Epidemiology, Risk Factors, Pathogenesis, and Natural History of Abdominal Aortic Aneurysm - UpToDate

9/11/2017 Epidemiology, risk factors, pathogenesis, and natural history of abdominal aortic aneurysm - UpToDate
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Epidemiology, risk factors, pathogenesis, and natural history of abdominal aortic aneurysm
Author: Jayer Chung, MD, MSc

Section Editors: John F Eidt, MD, Joseph L Mills, Sr, MD
Deputy Editor: Kathryn A Collins, MD, PhD, FACS
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2017. | This topic last updated: Sep 28, 2017.
INTRODUCTION — An abdominal aortic aneurysm (AAA) is a focal dilation (figure 1) 50 percent greater than the normal diameter of the aorta.
The abdominal aorta is the most common site of true arterial aneurysm affecting predominantly the segment of aorta below the renal arteries
(infrarenal aorta) [1]. Well-defined risk factors are associated with the development of AAA and include advanced age, male gender, Caucasian
race, a positive family history, smoking, the presence of other large vessel aneurysms, and atherosclerosis [2,3]. The Centers for Disease
Control ranked AAA as the 15th leading cause of mortality in the United States in 2013 in adults between 60 and 64 years of age [4].
AAAs progressively dilate over time. While expansion rates vary, large aneurysms generally expand at a faster rate than small aneurysms
[2,3]. Mechanisms for the development, expansion, and rupture of AAA have been validated in animal models. However, the relative
contribution of these in humans is unclear [5]. The main risk factors associated with expansion and rupture of AAA are somewhat different from
those that contribute to the development of AAA and include large aneurysm diameter, rapid expansion, smoking, hypertension, elevated peak
wall stress, a history of cardiac or renal transplant, decreased forced expiratory volume, and female gender [2,3]. While there is significant
overlap, the epidemiology, risk factors, pathogenesis, and natural history of the development of AAA differ somewhat from the natural history of
expansion and rupture and will therefore be discussed separately.
The epidemiology, risk factors, pathogenesis, and natural history of AAA are reviewed here. The diagnosis, management, and treatment of
AAA are discussed in detail elsewhere. Definitions of aneurysms by their location relative to the visceral vessels, involvement of the vessel
layer walls, morphology (saccular versus fusiform), and diameter (small versus large) are described in detail elsewhere. (See "Clinical features
and diagnosis of abdominal aortic aneurysm", section on 'Aneurysm definition and anatomy' and "Management of asymptomatic abdominal
aortic aneurysm", section on 'Introduction'.)
DEVELOPMENT OF AAA
Epidemiology — The prevalence of abdominal aortic aneurysm (AAA) is 4 to 8 percent in screening studies, affecting predominantly males [6-
9]. However, AAAs found on screening are generally small; those measuring ≥5.5 cm or greater are found in only 0.4 to 0.6 percent of those
screened [10]. Because the incidence of AAA rises sharply in individuals over 60 years of age, the future prevalence of AAA could increase
substantially in association with the aging population [11]. On the other hand, some suggest that a reduction in the prevalence of smoking
could have the opposite effect (figure 2), with several studies citing a lower prevalence of AAA in 65- to 80-year-old Caucasian adults [12-14].
The annual incidence of new AAA diagnoses is approximately 0.4 to 0.67 percent in Western populations. This equates to 2.5 to 6.5
aneurysms per 1000 person-years [15-18]. Age significantly impacts the incidence. As an example, in one study, among men aged 65 to 74
years, the incidence was 55 per 100,000 person-years, increasing to 112 per 100,000 person-years for men aged 75 to 85 years, and further
increasing to 298 per 100,000 person-years for those older than 85 [19].
Risk factors for the development of AAA — There is significant overlap between the risk factors that contribute to the development of AAA
and the risk factors that contribute to the expansion and rupture of AAA. However, the relative contribution of each risk factor to either the
development or the expansion and/or rupture of AAA varies. Tobacco abuse appears to be the main modifiable risk factor for the development
of AAA. Protective factors for the development of AAA include female gender, non-Caucasian race, diabetes, and moderate alcohol
consumption [20]. (See "Management of asymptomatic abdominal aortic aneurysm", section on 'Therapies to limit aortic expansion'.)
Advanced age and male gender — The incidence and prevalence are not significant in populations aged less than 60 years [6-9,19].
Among males aged between 65 and 80 years, the prevalence of AAA is 4 to 8 percent [6-9]. Aneurysms are rare in women less than 50 years
of age. The prevalence of AAA in 65- to 80-year-old women is four to six times lower compared with their male counterparts [21]. In a
systematic review of screening studies, the overall prevalence of AAA in women ranged from 0.37 to 1.53 percent [22]. Since prevalence
studies have defined aneurysm as aortic diameter ≥30 mm, the true prevalence of AAA in women may be underestimated because of
differences in body size [23].
Caucasian race — AAA occurs most frequently among non-Hispanic white Americans or Caucasians of European descent. The incidence
is 10-fold lower in Asian populations, at 0.45 percent in Asian men over 65 years in age [24]. Among Black Americans, AAA occurred half as
https://aplicacionesbiblioteca.udea.edu.co:3925/contents/epidemiology-risk-factors-pathogenesis-and-natural-history-of-abdominal-aortic-aneurysm/p… 1/15
frequently as in their Caucasian counterparts [25]. The Life Line Screening cohort study also showed a reduced risk for the development of
AAA among Hispanics (odds ratio [OR] 0.69), and confirmed the decreased risk of AAA among Asian-Americans and Black-Americans [26].
Family history — A genetic predisposition for the development of AAA has been suspected since the first report of three brothers who
each underwent surgery for ruptured AAA [27]. Since this report, multiple other familial clusters have been identified, further suggesting a
genetic predisposition [28,29]. Family history appears to increase the risk of the development of AAA by two- to fivefold [28-31]. These are
variable with polygenetic inheritance patterns [32]. Syndromic monogenetic disorders, such as Marfan syndrome (fibrillin-1 defect) or Ehlers-
Danlos syndrome type IV (abnormal type III procollagen), are more commonly associated with thoracoabdominal aortic aneurysms [33]. (See
"Epidemiology, risk factors, pathogenesis, and natural history of thoracic aortic aneurysm", section on 'Genetic predisposition'.)
Smoking — Tobacco smoking is the modifiable risk factor most strongly associated with the development of AAA. Among screened
patients found to have small AAAs, 18 to 25 percent are current smokers [25,26,34]. Current smokers also initially present with larger
aneurysms. The number of pack-years is positively associated with increased odds of AAA being found on screening [26,34]. Men who smoke
over one pack per day also have a 15-fold increased risk of AAA compared with age-matched males who do not smoke [35]. Smoking
cessation decreases the subsequent odds of AAA being identified on screening, with the greatest benefit among those who have quit for more
than 10 years. Unfortunately, the odds never return to the baseline of nonsmokers, indicating that some degree of damage inflicted by tobacco
use is permanent [26].
Presence of other large vessel aneurysms — Patients with other large vessel aneurysms (such as iliac, femoral, popliteal, or carotid
artery aneurysms) have an increased risk for AAA. Patients with a femoral artery aneurysm are found to have a concomitant AAA 85 percent
of the time. Subjects with popliteal aneurysms have a concomitant AAA 60 percent of the time [36,37]. Up to 25 percent of subjects have
combined thoracic and abdominal aortic aneurysms [38,39]. Compared with men, more women have combined thoracic aortic aneurysms and
AAA (48 versus 28 percent) [38]. AAA has also been found to coexist with intracranial aneurysm; AAA screening is advocated by some for
patients found to have intracranial aneurysm [40-42].
Atherosclerotic risk factors — Systemic atherosclerosis is present concurrently with AAA in multiple studies corroborating the significant
overlap in the risk factors between the two disease processes [25,26,43].
● Coronary artery disease is present in over 25 percent of individuals with AAA.

● Peripheral arterial disease is found in over 12 percent of those with AAA.
However, it is important to note that there are patients with aneurysmal disease with a low burden of peripheral artery disease (PAD).
Moreover, the incidence of PAD is low in those with familial aortic aneurysm [44]. The pathophysiology responsible for AAA formation is felt to
be distinct from atherosclerosis. (See 'Pathophysiology of AAA' below.)
With respect to the major risk factors associated with atherosclerosis, the roles of male gender and tobacco use are discussed above.
Hypertension and hyperlipidemia are frequently cited as etiologic risk factors for the development of AAA [25,26,45,46]. Intuitively, chronically
elevated blood pressure would weaken the aortic wall, as would lipid-laden atherosclerotic plaques.
Other factors
● Obesity – There is inconsistency in the literature regarding the association of obesity with the presence of AAA [47-49]. If there is an
association, it is mildly positive, increasing the odds of AAA by 22 percent in a large cohort from Australia [48]. Obesity may be more
significant in conjunction with atherosclerotic disease, amplifying the odds of the development of AAA by twofold relative to nonobese
atherosclerotic patients [49].
● Diet and alcohol consumption – Data regarding moderate alcohol consumption are inconsistent, with several studies citing a moderate
protective effect (hazard ratio [HR] 0.57 to 0.80) [50]. Conversely, with higher levels of alcohol intake (≥30 grams/day; ≥2 drinks/day) there
appears to be an increased risk of AAA [35]. This decreased risk of AAA with modest alcohol intake seemed to be most pronounced with
beer and wine; however, larger studies are required to corroborate these findings.
Fruit and vegetable consumption appears to be mildly associated with less AAA development [26,51]. The Lifeline Registry in the United
States showed that individuals who adhered to a diet of fruit and nuts ≥3 servings/week decreased their odds of developing AAA by
approximately 10 percent [26]. The effect appears stronger with higher fruit intake. Among a Swedish cohort of 80,426 participants, a
higher consumption of fruits (>2 servings/day) was associated with a 25 percent decreased risk of AAA relative to those with lower fruit
intake (0.7 servings/day) [51].
Negative risk factors — While diabetes mellitus is positively associated with the presence of atherosclerosis, it is negatively associated
with AAA [25,26,46,52-54]. Studies estimate the odds of AAA among diabetics compared with nondiabetics to be between 0.52 and 0.75
[25,26,53]. The lack of association between diabetes and AAA suggests that the development of AAA and atherosclerosis are distinct
processes, despite the significant overlap of risk factors. Moreover, the medications used to treat diabetes mellitus may exert a potential
protective effect with respect to AAA development [55].
Pathophysiology of AAA — AAA is the focal manifestation of a systemic process highlighted by inflammation, smooth muscle cell apoptosis,
and extracellular matrix degradation. The embryologic origins of the infrarenal aorta may also play a role. Although there is significant overlap
of risk factors and prevalence of disease with atherosclerosis, the etiology of AAA is distinct from atherosclerosis. The processes driving the
initiation of AAA, and the ultimate expansion and/or rupture of an AAA, are somewhat different and are discussed separately. (See 'Expansion
and rupture of AAA' below.)
Much of the knowledge of the pathogenesis of human aortic aneurysms is extrapolated from animal models. No known treatment can induce
regression once AAA has formed, and most therapies are aimed at limiting further expansion. (See "Management of asymptomatic abdominal
aortic aneurysm", section on 'Therapies to limit aortic expansion'.)
Embryology and histology of the infrarenal aorta — The embryology and histology of the infrarenal abdominal aorta helps to explain the
predisposition of this anatomic site to aneurysm formation (picture 1).
The smooth muscle cell composition of the infrarenal aorta is derived from the paraxial mesodermal somites, which is distinct from other parts
of the aorta or iliac arteries. This is significant as areas derived from somites appear more susceptible to aneurysmal degeneration [56]. The
thickness and number of elastic lamellae in the media gradually decrease along the length of the aorta from the aortic root to the iliac
bifurcation such that at the level of the conus arteriosus to the bifurcation of the iliac arteries, there is a 10-fold decrease in the amount of
elastin [57]. Transforming growth factor-beta (TGFB) appears critical to mediating the differences in the smooth muscle cell phenotype in
different parts of the aorta due to differential responses depending upon the embryologic cell of origin [58,59]. There is also less collagen in the
infrarenal aorta relative to other portions of the aorta [60]. Finally, the vasa vasorum is somewhat fragile, rendering the blood supply to the
media relatively meager [61].
Hemodynamic susceptibility — The unique hemodynamic pressures exerted on the infrarenal aorta upregulate proteins that are important
in the development of AAA. As the aorta tapers and gives off its major branches, the pulse wave increases from the heart toward the infrarenal
aorta [62]. The bifurcation of the aorta also results in turbulence and areas of high and low shear stress [63]. In regions of high shear stress,
endothelial cells increase the production of endothelial nitric oxide, and production of matrix metalloproteinase-2 and -9 and TGFB are
upregulated [64]. In areas of low stress, endothelial cells produce nuclear factor kappa-light-chain-enhancer of activated B cells (ie, nuclear
factor-KB) and endothelin-1 [65].
Inflammation and the Th2 response — There is a transmural infiltration of inflammatory cells in AAA, such as polymorphonuclear
neutrophils, T-cells, B-cells, macrophages, mast cells, and natural killer cells [66-69]. The predominant cell types are CD4+ T-cells, B-cells, and
macrophages [70], indicative of a shift toward a T-helper type 2 (Th2) response. (See "T helper subsets: Differentiation and role in disease",
section on 'T helper subsets in disease'.)
In contrast, the T-helper type 1 (Th1) response is more frequently found in atheroma and may explain the different mechanisms of AAA despite
the overlap of risk factors between atherosclerosis and AAA [71]. This results in the secretion of interleukins (IL-4, IL-5, IL-10, and IL-13) and
inhibition of interferon (IFN-γ), which have pleiotropic effects upon smooth muscle cells, extracellular matrix, and other inflammatory cells that
mediate and regulate AAA development [72,73]. IFN-γ blockade appears particularly important, as the IFN-γ appears to protect against IL-4-
mediated collagenolysis and elastolysis [73].
Reactive oxygen species (ROS), particularly superoxide anion (O2-), are significantly increased in aneurysmal tissue. ROS are especially
important in the pathogenesis of AAA in the presence of tobacco abuse. These species are produced by the inflammatory cell infiltrate and
appear to predispose toward the Th2 inflammatory phenotype [74]. ROS are mediated via nicotinamide adenine dinucleotide phosphate-
oxidases and contribute directly to smooth muscle cell degeneration as well as to amplify the Th2 inflammatory response that mediates AAA
development [75].
Despite the presence of inflammatory infiltrate in AAA, radiologic findings of inflammation inconsistently predict aneurysmal expansion or
rupture [76]. Ultrasmall superparamagnetic particles of iron oxide (USPIO)-enhanced magnetic resonance (MR) imaging is one modality that
can identify aortic wall cellular inflammation in those with AAA [77,78]. In a multicenter cohort study that monitored 342 individuals with AAA ≥4
cm for over two years, USPIO enhancement was identified in 42.7 percent of participants, absent in 55.8 percent, and indeterminant in 1.5
percent [78]. Compared with those without uptake, patients with USPIO enhancement had higher rates for the primary outcome of aneurysm
rupture or repair (47.3 versus 35.6 percent). Patients with USPIO enhancement also had increased rates of aneurysm expansion compared
with those without uptake (3.1 versus 2.5 mm/year), although this was not independent of current smoking habit. Baseline AAA diameter and
current smoking habit also predicted the primary outcome, and the addition of USPIO enhancement to the multivariate model did not improve
prediction of adverse AAA-related events over clinical features alone. 18F-fluorodeoxyglucose positron emission tomography (FFDG-PET) is
similarly inconsistent for predicting AAA expansion or rupture [76,77]. Further study is needed to more accurately quantify associations
between inflammation within AAA on imaging and subsequent expansion or rupture before these become clinically useful.
Smooth muscle cell apoptosis — The Th2 inflammatory cells also secrete Fas ligand and Fas-associated phosphatase-1 (FAP-1). These
mediate apoptosis of vascular smooth muscle cells as well as the Th1-lymphocytes [71,79]. IL-4 will also accelerate the Th2 inflammatory
phenotype as it promotes the survival of Th2 lymphocytes while failing to rescue Th1 lymphocytes. This favors the cytokine environment further
toward the Th2 phenotype, which then accelerates vascular smooth muscle cell apoptosis (picture 2) [80].
Extracellular matrix degradation — Further degradation of the extracellular matrix contributes to the development of AAA. In particular,
matrix metalloproteinases (MMPs) and elastases are critical to degrade and fragment the medial elastic lamellae and type I and III collagen.
These are secreted by the inflammatory cell infiltrate, smooth muscle cells, and endothelial cells of the aorta. (See "Vascular endothelial
function and fundamental mechanisms of fibrinolysis (thrombolysis)".)
The most important inflammatory cell appears to be the macrophage, which is particularly vital for the production of MMP-9 [68,81]. MMP-12
production is augmented by IL-4 and gamma interferon blockade and appears to be important for the early stages of AAA development [73].
The proteases found most frequently are MMP-1, -2, -3, -8 -9, -12, and -13; serine proteases (tissue-type plasminogen activator [t-PA],
urokinase [u-PA], plasmin and neutrophil elastase); and cysteine proteases (cathepsin D, K, L, and S). Elastin has a long half-life and
decreases with aging and in aneurysms. These are responsible for the destruction of type I and III collagen and elastin and the elastic
lamellae, which are the hallmark of histological specimens of AAA [82,83].
EXPANSION AND RUPTURE OF AAA — The risk factors associated with expansion and rupture of abdominal aortic aneurysm (AAA) overlap
somewhat with those associated with the development of AAA, though there are some significant differences. These risk factors include large
baseline aneurysm diameter, rapid expansion, tobacco use, hypertension, elevated peak wall stress, a history of cardiac or renal transplant,
decreased forced expiratory volume (FEV1), and female gender [2,3]. Most of these risk factors are intuitive, though the role of female gender
requires further explanation.
Epidemiology of AAA rupture — In 2013, statistics compiled by the United States Centers for Disease Control found that AAA is the 15th
leading cause of death among adult Americans aged 60 to 64 years of age [4]. This represented a rate of 4.1 deaths per 100,000 people [4].
When stratified by gender, most of the deaths were found to be in men, where AAA remained the 15th leading cause of death in men aged 60
to 64 [4]. AAA is the cause of death in 0.13 percent of males, compared with 0.07 percent of females. The rates of rupture do not appear to be
declining [84] and may in fact be increasing in certain populations [85].
Risk factors for AAA rupture
Baseline aortic diameter — Baseline diameter is the most validated parameter associated with AAA rupture. Rupture risk at 12 months, as
stratified by baseline aortic diameter, is summarized below [2,3]:
● <1 percent rupture risk for AAA baseline diameter 30 to 39 mm

● 1 percent rupture risk for AAA baseline diameter 40 to 49 mm
● 1 to 11 percent rupture risk for AAA baseline diameter 50 to 59 mm
● 10 to 22 percent rupture risk for AAA baseline diameter 60 to 69 mm
● 30 to 33 percent rupture risk for AAA baseline diameter >70 mm
Rapid expansion — While the expansion of aneurysms is largely predictable, individual aneurysms may undergo unpredictable stochastic
expansion (eg, expanding for a time, then not expanding, then expanding again). Larger aneurysms expand at more rapid rates compared with
smaller aneurysms [86-88]. In the United Kingdom Small Aneurysm Trial, the mean expansion rates were as follows [88]:
● 1.9 mm per year for AAA baseline diameter 2.8 to 3.9 cm

Rapid expansion has been defined as aneurysms that increase in size ≥5 mm over a six-month time-period or ≥10 mm over a 12-month period
[2]. However, several studies have shown that the definition of rapid expansion depends upon the initial baseline diameter as well, with larger
aneurysms requiring larger interval increases in diameter to be defined as "rapidly" expanding [89]. Moreover, it is unclear whether rapidly
expanding aneurysms increase the risk of rupture independent of the diameter of the aneurysm.
Smoking — Tobacco use is associated with the development of AAA, more rapid expansion, and increased risk of AAA rupture [86-88] and
represents the single most effective nonsurgical intervention to reduce the risk of aneurysm-related complications and/or death [90]. Data from
the Aneurysm Detection and Management (ADAM) Study Group suggest that current smoking increases the mean expansion rate of AAA by
an additional 0.05 cm/year [86]. A meta-analysis found that current smoking increased the AAA expansion rate by 0.35 mm/year and was
associated with a twofold increased risk of rupture [91].
Hypertension — Data regarding the role of hypertension in AAA expansion are somewhat inconsistent. Elevated diastolic blood pressure is
associated with a 0.02 cm/year increase in diameter for every 10 mmHg in the Aneurysm Detection and Management Study [86]. Data from
the United Kingdom failed to show an association between hypertension and aneurysm enlargement [88] but did show an association between
hypertension and AAA rupture [92]. Overall, the data most consistently support the association between AAA rupture and hypertension. The
association between AAA expansion and hypertension is less clear.
Elevated peak aortic wall stress — Unfortunately, there are limits to using baseline AAA diameter to predict rupture risk [93]. In one
review of 24,000 consecutive autopsies performed over 23 years, 473 AAAs were identified, of which 118 were ruptured. Interestingly, 40
percent of AAAs with a diameter between 7 and 10 cm were not ruptured. Moreover, 13 percent of aneurysms <5 cm had ruptured. These data
have led investigators to seek other factors associated with AAA rupture. One of the more popular investigational methods uses finite element
analysis to quantify peak wall stress at given points of an aneurysm based upon computed tomographic (CT) images [94]. Later iterations of
these analyses have become more complex and incorporate the peak wall stress with wall stiffness, the patient's diastolic pressure,
morphology of the aneurysm, diameter, expansion rate, and gender to improve the precision of the predicted models [95,96]. Further research
into this area is necessary, however, and these methods are not yet available for generalized clinical use.
History of cardiac or renal transplant — Cardiac and abdominal organ transplant appears to increase the prevalence of AAA, the rate of
expansion, and the risk of rupture post-transplantation [97,98]. Immunosuppressant and corticosteroid treatment have been associated with
AAA development, expansion, and rupture in animal models, though more study is required to clarify the mechanisms of AAA expansion and
rupture after transplantation [97,98].
For heart transplant patients, 10 percent of subjects were found to have AAA. Among those heart transplant recipients without preexisting
aneurysms, the diagnosis of AAA was made at a mean of six years after transplantation. Older age at the time of transplantation, male gender,
and ischemic heart disease prior to transplantation were positively associated with the development of AAA [97]. In a large series of liver
and/or kidney transplant patients, the prevalence of AAA was approximately 1 percent. AAA expansion rates were higher relative to
pretransplantation rates, with rupture occurring only post-transplantation [98].
Decreased forced expiratory volume (FEV1) — Individual studies suggest that subjects with severe chronic obstructive pulmonary
disease (COPD) may have an elevated risk of AAA rupture [92,99]. A lower FEV1 was independently associated with an increased risk of
aneurysm rupture after three years of surveillance of AAA in one study [92]. Another study similarly found that those with severe COPD had an
increased risk for ruptured AAA [99]. Data are mixed as to whether mild-to-moderate disease increases the risk of rupture.
Female gender — Although the prevalence of AAA is lower among females, multiple studies have quantified that female gender is one of
the strongest predictors of AAA rupture [2,3,92,100,101]. Data from the United Kingdom Small Aneurysm trial suggest that the risk of death
from rupture in females may be four times higher compared with males with similar-diameter aneurysms during surveillance [92].
AAAs in females also expand more rapidly, and rupture occurs at AAA diameters that are 5 to 10 mm smaller compared with males when
controlling for other known covariates known to influence rupture risk [100,101]. This may be due to a decreased tensile strength in female
aortas as well as due to increased peak wall stress within female AAA [102,103]. Differentiating gender from effect of a smaller body habitus
has been difficult and requires further research to develop a nomogram to predict rupture risk adjusted for body size, similar to that which is
being developed for thoracic aortic aneurysms [104].
Other factors
● Saccular aneurysms have been posited to be at an increased risk of rupture. This is based on the theoretical increased risk of rupture in
the transition zone between healthy aorta and the aneurysm itself, which is more pronounced in saccular aneurysms. This risk has not
been well quantified in the literature. One study failed to find an association between peak wall stress and saccular aneurysms [105].
● The influence of recent prior surgery upon AAA rupture has also been reported in small series. In a small series of 33 patients with a
known AAA who underwent a variety of unrelated operations, 3 percent of AAA >5 cm ruptured postoperatively [106]. The risk may be
higher with cardiac surgery [107]. The mechanisms of this increased risk are unclear, though they may be related to the stress of surgery.
● When AAA occurs in patients with diabetes mellitus, diabetes appears to protect against expansion of AAA [86,91]. The decrease in the
expansion rate ranges between 25 and 40 percent in patients with diabetes compared with nondiabetics [86,91]. The mechanisms for this
remain unclear, but this is consistent also with the protective effect of diabetes upon the development of AAA. Some authors posit that the
protective effect may be mediated by the increased arterial stiffness induced by diabetes upon the aorta [108]. It is unclear whether
diabetes decreases rupture risk when controlling for aneurysm diameter.
● Although coronary artery disease and systemic atherosclerosis appear to be associated with the development of AAA, coronary artery
disease may not be associated with expansion or rupture of AAA. A meta-analysis found a negative association between a history of
coronary artery disease and AAA expansion [109]. Future appropriately powered studies that clearly define the severity of systemic
atherosclerosis will be required to quantify the true role of atherosclerosis upon AAA expansion and rupture.
SUMMARY AND RECOMMENDATIONS
● Abdominal aortic aneurysm (AAA), which is a focal dilation more than 50 percent greater than the normal diameter of the aorta (figure 1),
is a common but potentially lethal condition. The abdominal aorta is the most common site of true arterial aneurysm affecting
predominantly the segment of aorta below the renal arteries (infrarenal aorta). (See 'Introduction' above.)
● Ultrasound screening studies have found that 4 to 8 percent of older men have an occult AAA. Although the prevalence of AAA is four to
six times lower for women compared with men, women present with rupture more often than men. (See 'Epidemiology' above and
'Epidemiology of AAA rupture' above.)
● The main risk factors for developing AAA include advancing age, male gender, Caucasian race, family history, smoking, the presence of
other large vessel aneurysm, and atherosclerotic risk factors. Although diabetes mellitus is consistently a strong risk factor for
atherosclerosis, it is negatively associated with the development of AAA. (See 'Risk factors for the development of AAA' above.)
● Aneurysmal degeneration of the abdominal aorta is a multifactorial systemic process due to alterations in vascular wall biology. AAAs are
characterized by transmural inflammatory changes, abnormal collagen remodeling and cross-linking, and loss of elastin and smooth
muscle cells, which results in progressive thinning and weakening of the aortic wall and enlargement of the aortic diameter. (See
'Pathophysiology of AAA' above.)
● Multiple factors influence aortic expansion and the risk of rupture, the most important of which are aortic diameter and ongoing smoking.
Small and medium-sized AAAs (<5.5 cm) expand at an average rate of 2 to 3 mm/year while larger AAAs expand at approximately 3 to 4
mm per year. AAAs that exhibit rapid diameter expansion ≥5 mm over six months or >10 mm over one year of follow-up have an increased
risk for rupture. (See 'Expansion and rupture of AAA' above.)
ACKNOWLEDGMENT — We are saddened by the death of Emile R Mohler, III, MD, who passed away in October 2017. UpToDate wishes to
acknowledge Dr. Mohler's past work as an original contributor for this topic, as well as his work as our Section Editor for Vascular Medicine.
Use of UpToDate is subject to the Subscription and License Agreement.
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Topic 15190 Version 16.0
https://aplicacionesbiblioteca.udea.edu.co:3925/contents/epidemiology-risk-factors-pathogenesis-and-natural-history-of-abdominal-aortic-aneurysm/… 10/15
GRAPHICS
Anatomy abdominal aortic aneurysm
Graphic 60682 Version 13.0
Rise and fall of AAA incidence and smoking
US annual adult per capita cigarette consumption and US age-adjusted AAA mortality per 100,000 white men
by year [1,2]. For 1951 to 1978, rates are standardized to the US 1960 population as calculated by Lilienfeld et
al [3], and from 1979 onward to the US 1970 population from CDC Wonder [4]. Rates include abdominal,
thoracoabdominal, and unspecified aortic aneurysm, both ruptured and nonruptured, but exclude thoracic
aneurysm and dissection. Because all non-syphilitic aortic aneurysms and dissections were combined before
1968, and 1967 to 1968 data indicate that thoracic aneurysm and dissection accounted for 20 percent of
total, pre-1968 values.
US: United States; AAA: abdominal aortic aneurysm; CDC: Centers for Disease Control (United States).
Data from:
1. Centers for Disease Control and Prevention. Surveillance for selected tobacco-use behaviors - United States,
1900-1994. MMWR 1994; 43:1.
2. Economic Research Service, US Department of Agriculture (USDA). Tobacco Outlook October 24, 2007, TBS-
263. Available at: http://usda. mannlib.cornell.edu/MannUsda/viewDocumentInfo.do?documentID1389.
Accessed July 2011.
3. Lilienfeld DE, Gunderson PD, Sprafka JM, Vargas C. Epidemiology of aortic aneurysms, I: mortality trends in
the United States, 1951 to 1981. Arteriosclerosis 1987; 7:637.
4. Centers for Disease Control and Prevention. Compressed Mortality File 1979-1998 and 1999-2007. CDC
WONDER On-line Database. Available at: http://wonder.cdc.gov. Accessed July 2011.
Reproduced with permission from: Lederle FA. The rise and fall of abdominal aortic aneurysm. Circulation 2011;
124:1097. Copyright © 2011 Lippincott Williams & Wilkins.
Staining to show tissue destruction in aortic aneurysm
Verhoeff's elastic staining at 10x magnification (B) and 20x magnification (D) shows elastic fiber
destruction in aortic aneurysm compared with control aorta specimens at 10x magnification (A) and 20x
magnification (C).
Reproduced with permission from: Jayer Chung, MD, MSc, Baylor College of Medicine.
Staining to show muscle loss in abdominal aortic aneurysm
Hematoxylin and eosin staining of aortic specimens. Panels (A), (B), and (C) are magnified 100x; panels (D), (E), and (F) are magnified 200x. Control
segments of the aorta (A,D) exhibit an abundance of vascular smooth muscle cells with dark nuclei apparent and thick, well-ordered layers of elastin. By
contrast, the segment of aortic aneurysm (B,D) shows depletion of smooth muscle cells, as shown by marked decrease in nuclei and vacuolization
(prominent in B). The elastin fibrils are also thinned and disordered (C,F).
Reproduced with permission from: Jayer Chung, MD, MSc, Baylor College of Medicine.
Contributor Disclosures
Jayer Chung, MD, MSc Nothing to disclose John F Eidt, MD Nothing to disclose Joseph L Mills, Sr, MD Grant/Research/Clinical Trial
Support: Cesca Therapeutics [Critical limb ischemia (Hepatocyte growth factor)]; Voyager Trial [Peripheral artery disease (Rivoxaraban)].
Consultant/Advisory Boards: AnGes [Critical limb ischemia (Hepatocyte growth factor)]; AstraZeneca [Peripheral artery disease (ticagrelor)].
Other Financial Interest: Elsevier; Rutherford [Vascular surgery (Rutherford and Comprehensive Vascular and Endovascular Surgery
textbooks)]. Kathryn A Collins, MD, PhD, FACS Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a
multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is
required of all authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

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9/11/2017 Epidemiology, risk factors, pathogenesis, and natural history of abdominal aortic aneurysm - UpToDate

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Author: Jayer Chung, MD, MSc

● Coronary artery disease is present in over 25 percent of individuals with AAA.

Risk factors for AAA rupture

● <1 percent rupture risk for AAA baseline diameter 30 to 39 mm

● 1.9 mm per year for AAA baseline diameter 2.8 to 3.9 cm

SUMMARY AND RECOMMENDATIONS

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Topic 15190 Version 16.0

Anatomy abdominal aortic aneurysm

Graphic 60682 Version 13.0

Rise and fall of AAA incidence and smoking

Graphic 87502 Version 4.0

Staining to show tissue destruction in aortic aneurysm

Graphic 109210 Version 1.0

Staining to show muscle loss in abdominal aortic aneurysm

Graphic 109211 Version 1.0

Conflict of interest policy

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