35. 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;39:1488–1493.

36. Zhu L, Vranckx R, Khau Van Kien P, et al. Mutations in myosin heavy chain 11 cause a syndrome

associating thoracic aortic aneurysm/aortic dissection and patent ductus arteriosus. Nat Genet

2006;38:343–349.

37. Pannu H, Tran-Fadulu V, Papke C, et al. MYH11 mutations result in a distinct vascular pathology

driven by insulin-like growth factor 1 and angiotensin II. Hum Mol Genet 2007;16:3453–3462.

38. Pannu H, Fadulu VT, Chang J, et al. Mutations in transforming growth factor-beta receptor type II

cause familial thoracic aortic aneurysms and dissections. Circulation 2005;112:513–520.

39. Jarrett F, Darling RC, Mundth ED, et al. Experience with infected aneurysms of the abdominal

aorta. Arch Surg 1975;110:1281–1286.

40. Bakker-de Wekker P, Alfieri O, Vermeulen F, et al. Surgical treatment of infected pseudoaneurysms

after replacement of the ascending aorta. J Thorac Cardiovasc Surg 1984;88:447–451.

41. Bachet JE, Termignon JL, Dreyfus G, et al. Aortic dissection. prevalence, cause, and results of late

reoperations. J Thorac Cardiovasc Surg 1994;108:199–205.

42. Bernard Y, Zimmermann H, Chocron S, et al. False lumen patency as a predictor of late outcome in

aortic dissection. Am J Cardiol 2001;87:1378–1382.

43. Elefteriades JA, Lovoulos CJ, Coady MA, et al. Management of descending aortic dissection. Ann

Thorac Surg 1999;67:2002–2005.

44. Marui A, Mochizuki T, Mitsui N, et al. Toward the best treatment for uncomplicated patients with

type B acute aortic dissection: a consideration for sound surgical indication. Circulation 1999;100(19

Suppl):II275–II280.

45. Juvonen T, Ergin MA, Galla JD, et al. Risk factors for rupture of chronic type B dissections. J

Thorac Cardiovasc Surg 1999;117:776–786.

46. Borst HG, Walterbusch G, Schaps D. Extensive aortic replacement using “elephant trunk” prosthesis.

Thorac Cardiovasc Surg 1983;31(1):37–40.

47. Huynh TT, Miller CC 3rd, Estrera AL, et al. Determinants of hospital length of stay after

thoracoabdominal aortic aneurysm repair. J Vasc Surg 2002;35:648–653.

48. Cambria RP, Clouse WD, Davison JK, et al. Thoracoabdominal aneurysm repair: results with 337

operations performed over a 15-year interval. Ann Surg 2002;236:471–479.

49. Kouchoukos NT, Daily BB, Rokkas CK, et al. Hypothermic bypass and circulatory arrest for

operations on the descending thoracic and thoracoabdominal aorta. Ann Thorac Surg 1995;60:67–76.

50. Svensson LG, Crawford ES, Hess KR, et al. Experience with 1509 patients undergoing

thoracoabdominal aortic operations. J Vasc Surg 1993;17(2):357–368; discussion 368–370.

51. Shah PJ, Estrera AL, Safi HJ. Thoracoabdominal aortic aneurysm: current surgical trends. In: Safi

HJ, McPherson D, eds. Houston Aortic Symposium. 2008.

52. Safi HJ, Miller CC 3rd, 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):372–381.

53. Miller CC 3rd, Porat EE, Estrera AL, et al. Analysis of short-term multivariate competing risks data

following thoracic and thoracoabdominal aortic repair. Eur J Cardiothorac Surg 2003;23:1023–1027.

54. Coselli JS, Lemaire SA, Koksoy C, et al. Cerebrospinal fluid drainage reduces paraplegia after

thoracoabdominal aortic aneurysm repair: results of a randomized clinical trial. J Vasc Surg

2002;35:631–639.

55. Hollier LH, Money SR, Naslund TC, et al. Risk of spinal cord dysfunction in patients undergoing

thoracoabdominal aortic replacement.Am J Surg 1992;164:210–213.

56. Jacobs MJ, de Mol BA, Elenbaas T, et al. Spinal cord blood supply in patients with

thoracoabdominal aortic aneurysms. J Vasc Surg 2002;35:30–37.

57. Safi HJ, Harlin SA, Miller CC 3rd, et al. Predictive factors for acute renal failure in thoracic and

thoracoabdominal aortic aneurysm surgery. J Vasc Surg 1996; 24: 338–344.

58. Safi HJ, Miller CC 3rd, Carr C, et al. Importance of intercostal artery reattachment during

thoracoabdominal aortic aneurysm repair. J Vasc Surg 1998;27(1):58–66; discussion 66–68.

59. Huynh TT, Miller CC 3rd, Safi HJ. Delayed onset of neurologic deficit: significance and

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management. Semin Vasc Surg 2000;13:340–344.

60. 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;43:239–246.

61. Kawanishi Y, Munakata H, Matsumori M, et al. Usefulness of transcranial motor evoked potentials

during thoracoabdominal aortic surgery. Ann Thorac Surg 2007;83:456–461.

62. Keyhani K, Miller CC 3rd, Estrera AL, et al. Analysis of motor and somatosensory evoked potentials

during thoracic and thoracoabdominal aortic aneurysm repair. J Vasc Surg 2009;49:36–41.

63. Crawford ES, Mizrahi EM, Hess KR, et al. The impact of distal aortic perfusion and somatosensory

evoked potential monitoring on prevention of paraplegia after aortic aneurysm operation. J Thorac

Cardiovasc Surg 1988;95:357–367.

64. Azizzadeh A, Huynh TT, Miller CC 3rd, et al. Reversal of twice-delayed neurologic deficits with

cerebrospinal fluid drainage after thoracoabdominal aneurysm repair: a case report and plea for a

national database collection. J Vasc Surg 2000;31:592–598.

65. Safi HJ, Miller CC 3rd, Azizzadeh A, et al. Observations on delayed neurologic deficit after

thoracoabdominal aortic aneurysm repair. J Vasc Surg 1997;26:616–622.

66. Widmann MD, DeLucia A, Sharp J et al. Reversal of renal failure and paraplegia after

thoracoabdominal aneurysm repair. Ann Thorac Surg 1998;65:1153–1155.

67. Estrera AL, Miller CC 3rd, Huynh TT, et al. Preoperative and operative predictors of delayed

neurologic deficit following repair of thoracoabdominal aortic aneurysm. J Thorac Cardiovasc Surg

2003;126(5):1288–1294.

68. Azizzadeh A, Huynh TT, Miller CC 3rd, et al. Postoperative risk factors for delayed neurologic

deficit after thoracic and thoracoabdominal aortic aneurysm repair: a case-control study. J Vasc Surg

2003;37(4):750–754.

69. Huynh TT, van Eps RG, Miller CC 3rd, et al. Glomerular filtration rate is superior to serum

creatinine for prediction of mortality after thoracoabdominal aortic surgery. J Vasc Surg

2005;42(2):206–212.

70. Kouchoukos NT, Masetti P, Mauney MC, et al. One-stage repair of extensive chronic aortic

dissection using the arch-first technique and bilateral anterior thoracotomy. Ann Thorac Surg

2008;86:1502–1509.

71. Kouchoukos NT, Masetti P, Murphy SF. Hypothermic cardiopulmonary bypass and circulatory arrest

in the management of extensive thoracic and thoracoabdominal aortic aneurysms. Semin Thorac

Cardiovasc Surg 2003;15:333–339.

72. Tabayashi K, Motoyoshi N, Saiki Y, et al. Efficacy of perfusion cooling of the epidural space and

cerebrospinal fluid drainage during repair of extent I and II thoracoabdominal aneurysm. J

Cardiovasc Surg 2008;49:749–755.

73. Coselli JS, Bozinovski J, LeMaire SA. Open surgical repair of 2286 thoracoabdominal aortic

aneurysms. Ann Thorac Surg 2007;83:S862–S864.

74. Lemaire SA, Jones MM, Conklin LD, et al. Randomized comparison of cold blood and cold

crystalloid renal perfusion for renal protection during thoracoabdominal aortic aneurysm repair. J

Vasc Surg 2009;49(1):11–19; discussion 19.

75. Conrad MF, Crawford RS, Davison JK et al. Thoracoabdominal aneurysm repair: a 20-year

perspective. Ann Thorac Surg 2007;83:S856–S861.

76. 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;43:217–

222.

77. Quinones-Baldrich WJ. Descending thoracic and thoracoabdominal aortic aneurysm repair: 15-year

results using a uniform approach. Ann Vasc Surg 2004;18:335–342.

78. Fehrenbacher JW, Hart DW, Huddleston E, et al. Optimal end-organ protection for thoracic and

thoracoabdominal aortic aneurysm repair using deep hypothermic circulatory arrest. Ann Thorac

Surg 2007;83:1041–1046.

79. Etz CD, Halstead JC, Spielvogel D, et al. Thoracic and thoracoabdominal aneurysm repair: is

reimplantation of spinal cord arteries a waste of time? Ann Thorac Surg 2006;82:1670–1677.

80. Etz CD, Di Luozzo G, Bello R, et al. Pulmonary complications after descending thoracic and

thoracoabdominal aortic aneurysm repair: predictors, prevention, and treatment. Ann Thorac Surg

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2007;83:S870–S876.

81. Safi HJ, Miller CC 3rd, Estrera AL, et al. Staged repair of extensive aortic aneurysms: morbidity

and mortality in the elephant trunk technique. Circulation 2001;104:2938–2942.

82. Svensson LG, Crawford ES, Hess KR, et al. Variables predictive of outcome in 832 patients

undergoing repairs of the descending thoracic aorta. Chest 1993;104:1248–1253.

83. Okita Y, Tagusari O, Minatoya K, et al. Is distal anastomosis only to the true channel in chronic

type B aortic dissection justified? Ann Thorac Surg 1999;68:1586–1591.

84. Gilling-Smith GL, Worswick L, Knight PF, et al. Surgical repair of thoracoabdominal aortic

aneurysm: 10 years’ experience. Brit J Surg 1995;82:624–629.

85. Dudra J, Shiiya N, Matsui Y, et al. Operative results of thoracoabdominal repair for chronic type B

aortic dissection. J Cardiovasc Surg 1997; 38: 147–151.

86. Safi HJ, Miller CC 3rd, Estrera AL, et al. Chronic aortic dissection not a risk factor for neurologic

deficit in thoracoabdominal aortic aneurysm repair. Eur J Vasc Endovasc Surg 2002;23:244–250.

87. Safi HJ, Miller CC 3rd, Reardon MJ, et al. Operation for acute and chronic aortic dissection: recent

outcome with regard to neurologic deficit and early death. Ann Thorac Surg 1998;66:402–411.

88. 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;331:1729–1734.

89. Quiñones-Baldrich WJ, Panetta TF, Vescera CL, et al. Repair of type IV thoracoabdominal aneurysm

with a combined endovascular and surgical approach. J Vasc Surg. 1999;30:555–560.

90. Zhou W, Reardon M, Peden EK, et al. Hybrid approach to complex thoracic aortic aneurysms in

high-risk patients: surgical challenges and clinical outcomes. J Vasc Surg 2006;44:688–693.

91. Patel R, Conrad MF, Paruchuri V, et al. Thoracoabdominal aneurysm repair: hybrid versus open

repair. J Vasc Surg. 2009;50:15–22.

92. Böckler D, Kotelis D, Geisbüsch P, et al. Hybrid procedures for thoracoabdominal aortic aneurysms

and chronic aortic dissections – a single center experience in 28 patients. J Vasc Surg. 2008;47:724–

732.

93. Lee CW, Beaver TM, Klodell CT Jr, et al. Arch debranching versus elephant trunk procedures for

hybrid repair of thoracic aortic pathologies. Ann Thorac Surg. 2011;91(2):465–471.

94. Chiesa R, Tshomba Y, Melissano G, et al. Hybrid approach to thoracoabdominal aortic aneurysms in

patients with prior aortic surgery. J Vasc Surg 2007;45:1128–1135.

95. Milewski RK, Szeto WY, Pochettino A, et al.. Have hybrid procedures replaced open aortic arch

reconstruction in high-risk patients? a comparative study of elective open arch debranching with

endovascular stent graft placement and conventional elective open total and distal aortic arch

reconstruction. J Thorac Cardiovasc Surg. 2010;140(3):590–597.

96. Lobato AC, Camacho-Lobato L. Endovascular treatment of complex aortic aneurysms using the

sandwich technique. J Endovasc Ther. 2012;19(6):691–706.

97. Orr N, Minion D, Bobadilla JL. Thoracoabdominal aortic aneurysm repair: current endovascular

perspectives. Vasc Health Risk Manag. 2014;10:493–505.

98. Tolenaar JL, van Keulen JW, Trimarchi S, et al. The chimney graft, a systematic review. Ann Vasc

Surg. 2012;26(7):1030–1038.

99. Greenberg R, Eagleton M, Mastracci T. Branched endografts for thoracoabdominal aneurysms. J

Thorac Cardiovasc Surg. 2010; 140(Suppl 6):S171–S178.

100. Marzelle J, Presles E, Becquemin JP. Results and factors affecting early outcome of fenestrated

and/or branched stent grafts for aortic aneurysms: a multicenter prospective study. Ann Surg. 2015;

261(1):197–206.

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Chapter 96

Abdominal Aortic Aneurysms

Adam W. Beck, Kristina A. Giles, and Thomas S. Huber

Key Points

1 An aneurysm is defined as a permanent, focal dilation of an artery that exceeds 1.5 times the normal,

expected diameter.

2 The risk factors for abdominal aortic aneurysm include age, male gender, smoking, family history,

hypertension, chronic obstructive pulmonary disease and the presence of other aortoiliac or

peripheral aneurysms.

3 The diameter of an aneurysm is the greatest predictor of rupture as predicted by the tangential stress

of the vessel wall.

4 The natural history of abdominal aortic aneurysms is to increase in size with a mean growth rate of

0.4 cm/yr.

5 The treatment of abdominal aortic aneurysm represents a balance between the risk of rupture and

the operative mortality rate.

6 Infrarenal abdominal aortic aneurysms should be repaired in men when their diameter reaches 5.5

cm and in women when the diameter reaches 5 cm provided they are a reasonable operative risk.

7 CT arteriography is both the diagnostic study of choice and the sole imaging study required for

operative planning.

8 Endovascular repair is the preferred choice by both patients and providers in the United States.

9 Endovascular aneurysm repair mandates long-term follow-up with serial imaging to confirm the

integrity of the device and repair.

Abdominal aortic aneurysms (AAAs) are a common problem in developed countries and represent a

significant public health concern globally. Operative repair is the only means to reduce the risk of

rupture and the associated mortality. The treatment algorithm represents a balance between the risk of

repair and the ongoing risk of rupture. The open technique has been the traditional approach since its

description by Dubost et al.1 in the early 1950s. The endovascular approach has emerged as the

preferred treatment since its commercial release at the turn of the 21st century and has truly

revolutionized the care of patients with AAAs.

DEFINITIONS AND CLASSIFICATIONS

1 An aneurysm is defined as a permanent, focal dilation of an artery that exceeds 1.5 times the normal,

expected diameter.2 The diameter of a normal abdominal aorta in an adult male is approximately 2 cm

(range, 1.4 to 3 cm), and, therefore, a 3-cm aorta would be considered aneurysmal.3 The abdominal

aorta is consistently larger in men than in women and increases slightly with age for both genders.4

AAAs should be differentiated from other conditions in which the size of the aorta is increased,

including ectasia and arteriomegaly. In aortic ectasia, the diameter is increased by less than 1.5 times of

the normal, expected diameter. The term arteriomegaly refers to a diffuse (nonfocal) enlargement of

several arterial segments with increases in diameter greater than 50% of the normal expected diameter.

Arterial segments in patients with arteriomegaly may be considered aneurysmal if the diameter of a

segment is increased by more than 50% of the diameter of an adjacent segment. The term aneurysmosis

denotes the presence of multiple aneurysmal segments separated by either normal, occluded, or

arteriomegalic segments.

AAAs are classified primarily according to how far they extend cephalad (Fig. 96-1). More than 95%

of all abdominal aortic aneurysms are classified as infrarenal.5 These aneurysms start below the renal

arteries, and may be termed “juxtarenal” when closely approximating the renal arteries, generally less

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than 10 mm along the centerline of flow below the renal orifices. AAAs classified as suprarenal extend

above the renal orifices to the level of the superior mesenteric or celiac arteries. Aneurysms involving

the thoracic and abdominal aorta are designated as thoracoabdominal aortic aneurysms and are

classified according to how far they extend both cephalad and caudal (extent 1 through 4). Aneurysms

that extend above the renal arteries are more complicated for both endovascular and open repair, and

can be associated with greater morbidity. Some centers report similar outcomes for open juxtarenal and

type IV thoracoabdominal aneurysm repair compared to infrarenal aneurysms; however, national results

are more discrepant.5–7 New techniques and endograft design have expanded the indications for

endovascular repair to include select juxtarenal and thoracoabdominal aneurysms.8–10

Approximately 10% to 20% of all AAAs are associated with aneurysms of the iliac arteries.11,12

Aneurysm involvement of the iliac vessels is usually confined to the common or internal iliac arteries,

with aneurysmal involvement of the external iliac arteries being very rare. The management of AAAs

associated with common iliac artery aneurysms may complicate both open and endovascular repair.

MAGNITUDE OF THE PROBLEM

AAAs and their sequelae are common problems in developed countries. The incidence of AAAs in the

United States ranges from 1.5% in autopsy series to 3.2% among unselected adult patients screened with

ultrasonography.13 Predictably, the incidence increases among subsets of patients with defined risk

factors for AAAs and approximates 50% among patients with either femoral or popliteal artery

aneurysms.13 It should be emphasized that these rates have been determined with the broad definition

of an aneurysm (i.e., 1.5 times the normal vessel diameter) and do not necessarily reflect aneurysms

that are of sufficient size to merit repair. Furthermore, the incidence of AAAs increased up until the end

of the 20th century then has more recently plateaued and even started to decline.14–16 Changes in

incidence may be reflective of smoking trends in the United States.17 A total of 10,597 deaths were

caused by AAAs and/or dissections during 2009 and this corresponded to death rate of 3.5/100,000 as

reported by the Centers for Disease Control and Prevention.18 These numbers may be underestimated

because a significant number of sudden deaths in elderly patients may be secondary to undiagnosed

ruptured aneurysms. Of note, spanning the time period of the introduction of endovascular AAA repair,

death rates from AAA have declined by nearly 50%.19

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Figure 96-1. Classification of abdominal aortic aneurysms. More than 95% of all abdominal aortic aneurysms are infrarenal.

Juxtarenal aneurysms extend to the level of the renal arteries, and suprarenal aneurysms to the level of the superior mesenteric.

Aneurysms extending above the superior mesenteric artery and above are designated as thoracoabdominal aneurysms and are

classified (Crawford extent I–IV) according to how far they extend cephalad and caudal.

PATHOGENESIS AND RISK FACTORS

The pathogenesis of AAAs remains unresolved, although it is an intense area of both experimental and

clinical investigation. Multiple potential etiologic factors have been implicated including

atherosclerosis,20 hemodynamics,21 collagen,22 collagenase,23 elastin,24 elastase,25 metalloproteinases,26

protease inhibitors,27 programmed cell death (apoptosis),28 neutrophils,29 and inflammatory

mediators.30 The etiology is likely multifactorial with interaction between both environmental and

genetic factors. Unfortunately, investigation into the potential mechanisms has not resulted in any

effective biologic therapies. Elucidation of the pathogenesis has been complicated by the older age of

patients at presentation and the absence of suitable animal models.

2 Multiple risk factors have been identified for the development of AAAs, including age, sex, race,

smoking, hypertension, hyperlipidemia, peripheral vascular disease, myocardial infarction, and family

history.31,32 Identification of these risk factors is important to facilitate screening high-risk patient

populations. AAAs are a disease process of aging and are rare among persons less than 50 years of age.

Indeed, the mean age among patients undergoing repair across the country was 75.5 years in a recent

Medicare population study.19 A meta-analysis of the population-based screening studies for AAAs

reported that male sex had the strongest association (odds ratio, 5.69).33 The incidence of death

resulting from AAAs for men of 60 to 64 years of age is 11-fold higher than that for women of the same

age, but it is only 3-fold higher for men between 85 and 90. Furthermore, men account for

approximately 80% of all AAA repairs performed nationally.19,34 The Aneurysm Detection and

Management Veterans Affairs Cooperative Study Group (ADAM) reported that smoking was the

strongest modifiable risk factor associated with AAAs >4 cm (odds ratio, 5.57) among the 73,451

veterans screened.35 Similarly, Wilmink et al.36 reported that abdominal aneurysms were 7.6 times

more likely to develop in current smokers than in nonsmokers and that the duration of smoking rather

than level of exposure appeared to correlate with their development. Decreasing prevalence of smoking

has correlated with decreasing AAA deaths in the US and European population.17,37 Darling et al.38

prospectively analyzed patients undergoing repair of AAAs and reported that 15.1% had a first-degree

relative with an aneurysm, in contrast to only 1.8% in the control group. Interestingly, the presence of a

female family member with an aneurysm correlated with an increased risk for rupture. Larsson et al.39

reported from a population-based control study in Sweden that the relative risk of an AAA in firstdegree relatives was 1.9 (95% CI, 1.6–2.2). However, the risk of an aneurysm was not affected by the

gender of the index individual or relative.

The presence of an aneurysm in the aorta, iliac, femoral, or popliteal arteries dramatically increases

the risk for a new or additional AAA. Metachronous aneurysms may develop anywhere in the remaining

native aorta, and are commonly seen during follow-up within the residual infrarenal aortic cuff. When

this occurs, the etiology of the aneurysm is often unclear and may be related to degeneration of the

native aorta, or a pseudoaneurysm that develops at the anastomosis. The incidence of aortoiliac

aneurysms in patients with popliteal or femoral artery aneurysms is approximately 50%.13 Importantly,

all patients found to have one of these peripheral artery aneurysms should undergo a computed

tomography (CT) scan of the entire aorta from thorax to the iliac vessels to exclude a synchronous

aneurysm in addition to being screened for other peripheral aneurysms. Interestingly, the reverse

scenario is not true; patients with aortic or iliac artery aneurysms have a <5% chance of having a

peripheral artery aneurysm, and evaluation beyond physical examination is likely not justified.40

The incidence of AAAs is increased among patients with an aortic dissection. Late or repeated

operations are required in approximately 20% of patients by 10 years after an acute aortic dissection.41

The aneurysms may develop in either the thoracic or abdominal aorta, although the former site is more

common. The term dissecting aneurysm is frequently used to describe fusiform degenerative aneurysms,

although it is a misnomer; dissection and aneurysm degeneration are separate processes, but can occur

in the setting of the other. Aneurysm false lumen degeneration can occur after a dissection, and

dissection of the aorta involved in an existing aneurysm can also occur. Simply, a dissection is a tear

within the aortic intima itself that leads to blood flow between the layers of the aorta (within the

2718