Oxford Textbook of Fundamentals of Surgery

William E. G. Thomas (ed.) et al.

https://doi.org/10.1093/med/9780199665549.001.0001
Published: 2016 Online ISBN: 9780191810817 Print ISBN: 9780199665549

CHAPTER

2.7.4 Aneurysms 

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Robert Davies, Robert Sayers

https://doi.org/10.1093/med/9780199665549.003.0043 Pages 343–348

Published: July 2016

Abstract
An arterial aneurysm is de ned as a 50% or greater increase in the diameter of a vessel. The infrarenal
aorta and popliteal artery are the commonest locations for arterial aneurysms accounting for more
than 12 000 hospital admissions per year in England. The majority of arterial aneurysms are
asymptomatic at the time of presentation having been identi ed incidentally during routine health
checks or investigations for other pathologies.

Keywords: abdominal aortic aneurysm, femoral artery aneurysm, popliteal artery aneurysm,
endovascular aneurysm repair, rupture
Subject: Surgery, Vascular Surgery, Urology, Paediatric Surgery, Cardiothoracic Surgery, Peri-operative
Care, Trauma and Orthopaedic Surgery, Upper Gastrointestinal Surgery, Colorectal Surgery, Surgical
Oncology, Neurosurgery, Breast Surgery, Transplant Surgery, Surgical Skills
Series: Oxford Textbooks in Surgery

Introduction

An arterial aneurysm is de ned as a 50% or greater increase in the diameter of a vessel whereas an increase
of less than 50% is ectasia. The infrarenal abdominal aorta is the commonest site for an arterial aneurysm
and abdominal aortic aneurysms (AAAs) account for almost 12 000 hospital admissions per year in England.
Popliteal artery aneurysm (PAA) is the most common peripheral artery aneurysm.

Arterial aneurysms rarely occur in isolation and their aetiology is multifactorial, including a genetic
preponderance. The majority of arterial aneurysms are asymptomatic at the time of presentation, but the 5-
year complication rate of aneurysms that are more than twice the size of the normal vessel diameter is high.

Complications associated with aneurysms relate to their size, including mass e ect on surrounding
structures and rupture, and thromboembolization. Aneurysm rupture is a life-threatening event and 6000
deaths per year in England and Wales result from ruptured AAA. Therefore, the general principle for treating
all asymptomatic arterial aneurysms is quantifying the risk of an aneurysm developing complications and
weighing this up against the risk associated with elective repair.
Abdominal aortic aneurysm

Incidence
The incidence of AAA, de ned as an enlargement of at least 3 cm, increases with age and a ects
approximately 4% of the elderly general population (≥ 65 years) within the United Kingdom. The age-
speci c prevalence is six times greater in men than women with an estimated prevalence of 5–8% for men
1,2,3
aged 65–80 years old.

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Pathophysiology
AAA represents a chronic in ammatory pathology and is usually characterized by the presence of a
4
biologically active mural thrombus directly proportional to the maximum AAA diameter. Ten per cent of
AAAs are classed as ‘in ammatory’ referring to the presence of a dense retroperitoneal in ammatory
reaction with a thick ‘rind’ of bro-in ammatory tissue overlying the native vessel.

Patients with an AAA demonstrate a high incidence of cardiovascular disease and associated risk factors
including male gender, cigarette smoking, hypercholesterolaemia, and hypertension. Diabetes mellitus
appears to be protective for AAA. There appears to be a genetic preponderance for the development of AAA
with 20% of patients having a positive family history; a variant in the LRP1 gene has recently been
implicated as a potential causal gene.

Symptoms and signs

The majority of AAAs a ect the infrarenal aorta and 75% are asymptomatic at the time of presentation
having been identi ed incidentally during routine health checks or investigations for other pathologies.

Alternatively, the patient with a symptomatic non-ruptured AAA may present with (a) symptoms/signs
resulting from the growth/mass e ect of the AAA itself, for example, lumbar-sacral or loin pain,
constitutional illness including malaise and fatigue, and a pulsatile abdominal mass, or (b) acute or chronic
limb ischaemia resulting from distal embolization. In ammatory aneurysms associated with
retroperitoneal brosis may cause ureteric or duodenal obstruction. The patient with a ruptured AAA
presents with the classic triad of lumbar/loin pain, haemodynamic instability/collapse, and a pulsatile
abdominal mass. Rarely AAAs present with primary aortoenteric or aortocaval stulae.

Management

When to repair
The natural history of AAA is that of gradual accelerating, asymptomatic expansion until rupture occurs.
The best-known predictor of rupture rate is the maximum AAA diameter; the annual risk of rupture for an
5
aneurysm with a diameter greater than 7 cm may be as high as 25% (Table 2.7.4.1).
Table 2.7.4.1 AAA rupture rates based on maximum transverse diameter

Diameter 5-year risk of rupture

<5 cm 5%

5–6 cm 25%

6–7 cm 35%

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>7 cm 75%

Source: data from The Lancet, Volume 352, Issue 9141, The UK Small Aneurysm Trial Participants, Mortality results for
randomised controlled trial of early elective surgery or ultrasonographic surveillance for small abdominal aortic aneurysms, pp.
1649–55, Copyright © 1998 Elsevier Ltd, http://www.sciencedirect.com/science/journal/01406736 10.1016/S0140-
6736(98)10137-X

Approximately 2500 men aged 60 years or older die as a result of a ruptured AAA (rAAA) in England and
Wales per year; 2.5% of all deaths in males aged 60 years or older. Of these deaths, approximately half occur
5,6
prior to hospital treatment. For patients who survive to reach hospital alive, despite advances in
perioperative management, in-hospital mortality rates following emergency open surgery for rAAA remain
7
devastatingly high. Open surgical repair of rAAA is associated with an in-hospital mortality rate of 40%.
Therefore in the United Kingdom elective repair of an infrarenal AAA, in a suitably t patient, is
recommended when the aneurysm measures 5.5 cm or more, or greater than 4.5 cm with a growth rate
5
greater than 0.5 cm/6 months.

Preoperative investigation
Investigation of the patient with an AAA is aimed at (a) assessing the AAA, and (b) assessing the
physiological tness of the patient.

Assessing the AAA

Duplex Doppler ultrasonography (DDU) is an ideal imaging modality to con rm or screen for the presence
of an AAA and can be performed within the emergency department. In skilled hands, aneurysm morphology
and relationship to the renal arteries can be assessed although views may be limited as a result of obesity or
overlying bowel gas. A computed tomographic aortogram (CTA) that includes the arterial tree from the
aortic arch to the femoral arteries should be performed in all patients found to have a large AAA (≥5.5 cm).
Precise AAA anatomical con guration is vital when assessing the suitability of an AAA for endovascular
aneurysm repair (EVAR). For patients found not to be anatomically suitable for EVAR, CTA provides valuable
information for planning an open surgical repair including the presence of anatomical variants such as a
retro-aortic left renal vein or horseshoe kidney. AAAs are frequently associated with aneurysmal disease
a ecting the peripheral arteries with 10% and 5% of patients found to have concomitant popliteal and
femoral artery aneurysms respectively.
Assessing the patient

Both open surgical repair and EVAR cause considerable physiological insult to patients’ cardiorespiratory
and renal systems; 20–25% of patients undergoing elective open AAA repair or EVAR su er perioperative
myocardial injury as determined by raised cardiac troponin levels. Thus, it is vitally important to assess a
patient’s physiological tness and ability to survive a major operation, and weigh this up against the risk of
not intervening, that is, risk of rupture. Recently, cardiopulmonary exercise testing has been trialled as a
risk strati cation tool. Anaerobic exercise threshold and maximum oxygen uptake (VO2) are measured
preoperatively as a measure of cardiopulmonary function. Although initial reports are encouraging, further
robust and standardized studies are required before its widespread adoption can be fully supported.

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Identifying, investigating, and physiologically optimizing at-risk patients should be undertaken in the
multidisciplinary team setting involving surgeons, radiologists, anaesthetists, and, when indicated,
cardiologists, respiratory physicians, and nephrologists.

Open surgical repair

Open surgical repair is traditionally performed transperitoneally through a midline or transverse incision
under general anaesthesia. The posterior peritoneum is incised with the duodenum and small bowel
retracted to the right and the transverse colon superiorly. The left renal vein is identi ed and the underlying
aortic neck is dissected su ciently to allow the safe application of a clamp. Dependent on the extent of the
AAA, the common iliac arteries or iliac bifurcations are dissected and controlled. The iliac arteries are then
clamped, followed by the aorta. The aneurysm sac is opened longitudinally and any back-bleeding from the
lumbar or inferior mesenteric arteries oversewn. Inlay graft reconstruction using a straight or bifurcated
prosthetic graft is then performed. It is important to note that cross-clamping of the aorta places
considerable strain on the myocardium by dramatically increasing systemic vascular resistance and arterial
pressure. Furthermore, upon re-establishing ow into the lower limbs, signi cant hypotension may occur
resulting in further myocardial or nephric injury.

Elective, open infrarenal AAA repair is associated with a perioperative mortality rate of 3–10%, with the
majority secondary to micro- and macrovascular thrombosis causing myocardial injury, thromboembolism,
8,9,10,11,12
and multiple organ failure. Meticulous preoperative planning, intraoperative technique, and
postoperative care are vital to achieve good outcomes. The use of preoperative beta blockers, intraoperative
cell salvage, and heparin, and early postoperative extubation has been reported to improve results.

Endovascular aneurysm repair

EVAR provides a less invasive and safer alternative treatment to open surgical repair in the t and
anatomically suitable patient. The EVAR-1, EVAR-2, and DREAM trials reported EVAR was associated with a
3% absolute risk reduction in perioperative mortality when compared to open surgical repair. However,
exponents have argued that these initial operative mortality bene ts are o set by the long-term economic
cost due to late graft-related complications.

Endoleak is a complication unique to EVAR and results in perfusion of the aneurysm sac and subsequent risk
of rupture (Table 2.7.4.2). The EVAR-1 trial reported 22% of EVARs were complicated by endoleak and 35%
require a secondary procedure to maintain complete aneurysm exclusion within 3 years of the procedure.
However, the endoleak rate is in uenced by a variety of factors including preprocedural planning, type of
13
stent graft deployed, aortic morphology, and technical expertise. For these reasons, and the risk of other
stent-related complications including stent migration, regular outpatient follow-up with CTA or DDU
combined with abdominal radiographs is necessary to identify aneurysm exclusion failure. Thus, the short-
term perioperative mortality/morbidity bene ts of EVAR may be outweighed by its long-term morbidity in
terms of re-intervention as well as the associated economic burden.

Table 2.7.4.2 Classification of endoleak

Type Failure of stent gra to seal against the aortic wall proximally (type Ia) or against the iliac arteries distally (type Ib)
I

Type Retrograde blood flow through one (type IIa) or more (type IIb) normal branches of the excluded aortic segment, e.g.

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II inferior mesenteric artery or lumbar arteries

Type Structural failure of the stent gra secondary to fabric disruption (type IIIa), separation of modular components (type
III IIIb), suture holes in fabric (type IIIc)

Type Caused by gra porosity typically identified at the time of stent gra deployment
IV

The UK National Health Service AAA screening programme has recently been implemented in an attempt to
reduce the risk of death from AAAs in men aged 65 years and over by 50%. Men in their 65th year are invited
to attend screening, which consists of a DDU of the abdominal aorta. It is calculated that 192 men need to be
scanned to prevent one rupture AAA death over a 10-year period. However, for every 1660 men scanned, one
extra postoperative death will occur. Therefore, for every 10 000 men scanned, 65 AAA ruptures will be
prevented saving 52 lives over a 10-year period.

Femoral artery aneurysms

Incidence
Femoral artery aneurysms (FAAs) are the second most common peripheral artery aneurysm to popliteal
artery aneurysms. They are ten times more common in males and predominantly occur in patients aged
14
over 65 years of age with risk factors for cardiovascular disease. FAAs rarely occur in isolation (<10%) and
are frequently associated with a contralateral aneurysm or/and aneurysmal disease a ecting the aorta or
other peripheral arteries.

Pathophysiology
Although not well understood, it is theorized that the initiating element for the majority of FAAs is
atherosclerotic constriction at the level of the inguinal ligament causing a poststenotic dilatation of the
common femoral artery (CFA). The resulting turbulent ow and pressure uctuations within the CFA results
in arterial wall vibration, clinically evident as a bruit or thrill. The arterial wall, pre-weakened by
atherosclerosis, and subjected to long-term vibratory forces, progressively weakens and undergoes
15,16
aneurysmal degeneration.
Symptoms and signs
The majority of patients with FAAs present with localized symptomatology or lower limb ischaemia,
although a third are asymptomatic and identi ed incidentally. FAAs are classically felt as smooth, fusiform,
pulsatile swellings in the groin that may or may not be tender. Compression of adjacent neurovascular
structures may result in lower limb chronic venous hypertensive changes, but dysaesthesia/paraesthesia
from resultant femoral nerve compression is rare.

As with all aneurysms, thrombosis, distal embolization, and rupture may occur. In the case of FAAs,
thromboembolization occurs more commonly than rupture re ecting the protective nature of the

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constraining femoral sheath. In cases of acute thrombosis, patients may present with a ‘threatened’ leg that
requires emergency treatment, which is often made more complex due to previous ‘silent’ embolic
occlusion of the crural vessels.

Investigation
17
Only 20% of FAAs are reliably identi ed on clinical examination. Thus a high index of suspicion is required
and all patients with AAAs or peripheral artery aneurysms should undergo imaging assessment of their
lower limb vasculature as routine.

DDU is an adequate screening tool in both the emergency and elective setting. Upon identi cation, the
authors recommend further assessment of the lower limb arterial tree utilizing CTA and/or magnetic
resonance angiography (MRA) to allow accurate planning of future interventions. In the acutely ischaemic
limb, lengthy preoperative investigations may be detrimental to the success of limb salvage surgery; in
these circumstances a combination of DDU and on-table angiography are key.

Management
All symptomatic aneurysms, or aneurysms complicated with thromboembolism or rupture, should be
o ered primary surgical repair. There is considerable debate relating to the treatment of asymptomatic
FAAs, as their natural history is unknown. In practice, modern vascular surgeons will consider a FAA
measuring greater than 2.5 cm or enlarging on serial imaging for elective repair.

The majority of FAAs are isolated to the CFA (type I). These are best repaired with a straight inlaid,
interposition graft with the redundant sac plicated over the graft. Autologous vein should be utilized where
there is a suspicion of infection otherwise a prosthetic conduit may be used. Aneurysms that extend into the
super cial femoral artery or profunda femoris artery (type II) require individually tailored solutions
depending on the anatomy. Similarly, for those patients in whom multilevel aneurysmal disease occurs, the
most clinically pressing disease should be addressed at the initial operation whilst simultaneously planning
for any necessary future vascular reconstructions.

Femoral artery pseudoaneurysms

Pathophysiology
The wall of a pseudoaneurysm consists of thin brous tissue as opposed to all three tunica (intima, media,
and adventitia) layers, as is the case with a true aneurysm. This brous pseudocapsule develops as a result
of an arterial wall or anastomotic defect that allows extravasation of blood at systemic pressure into the
perivascular soft tissues.
Iatrogenic, post-catheterization pseudoaneurysm formation is the commonest cause of femoral artery
18,19
pseudoaneurysms (FAPs) with a reported incidence of 1–6%. Risk factors include coagulopathies,
including antiplatelet and warfarin therapy, hypertension, and factors that reduce the e ectiveness of post-
procedural vessel compression or closure devices including obesity, heavily calci ed arteries, cannulation of
20
the super cial femoral or profunda femoris arteries, and a sheath size greater than 7 Fr.

Infection, particularly in the drug abuser population, and femoral para-anastomotic failure may also lead to
pseudoaneurysm formation. Anastomotic pseudoaneurysms complicate 8% of aortobifemoral bypasses and
21,22
2.5% of all femoral anastomoses at a median follow up of 8 years.

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Symptoms and signs
FAP may present as a pulsatile groin mass that may or may not be painful. The weakened pseudocapsule
when subjected to systemic blood pressure may gradually expand causing localized compression and/or
erosion of adjacent structures, distal embolization, or rupture. Mycotic aneurysms present as a painful,
erythematous groin mass often with a concurrent purulent/sanguineous discharge and represent a surgical
emergency due to the high risk of bleeding.

Investigation
Investigation is primarily aimed at (1) con rming the clinical diagnosis, (2) assessing the size of the
pseudoaneurysm, and (3) assessing the size and location of the arterial/anastomotic defect. DDU is the
initial investigation of choice and can be used to plan treatment in isolation when an uncomplicated post-
catheterization pseudoaneurysm occurs. In cases in which complex reconstructive surgery may be required,
for example, anastomotic pseudoaneurysm, CT angiography should be utilized as an adjunct to DDU.

Treatment
The majority of small post-catheterization pseudoaneurysms undergo spontaneous thrombosis.
Pseudoaneurysm size and anticoagulation status are the two most important predictors of spontaneous
thrombosis; approximately 90% of pseudoaneurysms measuring 3 cm or less thrombose within 1 month
23
without intervention. Thus an initial conservative management strategy for small pseudoaneurysms (≤3
cm) with serial DDU remains advocated by some authors.

The use of minimally invasive techniques for treating FAP, particularly iatrogenic, post-catheterization
pseudoaneurysms, has gained widespread acceptance. Ultrasound-guided compression in isolation has
20
reported success rates of 63–100%. Concomitant systemic anticoagulation and/or pseudoaneurysm size
greater than 3 cm are independent predictors of failure, and complications including pseudoaneurysm
20
rupture, femoral vein thrombosis, and acute limb ischaemia have been reported in up to 4% of cases.

The use of ultrasound-guided percutaneous thrombin injection into the pseudoaneurysm sac is now
widespread with reported success rates of greater than 90%. Unlike ultrasound-guided compression, the
24
patient’s anticoagulation status does not adversely a ect outcome. Complications including distal
embolization are reported in 4% or less of cases and may be further reduced with the adjunct use of an
intra-arterial balloon protection devices in pseudoaneurysms with wide necks.

Minimally invasive percutaneous treatments have con ned the indications for open surgical repair to those
pseudoaneurysms that are rapidly expanding, mycotic, causing neurovascular compression, skin necrosis,
or have undergone failed percutaneous treatment—complex pseudoaneurysms. Non-infected
pseudoaneurysms are repaired primarily with interrupted non-absorbable sutures or with an autologous
vein patch-angioplasty depending on the size of the arterial defect. However, the surgical treatment of
mycotic pseudoaneurysms is more complex with surgical goals being (a) the excision of infected tissues,
and (b) preservation of the distal circulation. The use of extra-anatomical autologous vein grafts is often
required, whilst in some cases of gross suppurative infection and systemic decompensation, primary
ligation of the femoral vessels as a ‘bail-out’ procedure may become necessary with a 30% risk of
subsequent amputation.

Popliteal artery aneurysms

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Incidence
PAAs are the most common peripheral artery aneurysm being diagnosed predominantly in males during
their seventh decade of life. The presence of a PAA often re ects a systemic aneurysmal preponderance;
50% are bilateral and 40% are associated with an AAA. Conversely, 10% of patients with an AAA have a
concomitant popliteal artery aneurysm.

Pathophysiology
The majority of PAAs result from atherosclerotic disease a ecting the tunica media. Non-atherosclerotic
causes of aneurysmal degeneration are infrequent and include the vasculitides and connective tissue
disorders. Mechanical causes including poststenotic dilatation secondary to popliteal entrapment syndrome
or repetitive trauma, as in the case of horse riding boots, may also result in aneurysmal change.

Symptoms and signs

Two-thirds are symptomatic at the time of diagnosis, with 90% of patients presenting with features of limb
ischaemia; symptoms secondary to neurovascular compression or aneurysm rupture are rare.

Clinical examination may reveal an obvious pulsatile mass arising from the popliteal fossa. However, more
often than not it is the clinical symptomatology in conjunction with the absence of the normal concavity of
the popliteal fossa on examination that alerts the clinician to the possibility of a PAA. Di erential diagnoses
should include Baker cyst, lymphadenopathy, and pseudoaneurysm.

Acute thrombosis and/or distal embolization causing critical limb ischaemia are the most common
complications of PAAs. Occasionally, a more insidious onset of claudication and critical limb ischaemia may
occur due to repeated ‘showering’ of emboli into the distal arterial tree. Asymptomatic ‘silent’ thrombosis
and/or embolization may be identi ed through reduced ankle–brachial pressure indices or loss of pedal
pulses during a routine medical check-up.

Large aneurysms may compress surrounding neurovascular structures causing lower limb swelling and
paraesthesia. However, due to the relative mobility of the popliteal artery, tethered at the adductor hiatus
proximally and the soleal muscular arch distally, rupture is rare. When aneurysm rupture does occur, limb
salvage rates are poor with more than two-thirds of patients undergoing subsequent amputation (Figure
2.7.4.1).
Fig. 2.7.4.1

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Diagrammatic representation of a right popliteal artery viewed from behind.

Investigation
Radiological investigations are aimed at (a) con rming the clinical diagnosis, (b) assessing the extent of the
aneurysm, and (c) assessing the in ow and run-o vessels for concomitant stenotic/occlusive or
aneurysmal disease. DDU performed by a skilled sonographer can provide excellent and expedient
information regarding in ow, out ow, diameter, sac thrombus, and venous thrombosis compression. The
authors recommend the use of CTA or MRA to further assess the proximal and distal arterial trees in line.
Speci cally, detailed assessment of the run-o vessels is required as they directly relate to the urgency and
success of future surgical and endovascular reconstruction.

Management
There are no randomized controlled trials to establish clear indications for intervention for PAAs. It is
widely accepted that all symptomatic PAAs require intervention to prevent limb loss; however, indications
for intervention in an asymptomatic popliteal aneurysm remain controversial. It is reported that the
majority of asymptomatic popliteal artery aneurysms eventually develop thromboembolic complications
25,26
with associated amputation rates of 67%. Furthermore, graft patency and limb salvage rates are much
better when performed in the asymptomatic limb with results superior to that for occlusive disease. Thus,
the authors would recommend all t patients with a PAA measuring 2 cm or more in maximum diameter
with an available suitable autologous conduit be considered for intervention.

Surgical reconstruction
The two main approaches to the popliteal aneurysm are the medial and posterior approach.
The posterior approach involves an ‘S’-shaped incision in the popliteal fossa with dissection of the aneurysm
from other popliteal structures followed by inlay, interposition grafting. The advantages of the posterior
approach are (a) the ability to freely ligate feeding geniculate branches thereby preventing future endoleak
and sac expansion that may occur following simple ligation and bypass, and (b) the sac may be excised
which is especially important in cases of neurovascular compression. The disadvantage of this approach,
however, is the di culty in exposing the crural vessels and the super cial femoral artery should the extent
of reconstruction be more complex that preoperatively anticipated. Harvesting the long saphenous vein for
use as a conduit is more di cult in the prone position; a preoperatively marked basilic vein may be utilized
as an alternative in these cases.

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The medial approach employs the same exposure technique as one would use for a femoral below-knee
popliteal bypass and is thus considered more familiar if not easier by some surgeons. The popliteal artery is
ligated above and below the aneurysm with a non-absorbable suture and a femoral below-knee popliteal
bypass reconstruction is performed. This approach should be employed for aneurysms that are not isolated
to the popliteal artery or in cases where femoral-distal arterial reconstruction is anticipated. Although
technically challenging, it is possible to ligate the geniculate vessels utilizing this approach and thus the
perceived drawback to this approach of potential sac expansion due to an ‘endoleak’ is negated if
endoaneurysmorrhaphy is performed.

Both techniques can be combined with intra-arterial thrombolysis or crural vessel thromboembolectomy in
the acutely ischaemic limb. In a chronically ischaemic leg, thrombolysis and/or embolectomy are unlikely to
resolve a mature (>21 days) thromboembolic occlusion in the run-o vessels and therefore a crural or pedal
bypass may be required.

Endovascular reconstruction
A preoperatively planned covered stent (endograft) is deployed through a transfemoral approach with
‘landing zones’ being healthy artery proximal and distal to the aneurysm. Endograft reconstruction is less
traumatic than open reconstruction, resulting in smaller wounds, a reduced hospital stay, and therefore
reduced cost in the short term. Furthermore, initial reports of early stent kinking/fracture/thrombosis as a
result of repeated knee extension and exion have diminished with stent technology improvements.
However, there remains a paucity of evidence, particularly long-term follow-up data, to support the use of
endograft and the authors reserve their use to the ‘un t’ symptomatic patient.
Further reading
Antonello M, Frigatti P, Battocchio P, et al. Open repair versus endovascular treatment for symptomatic popliteal artery
aneurysm: results of a prospective randomized study. J Vasc Surg 2005; 42(2):185–93. 10.1016/j.jvs.2005.04.049
Google Scholar WorldCat Crossref PubMed

Davies RS, Wall M, Rai S, et al. Long-term results of surgical repair of popliteal artery aneurysm. Eur J Vasc Endovasc Surg 2007;
34(6):714–18. 10.1016/j.ejvs.2007.06.019
Google Scholar WorldCat Crossref PubMed

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EVAR trial participants. Endovascular aneurysm repair and outcome in patients unfit for open repair of abdominal aortic
aneurysm (EVAR trial 2): randomised controlled trial. Lancet 2005; 365(9478):2187–92. 10.1016/S0140-6736(05)66628-7
WorldCat Crossref

EVAR trial participants. Endovascular aneurysm repair versus open repair in patients with abdominal aortic aneurysm (EVAR trial
1): randomised controlled trial. Lancet 2005; 365(9478):2179–86. 10.1016/S0140-6736(05)66627-5
WorldCat Crossref

Galland RB, Magee TR. Management of popliteal aneurysm. Br J Surg 2002; 89(11):1382–5. 10.1046/j.1365-2168.2002.02221.x
Google Scholar WorldCat Crossref PubMed

Lederle FA, Wilson SE, Johnson GR, et al. Immediate repair compared with surveillance of small abdominal aortic aneurysms. N
Engl J Med 2002; 346(19):1437–44. 10.1056/NEJMoa012573
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Prinssen M, Verhoeven EL, Buth J, et al. A randomized trial comparing conventional and endovascular repair of abdominal aortic
aneurysms. Dutch Randomized Endovascular Aneurysm Managemtn (DREAM) Trial Group. N Engl J Med 2004; 351(16):1607–
18. 10.1056/NEJMoa042002
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Thompson SG, Ashton HA, Gao L, et al. Multicentre Aneurysm Screening Study Group. Screening men for abdominal aortic
aneurysm: 10 year mortality and cost e ectiveness results from the randomised Multicentre Aneurysm Screening Study. BMJ
2009; 338:b2307. 10.1136/bmj.b2307
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Young EL, Karthikesalingam A, Huddart S, et al. A systematic review of the role of cardiopulmonary exercise testing in vascular
surgery. Eur J Vasc Endovasc Surg 2012; 44(1):64–71. 10.1016/j.ejvs.2012.03.022
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