CAROTID ARTERY DISEASE

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CAROTID ARTERY DISEASE

• Vic Vernenkar, D.O.
• St. Barnabas Hospital
• Dept. of Surgery

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Epidemiology

• 3rd most common cause of death in the US
• Most common cause of long term disability
• 500,000 CVAs annually
• Contributes 200,000 deaths annually
• Of those that survive, 2/3 have disability, 1/3
  require hospitalization for it.
• 16 trillion a year in costs

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Risk Factors Nontreatable

• Age
• Ethnicity
• Gender
• Family History
• Genetics

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Risk FactorsTreatable

• Hypertension
• TIAs
• Previous CVAs
• Asx Bruit or Stenosis
• Cardiac Disease
• Aortic Arch atheromatosis

• Diabetes Mellitus
• Cigarette Smoking
• ?fibrinogen, ?homocysteine ?anticardiolipin
• Oral contraceptives
• Obesity

5
Anatomy

• Brain 2 of body weight but 17 of CO and 20 of
  O2 supply.so neural tissue can become necrotic
  within minutes
• Branches of aortic arch inominate
  (Brachiocephalic), L common carotid and L
  subclavian.

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Anatomy

• Inominate branches to form R subclavian and R
  common carotid.
• 10 of population L common comes of inominate.

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Anatomy

• Brain supplied by 2 internals and 2 vertebrals.
  The internal supply 80-90 of total blood flow.
• The common carotids bifurcate at angle of
  mandible into external and internal.
• Branches if external are lingual, ascending
  pharyngeal, superior thyroid, occipital,
  posterior auricular. The terminal branches are
  int. maxillary and superficial temporal a.

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Anatomy

• Extensive collaterals between external and
  vertebrals in case of occlusion
• Periorbital collaterals connect through
  ophthalmic artery to internal carotid in case of
  occlusion in neck.
• Extensive side to side collaterals between L and
  R externals and L and R vertebrals.

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Anatomy

• Internals branch into anterior cerebral and
  middle cerebral arteries
• The L and R middle cerebrals connect at the
  circle of Willis via anterior and posterior
  communicating arteries.
• 15 have no connections between ant and post
  cerebral circulations, 35 lack connection
  between the two hemispheres.

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Anatomy

• Vertebrals arise from first portion of subclavian
  artery and enter 6th cervical vertebra and ascend
  in foramen. Unite to form Basilar artery. The
  Basilar terminates as L and R posterior cerebral
  arteries ? posterior communicating arteries of
  the circle of Willis.

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Anatomy

• Branches of external carotid can anastamose with
  orbital arteries? supply internal carotid artery
  in case of proximal occlusion
• Collateral between external and ophthalmic are
  most important of these.

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Anatomy

• Vertebral gives off branches to muscles of
  neckif proximal vertebral gets occluded, the
  external can supply the distal vertebral via
  these branches.
• If common occluded, blood can go from vertebral
  to external branches to internal
• Finally branches of the L and R external can
  anastamose freely across the face.

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Pathophysiology

• Complication of atherosclerosis (most common)
• High shear stress (bifurcations)
• Intimal injury
• Carotid bulb plaques
• Aneurysms, kinks, coiling.
• FMD (thickened,beaded), Takayashu (women,
  branches of aorta) arteritis, Temporal arteritis
  (elderly, blindness).
• Trauma

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Atherosclerosis

• Locations of turbulence, like bifurcations
• The common carotid is most common spot in the
  cerebral circulation
• Occur along the outer wall of bifurcation, and
  only proximal portion of external.

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Atherosclerosis

• At bifurcation you get separation of flow,
  disruption of laminar flow, flow stasis,
  prolonged residence time, shear stress
• Grossly the plaque is thickest at the
  bifurcation, extending 2cm into distal internal
  carotid.

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Atherosclerosis

• The plaque occupies the media and intima, sparing
  the outer media and adventitia.
• The plaque tapers from the media into the normal
  intima.
• Mature plaques are characterized by a
  heterogeneous core and fibrous cap. Disruption of
  the cap leads to embolization and thrombosis.
  Also exposes the non-endothelized intima to
  platelets (ulcer).

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Plaque Composition

• Fibroblast proliferation
• Lipid accumulation
• Calcification
• Ulceration
• Sub-intimal hemorrhage
• Thrombosis

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Clinical Presentation

• TIA resolves within 24h. Can present as a
  transient hemispheric event or monocular
  blindness (amaurosis fugax). A hemispheric attack
  presents with contralateral combined sensory and
  motor deficit or purely motor or purely sensory
  deficit.

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Clinical Presentation

• When ischemia occurs in the posterior
  circulation, it causes vertebrobasilar
  insufficiency presenting as vertigo, drop
  attacks, binocular vision loss, dysarthria,
  dysphagia, incoordination.
• A stroke lasts more than 24h. Most are a result
  of emboli to branches of middle cerebral artery

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Evaluation

• Physical Exam
• Duplex (most accurate in gt50 stenosis)
• MRA
• Angiography (gold standard, but risks)

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Duplex

• Excellent screen for neurologic sympt.
• peak sys. Velocity gt 220cm/sec
• end dias. Velocity gt 80cm/sec
• post stenotic turbulence
• Less reliable in anatomic variants
• Operator dependant

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Carotid Angiography

• Gold Standard
• Remains the most definitive tool for decision to
  operate
• Complications 1-4
• Pseudoaneurysm
• Stroke
• Dissection

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Natural History- Symptomatic Dz

• Cumulative risk for stroke at 5 years after a TIA
  is 30-50.
• 1/3 patients die within 5y of TIA, usually of
  CAD.
• Risk for stroke following TIA 10-30 in first
  year, 6 risk subsequent years.
• After stroke, a 20-30 mortality, risk of
  recurrent is 5-40, with 30 of these fatal.

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Asymptomatic Disease

• Only 10 of stroke patients have had a TIA prior.
• Asymptomatic bruits are present in 5 of
  populationgt50
• Bruits are not diagnostic of significant
  stenosis. (only 23 have gt50 stenosis)

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Asymptomatic Disease

• Risk of stroke is proportional to degree of
  stenosis (greatest over 80 stenosis)
• For patients with 75-80 stenosis, risk of stroke
  18-46.

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Asymptomatic Disease

• Risk of stroke elevated in patients undergoing
  major surgical procedures such as CABG, vascular
  surgery.
• Stroke is not increased with unilateral
  asymptomatic high grade carotid disease during
  CABG, but it is in bilateral high grade stenoses.

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Medical Treatment

• Control risk factors
• No drug therapy has been shown to reduce the risk
  of stroke in asymptomatic disease.

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Medical Treatment

• No study has provided definitive evidence that
  systemic anticoagulation reduces the risk of
  stroke in patients who have had a stroke or TIA.
• ASA has been shown to decrease the morbidity and
  mortality from symptomatic disease
• In patients with TIA or stroke, ASA demonstrated
  a 22 risk reduction in recurrent strokes, TIA,
  MI, or vascular death, compared with controls.
• Plavix and ASA offers no added benefit.

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Symptomatic Disease

• Degree of ICA stenosis is most important
  predictor of CVA
• Severity of stenosis is proportional to Risk of
  Stroke
• Definite benefit of surgery in symptomatic pts
  with gt 70 stenosis is established in three major
  studies (NASCET, ECST, VATCE)

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NASCET north american symptomatic carotid
endarterectomy trial

• Double armed, prospective trial
• Medical vs. Surgical therapy
• Pt.s developing sx.s during the trial were
  operated and excluded
• 5 yr trial terminated at two years due to end
  point
• Surgery 9, Medical 26

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NASCET (cont.)

• Risk of major CVA was ? by 80 at 2yr follow-up.
• CEA was beneficial in symptomatic pts with
  occlusion of contralateral carotid.

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ECST european carotid surgery trial

• Double armed prospective trial, 3y f/u
• Medical vs. Surgical therapy
• 70-99 stenosis
• 778 pts with carotid distribution CVA, TIA or
  retinal infarction
• Surgery 12.3, medical 22

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VATCE veterans affairs trial of carotid
endarterectomy

• Terminated early due to early endpoints in NASCET
  and ECST trials.
• Also showed Carotid Endarterectomy to be
  beneficial in symptomatic patients.
• Surgery 7, medical 20

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Symptomatic Trials Summary

• 0-29 CAS- medical therapy with anti-aggregate
  platelet therapy
• 30-69 CAS- medical therapy probably desirable in
  most patients
• 50-69- CAS- surgery provides modest benefit in
  hemispheric ischemia
• 70 CAS- surgical therapy indicated

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Asymptomatic Disease

• Prevalent in the elderly population
• Asymptomatic CAS gt70 rare
• Asymptomatic bruit 1.5 risk of CVA per year X 5
  yr.s
• lt75 1.3/yr.
• gt75 10.5/yr.

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CASANOVA carotid artery surgery asymptomatic
narrowing operation vs. aspirin

• Asymptomatic pt.s with CAS 50-90
• Prospective double armed trial
• Medical therapy (330 mg ASA QD 75mg
  dypyridamole TID)
• Surgical therapy- CEA

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CASANOVA (cont)

• No statistically significant difference in
  medical vs. surgically treated groups.

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ACAS asymptomatic carotid atherosclerosis study

• CEA, ASA and medical risk factor mgmt in patients
  lt 80y/o with CASgt60
• Risk of CVA reduced over 5 yrs by 5.9
• Absolute yearly reduction of 1
• Benefit negated by many factors.

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Asymptomatic Trials Summary

• Asymptomatic patients with CAS gt 80 will benefit
  from surgery assuming the surgeon has
  complication rate lt3
• Some investigators refrain from recommending
  surgery in any asymptomatic patient.

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Endovascular Treatment

• Problem of embolization from angioplasty
• Use of cerebral embolic protection devices
• 4 prospective randomized trials comparing endo
  and surgery. 3 were in adequate risk, 1 in high
  risk only. CAVATAS, Wallstent, Sapphire (only one
  with protection device), the other was stopped
  5/7 stroked after stenting!
• Long-term efficacy and durability is unknown.
• At present limited to high risk only