomplished with relatively good success.^44-46 In the absence of infection, salvaging the device or portions of the device is also possible. Although we have applied the aortic cross-clamp to a proximal aortic segment with an endovascular stent graft in place and repaired a distal segment in an open fashion, in cases in which the stent graft encroaches on the aortic arch, it may not be possible to place a cross-clamp, and hypothermic circulatory arrest may be needed. Suturing an existing stent graft to a standard Dacron graft in a hemostatic fashion is also feasible, particularly if the surrounding aortic tissue can be incorporated into the suture line. Notably, endovascular aortic repair in patients with connective tissue disorders is not supported by current US guidelines;²⁴ however, selective use as bridge to open repair or to treat late complications of open repair may be an appropriate strategy.^47,48

In each patient, the indications for operation discussed above are weighed against the risks posed by surgical intervention.^49,50 The Crawford classification of TAAA (Fig. 49-6) permits standardized reporting of the extent of aortic involvement, thereby allowing appropriate risk stratification, choice of specific treatment modalities according to the extent of the aneurysm, and a type-specific determination of the risks for neurologic deficits and other morbidities and mortality associated with TAAA repair. Extent I TAAA repairs involve replacing most or all of the descending thoracic aorta and the upper abdominal aorta. Extent II repairs involve most or all of the descending thoracic aorta and extend into the infrarenal abdominal aorta. Extent III repairs involve the distal half or less of the descending thoracic aorta and varying portions of the abdominal aorta. Extent IV repairs involve most or all of the abdominal aorta. In general, less extensive distal aortic repair (DTAA, extents III and IV TAAA) tend to pose less operative risk than more extensive distal aortic repair (extents I and II TAAA), although patient-specific disease, such as having a heavy atherosclerotic burden, can increase risk in lesser repairs.

Most commonly, patients with DTAA and TAAA meeting criteria for repair are in their mid-to-late 60s. Younger patients tend to include those patients with connective tissue disorders or chronic aortic dissection. Additionally, there appears to be substantial differences in patient characteristics by extent of repair. Regarding our comprehensive TAAA experience,⁵¹ about 10% of TAAA patients have a connective tissue disorder; however, this increases to 17% in extent II repairs and decreases to 5% in extent IV TAAA repair. Chronic aortic dissection is present in nearly a third of patients; this proportion is increased in extent I and II repairs (39 and 44%, respectively) and decreased in extent III and IV repairs (19 and 11%, respectively). Furthermore, while roughly a quarter of TAAA patients have had a prior distal aortic repair, this rate is increased in extent III and IV repairs (42 and 36%)—this speaks to the progressive nature of repair in extents III and IV, as many of these prior repairs were abdominal aortic repairs.

An adequate preoperative assessment of physiologic reserve is critical in evaluating operative risk. Many patients have significant comorbidities; chronic pulmonary obstructive disease, coronary artery disease, hypertension, cerebrovascular disease, and peripheral vascular disease are all relatively common in TAAA repair. Chronic elevated serum creatinine levels (>3.0 mg/dL) are relatively uncommon in patients undergoing TAAA repair, and affect 3% of patients in our experience.⁵¹ Unless they require emergency operation, patients undergo a thorough preoperative evaluation with emphasis on cardiac, pulmonary, and renal function.

Cardiac Status

Impaired myocardial contractility and reduced coronary reserve are common among elderly patients who undergo aortic reconstruction. Patients need substantial cardiac reserve in order to tolerate clamping of the thoracic aorta. Given the prevalence of preoperative cardiac disease and the physiologic strain of aortic clamping, it is not surprising that cardiac complications are a major cause of postoperative mortality. Reports indicate that cardiac disease has been responsible for 49% of early deaths and 34% of late deaths after TAAA repair, attesting to the importance of careful preoperative cardiac evaluation.^20,52

Several imaging techniques are useful in preoperative screening for cardiac disease. Transthoracic echocardiography is noninvasive and can satisfactorily evaluate both valvular and biventricular function. Dipyridamole-thallium myocardial scanning identifies regions of myocardium that are reversibly ischemic, and it is more practical than exercise testing in this generally elderly population, whose exercise capacity is often limited by concurrent lower-extremity peripheral vascular disease. In patients with evidence of reversible ischemia on noninvasive studies, and in those with a significant history of angina or an ejection fraction of 30% or less, cardiac catheterization and coronary arteriography are performed. Patients who have asymptomatic aneurysms and severe coronary artery occlusive disease (ie, significant left main, proximal left anterior descending, or triple-vessel coronary artery stenosis) undergo myocardial revascularization before aneurysm repair. In appropriate patients, percutaneous transluminal angioplasty is carried out before surgery. If clamping proximal to the left subclavian artery is anticipated in patients in whom the left internal thoracic artery has been used as a coronary artery bypass graft, a left-carotid-to-subclavian bypass is typically necessary to prevent cardiac ischemia when the aortic clamp is applied.⁵³

Renal Status

Preoperative renal insufficiency has been a major risk factor for early mortality throughout the history of TAAA repair.^49,54 It was among the predictive variables selected in Svensson et al’s⁵⁴ multivariable analysis of Crawford’s complete experience with TAAA surgery in 1509 patients treated between 1960 and 1991. Patients with severely impaired renal function who are not receiving long-term hemodialysis frequently require temporary hemodialysis early after operation and are clearly at increased risk for postoperative complications.

Although patients are not rejected as surgical candidates on the basis of renal function, careful assessment of renal function aids in estimating perioperative risk and adjusting treatment strategies accordingly. Renal function is assessed preoperatively by measuring serum electrolytes, blood urea nitrogen, and creatinine. Kidney size and perfusion can be evaluated by using the imaging studies obtained to assess the aorta. Patients who have poor renal function secondary to severe proximal renal artery occlusive disease are revascularized at operation by renal arterial endarterectomy, stenting under direct vision, or bypass grafting, with the expectation that renal function will stabilize or improve.⁵²

Because of the nephrotoxic effects of vascular contrast agents, surgery is delayed (if possible) for 24 hours or longer after CT scanning or aortography has been performed. This is especially important in patients with preexisting renal impairment. Strategies to reduce the risk of contrast-induced nephropathy include periprocedural administration of acetylcysteine and intravenous hydration. If renal insufficiency occurs or worsens after contrast administration, the surgical procedure is postponed until renal function returns to baseline or is satisfactorily stabilized.

Pulmonary Status