Seminar
`
`Lancet 2005; 365: 1577–89
`
`See Personal Account page 1590
`
`Department of Cardiovascular
`and Thoracic Surgery
`(N Sakalihasan MD,
`Prof R Limet MD), and
`Laboratory of Connective
`Tissues Biology
`(O D Defawe PhD), University of
`Liège, Sart-Tilman 4000 Liège,
`Belgium
`
`Correspondence to:
`Prof R Limet
`rlimet@ulg.ac.be
`
`Abdominal aortic aneurysm
`
`N Sakalihasan, R Limet, O D Defawe
`
`Abdominal aortic aneurysms cause 1·3% of all deaths among men aged 65–85 years in developed countries. These
`aneurysms are typically asymptomatic until the catastrophic event of rupture. Repair of large or symptomatic
`aneurysms by open surgery or endovascular repair is recommended, whereas repair of small abdominal aortic
`aneurysms does not provide a significant benefit. Abdominal aortic aneurysm is linked to the degradation of the
`elastic media of the atheromatous aorta. An inflammatory cell infiltrate, neovascularisation, and production and
`activation of various proteases and cytokines contribute to the development of this disorder, although the underlying
`mechanisms are unknown. In this Seminar, we aim to provide an updated review of the pathophysiology, current
`and new diagnostic procedures, assessment, and treatment of abdominal aortic aneurysm to provide family
`practitioners with a working knowledge of this disorder.
`
`Abdominal aortic aneurysms are a substantial burden on
`health care in more developed countries, occurring
`mostly among men older than 65 years of age. The
`disorder is the thirteenth leading cause of death in the
`USA.1 Although some patients have vague symptoms,
`such as back pain or abdominal pain, most abdominal
`aneurysms are asymptomatic until rupture, which leads
`to death in 65% of patients.2 An increased awareness of
`the characteristics of abdominal aortic aneurysm by first-
`contact practitioners might reduce the risk of a fatal
`outcome with this disorder. Here, we review the key
`aspects of
`this disorder,
`including epidemiology,
`pathogenesis, diagnosis, and treatment.
`
`Terminology
`the Greek ανευρυσµα
`from
`Aneurysm derives
`(aneurusma), meaning widening, and can be defined as
`a permanent and irreversible localised dilatation of a
`vessel. Although an aneurysm occurring in any portion
`of the infradiaphragmatic aorta could be termed an
`abdominal aortic aneurysm, common practice restricts
`this definition to an aneurysm of the infrarenal aorta.
`Aneurysms
`involving
`the renal ostia
`(intrarenal,
`suprarenal aorta) are also included under this term.
`The normal diameter of the abdominal aorta varies
`with age, sex, and bodyweight,3
`and decreases
`progressively from its entry into the abdominal cavity
`to the iliac bifurcation. In elderly men, the infrarenal
`abdominal aortic diameter is between 15 mm and
`24 mm.4 McGregor and colleagues5 proposed the
`definition of an abdominal aortic aneurysm as an
`aorta with an infrarenal diameter greater than 30 mm.
`In 1991, the Society for Vascular Surgery and the
`International Society for Cardiovascular Surgery Ad
`Hoc Committee on Standards in Reporting proposed
`as a criterion that the infrarenal diameter should be
`1·5 times the expected normal diameter.6 There is no
`definite consensus on the definition of abdominal
`aortic aneurysm; however, the disorder is conven-
`tionally diagnosed if the aortic diameter is 30 mm or
`more. This dilatation affects the three layers of the
`vascular tunic; otherwise, the dilatation is called a
`pseudoaneurysm. Most aneurysms are fusiform since
`
`the whole circumference of the artery is affected,
`whereas an aneurysm that includes only a part of the
`circumference is termed saccular. An inflammatory
`aneurysm is characterised by extensive perianeurysmal
`and retroperitoneal fibrosis and dense adhesions to
`adjacent abdominal organs.
`
`Epidemiology
`The incidence of abdominal aortic aneurysms has
`increased during the past two decades, due in part to
`the ageing of the population, the rise in the number of
`smokers, the introduction of screening programmes,
`and improved diagnostic tools. Rupture of these
`aneurysms causes about 8000 deaths per year in the
`UK and roughly 15 000 per year in the USA.1,7 The
`disorder is more common in men than in women, with
`prevalence rates estimated at between 1·3% and 8·9%
`in men and between 1·0% and 2·2% in women.8–12
`However, since smoking is one of the most important
`risk factors for abdominal aortic aneurysm13 and the
`number of female smokers is rising,14 the sex ratios for
`the prevalence of the disorder will probably change in
`the future.10,11 Most aneurysms discovered by screening
`are of small size and do not need immediate surgical
`repair.15–17 However, they can become enlarged with
`time at a mean rate that is initially slow and then
`increases exponentially.18
`In general, the risk of
`rupture increases as the diameter of the aneurysm
`enlarges.14,19,20 The overall mortality rate for patients
`with ruptured abdominal aortic aneurysms is between
`65% and 85%,2,7 and about half of deaths attributed to
`rupture occur before the patient reaches the surgical
`room.21,22
`
`Search strategy and selection criteria
`
`The primary source of references included MEDLINE searches
`for recent literature with many keywords for both clinical and
`basic research topics. We largely selected publications in the
`past 5 years, but did not exclude commonly referenced and
`highly regarded older publications. We also reviewed books
`and review articles pertaining to abdominal aortic aneurysm.
`
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`Seminar
`
`Aetiology and risk factors
`There are many causes of aneurysmal dilatation, but few
`abdominal aortic aneurysms are the direct consequence
`of specific causes such as trauma, acute infection
`(brucellosis,
`salmonellosis),
`chronic
`infection
`(tuberculosis),
`inflammatory diseases
`(Behçet and
`Takayasu disease),23,24 and connective tissue disorders
`(Marfan Syndrome, Ehlers-Danlos type IV).25 Thus, most
`abdominal aortic aneurysms are called non-specific.6
`Moreover, because this disorder is invariably associated
`with severe atherosclerotic damage of the aortic wall, it
`has been traditionally regarded as a consequence of
`atherosclerosis.26 This conventional view has been
`increasingly challenged in recent years. Clinical and
`basic research studies indicate that aneurysms arise
`through pathogenic mechanisms that differ, at least in
`part,
`from
`those responsible
`for athero-occlusive
`disease.27,28 Much published work lends support to this
`concept.29,30 Defawe and colleagues31 showed that two
`physiological inhibitors of proteases (TIMP-2 and PAI-1)
`were expressed less in abdominal aortic aneurysms than
`in athero-occlusive disease, suggesting a significant role
`for protease inhibitors during the divergent evolution of
`the
`initial atherosclerotic plaque
`towards either
`abdominal aortic aneurysm or athero-occlusive disease.
`Moreover, since not all patients with atherosclerosis
`develop an abdominal aortic aneurysm, even
`if
`atherosclerosis does have a role in the pathogenesis of
`the disorder, additional factors are probably involved in
`aneurysm development.
`There is a strong clinical association between tobacco
`smoking and aneurysm development.12,14,32,33 The
`prevalence of abdominal aortic aneurysms in tobacco
`smokers is more than four times that in life-long non-
`smokers.12 A report that compared relative risks for
`different diseases in chronic cigarette smokers showed
`that the risk of developing abdominal aortic aneurysms
`is three-fold greater than the risk for developing
`coronary artery disease and nearly five-fold greater than
`the risk for cerebrovascular disease.34 Based on these
`clinical observations, chronic
`tobacco smoking
`is
`probably the single most important environmental risk
`factor for development and progression of aortic
`aneurysms. The rate of growth of these aneurysms has
`been reported to be higher in current smokers than in
`non-smokers (2·83 mm per year vs 2·53 mm per year,
`respectively).35 The mechanisms by which smoking
`could promote aneurysm formation remain unknown
`and are being investigated.36 Beside tobacco smoking,
`other risk factors include male sex, age, hypertension,
`chronic obstructive pulmonary disease, hyperlipidaemia,
`and family history of the disorder.10–12,35,37
`The familial clustering of abdominal aortic aneurysms
`has drawn attention to non-environmental risk factors
`for the disorder. Since the first case report by Clifton in
`1977,38 several studies have lent support to the notion
`that abdominal aortic aneurysms are one of the most
`
`common familial diseases. The frequency of the disorder
`in first-degree relatives is 15–19% compared with only
`1–3% in unrelated patients.39 Familial abdominal aortic
`aneurysms are more frequently found when the proband
`is a female and rupture occurs more often and at a
`younger age than with sporadic aneurysms.40,41 Two
`research groups have attempted segregation analysis of
`abdominal aortic aneurysm. Majumder and co-workers,42
`in a segregation analysis based on 91 probands and
`including 13 familial cases, showed that the most likely
`genetic model was an autosomal locus with a recessive
`inherited gene for the disorder. An analysis undertaken
`in 313 pedigrees, by Verloes and colleagues,40 provided
`evidence for a single autosomal dominant inheritance. A
`multinational study identified 233 families with 653
`affected members;39
`the
`inheritance mode was
`autosomal recessive in 72% of families and autosomal
`dominant in 25% of families. Linkage between aortic
`aneurysm growth and a 4G/5G polymorphism in the
`plasminogen activator inhibitor (PAI-1) promoter has
`been recorded.43,44 Linkage of abdominal aortic aneurysm
`frequency to a locus on chromosome 19q13 has also
`been reported.45 Several candidate genes are present in
`this region of chromosome 19, such as LDL receptor-
`related protein 3 (LRP3), which is particularly relevant
`since conditional knockout mice for LRP1, another
`member of this gene family, developed atherosclerosis
`and arterial aneurysm.46
`familial clustering of
`As discussed by Powell,47
`abdominal aortic aneurysms is probably not due to
`chance alone. An underlying cause could be particular
`genetic background, as mentioned before, but probably
`in
`conjunction with environmental
`factors.
`In
`comparison, clear evidence was reported for the
`interaction between smoking and polymorphic variation
`in the nitric oxide synthase gene for the development of
`carotid artery disease.48 Familial clustering of abdominal
`aortic aneurysms could also result from exposure to
`common environmental factors, such as tobacco smoke.
`Parental smoking has been suggested to underlie
`familial clustering.47 Additionally, women who smoke
`tend to have infants of low birthweight who have a high
`risk of developing coronary diseases later in life.49
`
`Pathophysiology
`The development of abdominal aortic aneurysms is
`clearly associated with alterations of the connective
`tissue in the aortic wall. Elastic fibres and fibrillar
`collagens are the main determinants of the mechanical
`properties of the aorta. Elastin and associated proteins
`form a network of elastic fibres responsible for the
`viscoelastic properties. Elastin is stabilised by cross-links
`between the molecules and can be degraded by specific
`proteases that display elastase activity. Elastic fibres
`associated with smooth muscle cells are most abundant
`in the media of the aortic wall. Collagen, in polymeric
`form, is also a significant component of the media and
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`Seminar
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`remodelling through localised expression of various
`extracellular matrix proteins as well as proteases and
`their inhibitors. Additionally, smooth muscle cells have
`a protective role against inflammation and proteolysis.92
`In-vitro aortic smooth-muscle cells have been shown to
`produce less monocyte chemotactic protein-1 (MCP-1), a
`major inflammatory mediator in abdominal aortic
`aneurysms, under cyclic stretching than with static
`culture, which lends support to the notion of a protective
`paracrine function of smooth muscle cells.93
`The development of abdominal aortic aneurysms is
`also associated with a mural thrombus in most patients.
`By contrast with arterial occlusive diseases, blood flow is
`maintained in aortic aneurysms resulting in a persistent
`remodelling activity of the components of the thrombus.
`Evolution of aneurysmal diameter has been reported to
`correlate with plasma markers of fibrin formation and
`degradation94 as well as
`the circulating complex
`plasmin-␣
`2-anti-plasmin95
`potentially
`related
`to
`thrombus turnover. The role of an adherent thrombus in
`
`Figure 1: Ultrasonography of an infrarenal aortic aneurysm
`A: Sagittal section with parietal thrombus (arrow). B: Transaxial section without
`thrombus.
`
`the surrounding fibrous adventitia. Two specific types of
`fibrillar collagen (types I and III) provide tensile strength
`and help maintain the structural integrity of the vascular
`wall. Beside elastic and collagen fibres, proteoglycans are
`also implicated in the organisation of the aortic wall.50
`One of the most important histological features of
`aneurysmal tissue is the fragmentation of the elastic
`fibres and a decreased concentration of elastin during
`aneurysm growth until the time of rupture.51–53 The loss
`of elastic fibres seems to be an early step in aneurysm
`formation.54 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.
`According
`to Dobrin and Mrkvicka,54
`collagen
`degradation is the ultimate cause of rupture. Increased
`collagen turnover has been reported in abdominal aortic
`aneurysms in human beings,55 suggesting the existence
`of a repair process as shown in animal models.56 An
`imbalance between collagen degradation and
`its
`synthesis could create the catabolic conditions that lead
`to rupture.
`The alteration of elastin and collagen in the aortic wall
`is dependent on production of proteases by resident
`vascular wall cells (medial smooth muscle cells and
`adventitial fibroblasts) and by
`the cells of
`the
`lymphomonocytic infiltrate. These inflammatory cells in
`the media and adventitia come from the aortic blood and
`from a medial neovascularisation, which characterises
`abdominal aortic aneurysms.57–59 Leucocyte recruitment
`into the aortic wall is promoted by elastin degradation
`fragments as well as proinflammatory cytokines,
`chemokines, and prostaglandin derivates produced by
`both
`the
`resident mesenchymal cells and
`the
`inflammatory cells themselves.60–63 Immunity has been
`suggested to play a part in the development of
`abdominal aortic aneurysm.64,65 Elastic and collagen
`fibres are degraded by proteolytic enzymes mostly
`represented by matrix metalloproteinases (MMP) locally
`activated by either other MMP or by plasmin generated
`by plasminogen activators.30,31,66–79 The role of MMP and
`plasmin
`in the development of abdominal aortic
`aneurysms
`has
`been
`confirmed
`in
`animal
`models.70,76,77,80–84 The
`tissue
`inhibitors of matrix
`metalloproteinases (TIMP) are also increased in the wall
`of the aneurysm.69 However, the balance between
`proteases and antiproteases seems to be in favour of
`proteolysis.31,85,86 The importance of this imbalance in
`aneurysm development is reinforced by experimental
`studies in which the antiproteases are overexpressed or
`genetically inactivated.87–90
`Besides rarefaction of its extracellular matrix, the
`elastic media also undergoes a reduction in the density
`of smooth muscle cells, which is regarded as a key event
`in the development of abdominal aortic aneurysms.91
`Smooth muscle cells participate
`in vascular wall
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`Seminar
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`Abdominal standard radiography can incidentally be
`diagnostic, mainly in the transverse view, if calcifications
`are present in the aortic wall, which allows visualisation
`of dilatation. However, standard radiography is not the
`method of choice for the diagnosis of abdominal aortic
`aneurysms. Ultrasonography
`is
`the simplest and
`cheapest diagnostic procedure and can accurately
`measure the size of the aorta in longitudinal as well as in
`anteroposterior and transverse directions (figure 1) with
`an accuracy of 3 mm.99 Ultrasonography is largely used
`not only for the initial assessment and the follow-up
`
`Figure 2: CT images of abdominal aortic aneurysms
`A: Scan slices of a dextoconvex aneurysm in a female patient admitted with diagnosis of cholecystitis.
`B: Retroperitoneal haematoma (arrow) from a ruptured aneurysm. C: Bleeding in a parietal thrombus (arrow)
`observed in a symptomatic small aneurysm. D: Para-aortic fibrosis associated with ureterohydronephrosis.
`
`aneurysmal degeneration has also been investigated.
`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 neovascularisation and
`inflammation.96 The implication of the thrombus in
`aneurysmal evolution in terms of a source of proteases
`has also been proposed after an initial report of an
`enrichment of MMP-9 (gelatinase B) in the thrombus.68
`Furthermore, Fontaine and colleagues97 have provided
`evidence of polymorphonuclear neutrophils (PMN)
`trapping and storing MMP-9 within the aneurysmal
`thrombus. They also showed that plasminogen and its
`activator (u-PA) are present in the thrombus in the
`aneurysm wall, which might result in local generation of
`plasmin, an activator of MMP.
`
`Methods of diagnosis
`The examination for a pulsatile mass should be done by
`bimanual palpation of
`the supraumbilical area.
`Sensitivity of abdominal palpation for detection of
`abdominal aortic aneurysms increases with the diameter
`of the lesion: 61% for aneurysms 3·0–3·9 cm, 69% for
`those 4·0–4·9 cm, and 82% for those 5·0 cm and larger.
`The palpation sensitivity also depends inversely on the
`size of the abdominal waistline.98
`
`Figure 3: MRI of an abdominal aortic aneurysm
`A: 2D T1-weight post contrast MRI. B: Gadolinium-enhanced MRA in the same
`patient showing tortuous aorta and iliac arteries.
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`surveillance, but also for population screening. If the
`diameter of the aneurysm is such that surgical procedure
`is contemplated, CT is the next step to help determine
`which treatment should be used (endovascular or open
`surgery) (figure 2). Serial CT scans can be used to
`visualise the proximal neck (the transition between the
`normal and aneurysmal aorta), the extension to the iliac
`arteries, and the patency of the visceral arteries. They can
`also measure the thickness of the mural thrombus.
`Venous anomalies that can be hazardous during the
`access to the neck are also clearly indicated (left vena
`cava, posterior left renal vein). CT can also display the
`presence of blood within the thrombus (crescent sign),
`which has been regarded by some groups as a predictive
`marker of imminent rupture100–102 (figure 2 C). In case of
`inflammatory aneurysm, CT allows estimation of the
`thickness of the aortic wall outside of the calcified
`deposits and visualisation of the presence of para-aortic
`fibrosis potentially associated with ureterohydronephrosis
`(figure 2 D). Extravasation of contrast material is
`diagnostic of aneurysm rupture. With three-dimensional
`imaging, helical CT and CT angiography can provide
`additional anatomical details, especially useful
`if
`endovascular procedure is considered.103 MRI, combined
`with magnetic resonance angiography (MRA) (figure 3),
`is of little harm since non-nephrotoxic contrast material
`(eg, gadolinium)
`is used, whereas conventional
`arteriography uses nephrotoxic contrast material, which
`can lead to renal failure and distal embolisation. Because
`of
`the
`steady development of MRA and CT
`angiographies, there will be hardly any place left for
`conventional
`aortography
`during
`preoperative
`assessment of the disorder. The use of conventional
`aortography is mainly restricted to the placement of
`endovascular devices or when a horse-shoe kidney is
`diagnosed.
`
`Clinical presentation
`Unruptured abdominal aortic aneurysms
`Non-ruptured aneurysms are generally asymptomatic in
`most patients. They are essentially diagnosed incidentally
`during extensive clinical examination, especially in
`patients who complain of coronary, peripheral, or cerebro-
`vascular diseases, or during population screening.22
`Fleming and co-workers104
`reported that population
`screening in men aged 65–74 years significantly reduces
`mortality related to the disorder.
`Non-ruptured aneurysms might exceptionally be
`diagnosed after complications, such as distal embolisa-
`tion and, even more rarely, acute thrombosis. Minor and
`less specific symptoms include chronic vague abdominal
`and back pain, which can result from direct pressure or
`distension of adjacent structures. Recent onset of severe
`lumbar pain has been deemed to indicate impending
`rupture. Ureterohydronephrosis might also take place,
`especially if the aneurysm is inflammatory or involves
`the iliac bifurcation (figure 4).
`
`Figure 4: Ureterohydronephrosis associated with abdominal aortic aneurysm
`Ureteral stenosis (A) resulting in ureterohydronephrosis (B) in a case of inflammatory aneurysm with para-aortic
`fibrosis (C) or para-iliac (D) fibrosis.
`
`Ruptured abdominal aortic aneurysms
`Rupture of abdominal aortic aneurysms is heralded by
`the triad of sudden-onset pain in the mid-abdomen or
`flank (that may radiate into the scrotum), shock, and the
`presence of a pulsatile abdominal mass. However, the
`degree of shock varies according to the location and size
`of the rupture and the delay before the patient is
`examined. Rupture from the anterolateral wall into the
`peritoneal cavity (figure 5) is usually dramatic and most
`often associated with death at the scene. Most patients
`with a rupture who reach the clinic alive have a rupture
`of the posterolateral wall into the retroperitoneal space; a
`small tear can temporarily seal the rupture and the
`initial blood loss might be small. This initial event is
`systematically followed within hours by a larger rupture.
`This biphasic evolution emphasises the importance of
`the intermediate period after the initial event, which
`should be used for medical transfer and emergency
`repair.
`Anecdotically, the first episode of rupture could be
`definitely contained and become a chronic pulsatile
`extra-aortic haematoma. Very rarely, the aneurysm
`might spontaneously rupture
`into the duodenum
`(figures 5 and 6); an incidence rate at necropsy of 0·04%
`to 0·07% has been
`reported.105–107 More often,
`aortoduodenal fistula can occur after previous repair,
`with an incidence rate of 0·5% to 2·3%.108 Rupture into
`the vena cava can also take place with an apparent
`pattern of
`lower extremity oedema erroneously
`attributed to cavoiliac thrombophlebitis (figure 4).
`However, the development of high output congestive
`heart
`failure and
`the perception of continuous
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`4
`
`5
`
`1
`
`2
`
`3
`
`Figure 5: Different possible sites of rupture of an abdominal aortic aneurysm
`1: Anterolateral free rupture in the abdominal cavity. 2: Retroperitoneal rupture.
`3: Rupture of retroperitoneal sac. 4: Rupture into the duodenum. 5: Rupture
`into the inferior vena cava.
`
`is pathognomonic. The overall
`abdominal noise
`prevalence of aortocaval fistula is 3% to 6% of all
`ruptured aortic aneurysms.109
`
`Indications for treatment
`Although surgical treatment of non-ruptured abdominal
`aortic aneurysms relies on specific rare indications, such
`
`Figure 6: Rupture of an abdominal aortic aneurysm in the duodenum
`CT displaying a known large aneurysm leaking into the duodenum (A, arrow), and presenting an air bubble in the
`parietal thrombus, which is a sign of aorta enteric fistula (B, arrow). The 92-year-old patient and her family had
`refused any intervention.
`
`as distal embolisation, ureteral compression, or
`contained retroperitoneal haemorrhage, treatment of
`intact abdominal aortic aneurysm
`is essentially
`prophylactic and aimed at prevention of fatal rupture.
`Indication for surgical treatment is deduced from the
`estimated risk of rupture, the estimated risk of the
`surgical procedure, and the estimated life expectancy of
`the patient. Figure 7 shows a proposed management
`plan for asymptomatic abdominal aortic aneurysms.
`
`Risk of rupture
`The size of the aneurysm is a universally recognised
`factor to forecast rupture, and the general consensus is
`that patients with a large aneurysm should undergo
`surgery. The
`real
`controversy
`surrounds
`the
`management of small aneurysms. A study was
`undertaken in which patients with small aneurysms
`(diameter between 4·0 cm and 5·5 cm) were randomly
`assigned to two groups that underwent either early
`elective surgery or delayed repair after the diameter of
`the aneurysm had reached or exceeded 5·5 cm.110 The
`results show closely similar survival curves for the two
`groups of patients. A US Veterans Administration study
`led to similar findings despite a lower operative mortality
`(2·7% vs 5·8%) with early than with delayed repair.15 The
`conclusions of these two studies were similar: rigorous
`surveillance of infrarenal aortic aneurysms smaller than
`5·5 cm in diameter is safe, whereas early surgery is not
`associated with improved long-term survival.
`Rapid expansion of the aortic diameters preceding
`fissuration and rupture has been observed in abdominal
`aortic aneurysms independently of their initial size,18,20
`which suggests that the size of the aneurysm, whatever
`its practical significance, is probably not the sole useful
`determinant for risk of rupture. Active investigations
`have been and still are being done to identify markers
`other than size that would predict a risk of rupture. A
`possible candidate is the level of serum MMP-9, which
`has been directly
`implicated
`in
`the proteolytic
`degradation of the extracellular matrix of the aortic
`wall.68 The amount of circulating MMP-9 has not only
`been reported to be significantly higher in patients with
`abdominal aortic aneurysm,111 but has also been
`significantly associated with the size and expansion rate
`of these aneurysms.112 Another factor that has been
`investigated as a potential serum marker is the reduced
`level of ␣1-antitrypsin (␣1-AT) since it is the most
`abundant serum inhibitor of proteases. However, the
`importance of this marker for the prognosis of
`abdominal aortic aneurysms has not been defined
`because of contradictory findings.113
`Family history represents a risk factor for aneurysm
`rupture. A study of 313 pedigrees showed a four-fold
`higher rate of rupture in familial cases than in sporadic
`cases.40 Additionally, a significantly earlier age at rupture
`(65 years vs 75 years) was also reported in these familial
`cases. Another potential risk factor for rupture could be
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`Asymptomatic abdominal aortic aneurysm
`
`⬍4·5 cm
`
`4·5–5·0 cm
`
`5·0–5·5 cm
`
`⬎5·5 cm
`
`Follow-up
`Ultrasonography
`every 6 months
`
`Follow-up
`Ultrasonography
`every 3 months108
`or 6 months76
`
`Follow-up
`Ultrasonography
`every 3 months76,108
`or 6 months13
`
`Surgery
`Open or
`endovascular
`repair
`
`Surgery
`Open or
`endovascular
`repair if:
`•Female patients
`•Familial cases
`•"Proved" rapid growth
`•Positive PET scan
`•High serum markers
`(such as MMP–9)
`
`Figure 7: Proposed management of an asymptomatic abdominal aortic aneurysm
`
`mortalities occurring at the scene of rupture, during
`transfer, shortly after admission to the emergency
`department, and during surgery are combined, then
`only 18% of patients with ruptured aortic aneurysms
`survive.138 Prance and co-workers138 suggested five
`preoperative risk factors to predict the mortality rate of
`ruptured abdominal aortic aneurysms: (1) age older than
`76 years; (2) creatinine higher than 190 ␮mol/L; (3)
`haemoglobin below 9g/dL; (4) loss of consciousness;
`and (5) ECG evidence of ischaemia. In their study, the
`mortality rate was 100% when the patient had three or
`more risk factors and decreased to 48%, 28%, and 18%
`when the risk factor number decreased to two, one, or
`zero, respectively.138
`
`Management
`Open surgical treatment
`During open surgical treatment, the abdomen is entered
`either through a long midline or a wide transverse
`incision. A
`retroperitoneal approach has been
`
`Figure 8: PETof an abdominal aortic aneurysm
`Coronal section showing 18F-FDG uptake in the wall of an aneurysm 7 days before
`rupture.
`
`related to the sex of the patient. A report from the UK
`Small Aneurysm Trial has shown that the risk of rupture
`in women was four-times higher than in men.16
`Preliminary data obtained by PET
`imaging of
`abdominal aortic aneurysms have shown focal uptake of
`18-fluorodeoxyglucose (18F-FDG) within the aneurysm
`wall in patients with either large, rapidly expanding, or
`painful aneurysms (figure 8).114 The uptake of 18F-FDG is
`regarded as a functional image of the inflammatory
`infiltrate and thus as a potential non-invasive technique
`to identify unstable aneurysms that are prone to rupture.
`
`Risk of elective aneurysm repair
`Reported mortality rate related to elective aneurysm
`repair varies among hospitals and surgeons.115 Mean
`30-day mortality rate has been reported at between 1·1%
`and 7·0%.116–121 Between 1998 and 2003, 453 patients were
`admitted to the University Hospital of Liège, Belgium,
`for elective repair of an abdominal aortic aneurysm (397
`by open surgery and 56 by endovascular repair); the
`overall 30-day mortality, regardless of the risk factors,
`after open surgery and endovascular repair was 2·7%
`and 1·8%, respectively. Most deaths resulting from the
`repair occurred in the so-called high-risk patients. Factors
`of increased operative risk are renal failure, chronic
`obstructive pulmonary disease, and, most importantly,
`myocardial ischaemia. If these patients are excluded, 30-
`day mortality rate of elective repair should be expected to
`be as low as 2% in most hospitals.121–123
`Several reports have shown the high incidence
`(between 40% and 60%) of coronary artery disease in
`patients with abdominal aortic aneurysm, which could
`be explained by common risk factors (eg, tobacco
`smoking and hypertension).124–127 Complications related
`to coronary artery disease are the main cause of the
`operative mortality of
`aneurysm
`surgery.126,128–131
`However, the benefit of coronary artery revascularisation
`before surgery remains controversial. Simultaneous
`aneurysm repair and coronary artery revascularisation
`have been recommended in selected patients scheduled
`for elective or urgent repair.132–134 However, a large
`randomised study did not show any significant
`difference in the long-term outcome when coronary-
`artery revascularisation was undertaken before elective
`surgery.135 The investigators therefore suggested the
`restriction of preoperative coronary revascularisation to
`patients with unstable cardiac symptoms. As yet, there is
`no consensus on the optimum strategy for preoperative
`cardiac management in patients scheduled for major
`elective vascular surgery.136,137
`As far as emergency repair for ruptured abdominal
`aortic aneurysms is concerned, mortality depends on the
`haemodynamic status of the patient at the time of
`surgery. By contrast with the progress in elective repair
`mortality, no improvement in operative mortality of
`ruptured aneurysms has been reported during the past
`decades, remaining as high as 30–70%.2,22
`If the
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`Seminar
`
`Figure 9: Potential issues of endovascular aneurysm repair
`A: Rupture of an abdominal aortic aneurysm 2 years after endovascular repair. B and C: CT in another patient showing the normalisation of the diameter of an
`aneurysm 6 years after endovascular repair.
`
`recommended in patients with chronic obstructive
`pulmonary disease. Disadvantages of this approach
`include: first that the intraperitoneal content cannot be
`inspected; and second, access to the right iliac artery can
`frequently be difficult, especially if there is a large right
`iliac aneurysm. Once the abdominal cavity is opened, the
`neck of the aneurysm needs to be identified to control it.
`In the cases of a suprarenal or intrarenal neck, a clamp
`above the renal arteries might be needed briefly. The
`iliac arteries are controlled in much the same way. The
`inferior mesenteric artery is tied close to the aortic wall
`to keep it collateral to the superior mesenteric artery; in
`some instances, encircling the inferior mesenteric artery
`with a rubber to reimplant it on the aortic prosthesis via
`a Carrell patch could be wise to maintain direct flow for
`sigmoid and rectum.
`The vascular graft is a knitted synthetic textile s