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et al. 2009), although longer term ﬁgures demonstrate a

wider variability of 54–90% at up to 10 years (De Vries

et al. 2005; Farina et al. 1989; Schillinger et al. 2001; Henry

et al. 2010).

If a stent is to be used, consideration has to be given as to

whether to utilise a self-expanding or balloon mounted

device. The choice of stent-type depends primarily on the

location of the lesion, and generally balloon mounted stents

are used where accurate placement is required, e.g. for

ostial disease (Fig. 2). Self-expanding stents treat elastic

recoil but may lack the radial force to remain expanded in a

ﬁbrotic lesion. Some operators reserve stenting for cases

where there is suboptimal result from angioplasty due to

stenosis recoil or ﬂow-limiting dissection, but others use

primary stenting of all signiﬁcant subclavian and innomi-

nate lesions (Brountzos et al. 2004; Henry et al. 1999).

In theory, primary stenting reduces the risk of ﬂow-limiting

dissection and distal embolisation, although there is little

evidence to support this (Burihan et al. 2011). Post-

procedural luminal diameter following stenting is better

than with PTA alone, but some data suggest longer term

outcome might be less advantageous than PTA alone, with

reported primary patency of 73 and 60% at 1 and 4 years,

respectively (Rodriguez-Lopez et al. 1999; Schillinger et al.

2001). Secondary patency results are more satisfactory at

90–94% (Henry et al. 1999; Rodriguez-Lopez et al. 1999).

Further concern relates to the long-term structural integrity

of stents in the distal subclavian artery, where compression

between the ﬁrst rib and clavicle, and ﬂexion forces on arm

movement can lead to strut fracture and recurrent stenosis/

occlusion. It was hoped that self-expanding stents might

solve this problem, with their ability to conform to these

compressive forces, but this does not appear to prevent

breakage (Phipp et al. 1999). Fortunately, most subclavian

atheromatous lesions are prevertebral, and here, stent

disruption is much less likely.

For occlusions, there is some evidence that primary

stenting may be superior to PTA alone. Duber et al. (1992)

reported a poor patency rate of 43% at 16 months following

PTA in a small cohort of patients with subclavian artery

occlusion. By comparison, Martinez et al. (1997) found an

81% cumulative patency rate at 6 months following

Fig. 1 a, b Left subclavian artery stenosis (arrows). Note the

proximity of the origin of the vertebral artery (arrowhead). c Balloon

angioplasty of the stenosis with a supporting guidewire in the

subclavian and axillary artery (S) and a protection guidewire in the

vertebral artery (V). d Following angioplasty, the stenosis has

improved, but there is now absent ﬂow in the vertebral artery

(arrowhead), which is rectiﬁed e by subsequent angioplasty of the

vertebral artery origin

104 D. R. Turner and S. M. Thomas

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stenting of occlusions, similar to the 86% patency at 1 year

noted by Sadato et al. (2004). However, long-term data of

stent performance in proximal upper limb occlusions is

lacking.

The longest follow-up data available for endovascular

treatment for subclavian artery occlusive disease is in

abstract form only, and reports both stenoses and occlusions

together (Henry et al. 2010). These data, out of 10 years

follow-up, suggest that treatment with stents limit restenosis

and improve long-term results compared to PTA alone. A

recent Cochrane Review concluded that there is insufﬁcient

high quality evidence to show if stents are superior to

angioplasty alone for subclavian artery stenotic disease

(Burihan et al. 2011).

2.1.2 Other Diagnoses

Atherosclerosis is the major cause of chronic large vessel

occlusive disease in the upper limb, but other diseases have

a relatively larger role than in the lower limb.

The inﬂammatory arteritides such as Takayasu’s disease

and giant cell arteritis cause stenotic and occlusive lesions

by mural inﬂammation and ﬁbrosis. Medical therapy to

suppress active inﬂammation remains the cornerstone of

treatment.

Surgery or endovascular treatment is usually reserved for

the treatment of severely symptomatic stenoses in the

chronic ‘burnt out’ phase of the disease, although endo-

vascular intervention has been reported during active dis-

ease. Results are generally inferior to those reported for

atheromatous disease (Joseph et al. 1994; Kerr et al. 1994),

probably due to the transmural nature and greater extent of

involvement in inﬂammatory arteritis (Maškovic

et al.

1999). However, acceptable results have been demonstrated

in a number of small series, including some cases of active

disease where adjuvant systemic therapy was given to

reduce the risk of early restenosis (Amann-Vesti et al. 2003;

Sharma et al. 2000; Tyagi et al. 1998). Furthermore,

recurrent stenoses can be safely treated with further endo-

vascular intervention (Tyagi et al. 1998).

Previous radiotherapy, particularly in the axilla for nodal

metastases from breast carcinoma, or over the lung apex for

bronchogenic lesions, can cause large artery steno-

Fig. 2 a Arch aortography demonstrates occluded left subclavian

artery origin (arrow) and incidental minor innominate artery stenosis

(arrowhead). b Distal subclavian and axillary artery (arrows) ﬁll via

retrograde vertebral artery ﬂow (arrowhead). c The occlusion was

crossed with a wire from the brachial approach, which was snared from

below to allow transfemoral stenting via a long 8-F sheath (d, e, f)

Upper Limb Arterial Intervention 105

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occlusion, often over a long segment. Surgical bypass can

provide good results (Jindal and Wolfe 2005; Law et al.

1995; Ziomek et al. 1986). However, surgery to previously

irradiated tissue may be fraught with difﬁculties. Endovas-

cular techniques offer a potential solution to some of the

problems associated with surgery. Only small case series

exist: short-term results are good, but long-term results are

blighted by recurrent steno-occlusion (Liu et al. 1998;

McBride et al. 1994).

2.2 Acute Upper Limb Ischaemia

Symptomatic acute ischaemia of the upper limb is more

common than its chronic counterpart, and may lead to

severe ischaemia, occasionally necessitating amputation.

Eyers and Earnshaw (1998) found that 17% of all cases of

acute limb ischaemia occur in the arm, and is usually due to

macro-embolic disease, with 90% of cardiogenic origin.

Other causes of acute upper limb ischaemia are listed in

Table 2. The most common landing site (60–85%) for upper

limb emboli is the brachial artery (Hernandez-Richter et al.

2001; Kaufman 2004; Deguara et al. 2005). In general,

embolic occlusion of the brachial artery is not usually limb

threatening because of collateral ﬂow. Conservative therapy

with anticoagulation is often appropriate, particularly in

elderly patients, as there is a high incidence of comorbidi-

ties which contribute to signiﬁcant mortality rates of

between 5.6 and 19% at 30 days (Deguara et al. 2005;

Hernandez-Richter et al. 2001; Sultan et al. 2001) and 63%

at 5 years (Licht et al. 2004). However, severe ischaemia

requires urgent treatment; diagnosis is frequently clinically

apparent and the majority of cases are best and most easily

treated surgically, with or without angiographic conﬁrma-

tion. Technical success following surgical thrombectomy is

achieved in 65–94%, limb salvage rates are between 82 and

100% and residual symptom rates are reasonably low. Local

and general complications occur in up to 28% (Eyers and

Earnshaw 1998; Hernandez-Richter et al. 2001; Licht et al.

2004.; Deguara et al. 2005). If the limb is not immediately

threatened, endovascular therapy may be considered, usu-

ally with catheter directed thrombolysis. In the largest

published series of 55 patients, of whom 40 were deemed

suitable for intraarterial thrombolysis, the overall rate of

complete recanalisation was 55%. All patients had some

clinical improvement. Those with successful thrombolysis

required no further intervention, and those in whom

thrombolysis failed were treated medically (56%) or by

embolectomy (44%). All limbs were saved, with only mild

residual symptoms in 1.8% of the original 55 patients

(Cejna et al. 2001). These results are supported by Coulon

et al. (1994) who reported a complete recanalisation rate of

only 63%, but limb salvage in all 13 of their patients, 15%

of whom had mild residual symptoms. Patients with limited

surgical options for severe ischaemia because of very poor

distal runoff resulting from thromboembolism may also

beneﬁt from ﬁbrinolytic therapy (Johnson et al. 1999).

However, despite their reasonable results, these series

are small, there is no data that gives a true comparison with

surgical thromboembolectomy or conservative treatment,

and generally there is sparse evidence to guide endovascular

treatment in the acutely ischaemic upper limb.

Microembolism can present with vertebrobasilar symp-

toms, or with the classical ‘blue digit syndrome’, caused by

digital microinfarcts and splinter haemorrhages. Showers of

microemboli from ulcerated proximal atheromatous plaque

frequently lead to intermittent symptoms. Treatment

involves aggressive antiplatelet medication and PTA to treat

the responsible plaque, leading to remodelling and stabili-

sation (Gaines et al. 1999).

The other main circumstance when acute upper limb

ischaemia may be precipitated is during treatment with

thoracic aortic stent grafts, when the left subclavian artery

may be covered to ensure an adequate proximal landingzone.

Overall thelikelihood ofischaemia is lowdue to the presence

of excellent collateral ﬂow, often via the vertebral artery.

Management to avoid upper limb ischaemia and possible

increased risk of stroke and paraplegia are usually surgical

with carotid to subclavian artery bypass (Sepehripour et al.

2011; Chung et al. 2011; Lee et al. 2011). There have,

however, been some reports of endovascular fenestration

of thoracic stent grafts (McWilliams et al. 2004), and the use

Table 2 Causes of acute upper limb ischaemia

Embolus

Cardiogenic

Proximal atheroma

Aneurysm

Fibromuscular dysplasia

Vascular injury

Trauma

Thrombosis

Brachial/radial artery cannulation

Iatrogenic

Inadvertent in intravenous drug use

Occupational

Vasculitis

Spontaneous

Hypercoagulation syndrome

‘Steal’ from haemodialysis ﬁstula formation

Aortic dissection

Compartment syndrome

106 D. R. Turner and S. M. Thomas

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of custom made fenestrated devices are becoming more

common totry tomitigate problemsduring theperiprocedural

period when the left subclavian artery would otherwise be

compromised.

3 Trauma

Vascular injuries of the upper extremity occur more com-

monly than in the legs. A signiﬁcant proportion of upper

limb vascular trauma is iatrogenic, secondary to arterial

catheterisation or misplaced venous line insertion, with road

trafﬁc accidents and penetrating stab wounds other common

causes, but large series are rare (Barros D’Sa 1995; Deguara

et al. 2005). In certain parts of the world penetrating injuries

due to gunshot wounds and stabbing are more common

(Robbs and Baker 1978), and there are increasing reports of

the use of endovascular techniques for wartime vascular

trauma (Fox et al. 2005). Conservative measures are usually

appropriate for minor trauma, and imaging is not usually

required unless there are ‘hard’ signs of vascular damage.

Severe trauma can result in arterial transection or branch

avulsion leading to life-threatening haemorrhage. Surgical

intervention traditionally provides the mainstay of therapy,

but use of endovascular techniques has been reported in

small numbers of patients. The potential beneﬁts of avoid-

ing a ‘hostile’ surgical environment with its inherent risks

favour minimally invasive therapy, though logistics often

mean that surgery is the ﬁrst consideration. Endovascular

intervention is unlikely to be successful in the severely

disrupted artery because of the difﬁculties crossing the

traumatised vessel with a guidewire, but bleeding branch

vessels may be embolised using coils. If a guidewire can be

placed across a damaged segment of artery, an inﬂated

balloon catheter of appropriate size will tamponade the

lesion (Lin et al. 2000). This allows time for consideration

of other therapeutic options, or may indeed treat small

arterial wall defects. Stent grafts have been used to repair

actively bleeding axillary artery injuries (Dinkel et al.

2002), posttraumatic occlusion (Strauss et al. 2001), and

exclude arteriovenous ﬁstulae and false aneurysms

(Broadbent et al. 2003; Hilﬁker et al. 2000). Long-term

outcome is uncertain but emergency stent graft placement

for arterial damage may provide a valuable short-term

solution, allowing other, potentially more serious, injuries

to be stabilised before surgical repair.

Inadvertent arterial puncture during central venous

catheterisation can be treated by external pressure if the

puncture site is compressible, but if this is not possible, or

unsuccessful, endovascular treatment can be performed

using angioplasty balloon tamponade, stent-grafting

(Schoder et al. 2003) or use of commercially available

closure devices (Nicholson et al. 2004).

4 Thoracic Outlet Syndrome

Thoracic outlet syndrome (TOS) describes a number of

different symptoms related to compression of subclavian

vessels and the brachial plexus exiting the thoracic outlet,

typically occurring when the arm is abducted. There are a

variety of recognised causes including cervical ribs and

ﬁbrous bands, but many cases occur in the presence of

‘normal’ anatomy. Neurogenic symptoms are commonest

(90%), and arterial TOS is unusual accounting for only

1–2% of cases, and such arterial symptoms are often asso-

ciated with anatomical anomalies, such as a cervical rib or

band (Davidovic et al. 2003; Kaufman 2004). Symptoms

include positional ischaemia, a palpable pulsatile mass and

sequelae of distal embolisation. Diagnosis can be estab-

lished on duplex ultrasound, and angiography, where clas-

sically there is compression of the distal subclavian artery

upon provocative hyperabduction of the arm. However, this

is also seen in 30% of ‘normal’ individuals. More sensitive

indicators to pathological involvement include persistent

stenosis and vessel irregularity in the neutral position,

occlusion and distal subclavian artery dilatation or aneu-

rysm formation. MRI or CT may be helpful in identifying

abnormal soft-tissue structures.

Endovascular options for treatment include thrombolysis

of in situ thrombus, stenting for stenoses, and stent-grafts

for aneurysm exclusion. However, because of the underly-

ing mechanism, stent/stent-graft devices are placed in a

position of high compressive stress, and mid- to long-term

results have been disappointing, with restenosis, occlusion

and device disruption (Phipp et al. 1999). Their use is

generally not recommended unless combined with surgical

decompression (Kaufman 2004). Surgical decompression

and repair/bypass probably remains the treatment of choice

at this time (Rigberg and Freishlag 2004). However, it

should be noted that 20% of patients show no improvement

following surgery.

Compression of the subclavian vein in the thoracic outlet

falls outside the scope of this chapter and produces a dif-

ferent set of challenges. However, there is an excellent

recent review of the approach to management for this

condition (Thompson et al. 2011).

5 Aneurysmal Disease

Aneurysms of the upper limb arteries are rare, accounting

for less than 2% of all peripheral aneurysms. The position of

the aneurysm may give some clue as to its aetiology.

Proximal subclavian and innominate artery lesions are most

likely to be degenerative, whereas distal subclavian and

proximal axillary artery aneurysms are usually secondary to

Upper Limb Arterial Intervention 107

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the rare arterial TOS. More distal aneurysms are highly

likely to be secondary to trauma. Mycotic lesions and

connective tissue disorders should always be considered.

Aberrant right subclavian arteries often have a patulous

origin, and are associated with proximal aneurysmal dila-

tation, which may lead to oesophageal compression (dys-

phagia lusoria) and a high risk of rupture (Lacroix et al.

2003).

Aneurysmal disease can thus lead to rupture, thrombosis,

distal embolisation or, particularly if intrathoracic, com-

pressive symptoms. Imaging is best performed with CTA/

MRA if proximal, and ultrasound if peripheral.

The rarity of upper limb aneurysms means no ﬁrm rec-

ommendations regarding treatment are available. Surgical

repair or bypass is well established, and may also treat the

underlying cause (e.g. decompression in TOS). However,

subclavian artery aneurysm repair can result in a compli-

cation rate as high as 46% (Salo et al. 1990), particularly if

transthoracic techniques are required. Endovascular repair

using stent grafts was ﬁrst reported in the mid 1990s (May

et al. 1993; Parodi 1996) and has subsequently has been

described in a number of small series, both as an elective

and emergency procedure (Lacroix et al. 2003; Schoder

et al. 2003) with good early results and low morbidity and

mortality. However, there remains little reported long-term

data on stent-graft durability and performance.

6 Conclusion

The circulation of the upper limb can be affected by a broad

variety of disorders. However, upper limb arterial disease is

markedly less common than that seen in the lower limb. As

a result, ﬁrm evidence regarding how speciﬁc lesions and

disorders should be treated is often lacking. It would appear,

however, that use of endovascular techniques in the man-

agement of upper limb arterial stenoses and occlusions is

associated with fewer complications than open surgery and

has acceptable patency rates. Endovascular therapy alone is,

however, not suitable for the treatment of arterial TOS,

because some form of surgical decompression is required.

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110 D. R. Turner and S. M. Thomas

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Carotid and Vertebral Artery Intervention

Stephen D. Goode and Trevor J. Cleveland

Contents

1 Carotid Artery Intervention............................................... 111

1.1 Surgery Trials and Role of Carotid Intervention

in Stroke Prevention .............................................................. 111

1.2 Carotid Artery Stenting Versus Carotid Endarterectomy .... 112

2 Indications for CAS............................................................. 113

3 Cerebral Protection Devices............................................... 114

4 Technical Aspects ................................................................ 114

5 Post-procedure Care............................................................ 115

6 Complications Following CAS ........................................... 115

7 Limitations of and Contraindications to CAS ................. 115

8 Vertebral Artery Intervention ........................................... 116

9 Pathology .............................................................................. 117

10 Indications for Vertebral Artery Intervention ................ 117

11 Technical Aspects ................................................................ 118

12 Post-procedural Care .......................................................... 118

13 Complications ....................................................................... 119

14 Conclusion ............................................................................ 119

References...................................................................................... 119

Abstract

Stroke is the third most common cause of death

worldwide. Current treatments for signiﬁcant carotid

artery stenotic disease include carotid endarterectomy

and carotid artery stenting. We present a synopsis of the

current evidence available comparing these two treat-

ments in addition to indications, technical aspects and

post-procedural care for patients undergoing carotid

artery stenting. Similarly we present the indications,

technical aspects and post-procedural details for verte-

bral artery intervention.

1 Carotid Artery Intervention

Stroke is the third most common cause of death worldwide.

Carotid artery disease accounts for approximately 25% of

all ischaemic strokes and is deﬁned as the narrowing or

occlusion of the artery due to atherosclerotic plaque build

up. The slow build up of plaque is caused by high blood

pressure, diabetes mellitus, smoking, high cholesterol, and

other mostly modiﬁable vascular risk factors. A severely

stenotic carotid artery is an independent risk factor for

ipsilateral future stroke.

1.1 Surgery Trials and Role of Carotid

Intervention in Stroke Prevention

Treatment of a stenotic lesion in the carotid artery is per-

formed mainly to prevent embolic stroke. A series of ran-

domized controlled trials in the 1990s began to clarify the

beneﬁts and risks of carotid surgery. The two landmark

trials were the North American Symptomatic Carotid End-

arterectomy Trial (NASCET) and the European Carotid

Surgery Trial (ECST) both of which randomised patients to

carotid endarterectomy (CEA) or contemporary best medi-

cal therapy (Barnett et al. 1998; Rothwell et al. 2003; ECST

1998). Differences between the trials in the method of

S. D. Goode (&)  T. J. Cleveland

Shefﬁeld Vascular Institute, Northern General Hospital,

Herries Road, Shefﬁeld, UK

e-mail: s.goode@shefﬁeld.ac.uk

M. G. Cowling (ed.), Vascular Interventional Radiology, Medical Radiology. Diagnostic Imaging,

DOI: 10.1007/174_2011_512,  Springer-Verlag Berlin Heidelberg 2012

111

https://t.me/med1917

measurement of carotid stenosis and in the deﬁnition of

outcome events meant that they were not directly compa-

rable. However, reanalysis of the individual patient data and

reassessment of the carotid angiograms have enabled the

results of the trials to be collated by Rothwell et al. (2003).

They published this reanalysis of the pooled trial data

(6,092 patients) from ECST and NASCET trials, showing

that the two trials had consistent results. Carotid endarter-

ectomy, over best medical therapy, is not beneﬁcial in

patients with 0–49% stenosis or occlusion. However, in

those patients with a high-grade carotid stenosis of 70–99%

CEA conferred an absolute risk reduction of 16% over

5 years as compared to best medical therapy (for ipsilateral

ischaemic stroke and operative stroke or death), with six

patients needing to undergo CEA to prevent 1 stroke. A

signiﬁcant beneﬁt from surgical intervention was also found

in those patients with 50–69% stenosis although the beneﬁts

were less marked; CEA conferred an absolute risk reduction

of 4.6% over 5 years with 22 patients requiring CEA to

prevent 1 stroke (Rothwell et al. 2003).

Overall the operative risk of stroke and/or death within

30 days after surgery was 7.1%. Patients undergoing sur-

gical correction of high-grade stenoses gained a durable

beneﬁt for more than 8 years. Increased efﬁcacy was found

with increased degree of stenosis, previous stroke, and

plaque ulceration. It is notable that following surgery, there

were other complications including cranial nerve palsy in

7.6%, neck wound haematoma in 5.5%, and wound infec-

tion in 3.4% of patients. The total perioperative morbidity

and mortality rate was 26.2%.

The asymptomatic carotid atherosclerosis study (ACAS)

results were released in late 1994 (Executive Committee for

ACAS 1995), which suggested that the indications for

carotid intervention could be broadened to include asymp-

tomatic patients with carotid artery disease of greater than

60%. The ACAS demonstrated a 5.9% absolute reduction in

the 5-year risk of ipsilateral ischaemic stroke in patients

who underwent endarterectomy of severe carotid stenosis

compared with those medically treated. The operative all-

stroke and death rate was 2.3%. The asymptomatic carotid

surgery trial (ACST) (Halliday et al. 1994; Halliday et al.

1995; Rothwell et al. 2004; Rothwell and Goldstein 2004;

Sleight et al. 2002; Halliday et al. 2004) results were pub-

lished in 2004 and demonstrated that in asymptomatic

patients with[70% stenosis, immediate CEA halved the net

5-year stroke risk from 12 to 6%; the absolute risk reduction

being 5.4% over 5 years. Practical considerations about the

effectiveness of surgery in these patients suggest that even

when considering the average 2% risk of ipsilateral stroke

per year, 85 asymptomatic patients would have to be

operated upon to prevent 1 stroke per year. More recently

the 10-year results of the ACST (Halliday et al. 2010) were

published which conﬁrm the superiority of immediate CEA

versus best medical therapy with a maintained beneﬁt at

10 years. The 10-year risk of non-perioperative stroke was

10.8% in the CEA group versus 16.9% in the best medical

therapy group.

Traditionally CEA has been used to remove the athero-

sclerotic plaque from the carotid artery via open neck sur-

gery, performed under local or general anaesthetic.

However, in recent years, the alternative technique of

stenting the carotid artery has been introduced. Given the

evolution of the treatment of patients with peripheral arte-

rial disease with percutaneous transluminal angioplasty

(PTA) and stents, the endovascular treatment of carotid

artery disease became feasible and, despite the proven

efﬁcacy of CEA, carotid artery stenting (CAS) has emerged

as an alternative therapy. The ﬁrst balloon angioplasty for

carotid stenosis was performed in 1979, and was followed

by further published case reports in the 1980s (Bocken-

heimer and Mathias 1983; Courtheoux et al. 1987). Since

these ﬁrst few case reports the endovascular treatment of

carotid artery disease has evolved and stenting is now the

treatment of choice as opposed to balloon angioplasty.

Dedicated carotid artery stents and cerebral protection

devices are now used routinely for intervention.

1.2 Carotid Artery Stenting Versus Carotid

Endarterectomy

Over recent years there have been a number of randomised

clinical trials comparing CEA and CAS. The Leicester

study was the ﬁrst prospective randomised single centre

trial investigating CAS versus CEA in symptomatic patients

(Naylor et al. 1998). The study was terminated after

enrolment of only 17 patients as the interim safety analysis

showed that 70% of all patients in the CAS arm had neu-

rological complications, compared to uneventful CEA.

However, this was a single centre study with very small

numbers and therefore too small to draw any signiﬁcant

conclusions. The Carotid and Vertebral Artery Translumi-

nal Angioplasty Study (CAVATAS) (Brown et al. 2001)

was a multicentre randomised trial involving centres in

Europe, Australia, and Canada. It enrolled 504 patients

starting in 1992 and was published in 2001, 253 patients

were randomised to CEA and 251 patients to carotid artery

intervention (65 received a stent and the remainder under-

went balloon angioplasty). There was no signiﬁcant differ-

ence in rate of stroke and death between CEA (10%) and

CAS/PTA (9.9%). At 1-year ultrasound follow-up there were

signiﬁcantly more re-stenoses (70–90%) in the CAS/PTA

group (CAS/PTA 14% vs. CEA 4%), but there were more

symptomatic restenoses in the CEA arm. The Kentucky

randomised trials comparing CAS with CEA were

published in 2001 (Kentucky 1, symptomatic patients) and

112 S. D. Goode and T. J. Cleveland

https://t.me/med1917

2004 (Kentucky 2, asymptomatic patients). These studies

reported very low complication rates (Brooks et al. 2001,

2004).

The SAPPHIRE (Yadav et al. 2004) (Stenting and

angioplasty with protection in patients at high risk for

endarterectomy) trial was the ﬁrst non-inferiority, random-

ised, multicentre trial that compared stenting with distal

cerebral protection and with CEA, in 723 patients who were

at high risk for surgery. Ultimately only 334 patients were

randomised to CEA or CAS due to patientsbeing deemed too

unﬁt for intervention. In particular there were signiﬁcantly

higher number of patients with coronary disease and previ-

ous percutaneous transluminal coronary angioplasty. The

primary end point was 30-day myocardial infarction (MI),

stroke plus death rate and ipsilateral stroke to one year. This

was 12.2% in the CAS arm versus 20.1% in the CEA arm,

concluding that CAS was not inferior to CEA (p = 0.048).

There were no differences in stroke at 3 years. None of the

CAS patients had a cranial nerve injury,while approximately

5% of the surgical group did (p = 0.004). This trial included

a mix of symptomatic and asymptomatic patients.

Randomised trials published in 2006 included two fur-

ther non-inferiority trials which had recruited exclusively

symptomatic patients. The Stent-Protected Angioplasty

versus Carotid Endarterectomy (SPACE) trial included

1,183 symptomatic patients with a [70% stenosis of the

ICA (Ringleb et al. 2006), 599 in the CAS group, and 584 in

the CEA group. The primary endpoint was 30-day ipsilat-

eral stroke and death (6.84% for CAS versus 6.34% for

CEA—the non-inferiority test was not signiﬁcant

(p = 0.09)). The investigators concluded that CEA remains

the preferred treatment for patients with symptomatic ICA

stenosis. The endarterectomy versus stenting in patients

with symptomatic severe carotid stenosis (EVA-3S) trial

included 527 symptomatic patients with an ICA stenosis of

60–90% (Mas et al. 2006). The primary endpoint was 30-

day stroke and death. The systematic use of a cerebral

protection device was instituted during the trial by the

safety committee, and the trial was ended prematurely for

reasons of both ‘safety and futility’. Inclusion stopped after

enrollment of 527 patients, although power calculations

indicated that 872 patients were needed to reach a statistical

power of 80%. thirty-day all stroke and death rates were 9.6

and 3.9% for CAS and CEA, p = 0.01, although the study

was ended prematurely the inferiority question still remains.

More recently two large randomised clinical trials

comparing CAS and CEA, namely the ICSS (Ederle et al.

2010) and CREST (Brott et al. 2010) have been published.

ICSS was a multicentre, international, randomised con-

trolled trial where 1,713 patients with recently symptomatic

carotid artery stenosis were randomly assigned to CAS or

CEA. The 120-day rate of stroke, death, or procedural

myocardial infarction was 85% in the stenting group

compared with 52% in the endarterectomy group

(p = 0006). There was no signiﬁcant difference in major

stroke and death. The majority of the difference in stroke

rate arose from non-disabling stroke in the CAS arm, with

surprisingly low numbers of minor stroke in the CEA group.

A substudy of the ICSS trial (Bonati et al. 2009) examined

the rate of MRI detectable ischaemic brain injury using

diffusion-weighted imaging. They found three times more

patients in the stenting group than in the endarterectomy

group had new ischaemic lesions on post-treatment scans

and that protection devices did not seem to be effective in

preventing cerebral ischaemia during stenting. Following on

from the ICSS study, a ‘pre-planned’ meta-analysis has

recently been published Carotid Stenting Triallists Collab-

oration (2010) which includes 3,433 patients from the EVA-3S,

SPACE and ICSS studies. At 120 days all stroke and death

within the CAS group was 8.9 versus 5.8% in the CEA

group (p = 0.0006), again the differences occurring for

minor stroke. Cranial nerve palsy was, as expected, signif-

icantly more likely with CEA. There was no statistically

signiﬁcant difference in outcome for patients under 70 years

(CAS 5.8 vs. CEA 5.7%).

The most recent published study is the Carotid Revas-

cularization Endarterectomy versus Stenting Trial (CREST)

(Brott et al. 2010). This is the largest published prospective

multicentre randomised trial comparing CAS and CEA,

which enrolled 2,502 patients from 117 US and Canadian

centres. There was no signiﬁcant difference in the primary

endpoints of any stroke, MI, or death during the peri-pro-

cedural period, or ipsilateral stroke on follow-up between

CAS and CEA (CAS 7.2%, CEA 6.8%). The rate of minor

stroke was higher in the CAS group and the rates of MI and

cranial nerve palsies were higher in the CEA group.

2 Indications for CAS

The beneﬁts of CAS over CEA are due to its minimally

invasive nature, allowing consideration of treatment in

patients who are unﬁt for CEA due to severe comorbidities,

those with surgically ‘hostile’ neck morphology due to

previous surgery/radiotherapy, or in those patients who

have unfavourable anatomy (short neck, high carotid

bifurcation, and distal ICA stenoses). UK national guide-

lines produced by the National Institute for Health and

Clinical Excellence (NICE) (NICE 2011) have recom-

mended that CAS can be performed in patients with

symptomatic carotid artery disease. For patients with

asymptomatic disease there is little evidence to support

routine use of CAS; however, there is currently an ongoing

trial ACST-2 (Rudarakanchana et al. 2009) which will

hopefully clarify this issue over the coming years.

In addition carotid stenting can be used to treat patients with

Carotid and Vertebral Artery Intervention 113

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