CAROTID ARTERY DISEASE

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

Risk Factors Nontreatable

Age

Ethnicity

Gender

Family History

Genetics

Risk FactorsTreatable

Hypertension

TIA’s

Previous CVA’s

Asx Bruit or Stenosis

Cardiac Disease

Aortic Arch atheromatosis

Diabetes Mellitus

Cigarette Smoking

↑fibrinogen, ↑homocysteine ↑anticardiolipin

Oral contraceptives

Obesity

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.

Anatomy

Inominate branches to form R subclavian and R common carotid.

10% of population L common comes of inominate.

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.

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.

Anatomy

Internals branch into anterior cerebral and middle cerebral arteriesThe 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.

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.

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.

Anatomy

Vertebral gives off branches to muscles of neck…if 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 internalFinally branches of the L and R external can anastamose freely across the face.

PathophysiologyComplication of atherosclerosis (most common)High shear stress (bifurcations)Intimal injuryCarotid bulb plaquesAneurysms, kinks, coiling….FMD (thickened,beaded), Takayashu (women, branches of aorta) arteritis, Temporal arteritis (elderly, blindness).Trauma

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.

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.

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).

Plaque Composition

Fibroblast proliferation

Lipid accumulation

Calcification

Ulceration

Sub-intimal hemorrhage

Thrombosis

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.

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

Evaluation

Physical Exam

Duplex (most accurate in >50% stenosis)

MRA

Angiography (gold standard, but risks)

Duplex

Excellent screen for neurologic sympt.peak sys. Velocity > 220cm/sec

end dias. Velocity > 80cm/sec

post stenotic turbulence

Less reliable in anatomic variants

Operator dependant

Carotid Angiography

Gold Standard Remains the most definitive tool for decision to operate Complications ~ 1-4%

PseudoaneurysmStrokeDissection

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.

Asymptomatic Disease

Only 10% of stroke patients have had a TIA prior.

Asymptomatic bruits are present in 5% of population>50

Bruits are not diagnostic of significant stenosis. (only 23% have >50% stenosis)

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%.

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.

Medical Treatment

Control risk factors

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

Medical TreatmentNo 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 diseaseIn 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.

Symptomatic Disease

Degree of ICA stenosis is most important predictor of CVASeverity of stenosis is proportional to Risk of Stroke

Definite benefit of surgery in symptomatic pts with > 70% stenosis is established in three major studies (NASCET, ECST, VATCE)

NASCET north american symptomatic carotid endarterectomy trial

Double armed, prospective trial Medical vs. Surgical therapyPt.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%

NASCET (cont.)

Risk of major CVA was ↓ by 80% at 2yr follow-up.

CEA was beneficial in symptomatic pts with occlusion of contralateral carotid.

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%

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%

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

Asymptomatic Disease

Prevalent in the elderly population

Asymptomatic CAS >70% rare

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

<75% ~ 1.3%/yr.

>75% ~ 10.5%/yr.

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

CASANOVA (cont)

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

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.

Asymptomatic Trials: Summary

Asymptomatic patients with CAS > 80% will benefit from surgery assuming the surgeon has complication rate <3%

Some investigators refrain from recommending surgery in any asymptomatic patient.

Endovascular TreatmentProblem of embolization from angioplastyUse of cerebral embolic protection devices4 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