Aneurysms

By Mohit Bansal, Brian Koottappillil, Jacob Mandel

Edited by Jason Hoffman, M.D.

• Definitions:
o Aneurysm—permanent localized dilatation of a blood vessel to at least 50%
larger than the expected normal diameter, more commonly seen in arteries
§ True aneurysm—involves all three layers of an intact, but weakened
arterial wall
§ False aneurysm (pseudoaneurysm)—vascular wall defect that results in
the formation of a hole in the vessel wall such that blood flows “to-and-
fro” between the intravascular space and a contained extravascular
hematoma
• The wall of a pseudoaneurysm is formed by the surrounding tissue
that acts as a tamponade for the pulsatile blood flow
o Classification:
§ Fusiform—diffuse circumferential dilatation of an affected vascular
segment (e.g., abdominal aortic aneurysms are often fusiform)
• Most common anatomic type of aneurysm
§ Saccular—spherical outpouchings at a site of focal weakness in the
vascular wall (e.g., intracranial berry aneurysms)

Case #1:
A 70-year-old male presents with dizziness and abdominal and lower back pain. His past medical and surgical
history is significant for hypertension, COPD, and CABG. In addition, he has a 30 pack-year history of smoking.
On physical exam he appears pale and diaphoretic. Blood pressure is 80/40, heart rate 123/min. Radial pulses are
thready and equal bilaterally. A carotid bruit and abdominal pulses are noted.

Figure 1. Abdominal aortic aneurysm (Saad 2010)

Abdominal Aortic Aneurysm
• Definition—an abdominal aortic aneurysm (AAA) is a fusiform (or saccular)
enlargement of the aorta that is either:
o 1.5 times greater in diameter than the adjacent normal aorta
o Greater than 3 cm in diameter
• Epidemiology:
o Most common vascular aneurysm
o Affects between 1 and 5.4% of the population (Mastracci, 2007)
o Usually located below the renal orifices (infrarenal)
• Risk factors:
o Atherosclerosis and associated risk factors (i.e., hypertension, hyperlipidemia,
diabetes mellitus)
§ Main cause of AAA, nearly 90% are affected by atherosclerotic vascular
disease (Endovascular Repair, 2002)
o Smoking
o Increasing age
o Male gender
o White race
o Family history
o Peripheral vascular occlusive disease (PAD), coronary artery disease (CAD)
• Pathogenesis:
o Aneurysms occur when the structure or function of the vascular wall connective
tissue matrix is compromised
o Most commonly, intimal atherosclerosis (i.e., plaque) causes deficient delivery of
nutrients from the luminal blood to the arterial tunica media, leading to medial
degeneration and necrosis
o The media, which provides most of the structural integrity to the aorta, becomes
thin and susceptible to aneurysmal dilatation
• Clinical findings:
o Nonruptured AAAs are most commonly asymptomatic and discovered
incidentally on abdominal imaging for an unrelated condition (Figure 1)
o Classic AAA triad:
§ Hypotension
§ Abdominal, flank, or back pain
§ Pulsatile abdominal mass
o With increasing size, patients may become symptomatic due to:
§ Obstruction of branch vessels resulting in distal ischemia
• Renal arteries à acute kidney injury (AKI)
• Mesenteric arteries à bowel ischemia
• Spinal arteries à paresis/paralysis
§ Compression of adjacent structures
• Duodenum à early satiety, nausea, vomiting
• Ureter à hydronephrosis
• Iliocaval veins à venous thrombosis
• Vertebrae à erosion à back pain
 • Bowel à constipation
• Complications:
o Aneurysms promote turbulent flow, with areas of blood stasis, which can lead to
the formation of mural thrombi with subsequent distal embolization
o Ruptured AAA
§ Often occurs without warning
§ Rupture may be either free, contained, or into adjacent structures
• Free AAA rupture results in massive, potentially fatal
intraperitoneal/retroperitoneal hemorrhage
• Rupture into an adjacent vein (e.g., left renal vein, inferior vena
cava, or common iliac vein) may result in hematuria, flank pain, or
high-output cardiac failure
• Rupture into bowel can lead to aorto-enteric fistula with massive
gastrointestinal hemorrhage
o Other complications include:
§ Thrombosis à catastrophic ischemia
§ Infection
• Screening:
o Since asymptomatic AAAs are often not discovered until they rupture, targeted
ultrasound screening is recommended for people most at risk:
§ Older age
§ Male gender
§ Smoking history
§ Positive family history
o United States Preventive Services Task Force (USPSTF) Guidelines (June 2014)
suggest:
§ One-time ultrasound screening for AAA for men ages 65-75 with a
smoking history
• Diagnosis:
o Diagnosis can be suspected on routine abdominal exam by palpation of a
pulsatile, nontender abdominal mass
o Abdominal B-mode ultrasonography (US)
§ Least expensive, least invasive, most frequently used examination for
initial confirmation and follow-up of small AAAs
§ Does not provide sufficient information for planning an intervention
§ Used to diagnose and monitor AAAs until the aneurysm is large enough
that repair may be considered
o Computed tomography (CT) scan (CT angiography)
§ Advantages
• More accurate measurement of diameter, relation to aortic branch
vessels, tortuosity, and angulation
§ Disadvantages:
• More expensive
• Requires intravenous contrast
• Radiation exposure
 § Imaging modality of choice to exclude suspected acute AAA rupture in
hemodynamically stable patients
o Conventional angiography
§ Diagnostic gold standard, but generally now replaced by CT angiography
§ Not necessary for most patients undergoing repair of AAA
o Standard guidelines for AAA treatment
§ <5.5 cm: Serial noninvasive imaging to monitor diameter, rate of growth,
and symptomatology
§ >5.5 cm: Elective repair of AAA with endovascular or open surgery
• Interventional option—endovascular abdominal aortic aneurysm repair (EVAR):
o Indications:
§ Provided adequate aortoiliac anatomy for an endovascular approach, the
following patients may benefit from EVAR with lifelong surveillance
rather than open repair:
• Older patients
• High perioperative risk
• Over time, EVAR has become much more commonplace and is no
longer reserved only for older, sicker patients
o Urgent indications:
§ Ruptured AAA
o Non-urgent indications:
§ Diameter >5.5 cm
§ Rapidly enlarging diameter—expanded by >0.5 cm within 6 months
§ Symptomatic patients (tenderness, abdominal or back pain, hypotension)
§ Repair of smaller AAAs may be justified in patients deemed to have high
risk of rupture (e.g., 5 cm diameter in a female with AAA)
o Contraindications:
§ Limitations to interventional approach due to aortoiliac anatomy:
• Short proximal neck
• Conical proximal neck
• >120O angulation of proximal neck
• Tortuosity of iliac vessels
§ Presence of a thrombus in the proximal landing zone, which is the region
of the aorta where the proximal stent is located following deployment
§ Significant iliac occlusive disease
§ Horseshoe kidney (depending on location of renal arteries)
o Procedure:
§ Preparation:
• Thromboprophylaxis
• Antibiotic prophylaxis
• Prophylaxis for post-implantation syndrome (PIS)
o Clinical features:
§ Fever
§ Elevated WBC count
§ Elevated inflammatory mediators (CRP, ESR)
• Commonly leads to reactive pleural effusion
§ Endograft placement
• Anesthesia options:
o General
o Regional
o Total intravenous anesthesia (TIVA)
o Local with conscious sedation
• Access options:
o Vascular cutdown
o Percutaneous
• Anticoagulation:
o Weight-based IV heparin dose of 80-100 units/kg
§ Goal of activated partial thromboplastin (aPTT)
time of >200 seconds
• Graft deployment
• Completion aortography
• Cutaneous closure
§ Postoperative care
• Endograft surveillance:
o CT angiography at 1- and 12-months post-EVAR
o If no signs of complications, Doppler ultrasonography
• Complications:
o Vascular injury during access or device deployment
o Endoleak
o Endograft separation, migration, kinking, collapse
o Injection
o Ischemic complications involving kidneys, bowel, pelvic
structures, and lower extremities due to
§ Thrombosis
§ Embolism
§ Dissection
§ Obstruction
• Endoleak (White et al.)
o Overview:
§ Identified during insertion of stent graft or during
follow-up surveillance imaging
§ Types I and III represent direct communication
between systemic blood flow and aneurysm sac
• Require immediate repair to prevent
aneurysm dilatation and risk of rupture
o Types:
§ Type Ia endoleak
• Definition—occurs at proximal endograft
attachment site
• Always repaired when detected
§ Type Ib endoleak
 • Definition—occurs at distal endograft
attachment site
• Always repaired when detected
§ Type II endoleak
• Definition—arise from branch vessels that
were excluded from the aneurysm sac during
graft placement
o These vessels feed the aneurysm via
retrograde flow
o Most commonly arise from the
inferior mesenteric artery or from a
lumbar artery
• If a type II endoleak is present without
increasing the size of the aneurysm sac,
immediate intervention is not warranted and
it can be allowed to spontaneously
thrombose
§ Type III endoleak
• Definition—caused by a defect in the graft
material or due to structural failure causing
separation between the graft components
due to inadequate overlap
• Require immediate repair due to direct
communication between systemic
circulation and aneurysm sac
• Requires placement of new graft component
across the defect followed by angioplasty for
remolding of the graft components
§ Type IV endoleak
• Definition—leakage through the graft wall
due to the quality (porosity) of the graft
material
• Often detected on post-deployment
angiogram
• Self-limited and resolve as patients’
coagulation returns to baseline
§ Type V endoleak
• Definition—enlarging aneurysm sac post-
EVAR without visible endoleak
o Management:
§ Repair of type II endoleaks is routinely done via a
transarterial or translumbar embolization
Thoracic Aortic Aneurysm
• Epidemiology:
o Aneurysms are less common in the thoracic than the abdominal aorta
o Incidence has been increasing, and is reported to be 10.4 per 100,000 person-
years (Clouse, 1998)
• Etiology:
o Degenerative (e.g., atherosclerosis)
o Genetic disease
o Bicuspid aortic valve
o Chronic dissection
o Vasculitis
o Infection
o Post-traumatic
o Post-coarctation repair
o Post-coronary artery bypass graft (CABG)
• Pathophysiology:
o The three most common types of pathology affecting the thoracic aorta
(Endovascular, 2005) are:
§ Thoracic aortic aneurysm
§ Aortic dissection
§ Penetrating ulcer
o Thoracic aortic aneurysms are defined by their location:
§ Ascending aorta
• Common causes:
o Younger patients
§ Collagen vascular disease
§ Vascular disease
§ Inflammatory disease
o Older patients:
§ Cystic medial degeneration
§ Aortic arch (transverse)
• Fusiform aortic arch aneurysms
o Most commonly degenerative
o Often contiguous with ascending or descending aortic
aneurysms
o Features:
§ Intimal calcification with bulky plaque or mural
thrombus
§ Elongation and tortuosity of the aortic arch
 § Deviation of mediastinal structures (e.g., trachea,
esophagus)
• Saccular aortic arch aneurysms
o Most commonly degenerative
o A focal aneurysm in an otherwise normal aortic arch may
be due to a contained thoracic aortic arch aneurysm rupture
caused by a penetrating ulcer
o An “aortic blister” may result from deep excavation of an
aortic plaque, with the formation of a localized aneurysm
that has not ruptured
o Irregular contour and perianeurysmal inflammation may be
caused by a mycotic aneurysm
§ One-third of cases of syphilic aortitis involve the
aortic arch and are most commonly saccular in
appearance
§ Descending aorta
• Most commonly degenerative
• Fusiform descending thoracic aortic aneurysms
o May be seen in patients with:
§ Takayasu arteritis
§ Vasculitides
§ Marfan syndrome
o These patients are usually young and do not have evidence
of coexistent atherosclerotic disease
• Saccular descending thoracic aortic aneurysms
o Usually not simple atherosclerotic lesions
o If a young patient presents with a saccular descending
thoracic aortic aneurysm localized to the proximal
descending thoracic aorta, consider chronic aortic
transection
§ Especially if the aneurysm is heavily calcified with
normal adjacent aorta
o Ductus aneurysm—aneurysms that arise from the underside
of the proximal descending aorta and burrow into the
middle mediastinum toward the pulmonary artery may be
derived from remnants of the ductus arteriosus
o Focal pseudoaneurysms may be due to penetrating ulcers,
as detailed above
§ Aortic ulcers are caused by atherosclerotic lesions
that ulcerate and penetrate the aortic wall
 • This may result in the formation of an
intramural hematoma (Bickerstaff, 1982)
§ Mycotic aneurysms may have a similar appearance
but are often multilobulated
§ When the aortic dilatation extends below the
diaphragm, the aneurysm is called a
thoracoabdominal aortic aneurysm
• Clinical features:
o Degenerative thoracic aortic aneurysms are often asymptomatic
§ Often discovered incidentally on chest imaging performed for other
reasons
o Large aneurysms may become clinically evidence due to:
§ Compression and/or stretching of adjacent structures
• Central airways
• Pulmonary arteries
• Superior vena cava
• Recurrent laryngeal nerve à vocal cord paralysis
o Thoracic aortic aneurysm rupture may result in:
§ Chest pain
§ Hypotension
§ Cardiovascular collapse
• Diagnosis:
o Symptomology and patient stability are essential, since rapid aneurysmal
expansion and/or rupture may be indicated acute or severe onset of:
§ Pain
§ Hoarseness
§ Hemoptysis
§ Dysphagia
o Management is heavily contingent upon aneurysm location and regional anatomy
§ Whether surgical and endovascular repair are sought is determined by the
relationship of the thoracic aortic aneurysm to the:
• Aortic valve
• Great vessels
• Abdominal visceral vasculature
§ This information can be obtained by imaging, highlighting its importance
o In acute situations, CT angiography is the preferred imaging modality for
assessing the thoracic aorta
§ Cross-sectional CT or MRI often provide satisfactory information for
following aneurysm progression, and for planning intervention
 • The large capacity of the aorta, tortuous anatomy, and cardiac
motion make conventional angiography difficult
o Thus, cross-sectional imaging is much easier and more
convenient for thoracic aneurysms
o The risk of rupture is higher for a penetrating aortic ulcer (40%) than type B
dissections (4%), so accurate diagnosis and treatment is crucial (Lee, 2004)
§ Imaging signs of imminent or ongoing rupture, rapid expansion, or
contained rupture include:
• New left pleural effusion in a patient with a descending thoracic
aortic aneurysm
• Acute onset of back pain
• Stranding of soft tissue in the mediastinum
• Extravasation of blood in the presence of a degenerative aneurysm
o Mycotic aneurysms are contained ruptures that may have a prominent
inflammatory response in the surrounding soft tissues
• Treatment:
o Medical therapy:
§ Antihypertensives
§ Beta-blockers
o Fusiform thoracic aortic aneurysms
§ Gold standard—surgical resection with synthetic graft replacement
(Findeiss, 2011)
o Risk of rupture, dissection, or death for patients with aneurysms >6 cm is as high
as 14.1% (Findeiss, 2011)
o Intervention is recommended for patients with:
§ Ascending thoracic aortic aneurysm diameter >5.5 cm
• If patient has Marfan syndrome, >5 cm
§ Descending thoracic aortic aneurysm diameter >6.5 cm
• If patient has Marfan syndrome, >6 cm
§ Aneurysm diameter is twice the normal aortic diameter (Dake, 1998)
§ Aneurysm growth >1 cm per year (Findeiss, 2011)
§ Symptomatic thoracic aortic aneurysm (Dake, 1998)
• Prognosis of a large thoracic aortic aneurysm is poor
o 3-year survival rate is as low as 25% (Olsson, 2006)
o Interventional options—thoracic endovascular aortic repair (TEVAR):
§ Overview:
• TEVAR utilizes an endovascular stent graft to exclude the
aneurysm sac from systemic circulation
 • By isolating the weakened aneurysm wall from the high-pressure
systemic circulation, rupture is less likely to occur, which
decreases mortality
• Short- and medium-term data demonstrate benefit of TEVAR over
open surgical repair for TAA with a lower 30-day mortality and
paraplegia rate, in addition to a shorter operative time, ICU stay,
and hospital stay (Endovascular, 2005)
§ Procedure:
• Thromboprophylaxis
• Antibiotic prophylaxis
• Prevention of AKI and contrast-induced nephropathy
• Cerebrospinal fluid (CSF) drainage
o Placing a drain into the subarachnoid space at the level of
the L3-L4 intervertebral disc space to decrease CSF
pressure increases the spinal cord perfusion pressure
gradient and decreases the risk of paralysis due to spinal
cord ischemia
o Indications:
§ Aneurysm with extensive involvement of the
thoracic aorta
§ History of prior open or endovascular aortic
aneurysm repair
§ Presence of internal iliac artery occlusive disease
• Endograft placement (Figure 2):
o General anesthesia
o Arterial access:
§ Femoral artery cut-down is historically preferred
due to a lack of devices that are labelled for
percutaneous use
o Introduction of guidewire and delivery of catheter under
fluoroscopic guidance
o Graft deployment under decreased mean blood pressure
o Completion aortography and closure
• Postoperative care
o Routine neurologic and vascular checks to detect:
§ Stroke
§ Spinal cord ischemia
§ Extremity ischemia
o Endograft surveillance
§ CT angiography at 1- and 6-months post-TEVAR
 • Annually thereafter
• Complications:
o Endoleak
§ The aneurysmal sac continues to receive blood
despite endoluminal stent graft placement
o Endograft failure
§ Separation
§ Migration
§ Kinking
§ Collapse
o Endograft infection
o Ischemic complications (thrombosis, embolism, dissection,
occlusion), most commonly involving the:
§ Spinal cord
§ Brain
§ Intestines
§ Upper extremities
Figure 2: Patient with a history of Hodgkin lymphoma with recent CT demonstrating a 6.5 cm descending thoracic
aortic aneurysm pre-TEVAR (a), post-TEVAR (b), and 7-years following graft placement with marked shrinkage of
the aneurysmal sac (c)
(Images courtesy of Kaiser Permanente Los Angeles Medical Center Vascular and Interventional Radiology
Department)
Peripheral Artery Aneurysm
• Etiology (Kaufman, 2013):
o Lower extremity aneurysms
§ Popliteal artery aneurysm
• Bilateral in 50% of cases
• 15:1 male:female ratio
• Associated with concomitant common femoral artery (CFA)
aneurysms in 40% of cases
• 40% patients with unilateral popliteal artery aneurysms have
concurrent AAA
o 75% of patients with bilateral popliteal artery aneurysms
have concurrent AAA
§ CFA aneurysm
• Normal CFA is ~9 mm in diameter
o 2 cm diameter is considered an aneurysm
• Most true CFA aneurysms are degenerative in origin
o More common in elderly men
o Bilateral in >70% cases
• Most pseudoaneurysms of the CFA are related to angiographic
procedures or surgical anastomoses
§ Lower extremity aneurysms in young patients, or involving the superficial
femoral (SFA), profunda femoris (PFA), or tibial arteries (TA) are rare
and should prompt investigation for an unusual etiology (e.g., Ehlers-
Danlos syndrome)
o Upper extremity aneurysms
§ Highly unusual, representing 2% of all peripheral artery aneurysms
§ Etiology:
• True upper extremity aneurysms
o Thoracic outlet syndrome
o Chronic dissection (originating in the aorta)
o Degenerative
o Marfan syndrome
o Vasculitides
• Upper extremity pseudoaneurysms
o Trauma
o Iatrogenic
o Infection
o Ehlers-Danlos syndrome
o Bechet disease
• Clinical presentation:
 o Popliteal artery aneurysms
§ Asymptomatic (40% cases)
§ Acute limb occlusion (25% cases)
• Caused by thrombosis or distal embolization of a mural thrombus
• One of the most feared complications
§ Claudication (25% cases)
§ Rupture (3% cases)
§ May cause deep vein thrombosis due to compression of adjacent deep
venous system
o CFA
§ Groin pain
§ Pulsatile mass
§ Compression of adjacent nerves or veins
§ Thrombosis (15% cases)
§ Distal embolization (10% cases)
§ Rupture (1-5% cases)
• Diagnosis:
o Lower extremity aneurysms
§ Popliteal artery aneurysm
• Ultrasound—excellent diagnostic modality for patients with
suspected popliteal artery aneurysms
• Work-up must include imaging of the abdominal aorta and both
popliteal arteries
§ CFA
• Ultrasound—excellent diagnostic modality for patients with
suspected CFA aneurysms
• When a degenerative or anastomotic aneurysm is found, MRA or
CTA should be obtained to evaluate the aortic and pelvic vessels
for additional aneurysms
o Upper extremity aneurysms
§ Ultrasound, CTA, and MRA are used to detect upper extremity aneurysms
and differentiate them from tortuous, but otherwise normal anatomy
• Management:
o Introduction
§ Conservative approach
• Used for small, asymptomatic popliteal artery aneurysms
• Medical management of cardiovascular risk factors
• Exercise therapy
• Trial of cilostazol
§ Antithrombotic therapy
 • Initiated immediately in patients diagnosed with popliteal artery
aneurysms who have evidence of:
o Acute thrombosis
o Distal embolization
o Chronic critical limb ischemia
§ Surveillance duplex ultrasound every 6- to 12-months
• For patients without indication for repair
o Indications for repair:
§ All symptomatic aneurysms that present with acute limb ischemia
§ Aneurysm diameter >2.0 cm
o Contraindications for repair:
§ Asymptomatic patients with complete aneurysm thrombosis
§ Nonambulatory patients
§ Acute aneurysm thrombosis with persistently poor runoff site despite
thrombolysis
o Endovascular aneurysm repair:
§ Definition—stent-graft placement to isolate the aneurysm from systemic
circulation and maintain perfusion to the distal extremity
§ Best suited for patients who:
• Are at high perioperative risk for surgery
• Have focal aneurysms that do not extend into the distal popliteal
artery
o At least 1 cm of normal artery should always be proximal
and distal to the aneurysm for adequate stent-graft fixation
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