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Chapter 4 Medical Management of Small Aortic Abdominal Aortic Aneurysms 67
14 . Matsumura JS , Brewster DC , Makaroun MS , et al. A multicenter controlled
clinical trial of open versus endovascular treatment of abdominal aortic aneurysm .
J Vasc Surg . Feb 2003 ; 37 (2) : 262 – 271 .
15 . Blankensteijn JD , de Jong SE , Prinssen M , et al. Two-year outcomes after conventional
or endovascular repair of abdominal aortic aneurysms . N Engl J Med . Jun 9 2005 ;
352 (23) : 2398 – 2405 .
16. The United Kingdom Small Aneurysm Trial Participants. Long-term outcomes of
immediate repair compared with surveillance of small abdominal aortic aneurysms.
N Engl J Med. May 9 2002;346(19):1445–1452.
17 . Lederle FA , Wilson SE , Johnson GR , et al. Immediate repair compared with surveil-
lance of small abdominal aortic aneurysms . N Engl J Med . May 9 2002 ; 346 (19) :
1437 – 1444 .
18 . O'Rourke MF , Nichols WW . Aortic diameter, aortic stiffness, and wave reflection
increase with age and isolated systolic hypertension . Hypertension . Apr 2005 ;
45 (4) : 652 – 658 .
19 . Lederle FA , Johnson GR , Wilson SE , et al. Relationship of age, gender, race, and
body size to infrarenal aortic diameter. The Aneurysm Detection and Management
(ADAM) Veterans Affairs Cooperative Study Investigators . J Vasc Surg . Oct 1997 ;
26 (4) : 595 – 601 .
20 . Lawrence-Brown MM , Norman PE , Jamrozik K , et al. Initial results of ultrasound
screening for aneurysm of the abdominal aorta in Western Australia: relevance for endo-
luminal treatment of aneurysm disease . Cardiovasc Surg . Jun 2001 ; 9 (3) : 234 – 240 .
21. Mortality results for randomised controlled trial of early elective surgery or ultra-
sonographic surveillance for small abdominal aortic aneurysms. The UK Small
Aneurysm Trial Participants. Lancet. Nov 21 1998;352(9141):1649–1655.
22 . Norman PE , Powell JT . Abdominal aortic aneurysm: the prognosis in women is
worse than in men . Circulation . Jun 5 2007 ; 115 (22) : 2865 – 2869 .
23 . Dillavou ED , Muluk SC , Makaroun MS . Improving aneurysm-related outcomes:
nationwide benefits of endovascular repair . J Vasc Surg . Mar 2006 ; 43 (3) : 446 – 451 ;
discussion 451–442 .
24 . Fleming C , Whitlock EP , Beil TL , et al. Screening for abdominal aortic aneurysm:
a best-evidence systematic review for the U.S. Preventive Services Task Force . Ann
Intern Med . Feb 1 2005 ; 142 (3) : 203 – 211 .
25 . Alcorn HG , Wolfson SK , Jr. , Sutton-Tyrrell K , et al. Risk factors for abdominal
aortic aneurysms in older adults enrolled in The Cardiovascular Health Study .
Arterioscler Thromb Vasc Biol . Aug 1996 ; 16 (8) : 963 – 970 .
26 . Wilmink AB , Forshaw M , Quick CR , et al. Accuracy of serial screening for
abdominal aortic aneurysms by ultrasound . J Med Screen . 2002 ; 9 (3) : 125 – 127 .
27 . Wilmink AB , Hubbard CS , Quick CR . Quality of the measurement of the infrarenal
aortic diameter by ultrasound . J Med Screen . 1997 ; 4 (1) : 49 – 53 .
28 . Wassef M , Baxter BT , Chisholm RL , et al. Pathogenesis of abdominal aortic
aneurysms: a multidisciplinary research program supported by the National Heart,
Lung, and Blood Institute . J Vasc Surg . Oct 2001 ; 34 (4) : 730 – 738 .
29 . Wassef M , Upchurch GR , Jr. , Kuivaniemi H , et al. Challenges and opportunities in
abdominal aortic aneurysm research . J Vasc Surg . Jan 2007 ; 45 (1) : 192 – 198 .
30 . Brady AR , Thompson SG , Fowkes FG , et al. Abdominal aortic aneurysm expan-
sion: risk factors and time intervals for surveillance . Circulation . Jul 6 2004 ;
110 (1) : 16 – 21 .
31 . Lederle FA , Johnson GR , Wilson SE , et al. Quality of life, impotence, and activity
level in a randomized trial of immediate repair versus surveillance of small abdominal
aortic aneurysm . J Vasc Surg . Oct 2003 ; 38 (4) : 745 – 752 .
32 . Yeung JJ , Kim HJ , Abbruzzese TA , et al. Aortoiliac hemodynamic and morphologic
adaptation to chronic spinal cord injury . J Vasc Surg . Dec 2006 ; 44 (6) : 1254 – 1265 .
33 . Vollmar JF , Paes E , Pauschinger P , et al. Aortic aneurysms as late sequelae of
above-knee amputation . Lancet . Oct 7 1989 ; 2 (8667) : 834 – 835 .
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68 B.T. Baxter
34 . MacSweeney ST , Ellis M , Worrell PC , et al. Smoking and growth rate of small
abdominal aortic aneurysms . Lancet . Sep 3 1994 ; 344 (8923) : 651 – 652 .
35 . Lindholt JS , Heegaard NH , Vammen S , et al. Smoking, but not lipids, lipoprotein(a)
and antibodies against oxidised LDL, is correlated to the expansion of abdominal
aortic aneurysms . Eur J Vasc Endovasc Surg . Jan 2001 ; 21 (1) : 51 – 56 .
36 . Bergoeing MP , Arif B , Hackmann AE , et al. Cigarette smoking increases aortic dila-
tation without affecting matrix metalloproteinase-9 and -12 expression in a modified
mouse model of aneurysm formation . J Vasc Surg . Jun 2007 ; 45 (6) : 1217 – 1227 .
37 . Gotto AM , Jr. Role of C-reactive protein in coronary risk reduction: focus on
primary prevention . Am J Cardiol . Mar 1 2007 ; 99 (5) : 718 – 725 .
38 . Steinmetz EF , Buckley C , Shames ML , et al. Treatment with simvastatin suppresses
the development of experimental abdominal aortic aneurysms in normal and hyper-
cholesterolemic mice . Ann Surg . Jan 2005 ; 241 (1) : 92 – 101 .
39 . Nagashima H , Aoka Y , Sakomura Y , et al. A 3-hydroxy-3-methylglutaryl coenzyme
A reductase inhibitor, cerivastatin, suppresses production of matrix metalloprotein-
ase-9 in human abdominal aortic aneurysm wall . J Vasc Surg . 2002 ; 36 (1) : 158 – 163 .
40. Evans J, Powell JT, Schwalbe E, et al. Simvastatin attenuates the activity of matrix
metalloprotease-9 in aneurysmal aortic tissue. Eur J Vasc Endovasc Surg. Jun 15 2007 .
41 . Sukhija R , Aronow WS , Sandhu R , et al. Mortality and size of abdominal aortic
aneurysm at long-term follow-up of patients not treated surgically and treated with
and without statins . Am J Cardiol. Jan 15 2006 ; 97 (2) : 279 – 280 .
42 . Hsia J , Langer RD , Manson JE , et al. Conjugated equine estrogens and coronary
heart disease: the Women's Health Initiative . Arch Intern Med . Feb 13 2006 ;
166 (3) : 357 – 365 .
43 . Boucek RJ , Gunja-Smith Z , Noble NL , et al. Modulation by propranolol of the
lysyl cross-links in aortic elastin and collagen of the aneurysm-prone turkey .
Biochem Pharmacol. Jan 15 1983 ; 32 (2) : 275 – 280 .
44 . Brophy C , Tilson JE , Tilson MD . Propranolol delays the formation of aneurysms
in the male blotchy mouse . J Surg Res . Jun 1988 ; 44 (6) : 687 – 689 .
45 . Gadowski GR , Pilcher DB , Ricci MA . Abdominal aortic aneurysm expansion rate:
effect of size and beta-adrenergic blockade . J Vasc Surg . Apr 1994 ; 19 (4) : 727 – 731 .
46 . Leach SD , Toole AL , Stern H , et al. Effect of beta-adrenergic blockade on the growth
rate of abdominal aortic aneurysms . Arch Surg . May 1988 ; 123 (5) : 606 – 609 .
47 . Lindholt JS , Henneberg EW , Juul S , et al. Impaired results of a randomised double
blinded clinical trial of propranolol versus placebo on the expansion rate of small
abdominal aortic aneurysms . Int Angiol . Mar 1999 ; 18 (1) : 52 – 57 .
48. Propranolol Aneurysm Trial Investigators. Propranolol for small abdominal aortic
aneurysms: results of a randomized trial. J Vasc Surg. Jan 2002;35(1):72–79.
49 . Liao S , Miralles M , Kelley BJ , et al. Suppression of experimental abdominal aortic
aneurysms in the rat by treatment with angiotensin-converting enzyme inhibitors .
J Vasc Surg . May 2001 ; 33 (5) : 1057 – 1064 .
50 . Daugherty A , Manning MW , Cassis LA . Angiotensin II promotes atherosclerotic
lesions and aneurysms in apolipoprotein E-deficient mice . J Clin Invest. Jun
2000 ; 105 (11) : 1605 – 1612 .
51 . Neptune ER , Frischmeyer PA , Arking DE , et al. Dysregulation of TGF-beta acti-
vation contributes to pathogenesis in Marfan syndrome . Nat Genet . Mar 2003 ;
33 (3) : 407 – 411 .
52. Comparison of two medications aimed at slowing aortic root enlargement in indi-
viduals with Marfan sndrome .
53 . Hackam DG , Thiruchelvam D , Redelmeier DA . Angiotensin-converting enzyme inhib-
itors and aortic rupture: a population-based case-control study . Lancet . Aug 19 2006 ;
368 (9536) : 659 – 665 .
54 . Lederle FA , Taylor BC . ACE inhibitors and aortic rupture . Lancet . Nov 4 2006 ;
368 (9547) : 1571 ; author reply 1572.
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Chapter 4 Medical Management of Small Aortic Abdominal Aortic Aneurysms 69
55 . Schouten O , van Laanen JH , Boersma E , et al. Statins are associated with a reduced
infrarenal abdominal aortic aneurysm growth . Eur J Vasc Endovasc Surg . Jul 2006 ;
32 (1) : 21 – 26 .
56 . Nieto FJ . Infective agents and cardiovascular disease . Semin Vasc Med . Nov 2002 ;
2 (4) : 401 – 415 .
57 . Lindholt JS , Ashton HA , Scott RA . Indicators of infection with Chlamydia pneu-
moniae are associated with expansion of abdominal aortic aneurysms . J Vasc Surg .
Aug 2001 ; 34 (2) : 212 – 215 .
58 . Grayston JT , Kronmal RA , Jackson LA , et al. Azithromycin for the secondary
prevention of coronary events . N Engl J Med . Apr 21 2005 ; 352 (16) : 1637 – 1645 .
59 . Burkhardt U , Zahn R , Hoffler U , et al. Antibody levels against Chlamydia pneu-
moniae and outcome of roxithromycin therapy in patients with acute myocardial
infarction. Results from a sub-study of the randomised Antibiotic Therapy in Acute
Myocardial Infarction (ANTIBIO) trial . Z Kardiol . Sep 2004 ; 93 (9) : 671 – 678 .
60 . Vammen S , Lindholt JS , Ostergaard L , et al. Randomized double-blind controlled
trial of roxithromycin for prevention of abdominal aortic aneurysm expansion . Br
J Surg . Aug 2001 ; 88 (8) : 1066 – 1072 .
61 . Petrinec D , Liao S , Holmes DR , et al. Doxycycline inhibition of aneurysmal degen-
eration in an elastase-induced rat model of abdominal aortic aneurysm: preserva-
tion of aortic elastin associated with suppressed production of 92 kD gelatinase .
J Vasc Surg . Feb 1996 ; 23 (2) : 336 – 346 .
62 . Petrinec D , Holmes DR , Liao S , et al. Suppression of experimental aneurysmal
degeneration with chemically modified tetracycline derivatives . Ann N Y Acad Sci .
Nov 18 1996 ; 800 : 263 – 265 .
63 . Longo GM , Xiong W , Greiner TC , et al. Matrix metalloproteinases 2 and 9 work
in concert to produce aortic aneurysms . J Clin Invest . Sep 2002 ; 110 (5) : 625 – 632 .
64 . Prall AK , Longo GM , Mayhan WG , et al. Doxycycline in patients with abdominal
aortic aneurysms and in mice: comparison of serum levels and effect on aneurysm
growth in mice . J Vasc Surg . May 2002 ; 35 (5) : 923 – 929 .
65 . Baxter BT , Pearce WH , Waltke EA , et al. Prolonged administration of doxycycline
in patients with small asymptomatic abdominal aortic aneurysms: report of a pro-
spective (Phase II) multicenter study . J Vasc Surg . Jul 2002 ; 36 (1) : 1 – 12 .
66 . Curci JA , Mao D , Bohner DG , et al. Preoperative treatment with doxycycline
reduces aortic wall expression and activation of matrix metalloproteinases in
patients with abdominal aortic aneurysms . J Vasc Surg . Feb 2000 ; 31 (2) : 325 – 342 .
67 . Mosorin M , Juvonen J , Biancari F , et al. Use of doxycycline to decrease the growth
rate of abdominal aortic aneurysms: a randomized, double-blind, placebo-control-
led pilot study . J Vasc Surg . Oct 2001 ; 34 (4) : 606 – 610 .
68 . Gibbons RJ , Smith SC , Jr. , Antman E . American College of Cardiology/American
Heart Association clinical practice guidelines: Part II: evolutionary changes in a con-
tinuous quality improvement project . Circulation . Jun 24 2003 ; 107 (24) : 3101 – 3107 .
https://t.me/med1917
Abstract Abdominal aortic aneurysm (AAA) rupture carries a 90% overall
mortality, and a 40–50% mortality for those patients who reach a hospital alive.
Because of this, the primary goal of AAA therapy is to avoid rupture. Treatment
of ruptured AAAs is very costly to the health care system. To date, there are two
effective methods to treat AAA, and thus exclude the AAA from pressurized blood
flow. The first is an open surgical exclusion of the AAA, along with an interposition
synthetic graft, while the second is an endoluminally placed covered stent graft
(endovascular aortic aneurysm repair, EVAR) that can be inserted either via the
femoral artery or the iliac artery. The most important factors that increase the risk
of open aneurysm repair are renal dysfunction with a creatinine level greater than
1.8 mg, congestive heart failure, jugular venous distention, ischemic electrocardio-
graphic changes with ST depression greater than 2 mm, history of a prior myocardial
infarction, pulmonary dysfunction including chronic obstructive pulmonary disease,
dyspnea on exertion or prior lung surgery, old age, and female gender. In the absence
of risk factors, elective open AAA carries an operative mortality of 3–5%, but the
risk rises as high as 40% if several of the aforementioned risk factors are present.
Keywords Infrarenal AAA , Preoperative risk , AAA , Operative mortality
AAA , endoluminal AAA repair , Retroperitoneal approach AAA , Postoperative
complications , AAA
Definition
Most medical dictionaries define an aneurysm as a localized widening or
ballooning of a portion of an artery, greater than 50% of the normal caliber of
the artery, commonly related to weakness in the wall of the blood vessel.
1
The
most common location of an extracranial aneurysm is the infrarenal abdominal
aorta. Using the above definition, an aorta with a diameter greater than 3 cm
can therefore be considered aneurysmal, although normal aortic diameters
vary with age, sex, and body habitus. Histologically, an abdominal aortic
Chapter 5
Surgical Treatment of Nonruptured
Infrarenal Abdominal Aortic
Aneurysms
Michael Wilderman and Gregorio Sicard
G. Upchurch and E. Criado (eds.) Aortic Aneurysms, Contemporary Cardiology
DOI: 10.1007/978-1-60327-204-9_5, © Humana Press, a part of
Springer Science + Business Media, LLC 2009
71
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72 M. Wilderman and G. Sicard
aneurysm (AAA) is characterized by macrophage degradation of the medial
elastin lamellar architecture by metalloproteinases.
2–
5
Historical Perspectives
Aneurysms have been recognized for thousands of years, in fact the Ebers
Papyrus in 2000 BC discusses traumatic aneurysms of the peripheral arteries.
6
In the second century AD, Antyllus wrote of the first elective procedure to treat
an aneurysm by proximal and distal ligation of the artery feeding the aneurysm,
along with opening the sac and evacuation of its contents.
7
Andreas Vesalius,
the sixteenth century Flemish anatomist, was the first to describe an AAA.
8
Antyllus’s technique remained the principal treatment method for at least the next
fifteen hundred years until Rudolph Matas, in 1923, performed the successful
technical ligation of a ruptured syphilitic infrarenal AAA.
9
Because of the high
mortality associated with aneurysm ligation, surgeons devised other therapies
such as inducing thrombosis of the aneurysm with wires, also with poor results.
10
In the early 1940s, surgeons utilized wrapping of the aneurysm with various
materials such as fascia lata, skin grafts, polyvinyl sponge, and even cellophane,
in an attempt to prevent aneurysmal rupture.
11–
13
The results of this method were
not good and the mortality and rupture rate of aneurysms remained quite high.
The current technique for AAA repair was conceptually devised in the early
twentieth century by the 1912 Nobel laureate Alexis Carrel.
14–
17
His method,
which he performed only in animals, consisted of replacing a segment of aorta
with a segment from another artery or vein. In 1951, Charles DuBost reported
retroperitoneal approach to replace the aneurysmal infrarenal aorta with an aortic
homograft.
18
In 1953, Michael DeBakey and Denton Cooley reported success
using a similar technique.
19
In the same year, Henry Bahnson described the tech-
nique described by DuBost to repair a ruptured AAA.
20
The use of homografts
was short-lived due to graft degeneration and subsequent graft rupture. The
next major breakthrough for AAA repair was the use of arterial protetics made
of Vinyon-N, originated in the work of Arthur Voorhees.
21
Blakemore placed
the first Vinyon-N graft in a patient with a ruptured AAA.
22
In 1954, Voorhees
and Blakemore described their results in 16 patients with AAA repaired using
Vinyon-N grafts with a 56% survival.
23,
24
These advances stimulated industry
to evaluate and develop arterial conduits. In 1958, Michael DeBakey’s group in
Houston reported excellent results on a large group of patients undergoing AAA
repair with knitted Dacron grafts.
25
Over the next two decades, many series were
reported with operative mortalities in the 10–15% range, using polyester grafts.
Prevalence and Incidence
AAA is typically a disease of elderly males, with increasing prevalence after
the sixth decade of life. AAA is two to six times more common in men than
women, and two to three times more common in white than African-American
population. The incidence of AAA varies from 3 to 117 per one hundred thou-
sand person years.
26–
29
Lederle et al.
30
reported that 2.6% of screened patients
with a normal ultrasound 4 years prior developed an AAA. They also reported
an incidence of AAA of 6.5 per thousand person years. In men, AAAs typi-
cally appear after age 50 and reach a peak incidence at age 80. In women, it
is usually later, around age 60, with a steady increase after that.
31–
33
Although
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Chapter 5 Surgical Treatment of Nonruptured Infrarenal Abdominal Aortic Aneurysms 73
AAAs fail to demonstrate a clear genetic predisposition or transmission pat-
tern, numerous reports suggest that 15–20% of first-order relatives of patients
with AAAs will have also have an aneurysm.
34–
36
Aortic aneurysm rupture is among the tenth leading causes of death in elderly
males. Most AAAs are found incidentally and only rarely cause symptoms
such as abdominal or back pain. Therefore, ruptured AAA may be the initial
form of presentation. Aortic aneurysm rupture carries a 90% overall mor-
tality, and a 40–50% mortality for those patients who reach a hospital alive.
The primary goal of AAA therapy is to avoid rupture. Treatment of ruptured
AAAs is very costly to the health care system. A study from Great Britain
found that about 2000 lives and nearly $50 million dollars could be saved if
AAAs were repaired prior to rupture.
37
Breckwoldt et al. suggested that emer-
gent interventions for patients with ruptured AAAs led to hospital losses of
$24,655 per patient.
38
Another study from the United Kingdom found that the
total costs of emergency AAA repair was 96,700 pounds, with a cost per life
saved of 24,175 pounds. The total cost of elective AAA repair was 76,583 with
a cost per life saved of 5470 pounds. The cost of emergency intervention was
found to be fivefold that of elective repair, per life saved, per year.
39
Diagnosis and Risk of Rupture
Since most AAAs are asymptomatic and patients may not present until their AAA
has ruptured, targeted screening of high risk population is recommended. A study
by Schermerhorn et al. showed that ultrasound screening for AAA was cost effec-
tive and beneficial for men 65–74 years of age with known risk factors such as
coronary artery disease (CAD), smoking, or a family history of AAA.
40
A report
by Derubertis et al. suggested a high incidence of AAA among women older than
65, with a history of smoking or heart disease. Women with such risk factors,
therefore, should also be considered for AAA screening.
41
Aneurysm screening
programs have been introduced in some countries.
42–
50
A large randomized trial
in the United Kingdom demonstrated an early mortality benefit of screening
ultrasonography for AAA.
51
Since January 2007, Medicare has offered coverage
of a one-time, ultrasound screening for senior males with a smoking history of
at least 100 cigarettes in their lifetime and for individuals with a family history
of AAA. In the Multicentre Aneurysm Screening Study, 70,495 men age 65–74
were randomized to ultrasound screening versus no screening for AAA. Of the
33,839 patients randomized to ultrasound screening, 80% were screened and 5%
had AAAs greater than 3 cm. At 4 years, there were 113 AAA-related deaths in
the nonscreened control group compared with 65 in the screened group. This trial
suggested a 32% reduction in AAA-related mortality in the screened group.
50
Currently, AAAs are more commonly found incidentally when patients are
imaged, either with ultrasound, CT scan, or MRI for other diseases or symp-
tomatology.
The Department of Veterans Affairs Aneurysm Detection and Management
(ADAM) study was designed to compare long-term AAA survival following
either surveillance or surgical treatment when aneurysm reached 5.5 cm versus
immediate open surgical repair for managing AAAs less than 5.5 cm. A total
of 1136 patients were enrolled and followed for a mean time of 4.8 years. No
significant difference was found between the two groups in terms of long-term
mortality, and the study concluded that there was no long-term survival advantage
by repairing AAA smaller than 5.5 cm. They thus recommended surveillance
of small AAAs until they reach a 5.5 cm diameter.
52
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74 M. Wilderman and G. Sicard
The UK Small Aneurysm Trial followed over 1000 patients for 10 years.
This study found no long-term survival benefit for early elective open repair
of small aneurysm between 4 and 5.4 cm of maximal diameter.
53
The refinement in the preoperative evaluation of patients undergoing AAA
repair during the last two decades has significantly decreased the mortality rate
of open AAA repair (Table 1 ).
54–
64
The risk of rupture of an AAA is estimated based on its maximal diameter.
Aneurysms between 3 and 5 cm have less than 1% per year risk of rupture.
A progressive risk of aneurysm rupture occurs with increasing aneurysm diameter.
An aneurysm growth rate greater than 0.5 cm in a 6-month period also appears
to increase the risk of rupture. Therefore, it is generally accepted that aneu-
rysms less than 5.5 cm can be safely followed with yearly ultrasound.
Most aneurysms, especially smaller ones, tend to grow at a rate of 0.3–
0.5 cm per year.
65–
67
Other factors that have been associated with increased expansion or rupture
rate are uncontrolled hypertension, chronic obstructive pulmonary disease
(COPD), female gender, severe CAD, a large volume of luminal thrombus,
and advanced age.
Fillinger et al. have reported that aortic wall stress is a key predictor of
rupture risk for AAA. A mathematical analysis of AAA geometry, known
as finite element analysis, has been suggested to be a better way to estimate
wall stress and the risk of rupture. Using this model, Fillinger’s group looked
at three groups of patients: those who presented with a ruptured AAA, those
who were symptomatic and required urgent surgery, and those who underwent
elective AAA repair. They found that peak wall stress was significantly higher
in ruptured AAA and symptomatic groups compared with that of the elective
repair group for diameter-matched subjects. They also found that the location of
maximal wall stress in their series was not at the site of maximal AAA diameter
but rather in the posterolateral location where most ruptures do occur.
68,
69
Table 1 Operative mortality following elective infrarenal abdominal
aortic aneurysm ( AAA ).
Authors
n
30-Day mortality (%)
Bush et al.
61
1580 (high risk) 5.2
Sicard et al.
64
61 (high risk) 5.1
Hua et al.
55
582 3.95
Lifeline Registry
82
334 1.4
Blankensteijn et al.
62
(randomized) 178 4.6
Anderson et al.
60
783 (2002) 4.21 (2002)
1043 (2001) 3.55 (2001)
1238 (2000) 4.12 (2000)
Greenhalgh et al.
63
(randomized) 539 4.7
Akkersdijk et al.
59
16,466 7.3
Lee et al.
58
4607 3.8
Hertzer et al.
57
1135 1.2
Huber et al.
56
16,450 4.2
Heller et al.
54
358,521 5.6
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Chapter 5 Surgical Treatment of Nonruptured Infrarenal Abdominal Aortic Aneurysms 75
Preoperative Risk Assessment
The principle behind surgical intervention for AAA is to prevent aneurysmal
rupture. To date, there are two effective methods to treat AAA, and thus
exclude the AAA from pressurized blood flow. The first is an open surgical
exclusion of the AAA, along with an interposition synthetic graft. The second
is an endoluminally placed covered stent graft (EVAR) that can be inserted via
either the femoral or the iliac artery. Each method has advantages and disad-
vantages, and therefore every situation must be assessed independently, based
on a patient’s age, infrarenal aortic anatomy, and comorbidities.
If a patient is discovered to have a symptomatic AAA (i.e., back or abdomi-
nal pain or hypotension), urgent or expedient surgical intervention is indicated.
Stable patients can undergo laboratory testing and cross-sectional imaging to
assess their potential for an endoluminal approach. If the patient is unstable,
then the patient should be taken to the operating room for an open repair.
Asymptomatic male patients with aneurysms greater than 5.5 cm or asympto-
matic female patients with aneurysms greater than 5.0 cm should undergo aneu-
rysm repair. Based on preoperative assessments such as aneurysmal anatomy,
along with the patient’s age and other comorbidities, the treatment strategy is
selected. The most important factors that increase the risk of open aneurysm
repair are renal dysfunction with a creatinine level greater than 1.8 mg, con-
gestive heart failure, jugular venous distention, ischemic electrocardiographic
changes with ST depression greater than 2 mm, history of a prior myocardial
infarction, pulmonary dysfunction including COPD, dyspnea on exertion or
prior lung surgery, old age, and female gender. In the absence of risk factors,
elective open AAA carries an operative mortality of 3–5%, but the risk rises as
high as 40% if several of the aforementioned risk factors are present.
70
Renal
failure alone is the strongest predictor of mortality with a 4- to 9-fold increase in
risk, whereas CAD carries a 2.5- to 5-fold increase in mortality.
71
Mortality is also affected by the given surgeon or hospital experience with
AAA repair. Larger centers with higher volumes have better outcomes than
less-experienced surgeons or small-volume centers.
72
Dimick et al. reported that
hospitals that perform more than 35 open AAA per year have a 30 day mortality
of 3%, as compared with lower volume centers that have a 30 day mortality of
5.5%. In general, they found that high-volume surgeons with vascular surgery
specialty training working at high-volume hospitals have the best outcomes.
73
To reduce overall operative mortality, perioperative cardiac optimization is
vital, especially since CAD is the principle cause of early and late mortality
after AAA.
74
The American College of Cardiology has standardized preopera-
tive cardiac evaluation for noncardiac surgery, and created categories for the
risk of the procedure and the clinical risk to the patient. Patients with unstable
coronary syndromes such as acute or recent MI (less than 30 days) or unstable
angina, decompensated CHF, significant arrhythmias such as high-grade AV
block or symptomatic ventricular arrhythmias, or severe valvular disease are
considered to have major cardiac risks. Intermediate-risk patients are those
with stable angina, prior MI by history or the presence of Q waves on an ECG,
compensated CHF, insulin-dependent diabetes mellitus, or renal insufficiency.
Patients with minor risk include those of advanced age, have an abnormal
ECG (left ventricular hypertrophy, left bundle branch block), have a history of
a prior stroke, or have uncontrolled hypertension.
75
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76 M. Wilderman and G. Sicard
Van Damme et al. found that in patients without clinical markers of CAD,
noninvasive cardiac testing did not predict cardiac complications. In patients
with definite clinical or ECG evidence of CAD, a negative stress test had a
high negative predictive value.
76
Poldermans et al. reported that in intermedi-
ate-risk patients, cardiac testing can be safely omitted, provided that patients
are treated with β -blockers to keep their heart rates until tight control.
77
In one
of the high-risk patients, it was found that coronary revascularization prior to
major vascular surgery did not improve overall 30-day outcomes.
78
The indication for cardiac testing and treatment prior to AAA repair are
the same as in the nonoperative setting, but the timing of such evaluations is
dependent upon the urgency of the surgery, patient risk factors, and surgery-
specific considerations. The preoperative evaluation aims at cardiac risk
stratification and treatment strategies to reduce the patient’s risk of cardiac
events.
75
Patients with a history of pulmonary insufficiency require preoperative pul-
monary function testing, and those who smoke should be encouraged to stop
smoking before surgery. Some patients with severe bronchospastic pulmonary
disease should be optimized with bronchodilator therapy or steroids prior to
open AAA repair.
In patients with a history of stroke or transient ischemic attack or in the pres-
ence of a carotid bruit, a carotid duplex scan should be performed. If a high-
grade stenosis is found in the internal carotid artery, carotid revascularization
should precede elective AAA repair.
Procedural Considerations
Juan Parodi reported the first endoluminal repair of an AAA in 1991.
79
Since
then, numerous endoluminal devices have been tested in clinical trials.
55,
59,
61–
64,
80–
83
Endovascular repair of AAA has been shown to reduce operative mor-
bidity, mortality, length of hospital stay, and postprocedure disability. Two
randomized trials, EVAR-1 and DREAM trials, demonstrated a significantly
lower mortality for EVAR when compared to open repair, but a higher reinter-
vention requirement for EVAR.
62,
63
To date, open repair has proven to be
more durable and requires less follow-up than endoluminal repair. Conrad et
al. reported on a large series of patients undergoing open AAA repair, with an
excellent 10 year survival for patients less than 75 years of age. In addition, the
freedom from graft-related reintervention is superior to EVAR.
84
A large series
published by Hertzer et al. also showed a low 30-day mortality and excellent
long-term survival with open AAA repair.
57
One issue for today’s vascular surgeons is the fact that with better endovas-
cular devices, fewer open infrarenal AAAs are being performed each year.
From 2001 to 2005, the mean volume of elective open infrarenal AAA repairs
declined by 27%. During that same period, EVAR procedures increased by
212% for vascular surgery trainees. Dillavou et al. reviewed a sample of
Medicare’s inpatient database from 2000 to 2003 and found a significant
increase nationwide in EVAR for elective repair of AAA and during that same
period, a concomitant decrease in operative mortality from 5.0% to 3.7%.
85
In
a review of the New York statewide discharge database, Anderson et al. found
a similar dramatic increase in EVAR for elective AAA repair and an associ-
ated decrease in operative mortality.
60
Similarly, large referral centers report
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Chapter 5 Surgical Treatment of Nonruptured Infrarenal Abdominal Aortic Aneurysms 77
over 80% use of EVAR in elective AAA repair. In 2005, 70% of all elective
infrarenal AAAs performed by vascular surgery trainees were endovascular
techniques. During the same period, the number of open ruptured repairs and
elective suprarenal AAA repairs has remained constant, although the numbers
have been low (Fig. 1 ). This has created a challenge for vascular surgery resi-
dents to achieve the necessary skills to perform complex aortic surgery.
86
Technical Considerations
Once a patient has been deemed medically suitable for open surgery, the specific
approach and operation is individualized based on several factors. The most
critical is the CT scan evaluation of the shape and configuration of the aneurysm.
The infrarenal neck, the portion of the aorta immediately below the renal arteries,
along with the iliac arteries must be assessed. If the iliac arteries have significant
occlusive disease, the graft may have to be anastomosed to the femoral arteries.
The presence of severe COPD is important because a laparotomy may not be
well tolerated in these patients. The history of previous abdominal surgeries
will also determine which approach is utilized. The two most frequently used
approaches for AAA repair are the left retroperitoneal and the midline transperi-
toneal. A transverse incision has also been described, especially for patients with
multiple upper abdominal surgeries (Fig. 2) .
For a transperitoneal exposure, the patient is placed in a supine position and
prepped and draped from his nipples to his knees. A long midline incision is
made extending from a patient’s xiphoid to pubis to provide maximal exposure
for an infrarenal repair. After entering the abdominal cavity, a full exploration
of the abdominal contents should occur to rule out other intra-abdominal
pathology that might have not been visible in the CT scan. If an unexpected
lesion is discovered, it must be evaluated and a surgeon must make a judgment
as to how best to proceed. Our group and others strongly discourage combining
a sterile vascular case with a potentially contaminated gastrointestinal case.
The next step is to retract superiorly the greater omentum and transverse colon.
The small bowel is eviscerated to the right side of the abdomen. This exposes
the base of the mesenteries of the left colon and the small intestine (Fig. 3).
Fig. 1 Treatment of abdominal aortic experience of vascular surgery residents in the
United States from 1994 to 2005
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