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Fig. 13.6 Omni-retractor setup, and exposure
when improved exposure of the distal arch and left subclavian is required. The eight or ninth space may be utilized to
approach an extent III aneurysm with little thoracic component. Oftentimes, both fth space and an eighth space entry
is required for an extent II aneurysm spanning the entire
thoracoabdominal aorta.
Once the ribs are reached, the scapular fascial plane just
above the ribs is mobilized all the way posteriorly. Staying
on the superior aspect of the rib the thoracic cavity is entered
and the posterior rib is shingled with a Guillotine. The undersurface of the diaphragm is encountered and dissecting further leads into the correct retroperitoneal plane. Once the
retroperitoneum is free, the endo-GIA blue staple load is utilized to staple and transect the diaphragm circumferentially,
taking care to avoid injuring the phrenic nerve. Leaving a
2–3cm cuff of diaphragm on the chest wall and marking the
staple line on either side with sutures facilitates later reapproximation of the diaphragm. This plane is then worked
caudally till the psoas muscle is reached. The peritoneum is
continually rolled toward the patient’s right side as this plane
is developed thereby executing a medial visceral rotation.
The Omni retractors are set up to provide adequate exposure within the abdominal cavity and the Finochietto rib
spreaders are placed to provide intercostal exposure
(Fig.13.6). Two rib spreaders are used if a higher intercostal
space (e.g., fourth interspace) is also entered for exposure.
Special care and attention is directed to padded retention of
the spleen to avoid capsular tear and injury.
A. Venkataraman and J. P. Schwartz
graft. Alternatively, an additional tube graft (10–12mm) can
be used to anastomose the intercostal vessels to the main
Dacron graft.
Repair oftheAbdominal Aortic Segment
The infrarenal abdominal aorta is clamped sequentially and
opened. The visceral vessels are identied and perfused with
cold blood via appropriately sized Pruitt balloon tipped catheters [33] (Figs.13.7 and 13.8). The visceral vessels are then
anastomosed to the Dacron graft either as an island patch or
individually by using short interposition bypass grafts.
Individual interposition bypass grafts tend to take longer for
the anastomoses to be completed but tend to be easier to
visualize and to be more hemostatic subsequently (Fig.13.9).
Fig. 13.7 Pruitt balloon tipped catheters
Repair oftheThoracic Aortic Segment
The thoracic aorta is clamped sequentially and the aorta
between clamps opened and a Dacron graft is sutured to the
proximal descending thoracic aorta. All lower intercostal
arteries from T8 to T12 are reattached either individually or
together as a patch to an elliptical incision in the Dacron
Fig. 13.8 Pruitt catheters utilized to perfuse individual mesenteric
vessels
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circulatory support. At our institution, we commonly
employ femoral–femoral cardiopulmonary bypass as
described below.
Femoral–Femoral Cardiopulmonary Bypass
Our preferred approach has been to cannulate the left femoral vein with an extended venous cannula that is extended to
the level of the right atrium under transesophageal guidance.
Arterial cannulation is also performed via the femoral artery
and full cardiopulmonary bypass is established.
Fig. 13.9 Individual grafts anastomosed to individual mesenteric ves-
sels and renal vessels
Fig. 13.10 Completely reconstructed thoracoabdominal aorta with
branch side grafts to visceral and renal vessels
If an island patch technique is used, typically the left renal
artery is located too far and requires a separate short interposition bypass graft. Once the visceral anastomosis is complete
the clamp is moved further down the graft and ow is reestablished to the viscera and kidneys (Fig.13.10).
Circulatory Support Options
A variety of strategies have been employed for circulatory
support or extracorporeal bypass for TAAA repair. Left
heart bypass (LHB) is considered the minimum and the
resultant decompression of the proximal circulation in
conjunction distal perfusion of the abdominal viscera, spinal cord, and lower extremities decreases complications
associated with ischemia. Many groups advocate left heart
bypass and use this technique as their preferred mode of
Left Heart Bypass
Left atrial drainage is established via the inferior pulmonary
vein. Arterial inow is established by cannulation of the iliac
system after exposure of the bifurcation, thereby providing
adequate retrograde ow to the visceral segment and the spinal cord via the internal iliac system and antegrade ow to
bilateral lower extremities.
Organ Protection
Neurologic Protection
The risk of postoperative neurologic decits (paraplegia and
paraparesis) has always plagued the repair of thoracoabdominal aneurysm with graft replacement since its inception. The development of a classication system for the
extent of an aneurysm had revealed that extent had a direct
correlation with neurological outcome in these operations.
In the era of simple cross-clamp techniques, immediate survival rates were fairly impressive, but the rate of neurologic
events (particularly in extent II aneurysms) remained persistently high. These poor neurologic outcomes were clearly
related to the aneurysm extent, rupture, clamp time, patient
age, and proximal disease. Over the years, several adjuncts
have been developed to improve upon these outcomes with
good results.
The technique of combined cerebrospinal uid (CSF)
drainage and distal aortic perfusion has consistently been
shown to provide superior neurological outcomes. The utilization of moderate hypothermia, active visceral cooling and
selective visceral perfusion, and aggressive intercostal artery
reattachments has further augmented the success of these
adjuncts [9]. Spinal catheters are inserted routinely by the
anesthesiology team in the third of fourth lumbar space. The
CSF pressure is kept at 10mmHg or less intraoperatively, and
the drain is kept in place usually for 3days postoperatively.
Because of the association of arterial blood pressure and oxy-
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A. Venkataraman and J. P. Schwartz
gen delivery to delayed neurologic decit, we maintain mean
arterial pressure (MAP) between 90mmHg and 100mmHg,
hemoglobin above 10 mg/dl, and a cardiac index above
2.0L/min. Urine output is closely monitored. In the event that
delayed neurologic decit occurs after removal of the CSF
drain, a new CSF drain is placed urgently and drained freely
for 2–3days and the CSF pressure kept below 10mmHg.
In current times, the overall rate of neurological events is
approximately 3% compared to 15% of patients during the
era of cross-clamp without adjuncts [9, 25]. The most noticeable result of adjuncts has been the signicant reduction in
neurologic decits in extent II repairs, 6.6% at present compared with previous incidence of 31% [25].
Renal andVisceral Protection
Distal aortic ischemia during TAA repair carries a formidable risk of perioperative morbidity and mortality. Renal dysfunction occurs in as many as 28% of patients undergoing
TAAA repairs, and necessitates dialysis in 4–11% of patients
[34]. With the advancement of surgical techniques and
adjuncts signicant improvements in open TAAA repair
have been achieved [35, 36]. The two primary approaches
that have emerged to maintain distal aortic perfusion and
selective visceral perfusion are that of left heart bypass
(LHB) and full cardiopulmonary bypass.
Left heart bypass (LHB) is used as a closed circuit with
the addition of a reservoir to salvage shed blood, and can be
used to maintain distal perfusion and pressure adjusted
accordingly to maintain stable hemodynamics. Visceral
perfusion can be provided using either isothermic (37°C)
or cold blood (4 °C) or crystalloid of all four branching
arteries [37].
Full cardiopulmonary bypass may also be used with a
wide range of protective hypothermic strategies such as mild
(34°C) to profound (18°C) systemic hypothermia, during
the repair. Partial cardiopulmonary bypass with three separate roller pumps for femoral–femoral bypass, celiac axis
and superior mesenteric artery perfusion, and bilateral renal
perfusion has also been described [38]. In some studies, cold
crystalloid perfusion was noted to protect against renal dysfunction over isothermic blood for renal perfusion [39]. In
studies comparing either cold blood versus cold crystalloid
for renal perfusion, no signicant difference was noted
between patients with regard to early death or renal failure
[37]. Recent aortic guidelines recommend the use of either
cold blood or cold crystalloid renal perfusion; however, the
exact techniques and additives vary amongst centers [19].
Concomitant visceral and renal artery occlusive disease is
present in a signicant proportion of patients with TAAAs
[40]. Techniques such as renal endarterectomy or the use of
balloon expandable stents to improve renal and visceral
blood ow have demonstrated benets such as fewer renal
failures in patients with preexisting renal dysfunction [26,
40]. The use of visceral stents in treating mesenteric and
renal occlusive disease is a new strategy that is gaining
acceptance [41]. The visceral stents prove useful in obliterating the false lumen associated with concomitant aortic dissections, keeping the ostia patent near patch anastomoses.
Although usually safe and effective, drawbacks include risk
of thrombosis, possibility of vessel perforation and stent
migration.
In the literature, the incidence of renal dysfunction is
highest after extent II TAAA repairs, which correlated with
prolonged protected and unprotected renal ischemia times.
Bowel ischemia occurred in only 1% of patients; however, it
had a substantial consequent attendant mortality of 88%
[34]. Thus, contemporary protective strategies enable
patients to undergo open TAAA repair with substantially
fewer renal and visceral ischemic complications than in previous decades.
Endovascular Repair
Endovascular aneurysm repair (EVAR) therapy offers a
potential alternative for patients who are physiologically
high risk for conventional surgery. Initially, advanced EVAR
was limited to short-necked abdominal aortic aneurysms,
but the development of the aortic endograft and bridging
stent graft technology has expanded its role to include further aortic coverage [42]. Early experience with application
of fenestrated and branched endografts to treat more extensive TAAA demonstrates acceptable outcomes [43]. The
rates of perioperative mortality, renal failure, and spinal
cord ischemia challenge outcomes attained for conventional
surgery in high-volume centers [44]. Renal failure and spinal cord ischemia (SCI) remain the most concerning postoperative morbidity in complex fenestrated branched
endovascular repair of TAAA.Renal failure occurred at a
rate of 2.8% in some series, with an incidence of 5.5% in the
subpopulation that underwent Type II repair [45]. SCI
symptoms developed in 8% of patients overall, but resolved
in nearly half the patients prior to hospital discharge in the
same series [45]. These outcomes are comparable with the
results contemporary open repair.
Staging of endovascular repair has been reported to be
associated with reduced incidence and severity of
SCI. Staging has its own risks. Before custom endografts
were available, staging was a necessity. However, a proportion of these patients die between stages (6%) and aneurysm
rupture is thought to be a causative factor [46]. From a technical standpoint, the need for the use of reinforced fenestrations in the endovascular treatment of complex TAAA may
be associated with higher rate of visceral and renal endoleaks
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197
and suboptimal patency rates [47]. Endoleaks also increase
the risk and need for reinterventions, but this has not appeared
to adversely affect longer-term outcomes. Evolving graft and
bridging stent design improvement may help to mitigate this
in future.
Hybrid Repair
The perioperative morbidity and mortality associated with
open surgical repair of TAAA has always remained signicant. The complications of acute renal failure (2–12%) and
cardiopulmonary (4–33%) and spinal cord ischemia (1–15%)
are signicant and are increased when preoperative pulmonary and renal impairment is present [48]. Complete endovascular exclusion of TAAA, while feasible, remains a
technique that is in evolution and has its shortcomings as
discussed above. Therefore, a hybrid approach mixing stable
endovascular exclusion of TAAAs after open visceral bypass
has evolved into a viable treatment option. The general
premise of the hybrid approach is based on the reduced physiologic stress of operating through one visceral cavity rather
than two (abdomen and thorax), thereby reducing complications and improving ultimate outcome.
Visceral hybrid TAAA repair utilizes retrograde revascularization of the visceral and renal arteries via an open
abdominal approach. This preparatory operation then enables
an endovascular stent-graft to exclude the TAAA including
the visceral aortic segment. Compared to open techniques,
this approach reduces visceral ischemia time. Spinal cord
ischemia, attributed to aortic cross-clamping, intraoperative
hypotension and reperfusion injury are theoretically minimized. The avoidance of a thoracotomy confers signicant
physiologic advantages in most patients, particularly those
with preoperative pulmonary impairment. There exists the
possibility of interval aneurysm degeneration and rupture
between two operations in the staged hybrid approach.
Proponents of this technique thus advocate its use in patients
considered high risk such as those with chronic obstructive
pulmonary disease, coronary artery disease, or chronic renal
insufciency [49]. These groups typically stage the open
debranching operation 2–4months prior to the endovascular
procedure, citing the avoidance of uid shifts and hemodynamic instability, which can result in a higher risk of paraplegia if performed concomitantly with endografting [49].
Summary
The outcomes of open TAAA repair have greatly improved
over the years and contemporary 30-day survival rates are
quoted over 90%. The highest survival rate published to
date was also the largest series ever reported, indicating
that high volume centers can achieve the best outcomes in
this complex disease process. Whilst sounding less invasive, hybrid and endovascular approaches still carry the signicant risk of morbidity and mortality compared with the
open procedures. It is reasonable to assume that with
increased use of endovascular techniques, an era will arrive
in which TAAAs may be more universally treated with less
invasive techniques. At present, open repair remains the
best option for the majority of patients to achieve good
long-term results.
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Abdominal Aortic Aneurysms
https://t.me/med1917
JoshuaD.Newman, AfaqMotiwala, AlexanderTurin,
AndrewChen, ValmikiRishiMaharaj, andRobertS.Dieter
14
Abbreviations
18
F-FDG
AAA Abdominal aortic aneurysm
ACE Angiotensin-converting enzyme
ADAM Aneurysm Detection and Management
CAD Coronary artery disease
CAESAR Comparison of surveillance versus aortic
CEUS Contrast-enhanced ultrasonography
CI Condence interval
COPD Chronic obstructive pulmonary disease
CTA Computed tomographic angiography
DREAM Dutch Randomized Endovascular Aneurysm
DUS Duplex ultrasound
EVAR Endovascular aneurysm repair
FAST Focused Assessment with Sonography in
HR Hazard ratio
IAAA Inammatory abdominal aortic aneurysm
MMP Matrix metalloproteinases
MRA Magnetic resonance angiography
MRI Magnetic resonance imaging
J. D. Newman (*) · A. Turin
Cardiology, Loyola University Medical Center, Maywood, IL, USA
A. Motiwala
Cardiovascular Diseases, Loyola University Medical Center,
Maywood, IL, USA
A. Chen
Cardiology, University of Nevada, School of Medicine,
Las Vegas, NV, USA
V. R. Maharaj
Internal Medicine, Loyola University Medical Center,
Maywood, IL, USA
R. S. Dieter
Interventional Cardiology, Vascular and Endovascular Medicine,
Loyola University Medical Center, Maywood, IL, USA
18
F-uoro-deoxy-glucose
endografting for small aneurysm repair
Management
Trauma
OR Odds ratio
OVER Open Versus Endovascular Repair
PAD Peripheral artery disease
PET Positron emission tomography
PIVOTAL Positive Impact of Endovascular Options for
treating Aneurysms Early
SPECT Single-photon emission computer
tomography
UKSAT UK Small Aneurysm Trial
US Ultrasound
USPSTF US Preventative Services Task Force
Introduction andDenitions
Aneurysm derives from the Greek word ανɛυρυσμα (aneurusma), meaning widening, and can be dened as a permanent and irreversible localized dilatation of a vessel. An
abdominal aortic aneurysm (AAA) is a permanent, localized
dilatation of the abdominal aorta that exceeds the normal
diameter by 50%.
The abdominal aorta begins at the level of the diaphragm
and extends to its bifurcation into the left and right common
iliac arteries. Normal aortic diameter varies with age, gender,
and body habitus, but the average diameter of the adult human
infrarenal aorta is about 2.0cm and typically less than 3.0cm.
Thus, for the majority of patients, an infrarenal aorta with a
maximum diameter≥3.0cm is considered aneurysmal [1].
Anatomy oftheAbdominal Aorta
The abdominal aorta is a retroperitoneal structure that begins
superiorly at the diaphragm and extends down to the level of
the forth lumbar vertebra, where it bifurcates into the right
and left common iliac arteries (Fig.14.1) [3]. The aorta lies
slightly left of midline, with the inferior vena cava adjacent
to it on the right. The branches of the aorta include (superior
to inferior) the left and right inferior phrenic arteries, left and
© Springer Nature Switzerland AG 2019
R. S. Dieter et al. (eds.), Diseases of the Aorta, https://doi.org/10.1007/978-3-030-11322-3_14
199
200
ar
in
arteries
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Fig. 14.1 Anatomy of the
abdominal aorta. (From
Tainter [2]. Reprinted with
permission from Elsevier)
J. D. Newman et al.
Diaphragm
Celiae artery
Left gastric
artery
Right renal
tery and vein
Superior
mesenteric
artery
Splenic artery
Common
hepatic artery
Left renal
artery and ve
Gonadal
arteries
Inferior
mesenteric
artery
Common iliac
arteries
lnternal iliac
arteries
External iliac
right middle suprarenal arteries, the celiac axis, superior
mesenteric artery, left and right renal arteries, left and right
gonadal arteries, inferior mesenteric artery, left and right
common iliac artery, middle sacral artery, and the paired
lumbar arteries. The common iliac artery bifurcates into the
external iliac and internal iliac arteries at the pelvic inlet.
Similar to other arteries, the aortic wall is divided into
three layers (from external to lumen): the tunica externa (or
tunica adventitia), tunica media, and tunica intima. The vascular supply to the tunica externa and tunica media is provided by an extensive network of small blood vessels known
as the vasa vasorum [3].
• Fusiform aneurysm: The circumference of the artery is
impacted by the aneurysm (most aneurysms are
fusiform).
• Saccular aneurysm: Only a part of the circumference of
the artery is impacted by the aneurysm.
• Inammatory aneurysm: Characterized by extensive perianeurysmal and retroperitoneal brosis and dense adhesions to adjacent abdominal organs [1].
• Infectious (mycotic) aneurysm: Aneurysm caused by an
infectious agent, most commonly bacterial (most commonly Staphylococcus aureus, Salmonella, and
Streptococcus pneumonia) [6].
Another commonly used classication modality is based
Classication
Aneurysms can be categorized by morphological characteristics, location, or etiology. The following are terms that
dene aneurysms based on morphology (Fig.14.2) [5].
on location within the aorta (Fig.14.3) [8]:
• Suprarenal aneurysm: Involves the origins of one or more
visceral arteries but does not extend into the chest.
• Pararenal aneurysm: The renal arteries arise from the
aneurysmal aorta; however, the aorta at the level of the
• True aneurysm: An aneurysm that involves all three layers
of the arterial wall (intima, media, and adventitia).
• False aneurysm (pseudoaneurysm): A collection of blood
or hematoma that has leaked out of the artery but is then
conned by the surrounding tissue.
superior mesenteric artery is not aneurysmal.
• Juxtarenal aneurysm: Originates just beyond the origins
of the renal arteries. There is no segment of nonaneurysmal aorta distal to the renal arteries, but the aorta at the
level of the renal arteries is not aneurysmal.
Tr ue aneurysm False (pseudo) aneurysm
Thoracoabdomina
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Fig. 14.2 Aneurysm
morphologies. (From
Netscher etal. [4]. Reprinted
with permission from
Elsevier)
201
Three normal vessel lamina
Fusiform aneurysm
Lack of three-layered structure
of normal blood vessel
Sacular aneurysm
Infrarenal Juxtarenal Pararenal
Fig. 14.3 Abdominal aortic aneurysms described by their location in relation to the renal arteries. (From Goldstone [7]. Reprinted with permis-
sion from Elsevier)
Suprarenal
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J. D. Newman et al.
• Infrarenal aneurysm: Originates distal to the renal arteries. There is a segment of nonaneurysmal aorta that
extends distal to the origins of the renal arteries.
• Thoracoabdominal aneurysm: Originates in the chest and
may involve the visceral or renal vessels.
Abdominal aortic aneurysms (AAA) most often affect the
segment of aorta between the renal and inferior mesenteric
arteries [9].
Pathophysiology
The development of abdominal aortic aneurysms is associated with alterations of the connective tissue in the aortic
wall. Elastic bers and brillar collagen are the main determinants of the mechanical properties of the aorta. Elastin
and associated proteins form a network of elastic bers
responsible for the viscoelastic properties of the aorta.
Elastin is stabilized by cross-links between the molecules
and is degraded by specic proteases that display elastase
activity. Elastic bers associated with smooth muscle cells
are most abundant in the media of the aortic wall. Collagen,
in polymeric form, is also a signicant component of the
media and the surrounding brous adventitia.
One of the major histological features of aneurysmal tis-
sue is fragmentation of elastic bers and a decreased concentration of elastin. The loss of elastic bers seems to be an
early step in aneurysm formation. Although elastin fragmentation and medial attenuation are the most important characteristics of the wall of an aneurysm, the adventitial tissue, in
which collagen is predominant, is responsible for the resistance of the aorta in the absence of medial elastin. Therefore,
while loss of elastin leads to aneurysm formation, collagen
degradation is thought to be the ultimate cause of aneurysm
rupture [5].
Collagen production continues throughout life and is even
increased in the aneurysmal wall. Besides enhanced collagen
synthesis, however, collagenolytic activity is increased in
AAA as well. This increased lytic activity is why several
hereditary connective tissue disorders (e.g., Ehlers-Danlos
and Marfan’s syndromes) are associated with aneurysm formation at an early age [8].
The alteration of elastin and collagen in the aortic wall is
dependent on production of proteases by nearby vascular
wall cells (medial smooth muscle cells and adventitial broblasts) and by the cells of the lymphomonocytic inltrate.
These inammatory cells in the media and adventitia come
from the aortic blood and from a medial neovascularization,
which characterizes abdominal aortic aneurysms. Leukocyte
recruitment into the aortic wall is promoted by elastin degradation fragments as well as proinammatory cytokines, chemokines, and prostaglandin derivatives produced by both the
resident mesenchymal cells and the inammatory cells
themselves. Elastic and collagen bers are degraded by proteolytic enzymes mostly represented by matrix metalloproteinases (MMP) locally activated by either other MMP or by
plasmin generated by plasminogen activators.
Besides rarefaction of its extracellular matrix, the elastic
media also undergo a reduction in the density of smooth muscle cells, which is regarded as a key event in the development
of abdominal aortic aneurysms. Smooth muscle cells participate in vascular wall remodeling through localized expression
of various extracellular matrix proteins as well as proteases
and their inhibitors. Additionally, smooth muscle cells have a
protective role against inammation and proteolysis.
The development of abdominal aortic aneurysms is also
associated with a mural thrombus in a number of patients.
By contrast with arterial occlusive diseases, blood ow is
maintained in aortic aneurysms resulting in a persistent
remodeling activity of the components of the thrombus.
Although the thrombus can substantially reduce aneurysmal
wall stress, its increasing thickness leads to local hypoxia at
the inner layer of the media, which can induce increased
medial neovascularization and inammation. This appears
to play a role in aneurysmal degeneration associated with an
adherent thrombus [1]. Some data suggests that thrombus
may actually increase risk of aneurysm rupture, presumably
due to localized tissue hypoxia and diminished wall strength
[10–13].
Risk Factors
The common risk factors of AAA are smoking, male gender,
white race, older age, chronic obstructive pulmonary disease
(COPD), hypertension, dyslipidemia, coronary artery disease
(CAD), peripheral artery disease (PAD), and positive family
history [14]. Interestingly, although diabetes mellitus is a risk
factor for PAD and CAD, it has been found to be a negative
risk factor for AAA development and growth [15, 16].
Age
Elastin is not synthesized in the adult aorta. With a half-life
of 70years, the amount of elastin in the aortic wall decreases
with age. The age-related alterations in the vessel wall affect
the mechanical properties of the aorta. This explains why
AAA is primarily a disease of the elderly [8].
Atherosclerosis
The historical association of AAA with atherosclerosis has
now expanded into a multifactorial causation for the disease.
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It is unclear why atherosclerosis, normally causing narrowing of the arterial lumen, should in some cases result in
dilation. There are epidemiological differences between
patients with obstructive vascular and aneurysmal disease.
Histological examination of the aneurysm wall reveals a
chronic adventitial and medial inammatory inltrate of
varying intensity. This distinguishes AAA from the purely
atherosclerotic aorta, in which inammatory cells are mainly
associated with plaque. Patients with obstructive peripheral
vascular disease also carry an increased risk for AAA.It is
also important to remember that both AAA and peripheral
arterial disease share many common risk factors (such as
age, gender, smoking, hypertension, and hyperlipidemia,
among others) [8].
Smoking
Smoking is the risk factor most strongly associated with
AAA.Men who currently smoke more than 25 cigarettes per
day have a 15-fold increased risk of AAA (hazard ratio [HR]
14.6, 95% CI 9.6–22) compared with men who have never
smoked [17]. A smoker’s risk of developing AAA continues
for at least 10years following smoking cessation. In spite of
this association, however, no causative link has been proven
between smoking and AAA formation. The mechanism by
which cigarette smoking contributes to aneurysm formation
is independent of atherosclerosis. Theories behind the pathophysiology include disruption in collagen synthesis, altered
expression of metalloproteinases, and the response to oxidative stress [18].
Patients with smoking history are more likely to develop
COPD.As is the case in AAA, COPD is driven by excess
matrix turnover and proteolysis. A large meta-analysis
recently showed a 1.8-fold increase prevalence and incidence
of AAA in patients with COPD compared to those without it
[19]. Further, some studies suggest that COPD increases the
risk of AAA rupture [20].
involved in pathogenesis [
rupture risk in patients with established AAAs [14].
5]. Hypertension also increases
Hyperlipidemia
High-serum total cholesterol has a positive association with
AAA prevalence, whereas high-density lipoprotein cholesterol has an inverse association. This correlation may be
related to the increased risk of atherosclerosis, or may in part
be a direct factor [21]. Similarly, obesity has also been shown
to be an independent risk factor [18].
Family History/Genetic Factors
Positive family history has been shown to be a major risk
factor for development of abdominal aortic aneurysm. A
study by Larsson and colleagues showed the overall relative
risk of AAA associated with family history compared to no
family history was 1.9 (95% condence interval [CI] 1.6–
2.2) [22].
The development of AAAs is unlikely to be related to a
single gene mutation, and multiple genetic factors are implicated. Susceptibility genes, rather than causal gene mutations, are likely to be important, particularly those regulating
inammatory mediators, tissue proteases, and smooth muscle cell biology [18].
Alcohol Intake
High levels of alcohol intake (>30g/day) have been associated with increased risk of AAA (OR 1.65, 95% CI 1.03–
2.64) [17]. The mechanism through which alcohol exposure
increases the risk of AAA is unclear, but could be through
upregulation of matrix metalloproteinases and focal elastin
degradation.
Gender
Men are at much higher risk of AAA than women. The reasons for this are unclear, but it is likely to be a function of
hormonal factors, genetic susceptibility, and risk factor
exposure [18].
Hypertension
Hypertension enhances the growth rate of aneurysms and is
associated with an increased prevalence of AAA, which indicates that an increased load on the aortic wall may be
Primary Disorders oftheAorta
A fraction of the cases of AAA are the direct consequence of
disorders of the aorta itself or disruptions in the integrity of
the aorta. Some of these causes include trauma, acute infection (bacterial or fungal), chronic infection (tuberculosis),
inammatory diseases (Behçet and Takayasu disease), and
connective tissue disorders (Marfan’s syndrome, EhlersDanlos type IV) [1].
In spite of the nomenclature, mycotic aneurysms are
most often caused by bacterial pathogens, with fungi rarely
being associated. The most commonly implicated organisms include Staphylococcus aureus, Salmonella, and
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