CAROTID ARTERY DISEASES, CAROTID STENTING

1. CAROTID ARTERY DISEASES
AND CAROTID STENTING
Dr VIRBHAN BALAI
FNB,DNB,MD,DLO,MBBS
MSSH,NEW DELHI

2. INTRODUCTION
 Stroke is the leading cause of adult disability
 Third leading cause of death in North America,
Europe, South America, and Asia.
 Most strokes (80% to 85%) are ischemic in
etiology.
 Atherosclerotic disease (affecting the
extracranial and intracranial arterial
circulation)accounts for approx 20% of
ischemic strokes .

3. Carotid Atherosclerosis and Stroke
 The carotid bifurcation has a predilection for the
development of atherosclerosis, typically at the origin
of ICA.
 Plaque = dense cap of CT, SMC`s, core of lipid &
necrotic debris.
 Vulnerabe plaque ; reduced amounts of collagen,
increased inflammation, thinning of the fibrous cap,
and increased cholesterol in the necrotic core.
 Plaque fissuring or rupture at the carotid bifurcation
 Occlusive or nonocclusive thrombus formation.

8. “near-occlusion ICA” String sign=Collapse of ICA

9. Natural History of Carotid Artery
Bifurcation Disease
 Two dominant factors determine the risk of
ischemic complications
 Symptomatic status of the lesion
 Severity of stenosis
 NASCET Trial = risk of any I/L stroke at 2-year F/U
in medically treated pt`s with symptomatic
stenoses of 70% to 99% was 26%.
 Among pt`s with symptomatic stenoses of 50% to
69%, the 5-year risk of any I/L stroke was 22.2%.

10. SYMPTOMATIC PATIENT

11. N Engl J Med. 1998;339[20]:1415–1425

12. Lancet. 2003;361:107–116.

13. Hazard of I/L ischemic stroke within 3 years after index TIA/Stroke
Cuffe et al, Stroke. 2006;37:1785-1791

14. Carotid artery disease
Definition
• Carotid artery stenosis = ≥ 50% stenosis of the
extracranial ICA
• ‘Symptomatic’ if associated with symptoms in
the preceding 6 months.
• ‘Asymptomatic’ if no prior symptoms or when
symptoms occurred >6 months ago.

15. Diagnosis
CLINICAL EVALUATION
• RISK FACTORS
– MODIFIABLE
– NON MODIFIABLE
• ISCHEMIC STROKE
• TIA (<1HR,NO INFARCTION)

17. Imaging
• DUS:- first-line carotid imaging modality to
assess extracranial ICA stenoses.
– Echolucency, intraplaque haemorrhage, surface
irregularity
– Doppler velocity (PSV,EDV) measurements
– Ratios (ICA/CCA PSV) for accurate estimation of
stenosis severity
– SRU Consensus
– Sonographic NASCET Index

18.  MRI – Plaque morphology,Vulnerable plaque
 CTA-Severe calcification may overestimate
stenosis severity.
 MRA- does not visualize vascular calcification,
an important issue in CAS.
 Transcranial Doppler- detection Spontaneous
embolisation (Uni directional high intensity
increase, short duration, random occurance,
“whistling” sound.

19. Recommendations for imaging of
extracranial carotid arteries

20. Treatment
• MEDICAL THERAPY
• ENDOVASCULAR THERAPY-CAS
• OPEN SURGERY- CEA

21. MEDICAL THERAPY

24. ENDOVASCULAR TECHNIQUES
 CAS - less invasive alternative to CEA
 Low risk of cranial nerve injury, wound
complications and/or neck haematoma
 Reduce perioperative MI

25. CAS Preffered Over CEA
• Hostile neck’ (prev radiation, rec stenosis),
• C/L recurrent laryngeal nerve palsy
• Challenging surgical access [very high ICA
lesions, proximal CCA lesions]
• Pt at high risk of perioperative MI

26. CAS disadvantage
• Access site complication
• Higher stroke

27. EMBOLIC PROTECTION DEVICES
 Controversial
 Meta-analysis of 24 studies - EPD use was
associated with a lower risk of perioperative
stroke (RR 0.59; P < 0.001).
Garg N et al,J Endovasc Ther 2009;16:412–427

28. • CREST : Carotid Revascularization
Endarterectomy versus Stenting Trial.
• ACT-1 : Asymptomatic Carotid Trial
– EPDs mandatory- best result with EPDs
 SPACE trial : Observed lower I/L stroke rates in
CAS pt`s without EPD (6.2%) vs. with EPD
(8.3%)

29. Recommendation on the use of EPD
during carotid stenting

30. Management of carotid artery disease
Asymptomatic carotid artery disease

31. Open surgery vs. medical therapy
• ACAS & ACST-1 compared CEA with medical therapy in
asymptomatic pt`s with 60–99% carotid stenosis.
 ACAS : 5-year rates of I/L stroke/death under CEA vs.
medical therapy were 5.1% vs. 11.0%, respectively (P =
0.0001, NNT = 18).
• 10-year risk of ‘any’ stroke rates were 13.4% vs. 17.9%,
respectively (P = 0.009, NNT = 22).
 ACST-1 : 5-year rates of any stroke 6.4% vs. 11.8%,
respectively (P < 0.0001, NNT = 19).
• Fatal/ disabling stroke rates were 3.5% vs. 6.1%,
respectively (P = 0.004, NNT = 38).

32. Features associated with increased risk of stroke in patients with
asymptomatic carotid stenosis treated medically

33. Carotid revascularization: surgery vs.
stenting
 Two biggest RCTs; CREST and ACT-1
 ACT-1; @30day death/stroke= 2.9%. Vs 1.7%
in CAS & CEA respectively (p=0.33).
 SAPPHIRE trial ; randomized symptomatic and
asymptomatic pt`s deemed ‘high risk for
surgery’ to either CEA or CAS (using EPDs
routinely

34. • The primary endpoint (30-day
death/stroke/MI and/or death or I/L stroke
between 31 days and 1 year) occurred in
12.2% of CAS pt`s and 20.1% of CEA pt`s (P =
0.053).
• At 3 years ; major I/L stroke (CAS 1.3% vs. CEA
3.3%), minor I/L stroke (6.1% vs. 3.0%) and
repeat revascularization (3.0% vs. 7.1%) were
not statistically different.

35. Recommendations for management of
asymptomatic carotid artery disease

37. Criteria Used to Define a High-Risk Population in
Studies of Carotid Artery Stenting

38. Clinical situations and anatomical findings when CAS is
preferred

39. Symptomatic carotid artery disease
Open surgery
 In a meta-analysis of all symptomatic pt`s
randomized within NASCET and ECST.
 NASCET; 0–49% stenosis gained no benefit from
surgery.
 CEA conferred a 7.8% ARR for stroke at 5 years in
pt`s with 50–69% stenoses (NNT = 13).
 Maximum benefit was seen in pt`s with 70–99%
ICA stenoses, where the ARR for stroke was
15.6% (NNT = 6).

40. Endovascular therapy vs. open surgery
 CAS - increased risk of any stroke but a
decreased risk of perioperative MI & cranial
nerve injury.
 Higher rates of perioperative stroke in pt`s >70
years of age undergoing CAS.
 Beyond the 30-day perioperative period, long-
term data after CAS are almost identical to
those after CEA.

42. Recommendations on revascularization in
patients with symptomatic carotid disease

44. Vertebral artery disease
• Up to 20% of ischaemic CVA involving the
posterior circulation are related to vertebral
artery disease

45. Imaging
• CTA/MRA have a higher sensitivity (94%) and
specificity (95%) than DUS (sensitivity 70%)
• MRA-Overestimate Vertebral ostial stenoses
• CTA - Underestimates the degree and
prevalence of ostial vertebral artery stenoses.
• DSA - rarely required for diagnostic purposes,
req in pt`s who are cond for revascularization.

46. Management of vertebral artery
disease
• Aspirin (or clopidogrel if aspirin is not
tolerated) and statins - irrespective of
symptoms.
• Most pt`s with asymptomatic vertebral artery
disease do not require any revascularization
• In pt`s with ischaemic events despite
antiplatelet therapy, revascularization may be
considered.

47. • VAST Trial - 162 randomized pt`s with vertebrobasilar
symptoms within the preceding 30 days and an extra-
or intracranial vertebral artery stenosis >50% to
stenting plus BMT (n = 57) or BMT alone (n = 58).
• 30 day ; Vertebrobasilar stroke or death occurred in 5%
of pt`s randomized to stenting and 2% in the medical
arm.
• At 3 years; 12% and 7% respectively
• Do not support routine endovascular interventions for
symptomatic vertebral artery stenoses unless
symptoms recur despite OMT

48. Recommendations for management of
vertebral artery stenoses

56. FUNDAMENTAL STEPS
1. Femoral access
2. Arch angiography
3. Selective catheterization target CCA
4. Wire placement in ECA
5. Sheath or GC placement in distal CCA
6. Placement of embolic protection device
7. Pre-dilation of lesion
8. Stent placement
9. Post-dilation of stent
10. Removal of EPD
11. Final angiography

57. Key steps in carotid stenting

58. Carotid Artery Stenting: The Procedure
PREPROCEDURAL ASSESSMENT
• Clinical assessment
• Advanced age -: >80 years has been associated
with significantly worse outcomes with CAS
• Decreased cerebral reserve -: presence of
dementia,cognitive impairment, and a H/O prior
strokes or lacunar infarcts increase the likelihood
that distal embolization and are relative CI for the
procedure.

59. • Anatomic assessments:
• CTA - higher spatial resolution, superior
visualization of the aortic arch compared with
MRA
• It allows an assessment of the degree of
calcification of the aortic arch and carotid
bifurcation, Not possible by MRA.

60. Anatomic Assessments Recommended Before Carotid Artery
Stenting and Their Impacts on Interventional Planning

61. Aortic arch type

62. Type Of Aortic Arch

63. Intubating the guiding catheter or
sheath into the CCA
• Type I or II aortic arch-; Enter the CCA using a
slightly curved catheter — JR or Headhunter
catheter
• Bovine arch- JL, IMA, or Simmons catheters.
• Type III aortic arch with calcification, difficult
to access; if access with a general catheter is
not feasible, use Simmons or Sidewinder
catheters.
• Contact the aortic arch as little as possible

64. Carotid Artery Stenting
Catheters for Angiography and Access

65. Engagement methods with the Simmons catheter

66. Baseline Angiography
• Femoral artery access
• Heparin bolus of 25 mg/kg
• Angiography of the carotid bifurcation
• Uncomplicated anatomy (i.e., type I aortic arch,
no tortuosity of the great vessels)- ; Bernstein
catheter.
• Complicated anatomies (e.g., type II or III arch,
tortuosity of the great vessels, bovine origin of
the left CCA);- Vitek or Simmons catheter.

67. Interventional Technique
• CAS steps:
1. Aspirin+ clopidogrel
2. Anticoagulation - UFH (ACT 275 - 300 Sec)
1. CI to heparin - direct thrombin inhibitor such as
bivalirudin
3. No sedation - To screen for any neurologic
change during the procedure.

68. Delivery of Sheath or Guide to the CCA
 6-Fr sheath or 8-Fr guide must be placed in the distal CCA
 Steps for delivery of a 6-Fr sheath in the CCA is as follows
1. CCA is engaged with a diagnostic catheter.
2. Stiff-angled Glidewire is advanced into the ECA, and the diagnostic
catheter is advanced over it.
3. Glidewire is exchanged for a superstiff Amplatz or SupraCore wire,
and then the diagnostic catheter is removed.
4. 6-Fr sheath and its dilator are delivered over the stiff wire to the
distal CCA, after which the dilator is removed.
 Guidewires and catheters should never be placed across the carotid
lesion to deliver the sheath or guide to the CCA.
 It is preferable to refer the pt for CEA than to persist in risky
attempts to deliver the guide or sheath.

69. Delivery of Embolic Protection Device
• Use of EPDs is currently considered the
standard of care during CAS.
• Filter-type EPD: most popular, user friendly,
allow continued antegrade flow
• Multiple filter-type EPDs have received FDA
approval, including Accunet, EmboShield,
Spider, Angioguard, FilterWire, and FiberNet
devices.

70. Filter-Type EPDs Used During Carotid
Intervention

71. EPDs

73.  Filter should be deployed in a straight and nondiseased
portion of the cervical ICA
 There must be at least 3 to 4 cm of distance between
the proximal margin of the filter and the distal margin
of the ICA lesion
 Filter-type systems have replaced distal occlusion
balloon EPDs, which were the first type of EPD used
during a carotid intervention (c.1998).
 Most recent group of EPDs developed for carotid
intervention are the proximal occlusion devices (e.g.,
the Parodi Antiembolism System from Gore Medical,
Flagstaff, AZ, and the MO.MA System from Medtronic).

74. Advantages and disadvantages of
EPDs

75. Carotid artery stent procedure

76. Angioplasty and Stenting
PREDILATION
 After placement of the EPD system, the lesion is
usually predilated to facilitate stent delivery.
 Low-profile coronary balloons with diameters of
3.0 - 4.0 mm are used.
 Attempts to deliver the stent without predilation
have been associated with a greater amount of
atheroembolism, likely related to increased
trauma to the lesion with forcible passage of the
stent across a tight stenosis.

77. Stent Selection and Placement
 Flexible self-expanding stents - conform to the
tortuous anatomy, changes in vessel shape
associated with neck movements.
 Nitinol, a nickel-titanium alloy, is the most
widely used material for carotid self-
expanding stents; because of its large elastic
range.

78. Self-Expanding Carotid Artery Stents

79.  Nominal diameter of the stent used should be 1 to 2 mm larger
than the diameter of the largest treated vessel (usually the CCA).
 Open-cell-design nitinol stents with large open-cell areas and highly
flexible interconnecting bridges (e.g., Precise stent, Cordis; Zilver
stent, Cook, Bloomington, IN)—may be optimal for treating lesions
in tortuous locations.
 Calcified lesions should be treated with stents that have a high
radial force and a moderate outward expansive force, such as
nitinol stents with a closed-cell design (e.g., Xact stent, Abbott).
 Lesions with the greatest risk for distal embolism should be treated
with stents that provide greater vessel scaffolding (closed-cell
nitinol or cobalt alloy stents; e.g., WALLSTENT, Xact).

80. POSTDILATION
• 4.5 - 5.5-mm diameter noncompliant balloon (e.g., Aviator,
Cordis; Sterling, Boston Scientific).
• Postdilation is associated with the greatest propensity for
plaque embolization; therefore experienced operators
advocate a conservative approach to postdilation.
• A residual stenosis of less than 20% is usually accepted.
• When filter-type EPDs are being used, “slow flow,” is an
important finding
• This phenomenon is caused by excessive distal
embolization of plaque elements that occlude the filter
pores, compromising antegrade flow through the filter .

81. Slow flow

82. Predictors of slow flow
– Treatment of symptomatic lesions
– Increased patient age
– Increased stent diameter
 To prevent distal embolization of debris at the time of
filter retrieval, use of an Export catheter to aspirate 40
to 60 mL of blood from the column of blood proximal
to the filter before retrieval of the filter EPD.
 If slow flow is observed after stent deployment,
poststent dilation is discouraged bcz it will probably
exacerbate the degree of embolization from the Tt site.

83. Removal of the EPDs and Final
Angiography
 Remove filter - type EPD by advancing a retrieval
sheath over the interventional wire and
collapsing the filter.
 The collapsed filter is then withdrawn carefully
across the stent and removed.
 Rarely, the pt have to turn head or external
compression may have to be applied to carotid.
 Final angiography at the Tt site, the EPD landing
zone, and the I/L anterior cerebral circulation.

84. Slow flow and rationale for aspiration
J Am Coll Cardiol. 2005;46[8]:1466–1472

85. Postprocedural Care and Follow-Up
 All pt`s should receive lifelong aspirin therapy
unless contraindicated.
 Clopidogrel is recommended for a minimum of 4
weeks after the procedure.
 Pt`s are seen at 1 month and 12 months after the
procedure for clinical assessment and a carotid
ultrasound study to screen for in-stent stenosis.
 Thereafter, yearly carotid ultrasound examination
is recommended.

86. Possible complications according to
the phase of the procedure

87. Predictors of complications during
coronary artery stenting

88. COMPLICATIONS OF CAROTID
INTERVENTION
STROKE
 Risk of periprocedural stroke is most strongly related to
the pt’s symptomatic status.
 Multiple observational studies of high-risk pt`s stroke
ranged from 2.3% - 6.9%.
 High-risk registry studies in recent years reporting
stroke rates of 2.3% - 4.4%.
 Approx 80% of these strokes I/L to the Tt site; --> 25% -
33% classified as major strokes (i.e., persistence of
neurologic deficit beyond 30 days).
 Majority of strokes occur at the time of the CAS
procedure.

89. Thirty-Day Outcomes From Randomized Trials of CAS and CEA in
Normal-Risk Pt`s

90.  After 30 days, the risk of I/L stroke with CAS is extremely
low.
 Most procedure-related strokes (>80%) are ischemic in
nature
 Mechanism ; distal embolization of plaque due to
manipulation of catheters and wires in the aortic arch/CCA
and embolization of plaque elements with angioplasty and
stent.
 Hemorrhagic strokes accounted for 15% - 20% of all strokes
in larger high-risk stent registries.
 Slightly later than that of ischemic strokes, and the
dominant mechanism is probably related to cerebral
hyperperfusion after CAS.

91. Hemodynamic Depression
• Baroreceptors are activated by increases in blood
pressure.
• Signals from these receptors are transmitted through
the glossopharyngeal nerve (cranial nerve IX) toward
the vasomotor center in the medulla, which in turn
activates the vagus nerve (cranial nerve X) and
reticulospinal tract, resulting in peripheral vasodilation,
bradycardia, and decreased cardiac contractility .
• Transient pressure from angioplasty and more
prolonged pressure from self-expanding stents
activates these baroreceptors, causing the hypotension
and bradycardia frequently associated with CAS.

93.  It is uncommon for significant effects to be seen beyond 48
to 72 hours, because the baroreceptors gradually adapt to
the pressure from the self-expanding stent.
 In a retrospective analysis of 500 consecutive CAS cases
from a single center, the frequency of procedural
hemodynamic depression—defined as a systolic blood
pressure less than 90 mm Hg or bradycardia of less than 60
beats/min—was 42%, with persistent hemodynamic
depression after the procedure in 17% of cases.
 Prophylactic measures include withholding
antihypertensive medications on the morning of the
procedure and ensuring adequate hydration with IV fluids
before and during the procedure.

94. Hyperperfusion Syndrome
 Cerebral hyperperfusion; bcz of improved flow to a
chronically ischemic cerebral territory.
 Caused by significant increases in cerebral blood flow
(>100% of baseline) after revascularization, which in
combination with impaired cerebral autoregulation
results in transudation of fluid into the brain’s
interstitium and cerebral edema .
 Clinically ; pt`s typically complain of a throbbing
headache I/L to the revascularization site. Associated
symptoms include nausea, vomiting, confusion, and
visual disturbances. In the most severe cases, patients
develop focal neurologic deficits and seizures.

95.  The feared complication of the hyperperfusion
syndrome is intracerebral or subarachnoid
hemorrhage, which is associated with a high
mortality rate (40% to 60%) and severe morbidity
among survivors.
 In 12 observational studies published since 2003,
the incidence of hyperperfusion syndrome was
1.3% (73 of 5431 cases).
 Most cases manifested within 24 hours after the
procedure, and cases beyond 2 to 4 days were
rare.

96. • Risk factors : for cerebral hyperperfusion after
CAS
– Include pre existing hypertension, postprocedural
hypertension, C/L carotid occlusion, critical I/L carotid
stenosis, and incomplete circle of Willis.
• Aggressive control of BP after CAS is
recommended in all pt`s to prevent it.
• Management of hyperperfusion syndrome are
prompt diagnosis and emergent institution of
therapy.

97.  Diagnosis is clinical, based on the pt’s symptoms.
 Several antihypertensive agents are
contraindicated bcz they are associated with
increased cerebral blood flow, including glycerol
trinitrate, nitroprusside, calcium channel
antagonists, and ACE inhibitors.
 Recommended agents :include β-blockers,
labetalol and clonidine which have favorable
effects on cerebral blood flow.

98. Lancet. 2005;4:877–888

99. Adverse Cardiac Events
 30-day incidence of MI has been in the range
of 0% - 2.4%.
 SAPPHIRE trial; CAS was compared with CEA
in high-risk pt`s,, significant and consistent
reduction in MI with CAS (2.4% vs 6.1%; P =
.04).
 CREST; 30-day MI rates of 1.1% in the CAS arm
and 2.3% in the CEA group (P = .03)

100. Restenosis
 ISR is an important late complication of CAS.
 Duplex ultrasound is used for screening
carotid ISR
 Incidence of severe ISR (≥80%) is 3% - 4% at
approx 18 months of F/U.
 ISR at 2 years in RCT`s of CAS and CEA was
11.1% (lower cutoff value i.e., ≥70% was used
to define it).