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Carotid Occlusive Disease
Presented By:
Dr. Rahul Jain
SR-2 Neurosurgery
Moderated by:
Dr V. C. Jha
Dr Nitish Kumar
Dr Gaurav Verma
Introduction
• Ischemic stroke remains a leading cause of death
and disability in the developed world.
• Atherosclerotic plaques of the cervical carotid
artery are relatively common and are a source of
emboli that place patients at risk of ischemic
stroke.
• Atherosclerosis is a disease of the arterial intima
that causes progressive narrowing of the vessel
lumen.
• The carotid bifurcation creates shear stress related
to turbulent, high-pressure arterial blood flow.
Turbulence causes endothelial damage and a focal,
recurrent inflammatory cascade.
• Focal, recurrent inflammatory cascade leads to
progressive deposition of atheromatous plaque and
gradual com-promise of the integrity of the carotid
arterial lumen.
• Transient ischemic attacks (TIAs) and strokes occur
when a portion of the plaque ruptures, migrates
distally into the intracranial circulation as
thromboembolism, and causes a focal arterial
occlusion or a broader, territorial infarct.
• clinical presentations of stroke or TIA are variable
• 10%–15% of those who suffer a stroke have a history of
sentinel TIA
• Amaurosis fugax is defined as acute, atraumatic
monocular visual loss, caused by retinal microemboli
or marginal perfusion related to diminished reti-nal
blood flow
• For symptomatic 70%–99% carotid stenosis, several
studies have defined the cumulative risk of
ipsilateral ischemic stroke as 20%–26% within 2–3
years
• Middle cerebral artery is the commonest site of
thromboembolic stroke. manifestations include
contralateral weakness and hemisensory loss.
Aphasia are associated with lesions of the
dominant hemisphere, hemineglect and apraxic
syndromes are associated with the nondominant
middle cerebral artery .
• Anterior cerebral artery infarctions involve
primarily contralateral lower extremity weakness,
poorly defined cognitive/psychiatric disturbances.
• Anterior choroidal artery
supplies the posterior limb
of the internal capsule, the
posterolateral thalamus, and
the lateral geniculate body;
infarctions present clinically
as a triad of contralateral
hemiparesis, hemisensory
loss, and homonymous
hemianopsia
Asymptomatic Extracranial Carotid Ds
• most commonly diagnosed by carotid ultrasound.
• Indications for non-invasive carotid evaluation may
include
• screening
• further investigation of a carotid bruit, or
• a thorough evaluation related to a previous stroke or
TIA.
• Current guidelines advise against routine screening
duplex sonograms for asymptomatic carotid
stenosis, because the incidence of clinically
significant internal carotid artery (ICA) stenosis
≥50% is <5% in the general population.
• In a prospective study of 339 asymptomatic patients
followed with serial Doppler examinations over 29
months, 2% of patients with 50%–80% stenosis, 8.3% of
those with 80%–99% stenosis, and 12.2% of those with
carotid occlusion experienced strokes.#
• Well-designed clinical trials involving asymptomatic
patients with 60%–99% carotid stenosis revealed an
11% stroke risk at 5 years in the medical cohorts.
North American Symptomatic Carotid
Endarterectomy Trial (NASCET)
defined the 5-year stroke risk
in the contralateral asymptomatic
Territory as
# Hennerici M, Hulsbomer HB, Hefter H, et al. Natural history of asymptomatic extracranial arterial disease. Results of a long-term
prospective study. Brain. 1987;110:777–791.
5 year stroke
risk
Degree of
stenosis
4.6% No disease
7.8% Stenosis <50%
12.9% Stenosis 50-59%
14.8% Stenosis 60-74%
18.5% Stenosis 75-94%
14.7% Stenosis 95-99%
9.4% occlusion
Symptomatic Carotid Disease
• Patients with carotid plaque ipsilateral to a previous TIA
or stroke have a higher risk of recurrent ischemic event
than their asymptomatic counterparts. 5 year stroke
risk
Degree of
stenosis
Rate of
Ipsilateral
stroke
Rate of Ipsilateral major
stroke
NASCET NASCET ECST
<50% 18.7% 4.7% 6%
50-69% 22.2% 7.2% 10.6%
70-99% 26% 13% 17.4%
• Data from the
medically treated
arms of NASCET and
ECST provide stroke
rates ipsilateral to the
symptomatic carotid
stenosis.
• One must be cautious in comparing data across
these two trials, however, because the degree of
carotid stenosis was measured differently and the
duration of follow-up was incongruous.
• The mean follow-up was 2 years in the severe
stenosis NASCET group, 5 years in the mild and
moderate stenosis NASCET groups, and
approximately 6 years in ECST.
MEDICAL MANAGEMENT
• Treatment of carotid stenosis includes risk factor
modification, pharmacologic therapy, and surgery
in some cases.
Risk Factor Treatment
Hypertension (HTN)
• increases the relative risk of stroke by
3- to 5-fold.
• most prevalent modifiable risk factor.
• One clinical trial indicated that a
reduction in diastolic blood pressure
(DBP) as little as 5–6 mm Hg may
decrease risk of stroke by 42%.
• Lifestyle modifications include salt
restriction and other dietary changes,
aerobic exercise, and weight loss.
Diabetes Mellitus
• increase the risk of stroke through acceleration of large-
artery atherosclerosis, adverse effects on plasma lipoprotein
levels, and promotion of plaque formation through
hyperinsulinemia.
• Authorities agree that the optimal fasting serum glucose
level is <126 mg/dL. The HbA1c value should be <6.5%.
Dyslipidemia
• statin therapy prevents carotid plaque progression and
reduces the incidence of transition from asymptomatic to
symptomatic carotid stenosis
• initial retrospective studies demonstrated improved
outcomes with perioperative statin therapy only among the
symptomatic population, recent prospective trials have
classified failure to prescribe a perioperative statin as an
independent risk factor for decreased survival, even among
asymptomatic patients.
• Two meta-analyses evaluating pooled outcomes
data on the effectiveness of statins in patients with
coronary artery disease showed a 27%–32%
reduction in stroke rate.
• All patients with carotid disease should be treated
with a statin, and the recommended low-density
lipoprotein level is <100 mg/dL.
Alcohol Consumption, Smoking, Obesity
• Obesity is associated with HTN and DM and should
be addressed as one component of a comprehensive
approach to risk factor treatment.
• Heavy alcohol consumption, cigarette smoking, and
obesity are modifiable risk factors that increase an
individual’s risk.
Antiplatelet Therapy
1. Aspirin
• Irreversibly inhibiting platelet cyclooxygenase, which
prevents the formation of thromboxane A2, both a
potent vasoconstrictor and an inducer of platelet
aggregation.
• In healthy individuals, a single aspirin results in 98%
inhibition of thromboxane A2 production within 1 hour.
• overview of trials of antiplatelet therapy in patients
with a history of TIA or stroke showed a 25% reduction
in the risk of nonfatal stroke, nonfatal myocardial
infarction (MI), and death from vascular causes
independent of age, sex, and other risk factors.
• best dose remains controversial, doses ranging
from 30 to 1500 mg/day.
• In the ASA and Carotid Endarterectomy (ACE) trial,
2804 patients who had undergone CEA were
randomized to compare the benefits of low-dose
(81–325 mg/day) to high-dose (650–1300 mg/day)
aspirin. Risk of stroke, MI, or death at 3 months
was 6.2% in the low-dose aspirin group compared
with 8.4% in the high-dose group
2. Adenosine Diphosphate Receptor Inhibitors
• Ticlopidine - significant hematologic side effects
limited its widespread use.
• Clopidogrel - more benign side effect profile.
• study enrolling more than 19,000 patients with
atherosclerotic disease manifesting as ischemic
stroke, MI, or symptomatic peripheral arterial
disease, 75 mg/day clopidogrel was found to be
more effective than 325 mg aspirin in reducing risk
of ischemic stroke, MI, and vascular death.
• 30% of patients may be considered clopidogrel
resistant, and more potent ADP receptor inhibitors
such as ticagrelor or prasugrel may be needed
Surgical Management
• In the early 1990s NASCET and ECST established
carotid endarterectomy (CEA) as highly effective
treatment symptomatic carotid stenosis >= 70%.
• Stenting and Angioplasty with Protection in
Patients at High Risk for Endarterectomy
(SAPPHIRE) trial and the Carotid Revascularization
Endarterectomy versus Stent Trial (CREST) carotid
artery stenting with the use of a distal protection
device should be the preferred operation for high-
risk patients who meet the surgical criteria outlined
in NASCET.
• However, inclusion of mild MI in the primary
outcome in CREST obscured the superiority of CEA
for stroke prevention.
• A Cochrane review of randomized trial data in 2012
supported CEA as the first-choice strategy when
surgery is indicated.
• CEA has been validated by multicentre randomized,
prospective clinical trials across at least two
generations of carotid surgeons as superior to
medical management alone for symptomatic
patients with >50% stenosis and asymptomatic
patients with >60% stenosis.
Carotid Endarterectomy
• first true CEA was performed by Michael E. DeBakey in
1953.
• Carotid Doppler ultrasonography provides a quick,
relatively cost-effective, and safe initial diagnostic
study, carries a sensitivity of 72% to 96% and a
specificity of 61% to 100% for high-grade stenosis.
• in the setting of significant calcification Doppler may
overestimate the degree of stenosis – CTA/MRA
• CTA with a sensitivity and specificity of 77% and 95%,
respectively, provides detailed information regarding
plaque-associated calcifications and the relationship of
the ICA bifurcation to the angle of the mandible, which
is used in determining candidacy for an endarterectomy
as opposed to endovascular therapies.
• MRA can provide value in detecting more detailed
characteristics of the atherosclerotic plaque,
including lipid content and intraplaque
hemorrhage.
• When there remains a discrepancy between
ultrasound and CTA or MRA, cerebral catheter
angiography may be performed, which carries a
nearly 100% sensitivity and specificity.
• Currently there is no recommendation for
widespread mass screening for carotid occlusive
disease in asymptomatic patients.
• Recently, the prevalence of moderate (≥50% to
69%) stenosis was found in 4.8% of men and 2.2%
of women younger than 70 years.
SURGICAL INDICATIONS AND
DECISION MAKING
Symptomatic Patients
• The results of the NASCET and the ECST had initially
provided level I evidence recommending surgical
intervention for symptomatic (amaurosis fugax,
hemispheric TIA, nondisabling stroke) patients with
greater than 70% stenosis on noninvasive imaging or
greater than 50% stenosis as demonstrated on catheter
angiography.
• In the analysis of Brott and colleagues pooled analysis
of the four largest clinical trials since the landmark
NASCET and ECST—the EVA-3S study, the SPACE study,
the ICSS, and the CREST- compared the efficacy of CAS
versus CEA in symptomatic patients.
• There were 129 periprocedural and 55 postprocedural
strokes in the CEA arm, whereas there were 206 and
57, respectively, in the CAS group.
• The preprocedural 120-day stroke and death was 3.2%
(unchanged from previous trials), and beyond 120 days
occurrence of stroke or death was infrequent, and rates
were similar between CAS and CEA.
• Long-term outcomes were similar for CEA (0.60%) and
CAS (0.64%); therefore, longterm outcomes of
periprocedural and postprocedural strokes still favor
CEA, underlining importance of improving CAS.
• With the assumption of a perioperative stroke and
death rate less than 6%, recommend performing an
early (within 2 weeks) CEA in all patients with
symptomatic ICA stenosis greater than 70% and
for older (>75 years), male patients with moderate
grade stenosis of 50% to 69%.
• Female patients with moderate stenosis should be
evaluated on an individual basis, and CEA is
contraindicated in patients with less than 50%
stenosis.
Asymptomatic Patients
• evidence is not nearly as convincing for
asymptomatic patients as it is for symptomatic
patients.
• Identifying specific factors that would place
asymptomatic patients at greater risk of stroke.
• High rates of radiographic progression of carotid
stenosis in asymptomatic patients have also been
shown to increase the risk of ipsilateral neurological
events.
• Assuming a perioperative risk of less than 3%, CEA
can be recommended for asymptomatic men below
age 75 with 60% to 99% stenosis.
Contralateral Stenosis
• The presence of a complete contralateral ICA
occlusion increases both the natural history risk of
stroke and perioperative morbidity.
• Perform an endarterectomy on the symptomatic
side first, or the side with a greater degree of
stenosis or concerning plaque characteristics in the
case of asymptomatic disease.
Carotid Artery Angioplasty and
Stenting
• CAS is a principal surgical tool in the management
of carotid atherosclerotic disease.
• Major impetus for the advancement of CAS came
with the publication of the results of SAPPHIRE
(stenting and angioplasty with protectionin
patients at high risk for endarterectomy) trial in
2004, which demonstrated the non-inferiority of
CAS compared with CEA in patients classified as
being at high risk for CEA, with significantly fewer
CAS patients requiring revascularization within 1
year of initial treatment.
CAROTID ARTERY STENTING TRIALS AND REGISTRIES
• CAVATAS (Carotid and Vertebral Artery
Transluminal Angioplasty Study)demonstrated no
statistically significant difference between
endovascular and surgical treatment in the rates of
dis abling stroke or death within 30 days (6.4% CAS
versus 5.9% CEA) and no significant difference in 3-
year ipsilateral stroke rates.
• The Wallstent trial was the first multicenter
randomized trial designed from its inception to
evaluate CEA and CAS equivalence. The trial was
halted by the Data Safety and Monitoring
Committee after an interim analysis demonstrated
worse outcomes for the CAS group. Distal
protection devices were not used in the Wallstent
trial.
• Carotid Revascularization Using Endarterectomy or
Stenting Systems (CaRESS) multicenter,
nonrandomized, prospective study. No statistically
significant difference between 30-day and 1-year death
or stroke rates was found between CAS and CEA.
• A major criticism of CaRESS, as opposed to randomized
trials, is that the low stroke and death rates may be
attributable to the ability of the treating physician to
consider patient-specific factors and successfully assign
each patient to the safest therapy.
• SAPPHIRE study established CAS as a treatment option
for high-risk patients (clinically significant cardiac
disease, severe pulmonary disease, contralateral
carotid artery occlusion, contralateral laryngeal nerve
palsy, previous radical neck surgery or radiation,
recurrent stenosis after CEA, or age >80 years).
• Stent-Supported Percutaneous Angioplasty of the
Carotid Artery Versus Endarterectomy (SPACE) trial
was undertaken to establish noninferiority for CAS
compared with CEA in patients with symptoms but
without high-risk features. The 30-day rates of
ipsilateral stroke or death were 6.84% for CAS and
6.34% for CEA (P = .09).
• Despite the results of CREST and ACT I
demonstrating noninferiority of CAS compared with
CEA in patients at low risk for adverse events with
CEA in terms of stroke, MI, and death, the CMS
continues to indicate CAS only for individuals at
high risk for CEA.
INDICATIONS FOR CAS
• current indications for CAS are principally based on
FDA and CMS approval for patients considered at
high risk for CEA.
• Therefore CAS is
presently approved for
patients with carotid
stenosis exceeding
70% and who are
considered at high risk
for CEA.
Carotid artery stenting procedure
5-French diagnostic catheter is advanced
into the external carotid artery of the
affected side
A 6- to 10-French guide
is then brought into the common carotid
artery over the exchange wire
The lesion is then crossed with a 0.014-
inch microwire (usually part of a distal
embolic protection
system). Once the lesion is crossed, a
distal embolic protection device is then
delivered through a microcatheter across
the lesion and, as the inset
indicates, unsheathed distal to the lesion.
The stent delivery system is then retrieved, and an
appropriately sized postdilation balloon is advanced
over the wire and inflated briefly to its
nominal pressure (left).
After this, the balloon is retrieved, and an
angiogram is performed to confirm satisfactory
revascularization.
Once success is
confirmed, the distal embolic protection device is
recaptured and withdrawn
SURGICAL TECHNIQUE for CEA
• Patients are positioned supine with the arms
tucked at the sides and the head on a soft
doughnut-shaped headrest and slightly extended
and turned 15 degrees contralaterally.
• The anteriorborder of the sternocleidomastoid
(SCM) muscle is palpated, and a curvilinear incision
is marked 1 cm below the mastoid and extending
inferiorly in a curvilinear fashion medially to join
with a skinfold two fingerbreadths above the
sternoclavicular joint.
• Venous structures encountered in a transverse direction
during this dissection include the retromandibular vein
draining into the external jugular vein and the
transverse facial vein draining into the internal jugular
vein (IJV).
• Dissection is maintained in a cranial-to-caudal direction
to expose the carotid bifurcation, ECA, and ICA.
• common carotid artery (CCA) is isolated first, and
umbilical tape is placed around the vessel proximal to
the plaque and clamped inferiorly, The umbilical tape is
also placed around the distal ICA past the plaque and
clamped.
• Once this is achieved, 5000 IU of heparin is administered
by the anesthesiologist intravenously. Approximately 3
minutes is taken to allow the heparin to be systemically
distributed prior to placing the clamps.
Complications of CEA
Cerebral hyperperfusion syndrome (CHS)
• lack of ischemia on radiography with objective
neurological findings.
• presents within 2 to 12 hours with sensorimotor
deficits, seizures, headaches, or altered mental
status; the incidence has been reported as between
0.2% and 18.9%.
• should be managed with normal to low systolic
blood pressure.
• postoperative neck hematoma- The goal in this
situation shouldnbe a rapid return to the operating
room, a controlled intubation, and expeditious
surgical exploration
• Cranial nerve injuries are the most common
complications associated with CEA. Injuries to the
hypoglossal, vagus, or facial nerve have been
reported in 3% to 23%. typically transient, resolving
in 3 to 6 months.
• Restenosis, frequently defined by a greater than
50% reduction in ICA luminal diameter as
determined by duplex ultrasound criteria. 10%, 3%,
and 2% risk of restenosis at 1, 2, and 3 years,
respectively, following CEA.
CONCLUSION
• Current literature is supportive of optimal medical
therapy, consisting of antiplatelet agents,
anticholesterol medications, and blood pressure
control, for all patients with carotid stenosis.
• CEA is a safe and effective treatment for selected
patients with asymptomatic and symptomatic stenosis;
however, the benefit is invariably greater in patients
with symptomatic disease.
• CAS continues to be refined. It is complementary to
CEA, particularly for those who are trained and
experienced in both techniques.
• With advancement in technology and experienceone
can expect the indications and applications of CAS to
expand.

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Carotid Occlusive Disease.pptx

  • 1. Carotid Occlusive Disease Presented By: Dr. Rahul Jain SR-2 Neurosurgery Moderated by: Dr V. C. Jha Dr Nitish Kumar Dr Gaurav Verma
  • 2. Introduction • Ischemic stroke remains a leading cause of death and disability in the developed world. • Atherosclerotic plaques of the cervical carotid artery are relatively common and are a source of emboli that place patients at risk of ischemic stroke. • Atherosclerosis is a disease of the arterial intima that causes progressive narrowing of the vessel lumen.
  • 3. • The carotid bifurcation creates shear stress related to turbulent, high-pressure arterial blood flow. Turbulence causes endothelial damage and a focal, recurrent inflammatory cascade. • Focal, recurrent inflammatory cascade leads to progressive deposition of atheromatous plaque and gradual com-promise of the integrity of the carotid arterial lumen. • Transient ischemic attacks (TIAs) and strokes occur when a portion of the plaque ruptures, migrates distally into the intracranial circulation as thromboembolism, and causes a focal arterial occlusion or a broader, territorial infarct.
  • 4. • clinical presentations of stroke or TIA are variable • 10%–15% of those who suffer a stroke have a history of sentinel TIA • Amaurosis fugax is defined as acute, atraumatic monocular visual loss, caused by retinal microemboli or marginal perfusion related to diminished reti-nal blood flow
  • 5. • For symptomatic 70%–99% carotid stenosis, several studies have defined the cumulative risk of ipsilateral ischemic stroke as 20%–26% within 2–3 years • Middle cerebral artery is the commonest site of thromboembolic stroke. manifestations include contralateral weakness and hemisensory loss. Aphasia are associated with lesions of the dominant hemisphere, hemineglect and apraxic syndromes are associated with the nondominant middle cerebral artery . • Anterior cerebral artery infarctions involve primarily contralateral lower extremity weakness, poorly defined cognitive/psychiatric disturbances.
  • 6. • Anterior choroidal artery supplies the posterior limb of the internal capsule, the posterolateral thalamus, and the lateral geniculate body; infarctions present clinically as a triad of contralateral hemiparesis, hemisensory loss, and homonymous hemianopsia
  • 7. Asymptomatic Extracranial Carotid Ds • most commonly diagnosed by carotid ultrasound. • Indications for non-invasive carotid evaluation may include • screening • further investigation of a carotid bruit, or • a thorough evaluation related to a previous stroke or TIA. • Current guidelines advise against routine screening duplex sonograms for asymptomatic carotid stenosis, because the incidence of clinically significant internal carotid artery (ICA) stenosis ≥50% is <5% in the general population.
  • 8. • In a prospective study of 339 asymptomatic patients followed with serial Doppler examinations over 29 months, 2% of patients with 50%–80% stenosis, 8.3% of those with 80%–99% stenosis, and 12.2% of those with carotid occlusion experienced strokes.# • Well-designed clinical trials involving asymptomatic patients with 60%–99% carotid stenosis revealed an 11% stroke risk at 5 years in the medical cohorts. North American Symptomatic Carotid Endarterectomy Trial (NASCET) defined the 5-year stroke risk in the contralateral asymptomatic Territory as # Hennerici M, Hulsbomer HB, Hefter H, et al. Natural history of asymptomatic extracranial arterial disease. Results of a long-term prospective study. Brain. 1987;110:777–791. 5 year stroke risk Degree of stenosis 4.6% No disease 7.8% Stenosis <50% 12.9% Stenosis 50-59% 14.8% Stenosis 60-74% 18.5% Stenosis 75-94% 14.7% Stenosis 95-99% 9.4% occlusion
  • 9. Symptomatic Carotid Disease • Patients with carotid plaque ipsilateral to a previous TIA or stroke have a higher risk of recurrent ischemic event than their asymptomatic counterparts. 5 year stroke risk Degree of stenosis Rate of Ipsilateral stroke Rate of Ipsilateral major stroke NASCET NASCET ECST <50% 18.7% 4.7% 6% 50-69% 22.2% 7.2% 10.6% 70-99% 26% 13% 17.4% • Data from the medically treated arms of NASCET and ECST provide stroke rates ipsilateral to the symptomatic carotid stenosis.
  • 10. • One must be cautious in comparing data across these two trials, however, because the degree of carotid stenosis was measured differently and the duration of follow-up was incongruous. • The mean follow-up was 2 years in the severe stenosis NASCET group, 5 years in the mild and moderate stenosis NASCET groups, and approximately 6 years in ECST.
  • 11. MEDICAL MANAGEMENT • Treatment of carotid stenosis includes risk factor modification, pharmacologic therapy, and surgery in some cases. Risk Factor Treatment Hypertension (HTN) • increases the relative risk of stroke by 3- to 5-fold. • most prevalent modifiable risk factor. • One clinical trial indicated that a reduction in diastolic blood pressure (DBP) as little as 5–6 mm Hg may decrease risk of stroke by 42%. • Lifestyle modifications include salt restriction and other dietary changes, aerobic exercise, and weight loss.
  • 12. Diabetes Mellitus • increase the risk of stroke through acceleration of large- artery atherosclerosis, adverse effects on plasma lipoprotein levels, and promotion of plaque formation through hyperinsulinemia. • Authorities agree that the optimal fasting serum glucose level is <126 mg/dL. The HbA1c value should be <6.5%. Dyslipidemia • statin therapy prevents carotid plaque progression and reduces the incidence of transition from asymptomatic to symptomatic carotid stenosis • initial retrospective studies demonstrated improved outcomes with perioperative statin therapy only among the symptomatic population, recent prospective trials have classified failure to prescribe a perioperative statin as an independent risk factor for decreased survival, even among asymptomatic patients.
  • 13. • Two meta-analyses evaluating pooled outcomes data on the effectiveness of statins in patients with coronary artery disease showed a 27%–32% reduction in stroke rate. • All patients with carotid disease should be treated with a statin, and the recommended low-density lipoprotein level is <100 mg/dL. Alcohol Consumption, Smoking, Obesity • Obesity is associated with HTN and DM and should be addressed as one component of a comprehensive approach to risk factor treatment. • Heavy alcohol consumption, cigarette smoking, and obesity are modifiable risk factors that increase an individual’s risk.
  • 14. Antiplatelet Therapy 1. Aspirin • Irreversibly inhibiting platelet cyclooxygenase, which prevents the formation of thromboxane A2, both a potent vasoconstrictor and an inducer of platelet aggregation. • In healthy individuals, a single aspirin results in 98% inhibition of thromboxane A2 production within 1 hour. • overview of trials of antiplatelet therapy in patients with a history of TIA or stroke showed a 25% reduction in the risk of nonfatal stroke, nonfatal myocardial infarction (MI), and death from vascular causes independent of age, sex, and other risk factors.
  • 15. • best dose remains controversial, doses ranging from 30 to 1500 mg/day. • In the ASA and Carotid Endarterectomy (ACE) trial, 2804 patients who had undergone CEA were randomized to compare the benefits of low-dose (81–325 mg/day) to high-dose (650–1300 mg/day) aspirin. Risk of stroke, MI, or death at 3 months was 6.2% in the low-dose aspirin group compared with 8.4% in the high-dose group
  • 16. 2. Adenosine Diphosphate Receptor Inhibitors • Ticlopidine - significant hematologic side effects limited its widespread use. • Clopidogrel - more benign side effect profile. • study enrolling more than 19,000 patients with atherosclerotic disease manifesting as ischemic stroke, MI, or symptomatic peripheral arterial disease, 75 mg/day clopidogrel was found to be more effective than 325 mg aspirin in reducing risk of ischemic stroke, MI, and vascular death. • 30% of patients may be considered clopidogrel resistant, and more potent ADP receptor inhibitors such as ticagrelor or prasugrel may be needed
  • 17. Surgical Management • In the early 1990s NASCET and ECST established carotid endarterectomy (CEA) as highly effective treatment symptomatic carotid stenosis >= 70%. • Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial and the Carotid Revascularization Endarterectomy versus Stent Trial (CREST) carotid artery stenting with the use of a distal protection device should be the preferred operation for high- risk patients who meet the surgical criteria outlined in NASCET.
  • 18. • However, inclusion of mild MI in the primary outcome in CREST obscured the superiority of CEA for stroke prevention. • A Cochrane review of randomized trial data in 2012 supported CEA as the first-choice strategy when surgery is indicated. • CEA has been validated by multicentre randomized, prospective clinical trials across at least two generations of carotid surgeons as superior to medical management alone for symptomatic patients with >50% stenosis and asymptomatic patients with >60% stenosis.
  • 19. Carotid Endarterectomy • first true CEA was performed by Michael E. DeBakey in 1953. • Carotid Doppler ultrasonography provides a quick, relatively cost-effective, and safe initial diagnostic study, carries a sensitivity of 72% to 96% and a specificity of 61% to 100% for high-grade stenosis. • in the setting of significant calcification Doppler may overestimate the degree of stenosis – CTA/MRA • CTA with a sensitivity and specificity of 77% and 95%, respectively, provides detailed information regarding plaque-associated calcifications and the relationship of the ICA bifurcation to the angle of the mandible, which is used in determining candidacy for an endarterectomy as opposed to endovascular therapies.
  • 20. • MRA can provide value in detecting more detailed characteristics of the atherosclerotic plaque, including lipid content and intraplaque hemorrhage. • When there remains a discrepancy between ultrasound and CTA or MRA, cerebral catheter angiography may be performed, which carries a nearly 100% sensitivity and specificity. • Currently there is no recommendation for widespread mass screening for carotid occlusive disease in asymptomatic patients. • Recently, the prevalence of moderate (≥50% to 69%) stenosis was found in 4.8% of men and 2.2% of women younger than 70 years.
  • 21. SURGICAL INDICATIONS AND DECISION MAKING Symptomatic Patients • The results of the NASCET and the ECST had initially provided level I evidence recommending surgical intervention for symptomatic (amaurosis fugax, hemispheric TIA, nondisabling stroke) patients with greater than 70% stenosis on noninvasive imaging or greater than 50% stenosis as demonstrated on catheter angiography. • In the analysis of Brott and colleagues pooled analysis of the four largest clinical trials since the landmark NASCET and ECST—the EVA-3S study, the SPACE study, the ICSS, and the CREST- compared the efficacy of CAS versus CEA in symptomatic patients.
  • 22. • There were 129 periprocedural and 55 postprocedural strokes in the CEA arm, whereas there were 206 and 57, respectively, in the CAS group. • The preprocedural 120-day stroke and death was 3.2% (unchanged from previous trials), and beyond 120 days occurrence of stroke or death was infrequent, and rates were similar between CAS and CEA. • Long-term outcomes were similar for CEA (0.60%) and CAS (0.64%); therefore, longterm outcomes of periprocedural and postprocedural strokes still favor CEA, underlining importance of improving CAS.
  • 23. • With the assumption of a perioperative stroke and death rate less than 6%, recommend performing an early (within 2 weeks) CEA in all patients with symptomatic ICA stenosis greater than 70% and for older (>75 years), male patients with moderate grade stenosis of 50% to 69%. • Female patients with moderate stenosis should be evaluated on an individual basis, and CEA is contraindicated in patients with less than 50% stenosis.
  • 24. Asymptomatic Patients • evidence is not nearly as convincing for asymptomatic patients as it is for symptomatic patients. • Identifying specific factors that would place asymptomatic patients at greater risk of stroke. • High rates of radiographic progression of carotid stenosis in asymptomatic patients have also been shown to increase the risk of ipsilateral neurological events. • Assuming a perioperative risk of less than 3%, CEA can be recommended for asymptomatic men below age 75 with 60% to 99% stenosis.
  • 25. Contralateral Stenosis • The presence of a complete contralateral ICA occlusion increases both the natural history risk of stroke and perioperative morbidity. • Perform an endarterectomy on the symptomatic side first, or the side with a greater degree of stenosis or concerning plaque characteristics in the case of asymptomatic disease.
  • 26. Carotid Artery Angioplasty and Stenting • CAS is a principal surgical tool in the management of carotid atherosclerotic disease. • Major impetus for the advancement of CAS came with the publication of the results of SAPPHIRE (stenting and angioplasty with protectionin patients at high risk for endarterectomy) trial in 2004, which demonstrated the non-inferiority of CAS compared with CEA in patients classified as being at high risk for CEA, with significantly fewer CAS patients requiring revascularization within 1 year of initial treatment.
  • 27. CAROTID ARTERY STENTING TRIALS AND REGISTRIES • CAVATAS (Carotid and Vertebral Artery Transluminal Angioplasty Study)demonstrated no statistically significant difference between endovascular and surgical treatment in the rates of dis abling stroke or death within 30 days (6.4% CAS versus 5.9% CEA) and no significant difference in 3- year ipsilateral stroke rates. • The Wallstent trial was the first multicenter randomized trial designed from its inception to evaluate CEA and CAS equivalence. The trial was halted by the Data Safety and Monitoring Committee after an interim analysis demonstrated worse outcomes for the CAS group. Distal protection devices were not used in the Wallstent trial.
  • 28. • Carotid Revascularization Using Endarterectomy or Stenting Systems (CaRESS) multicenter, nonrandomized, prospective study. No statistically significant difference between 30-day and 1-year death or stroke rates was found between CAS and CEA. • A major criticism of CaRESS, as opposed to randomized trials, is that the low stroke and death rates may be attributable to the ability of the treating physician to consider patient-specific factors and successfully assign each patient to the safest therapy. • SAPPHIRE study established CAS as a treatment option for high-risk patients (clinically significant cardiac disease, severe pulmonary disease, contralateral carotid artery occlusion, contralateral laryngeal nerve palsy, previous radical neck surgery or radiation, recurrent stenosis after CEA, or age >80 years).
  • 29. • Stent-Supported Percutaneous Angioplasty of the Carotid Artery Versus Endarterectomy (SPACE) trial was undertaken to establish noninferiority for CAS compared with CEA in patients with symptoms but without high-risk features. The 30-day rates of ipsilateral stroke or death were 6.84% for CAS and 6.34% for CEA (P = .09). • Despite the results of CREST and ACT I demonstrating noninferiority of CAS compared with CEA in patients at low risk for adverse events with CEA in terms of stroke, MI, and death, the CMS continues to indicate CAS only for individuals at high risk for CEA.
  • 30.
  • 31. INDICATIONS FOR CAS • current indications for CAS are principally based on FDA and CMS approval for patients considered at high risk for CEA. • Therefore CAS is presently approved for patients with carotid stenosis exceeding 70% and who are considered at high risk for CEA.
  • 32.
  • 33.
  • 34. Carotid artery stenting procedure 5-French diagnostic catheter is advanced into the external carotid artery of the affected side A 6- to 10-French guide is then brought into the common carotid artery over the exchange wire
  • 35. The lesion is then crossed with a 0.014- inch microwire (usually part of a distal embolic protection system). Once the lesion is crossed, a distal embolic protection device is then delivered through a microcatheter across the lesion and, as the inset indicates, unsheathed distal to the lesion. The stent delivery system is then retrieved, and an appropriately sized postdilation balloon is advanced over the wire and inflated briefly to its nominal pressure (left). After this, the balloon is retrieved, and an angiogram is performed to confirm satisfactory revascularization. Once success is confirmed, the distal embolic protection device is recaptured and withdrawn
  • 36. SURGICAL TECHNIQUE for CEA • Patients are positioned supine with the arms tucked at the sides and the head on a soft doughnut-shaped headrest and slightly extended and turned 15 degrees contralaterally. • The anteriorborder of the sternocleidomastoid (SCM) muscle is palpated, and a curvilinear incision is marked 1 cm below the mastoid and extending inferiorly in a curvilinear fashion medially to join with a skinfold two fingerbreadths above the sternoclavicular joint.
  • 37. • Venous structures encountered in a transverse direction during this dissection include the retromandibular vein draining into the external jugular vein and the transverse facial vein draining into the internal jugular vein (IJV). • Dissection is maintained in a cranial-to-caudal direction to expose the carotid bifurcation, ECA, and ICA. • common carotid artery (CCA) is isolated first, and umbilical tape is placed around the vessel proximal to the plaque and clamped inferiorly, The umbilical tape is also placed around the distal ICA past the plaque and clamped. • Once this is achieved, 5000 IU of heparin is administered by the anesthesiologist intravenously. Approximately 3 minutes is taken to allow the heparin to be systemically distributed prior to placing the clamps.
  • 38.
  • 39.
  • 40.
  • 41. Complications of CEA Cerebral hyperperfusion syndrome (CHS) • lack of ischemia on radiography with objective neurological findings. • presents within 2 to 12 hours with sensorimotor deficits, seizures, headaches, or altered mental status; the incidence has been reported as between 0.2% and 18.9%. • should be managed with normal to low systolic blood pressure.
  • 42. • postoperative neck hematoma- The goal in this situation shouldnbe a rapid return to the operating room, a controlled intubation, and expeditious surgical exploration • Cranial nerve injuries are the most common complications associated with CEA. Injuries to the hypoglossal, vagus, or facial nerve have been reported in 3% to 23%. typically transient, resolving in 3 to 6 months. • Restenosis, frequently defined by a greater than 50% reduction in ICA luminal diameter as determined by duplex ultrasound criteria. 10%, 3%, and 2% risk of restenosis at 1, 2, and 3 years, respectively, following CEA.
  • 43. CONCLUSION • Current literature is supportive of optimal medical therapy, consisting of antiplatelet agents, anticholesterol medications, and blood pressure control, for all patients with carotid stenosis. • CEA is a safe and effective treatment for selected patients with asymptomatic and symptomatic stenosis; however, the benefit is invariably greater in patients with symptomatic disease. • CAS continues to be refined. It is complementary to CEA, particularly for those who are trained and experienced in both techniques. • With advancement in technology and experienceone can expect the indications and applications of CAS to expand.