Carotid Stenting

Introduction

Carotid Artery Atherosclerotic Disease

Carotid artery stenosis is responsible

for 20-30% of ischemic stroke.

Cerebrovascular disease affects

750,000 people in US each year

Stroke is 3rd leading cause of death in

North America

168,000 deaths in US/year

Treatment:

Medical therapy

Aspirin, plavix, statins

Risk factor modification

Carotid Endarterectomy (CEA)

Carotid artery stenting (CAS)

Pathophysiology

Carotid disease is mostly due to atherosclerosis buildup of

cholesterol and fibrotic tissue in the arterial wall

results from both genetic and environmental influences

Usually unifocal, 90% of lesions are located within 2 cm

of the ICA origin.

The degree of carotid stenosis stroke risk.

Other uncommon causes: dissection, vasculitis,

fibromuscular dysplasia

symptoms :

progressive carotid stenosis leading to in-situ occlusion

and hypoperfusion,

intracranial arterial occlusion resulting from embolization

(more common)

Natural History and Risk

Stratification

Patients with asymptomatic carotid bruits are more common than

patients with symptomatic carotid stenosis.

A carotid bruit is identified in 4% to 5% of patients age 45 to 80 years,

(carotid stenosis 75%).

Carotid stenoses 50% have been identified in 7% of men and 5% of

women older than 65 years.

Bruit may be absent if there is slow flow through a severe stenosis.

The risk of progression of carotid stenosis is 9.3% per year;

risk factors for progression include

ipsilateral or contralateral ICA stenosis greater than 50%,

ipsilateral ECA stenosis greater than 50%,

systolic blood pressure greater than 160 mm Hg.

Stroke Risk In Symptomatic

Patients

Risk of stroke in the first year

11% for carotid stenosis 70% to 79%

35% for carotid stenosis greater than or equal to 90%.

Patients with carotid stenosis 70% to 99% had a 2-year ipsilateral

stroke risk of 26%.

Patients with near-occlusion have a lower stroke risk, ranging

from 8% at 5 years to 11% at 1 year.

Stroke Risk In Asymptomatic

Patients

Annual stroke risk is much lower than in symptomatic patients,

less than 1 % for carotid stenoses less than 60%

1% to 2.4% for carotid stenoses greater than 60%.

ACST (Asymptomatic Carotid Surgery Trial)

no relationship between the risk of stroke and increasing stenosis severity from 60% to 99%.

Patients referred for CABG high incidence of asymptomatic carotid stenosis (17% to 22% for
stenosis > 50% and 6% to 12% for stenosis > 80%.)

The risk of perioperative stroke after CABG

2% for carotid stenosis < 50%,

10% for carotid stenosis 50% - 80%,

19% for carotid stenosis > 80%.

Anatomic consideration

Anatomy: Transverse Aortic Arch

Brachiocephalic trunk or
Innominate Artery (1)

R common carotid artery

R subclavian artery

Vertebral artery

Left common carotid Artery (2)

Left subclavian artery(3)

L vertebral artery

True in about 70%

Common variant: L CCA

originating from innominate
artery

Anatomy: Common Carotid Artery

Located anterolaterally in the neck and

medial to the jugular vein

The carotid artery, jugular vein, and vagus

nerve are enclosed in connective tissue carotid sheath

Terminates as the carotid bifurcation

Internal carotid artery (ICA) and External
carotid artery (ECA)

At the vicinity of the superior border of the

thyroid cartilage or approximately at the
level of C4

Bifurcation has been described to be as low

as T2 and as high as C1.

External Carotid Artery

smaller of the two terminal branches of

the CCA

Has 8 branches : the superior thyroid,

ascending pharyngeal, lingual, facial,
occipital, posterior auricular, and the
terminal branches, the superficial
temporal, and the internal maxillary
artery.

The abundant number of anatomoses

between the branches of the ECA and the
intracranial circulation provides
important collateral pathway for cerebral
perfusion when significant disease is
present in the ICA

Internal Carotid Artery

The larger of the CCA terminal
branches
Divided into 4 main segments:

Cervical

begins at the CCA bifurcation and extends

to the base of the skull

normally has a slight dilation, termed the

carotid bulb and/or the carotid sinus

usually does not have branches

Petrous

inside the petrous part of the

temporal bone

Internal Carotid Artery

Cavernous

invested within the cavernous sinus

situated between the layers of the dura mater of

the cavernous sinus, but covered by the lining
membrane of the sinus

Cerebral
begins

after the artery perforates the

dura matter, passes between the optic
and oculomotor nerves, then proceeds
to the terminal bifurcation into

The Circle of Willis

Formed by branches from paired

carotid (anterior circulation) and
vertebral (posterior circulation)
arteries

the posterior cerebral, posterior

communicating, internal carotid,
anterior cerebral, and anterior
communicating arteries on each
side

Allows for collateral flow in the

setting of atherostenosis or
occlusive disease

Clinical Presentation

Clinical Presentation

The majority of patients asymptomatic

Diagnosis is made following auscultation of a carotid bruit or routine

ultrasound screening.

Transient ischemic attack (TIA) is the most common leading symptom,

absence of neurologic deficits careful history taking.

TIAs: temporary focal retinal and/or hemispheric neurological deficits

that resolve within 24 h.

If no therapy is instituted 11 %of patients developed a stroke within

90 days after TIA, one-half occurring within the first 2 days.

Patients with both retinal and hemispheric symptoms usually have

severe extracranial carotid disease.

Vascular Teritory of Brain

Occluded artery

Clinical manifestation

Opthalmic artery

Transient monocular blindness

Anterior choridal artery

Contralateral dense hemiparesis: face, arm, leg

Contralateral hemisensory loss (if lateral geniculate is involved, a contralateral

hemianopsia)

Recurrent artery of heubner

Mild weakness in the contralateral limb with dysarthria

Abulia with apathy and inertia of movement

Anterior cerebral artery

Contralateral weakness of the legs and shoulder

Cortical sensory deficit with poor touch localization and extinction with bilateral
stimuli (left arm apraxia only)

MCA-M1 Segment

Contralateral spastic hemiplegia, visual deficit

MCA-M2 Segment

Hemiparesis affecting the face and arm more than the legs Visual deficits

Left hemisphere MCA (superior

Motor aphasia (Brocas aphasia)

branch)

Also apraxia-both upper extremities

Oral buccal apraxia

Left hemisphere MCA (inferior

Receptive aphasia (Wernickes)

branch)
Nondominant hemisphere

Neglect-left side of space

Clinical syndromes associated with extracranial

carotid occlusive disease
Retinal syndromes

TIA

Amaurosis fugax or transient monocular blindness

Amaurosis fugax variants

Retinal infarction

Global cerebral syndromes

Bilateral or alternating TIAs

Bilateral simultaneous TLA,

suggesting

Central retinal artery occlusion

vertebrobasilar insufficiency

Branch retinal artery occlusion

Bilateral cerebral infarction

Anterior ischemic optic neuropathy

TIA = transient ischemic attack.

Hemispheric syndromes

TIA

Transient hemisphere attack

Limb-shaking TIA

Infarction (stroke)

Watershed infarction

Thromboembolic stroke

Evaluation of Patients with Carotid

Disease Imaging Studies

Carotid duplex US

Non invasive, virtually without

complications

Readily available and quick to do

Sensitivity ~70% when compared with

angiography

CT angiogram CT with IV contrast, very

thin sections

MR angiogram

Good resolution but requires expertise for

interpretation

Readily available (except in Jacobi) and

relatively quick to do

Claustrophobia-inducing machine patient

required to lie still for about 20-30 minutes

Digital subtraction angiography

gold standard

Good resolution but requires expertise

for interpretation

Invasive

Complications related to IV dye

Readily available and quick to do

Complications associated with IV dye

1% stroke risk associated with the

procedure

Carotid Duplex Ultrasound

The

degree of stenosis is
determined by the velocity
of blood flow through the
artery

the

higher the velocity, the

greater the degree of
stenosis

Carotid Duplex Ultrasound

Color doppler can demonstrate

the area of stenosis with
increased flow ( blue/ yellow
flow pattern in this image)

B-mode can demonstrate the

walls of the vessel and the area
of stenosis

Carotid Duplex Ultrasound

Can

identify other
pathology.
Carotid artery dissection
- the "false channel
(yellow-orange) is show,
distinct from the normal
lumen (red).

Carotid Duplex Ultrasound:

Interpretation
<50% stenosis

PSV < 125 cm/sec

50-79% stenosis

PSV>125 cm/sec

80-99% stenosis

EDV>140 cm/sec

>70% stenosis

ICA/CCA (PSV) >4

Occlusion

Absence of flow

with contralateral ICA

occlusion: ICA flow
velocity may be falsely
elevated

Other important
information:

extent of the plaque

plaque characteristics

patency of the distal ICA

CT Angioram

Using a 70% cutoff value for

stenosis, CTA compared to DSA

agreement in 96% of cases

sensitivity 100%

specificity 63%

negative predictive value was 100%

Interobserver agreement was higher

for CTA-measured stenosis than for
DSA-measured stenosis

Neurology. 2004;63:412-413, 457-460

CT Angioram

MR Angiogram

70% to 99% ICA stenoses

Time-of-flight MRA
Sensitivity 91.2% Specificity 88.3%

Contrast-enhanced MRA
Sensitivity 94.6%

ICA occlusion

Time-of-flight MRA
Sensitivity 94.5%

Specificity 99.6%

Moderate (50 to 69%) stenoses

Time-of-flight MRA
Sensitivity 37.9%

Specificity 92.1%

Contrast-enhanced MRA
Sensitivity 65.9%

Stroke. 2008;39:2237-2248

Specificity 99.3%

Contrast-enhanced MRA
Sensitivity 99.4%

Specificity 91.9%

Specificity 93.5%

MR Angiogram

Digital Subtraction Angiogram

CAROTID ARTERY INTERVENTION

Indications

Indications for carotid revascularization relating to symptomatic status and lesion severity are
similar for the endovascular and surgical strategies.

Current American Heart Association (AHA) 2006 and American College of Cardiology
Foundation (ACCF) 2007 guidelines recommend CEA

Symptomatic stenosis 50% to 99%, (risk of perioperative stroke or death < 6%).

Asymptomatic stenosis 60% to 99%, (risk of perioperative stroke or death < 3%).

some physicians delay revascularization until > 80% stenosis in asymptomatic patients

SAPPHIRE study potential safety advantages in high-risk patients with symptomatic

stenosis >50% and asymptomatic stenosis > 80%.

There is insufficient evidence to support CAS in high-risk patients with asymptomatic stenosis
less than 80% or in any patients without high-risk features.

The results of ongoing randomized trials will define the future role of CAS in low-risk patients.

Further study is needed in asymptomatic high-risk patients to determine the relative merits of
CAS compared with best medical therapy.

Criteria used to define high-risk in

carotid artery stent studies
Clinical
Age > 80 years
Congestive heart failure (class III/IV)
Known sever left ventricular sydfunction, LV EF < 30% Open heart surgery needed
within six weeks Recent MI (>24 hrs. and <4 weeks)
Unstable angina (CCS class III/IV)
Severe pulmonary disease Contralateral laryngeal nerve palsy
Anatomic
Previous CEA with recurrent stenosis
High cervical ICA lesions or CCA lesions below the clavicle
Contralateral carotid occlusion
Radiation therapy to neck
Prior radical neck surgery
Severe tandem lesions
ICA, internal carotid artery; CCA, common carotid artery; LV EF, left Ventricular ejection fraction; MI, myocardial infarction; CEA,
carotid endarterectomy.

Contraindications to carotid artery

stenting
Neurological

Major functional impairment

Significant cognitive impairment

Major stroke within 4 weeks

Clinical

Life expectancy <5 yrs

Contraindication to aspirin or
thienopyridines

Renal dysfunction precluding

safe contrast medium
administration

Anatomical

Inability to achieve safe vascular

access

Severe tortuosity of aortic arch

Severe tortuosity of CCA or ICA

Intracranial aneurysm or AVM

requiring treatment

Heavy lesion calcification

Visible thrombus in lesion

Total occlusion

Long subtotal occlusion (string

sign)

Patient Selection
Carotid Revascularization
Indicated

No

Medical therapy

Yes
Evaluate CEA risk
Low
CEA

Evaluate Carotid stent

risk
Low
High

High
CAS

Age
Cerebral reserve
Turtuosity
Cacification

Evaluate CEA risk

CAS

Low
CEA

High
Consider
Medical therapy

Clinical decision-making algorithm in the management of carotid artery stenosis based on estimated
procedural risks. (Roubin GS et al. Circulation. 2006;113:2021-30)

Clinical and angiographic features associated with

increased procedural risks after carotid stenting

Clinical

Risk Factors
Advanced age

Features
Age >80 y

Decreased cerebral
reserve

Dementia
Prior (remote) stroke
Multiple lacunar infarctions
Intracranial microangiopathy
>2 of 90 bends within 5 cm of
the lesion
Concentric circumferential
calcification width >3 mm

Angiographi Excessive tortuosity

c

Heavy calcification

CAROTID STENTING TECHNIQUES

Sheath/Guide placement

Crossing the lesion with a filter wire

Predilatation

Stent selection and deployment

Post dilatation

Embolic protection device removal

Final angiographic assessment

Potential complications of carotid

artery stenting
Cardiovascular

Neurological

Vasovagal reaction (5%-10%)

TIA(l%-2%)

Vasodepressor reaction (5%-10%)

Stroke (2%-3%)

Myocardial infarction (1%)

Intracranial hemorrhage (<1%)

Hyperperfusion syndrome (<1%)

Seizures (<1%)

Carotid artery

Dissection (<1%)

Thrombosis (<1%)

Perforation (<1%)

ECA stenosis or occlusion (5%-10%)

Transient vasospasm (10%-15%)

Restenosis (3%-5%)

General

Access site injury (5%)

Blood transfusion (2%-3%)

Contrast nephropathy (2%)

Contrast reactions (1%)

Death (1%)

ECA = external carotid artery; TIA = transient ischemic attack

Post-procedural care and followup

Clopidogrel (75 mg/day) for 1 month, except prior neck irradiation extended
to 1 year.

Aspirin (325 mg/day) is prescribed indefinitely.

Baseline ultrasound duplex study within 1 month after carotid stenting.

Not infrequently, flow velocities within the stent are elevated despite
documented good angiographic.

Long-term follow up evaluation of patients involves monitoring for evidence of

restenosis or progression of disease in the contralateral carotid artery.

Coronary artery stenting is associated with a low rate of restenosis (2% to 5%).

Ipsilateral stroke or TIA beyond the initial 2 weeks following carotid stenting are
extremely rare.