carotid artery disease-1

7/27/2019 Carotid Artery Disease-1

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CAROTID ARTERY

DISEASE

Vic Vernenkar, D.O.

St. Barnabas HospitalDept. 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 annuallyContributes 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

GenderFamily History

Genetics


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Risk Factors

Treatable

Hypertension

TIAs

Previous CVAsAsx Bruit or Stenosis

Cardiac Disease

Aortic Arch

atheromatosis

Diabetes Mellitus

Cigarette Smoking

fibrinogen,homocysteine

anticardiolipin

Oral contraceptives

Obesity


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Anatomy

Brain 2% of body weight but 17% of CO

and 20% of O2 supply.so neural tissue

can become necrotic within minutesBranches 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 ofinominate.


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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. maxillaryand superficial temporal a.


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Anatomy

Extensive collaterals between external and

vertebrals in case of occlusion

Periorbital collaterals connect throughophthalmic artery to internal carotid in case

of occlusion in neck.

Extensive side to side collaterals between Land R externals and L and R vertebrals.


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Anatomy

Internals branch into anterior cerebral andmiddle cerebral arteries

The L and R middle cerebrals connect at thecircle of Willis via anterior and posteriorcommunicating arteries.

15% have no connections between ant and

post cerebral circulations, 35% lackconnection 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 toform 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 occlusionCollateral between external and ophthalmic

are most important of these.


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Anatomy

Vertebral gives off branches to muscles ofneckif proximal vertebral gets occluded,the external can supply the distal vertebral

via these branches.

If common occluded, blood can go fromvertebral to external branches to internal

Finally branches of the L and R external cananastamose 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 circulationOccur 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 stressGrossly 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

CalcificationUlceration

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 hemisphericattack 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, dropattacks, 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 >50% stenosis)

MRAAngiography (gold standard, but risks)


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Duplex

Excellent screen for neurologic sympt.

peak sys. Velocity > 220cm/sec

end dias. Velocity > 80cm/secpost 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 operateComplications ~ 1-4%

Pseudoaneurysm

StrokeDissection


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Natural History- Symptomatic Dz

Cumulative risk for stroke at 5 years after aTIA is 30-50%.

1/3 patients die within 5y of TIA, usually ofCAD.

Risk for stroke following TIA 10-30% infirst year, 6% risk subsequent years.

After stroke, a 20-30% mortality, risk ofrecurrent 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% ofpopulation>50

Bruits are not diagnostic of significant

stenosis. (only 23% have >50% stenosis)


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Risk of stroke is proportional to degree of

stenosis (greatest over 80% stenosis)

For patients with 75-80% stenosis, risk ofstroke 18-46%.


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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 thatsystemic anticoagulation reduces the risk of strokein patients who have had a stroke or TIA.

ASA has been shown to decrease the morbidityand mortality from symptomatic disease

In patients with TIA or stroke, ASA demonstrateda 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 importantpredictor of CVA

Severity of stenosis is proportional to Riskof Stroke

Definite benefit ofsurgery in symptomaticpts with > 70% stenosis is established in

three majorstudies (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 wereoperated 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 ptswith 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 % stenosis778 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 bebeneficial 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 probablydesirable in most patients*

50-69%- CAS- surgery provides modest

benefit in hemispheric ischemia 70% CAS- surgical therapy indicated


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Prevalent in the elderly population

Asymptomatic CAS >70% rare

Asymptomatic bruit 1.5% risk of CVA peryear X 5 yr.s

75% ~ 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 + 75mgdypyridamole 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 < 80y/o with CAS>60%

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 > 80%

will benefit from surgery assuming the

surgeon has complication rate


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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 riskonly. CAVATAS, Wallstent, Sapphire (only onewith protection device), the other was stopped 5/7stroked after stenting!

Long-term efficacy and durability is unknown.At present limited to high risk only

carotid artery disease-1

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