carotid, subclavian, and vertebrobasilar disease kelley hodgkiss-harlow 9/30/2009

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Carotid, Subclavian, Carotid, Subclavian, and Vertebrobasilar and Vertebrobasilar Disease Disease Kelley Hodgkiss-Harlow Kelley Hodgkiss-Harlow 9/30/2009 9/30/2009

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Page 1: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Carotid, Subclavian, Carotid, Subclavian, and Vertebrobasilar and Vertebrobasilar DiseaseDisease

Kelley Hodgkiss-HarlowKelley Hodgkiss-Harlow

9/30/20099/30/2009

Page 2: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Carotid Disease: Carotid Disease: HistoryHistory

1875—Gowers case report of R 1875—Gowers case report of R hemiplegia/L blindnesshemiplegia/L blindness

1914—Hunt recognizes syndrome 1914—Hunt recognizes syndrome of TIAs as prodrome to strokeof TIAs as prodrome to stroke

1937—Moniz: Arteriography used 1937—Moniz: Arteriography used to diagnose carotid artery to diagnose carotid artery occlusionocclusion

1954—Eastcott publishes first 1954—Eastcott publishes first report of successful CEAreport of successful CEA

Page 3: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

PathologyPathology

Atherosclerosis: 90%Atherosclerosis: 90%– Deposition fatDeposition fat

intimaintimafatty plaque with fatty plaque with intermittent intermittent hemorrhage/ulcerationhemorrhage/ulceration

– Bifurcation Bifurcation predominance-secondary predominance-secondary to arterial geometry, to arterial geometry, velocity profile, and wall velocity profile, and wall shear stressshear stress

Other 10%:Other 10%:– FMDFMD– MechanicalMechanical– InflammatoryInflammatory– Radiation Radiation

Page 4: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

StrokeStroke

33rdrd leading cause of death in USA leading cause of death in USA Age is risk factor:Age is risk factor:

– Male:female ratio about 1.5:1Male:female ratio about 1.5:1– >65 y/o incidence 150-200/100,000>65 y/o incidence 150-200/100,000

High rate of recurrence if no intervention:High rate of recurrence if no intervention:– 10-20% within one year, 20-42% within 5 10-20% within one year, 20-42% within 5

yearsyears– Roughly accepted 10%/yr recurrence riskRoughly accepted 10%/yr recurrence risk

Majority recur within one yearMajority recur within one year High mortality rate with recurrenceHigh mortality rate with recurrence

– 35-65%35-65%

Page 5: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Stroke distributionStroke distribution

MCA: contralateral sensory/motor loss, head and MCA: contralateral sensory/motor loss, head and eye deviation toward infarcted sideeye deviation toward infarcted side– left—aphasia/neuropsych symptomsleft—aphasia/neuropsych symptoms

ACA: rare, contralateral lower extremity ACA: rare, contralateral lower extremity weakness/sensory, urinary incont, apathy, weakness/sensory, urinary incont, apathy, mutism, gait apraxiamutism, gait apraxia

PCA: mesencephalon, thalamus, occiptal and PCA: mesencephalon, thalamus, occiptal and temporal lobes—homonymous visual field deficit, temporal lobes—homonymous visual field deficit, alexia, prosopagnosia, amnesia, hallucinationsalexia, prosopagnosia, amnesia, hallucinations

Watershed areas: ACA/MCA and MCA/PCA Watershed areas: ACA/MCA and MCA/PCA bordersborders

Lacunar (brain stem, basal ganglia): pure motor, Lacunar (brain stem, basal ganglia): pure motor, pure sensory, ataxis hemiparesis, and dysarthria.pure sensory, ataxis hemiparesis, and dysarthria.

Page 6: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

TIA TIA

Definition: Transient focal neurologic Definition: Transient focal neurologic deficit of either anterior or posterior deficit of either anterior or posterior circulationcirculation

Rochester study: TIAs followed for five yrRochester study: TIAs followed for five yr– Incidence stroke 36%Incidence stroke 36%– 51% of these occurred within first year51% of these occurred within first year

Lit review: annual stroke incidence in pts Lit review: annual stroke incidence in pts with TIAs ranges from 5.3-8.6%/yr for first with TIAs ranges from 5.3-8.6%/yr for first 5 years5 years– Approx 1/3 pts with TIA will suffer stroke within Approx 1/3 pts with TIA will suffer stroke within

5 years5 years

Page 7: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

TIA IITIA II

Embolic theory of transient cerebral ischemia Embolic theory of transient cerebral ischemia (versus mechanical flow reduction)(versus mechanical flow reduction) Atheromatous debris, thrombus, or plt aggregatesAtheromatous debris, thrombus, or plt aggregates Ischemic attacks stop after occlusionIschemic attacks stop after occlusion

TIA vs small stroke? Cerebral infarction and TIA vs small stroke? Cerebral infarction and atrophy is correlated with percent stenosis atrophy is correlated with percent stenosis and h/o TIAsand h/o TIAs– 2% e/o stroke on CT with pts with ‘mild’ stenoses2% e/o stroke on CT with pts with ‘mild’ stenoses– 58% in pts with asymptomatic high-grade stenoses58% in pts with asymptomatic high-grade stenoses

Therefore, important to identify Therefore, important to identify asymptomatic lesions BEFORE TIA occursasymptomatic lesions BEFORE TIA occurs

Page 8: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Timing of CEATiming of CEA

Historically: weeks to months delay after TIA or strokeHistorically: weeks to months delay after TIA or stroke– ipsilateral hemorrhage and extension of the infarct ipsilateral hemorrhage and extension of the infarct

supported in several seriessupported in several series– Old data prior to current imaging studiesOld data prior to current imaging studies

No RCT addressing the questionNo RCT addressing the question Large meta-analysis 2003:Large meta-analysis 2003:

– No diff between rates of stroke or death for pts with No diff between rates of stroke or death for pts with stable stroke symptomsstable stroke symptoms when CEA performed when CEA performed early (<3-6 weeks) or delayed (>3-6 weeks)early (<3-6 weeks) or delayed (>3-6 weeks)

Pooled analysis of NASCET and ESCT dataPooled analysis of NASCET and ESCT data– Greatest benefit from surgery in group randomized Greatest benefit from surgery in group randomized

within 2 wks of surgery and this benefit decreased within 2 wks of surgery and this benefit decreased with further delay from symptom onsetwith further delay from symptom onset

Page 9: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Imaging StudiesImaging Studies

CT scan—90% cortical ischemic infarctions CT scan—90% cortical ischemic infarctions are detectable with a clinical neurologic are detectable with a clinical neurologic event after 24hevent after 24h– Hypodensities, mass effects, loss of Hypodensities, mass effects, loss of

distinction between cortical gray and distinction between cortical gray and subcortical white mattersubcortical white matter

– Hemorrhagic areas of reperfusionHemorrhagic areas of reperfusion– Only dx ~50% brainstem infarctsOnly dx ~50% brainstem infarcts

CTA vs. Angiography: Overal accuracy for CTA vs. Angiography: Overal accuracy for correct stenosis 90-96%, risks of correct stenosis 90-96%, risks of complications avoidedcomplications avoided

MRA: Sensitivity 83-97% and specificity 92-MRA: Sensitivity 83-97% and specificity 92-98% for detecting flow voids, tends to 98% for detecting flow voids, tends to overestimate when compared to angiographyoverestimate when compared to angiography

Page 10: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Symptomatic DiseaseSymptomatic Disease

NASCET:2226 pts randomized to NASCET:2226 pts randomized to medical care or CEA.medical care or CEA.– Patients had either a transient ischemic Patients had either a transient ischemic

attack or stroke within 4 months of attack or stroke within 4 months of enrollment and a 30-99% internal carotid enrollment and a 30-99% internal carotid artery stenosis. artery stenosis.

– For patients with a >=70% stenosis, For patients with a >=70% stenosis, carotid endarterectomy reduced the risk of carotid endarterectomy reduced the risk of any ipsilateral stroke from 26% to 9% at 2 any ipsilateral stroke from 26% to 9% at 2 years (P<0.001). years (P<0.001).

Conclusion: CEA better if symptomatic Conclusion: CEA better if symptomatic with stenosis >70%with stenosis >70%

Page 11: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Asymptomatic diseaseAsymptomatic disease

Natural history studies: 30-50% pts who Natural history studies: 30-50% pts who have suffered a stroke did NOT have TIA priorhave suffered a stroke did NOT have TIA prior– 20% pts with bruit will have hemodynamically 20% pts with bruit will have hemodynamically

significant stenosis of the carotid bulbsignificant stenosis of the carotid bulb ACAS trial (1995): Called off after 2.7 yrs f/uACAS trial (1995): Called off after 2.7 yrs f/u

– 5 yr risk for ipsi stroke, any periop stroke, and 5 yr risk for ipsi stroke, any periop stroke, and death was 5.1% surgical group c/w 11% medical death was 5.1% surgical group c/w 11% medical group.group.

– Absolute risk reduction of 5.9% and relative risk Absolute risk reduction of 5.9% and relative risk reduction of 53% in favor of CEA.reduction of 53% in favor of CEA.

– Combined neurologic morbidity and mortality Combined neurologic morbidity and mortality 1.52% for surgery.1.52% for surgery.

Page 12: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Asymptomatic Disease Asymptomatic Disease IIII Conclusion: CEA better if can offer with Conclusion: CEA better if can offer with

morbidity/mortality <1.5%, recc if >60% stenosismorbidity/mortality <1.5%, recc if >60% stenosis– Corresponds to 80% stenosis when using Corresponds to 80% stenosis when using

standardized duplex criteriastandardized duplex criteria ASCT (2004): 5 yr trial results confirm and ASCT (2004): 5 yr trial results confirm and

extend ACAS results.extend ACAS results.– 5 yr risk for ipsi stroke, any periop stroke, and 5 yr risk for ipsi stroke, any periop stroke, and

death was 6.4% surgical group c/w 11.8% death was 6.4% surgical group c/w 11.8% medical group.medical group.

– Benefit in pts >60% stenosisBenefit in pts >60% stenosis– Most benefit in pts >75 y/oMost benefit in pts >75 y/o

Page 13: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Duplex CriteriaDuplex Criteria

Individualized to each vascular Individualized to each vascular laboratory with a program of laboratory with a program of internal quality control.internal quality control.

ICA stenosis Peak Systolic Velocity

End diastolic velocity

<50% <125

50-74% >125 <125

>75% >125 (>300) >125

Page 14: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Pre-Op MedicationsPre-Op Medications

Antiplatelet TherapyAntiplatelet Therapy– Cochrane meta-analysis: ASA 81mg Cochrane meta-analysis: ASA 81mg

statistically significant benefit in reducing statistically significant benefit in reducing rate of stroke from any cause, but not death rate of stroke from any cause, but not death or cardiac eventsor cardiac events

– 81mg as effective as 325mg with less 81mg as effective as 325mg with less bleeding complications/risksbleeding complications/risks

StatinStatin– Reduction in in-hospital mortality, Reduction in in-hospital mortality,

perioperative stroke and death rates, but perioperative stroke and death rates, but not in-hospital cardiac eventsnot in-hospital cardiac events

– Multivariate analysis: 3-fold reduction in Multivariate analysis: 3-fold reduction in stroke, 5-fold reduction in deathstroke, 5-fold reduction in death

Page 15: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

CEA: TechniquesCEA: Techniques

Vertical vs. Horizontal IncisionVertical vs. Horizontal Incision Identification and Mobilization:Identification and Mobilization:

– Cervical lymph nodesCervical lymph nodes– Hypoglossal nerveHypoglossal nerve

Gaining distal ICA exposure:Gaining distal ICA exposure:– Digastric muscle divisionDigastric muscle division– Mandibular subluxationMandibular subluxation

Endarterectomy—Eversion vs. PatchEndarterectomy—Eversion vs. Patch No difference in rate of stroke/deathNo difference in rate of stroke/death Advantage—faster, less exposure, no suture line on Advantage—faster, less exposure, no suture line on

ICAICA Disadvantage—tech challenging, mobilization of bulb, Disadvantage—tech challenging, mobilization of bulb,

less visualization of endpoint, shunting cumbersomeless visualization of endpoint, shunting cumbersome Shunting—”snow plowing the intima”Shunting—”snow plowing the intima”

Page 16: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Selective ShuntingSelective Shunting

Local/Regional Anesthesia (0-1.1% Local/Regional Anesthesia (0-1.1% permanent deficit)permanent deficit)– 10% all procedures done10% all procedures done– Lesser fluctuations in blood pressureLesser fluctuations in blood pressure

EEG Monitoring (1.5-3.5%)EEG Monitoring (1.5-3.5%)– Wide threshold between EEG monitoring becoming Wide threshold between EEG monitoring becoming

abnormal vs. infarctionabnormal vs. infarction– ?sensitivity/specificity?sensitivity/specificity

Stump pressure measurements (0.8-2%)Stump pressure measurements (0.8-2%)– 50mmHg based on correlations with EEG 50mmHg based on correlations with EEG

monitoring, status of contralateral artery, and monitoring, status of contralateral artery, and reported outcomesreported outcomes

Page 17: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

To Shunt or Not To To Shunt or Not To ShuntShunt Clamping ischemia is Clamping ischemia is

uncommon cause of uncommon cause of perioperative stroke perioperative stroke – 93-96% pts tolerate 93-96% pts tolerate

carotid clamping carotid clamping without shunt under without shunt under local/regional local/regional anesthesiaanesthesia

Embolization or thrombosis Embolization or thrombosis usually due to technical usually due to technical difficulties difficulties

Shunt does not protect or Shunt does not protect or contribute to stroke risk—no contribute to stroke risk—no superiority in either superiority in either technique between technique between selective shunting vs. selective shunting vs. routine shunting. (Cochrane routine shunting. (Cochrane stroke group)stroke group)

RiskRisk Stroke Stroke raterate

Low: patent Low: patent contra ICA and contra ICA and stump pressure stump pressure >50mmHg>50mmHg

1.1%1.1%

Intermediate: Intermediate: occluded contra occluded contra ICA, pressure ICA, pressure >50mmHg>50mmHg

4%4%

High: occluded High: occluded contra ICA, contra ICA, pressure <50 pressure <50 mmHgmmHg

4%4%

Page 18: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Intraoperative Intraoperative AssessmentAssessment Operative ArteriographyOperative Arteriography

– If routinely performed, a reduction in mortality, If routinely performed, a reduction in mortality, stroke rate, and fatal strokes has been noted in stroke rate, and fatal strokes has been noted in several studiesseveral studies

AngioscopyAngioscopy– Direct visualization of the luminal surfaceDirect visualization of the luminal surface– Increases cross-clamp time, no info on patterns of Increases cross-clamp time, no info on patterns of

blood flowblood flow Duplex UltrasonographyDuplex Ultrasonography

– Detection and correction of turbulent blood flow Detection and correction of turbulent blood flow and anatomic defects lead to decreased occlusions and anatomic defects lead to decreased occlusions and restenosis and restenosis

Page 19: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

CEA vs. CASCEA vs. CAS

Randomized clinical trials to gain Randomized clinical trials to gain evidence on which to base clinical evidence on which to base clinical decisions.decisions.

CAS vs. CEACAS vs. CEAneed to enhance need to enhance our understanding of their roles.our understanding of their roles.

CAVATAS—angioplasty alone vs. CAVATAS—angioplasty alone vs. surgery, horrible results both surgery, horrible results both arms, of historical interest onlyarms, of historical interest only

Page 20: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

SAPPHIRE SAPPHIRE (Stenting and Angioplasty (Stenting and Angioplasty with Protection in Pts at High Risk for with Protection in Pts at High Risk for

Endarterectomy)Endarterectomy)

Initially, data showed results for stenting Initially, data showed results for stenting statistically significantly superior to those of statistically significantly superior to those of CEA….butCEA….but– Primary endpoint was amalgam of short and Primary endpoint was amalgam of short and

intermediate term results (periprocedural stroke, MI, intermediate term results (periprocedural stroke, MI, or death, and one year ipsilateral stroke or death)or death, and one year ipsilateral stroke or death)

– No statistically significant difference in outcome in No statistically significant difference in outcome in any individual endpoint (death, stroke, or MI).any individual endpoint (death, stroke, or MI).

– Majority of MI’s were non Q-wave and of doubtful Majority of MI’s were non Q-wave and of doubtful significance.significance.

<30% high-risk pts had symptomatic dz, <30% high-risk pts had symptomatic dz, treatment groups are not equal in terms of treatment groups are not equal in terms of comorbidities/agecomorbidities/age

No medical management armNo medical management arm

Page 21: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Symptomatic TrialsSymptomatic Trials

EVA-3S: >60% symptomatic stenosis EVA-3S: >60% symptomatic stenosis equally eligible ptsequally eligible pts– 30 day: Stroke/death rates 3.9% (CEA) vs. 30 day: Stroke/death rates 3.9% (CEA) vs.

9.6% (CAS)9.6% (CAS)– 6 months: 6.1% vs. 11.7%6 months: 6.1% vs. 11.7%– But…less experienced surgeons, no CPDBut…less experienced surgeons, no CPD

SPACE: symptomatic pts randomized SPACE: symptomatic pts randomized CEA vs. CAS, failed to prove “non-CEA vs. CAS, failed to prove “non-inferiority”inferiority”– CPD in only 27%CPD in only 27%

Page 22: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

CRESTCREST

2500 pts equally eligible for CEA vs. 2500 pts equally eligible for CEA vs. CAS, enrolled based on NASCET/ACAS CAS, enrolled based on NASCET/ACAS guidelines (50%/70%)guidelines (50%/70%)– Lead-in results suggest that older pts Lead-in results suggest that older pts

suffer worse outcomes (P=0.0006)suffer worse outcomes (P=0.0006)

Age (N)Age (N) Stroke/Death %Stroke/Death %

<60 (120)<60 (120) 2 (1.7%)2 (1.7%)

60-69 (229)60-69 (229) 3 (1.3%)3 (1.3%)

70-79 (301)70-79 (301) 16 (5.3%)16 (5.3%)

>= 80 (99)>= 80 (99) 12 (12.1%)12 (12.1%)

Page 23: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Conclusions: CAS vs. Conclusions: CAS vs. CEACEA The low morbidity and mortality rates in both The low morbidity and mortality rates in both

nonrandomized and randomized series nonrandomized and randomized series studying CEA for both asymptomatic and studying CEA for both asymptomatic and symptomatic pts must be equaled for CAS.symptomatic pts must be equaled for CAS.

30d stroke and stroke/mortality rates for CAS 30d stroke and stroke/mortality rates for CAS appear to be marginally statistically appear to be marginally statistically significantly higher than those associated with significantly higher than those associated with CEA (1.3%)CEA (1.3%)

Accepted indications:Accepted indications:– Surgically inaccessible lesionSurgically inaccessible lesion– Hostile NeckHostile Neck– RestenosisRestenosis– Medical high risk (hard to define)Medical high risk (hard to define)– Participation in RCTParticipation in RCT

Page 24: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Vertebrobasilar Vertebrobasilar IschemiaIschemia Symptoms: Commonly manifested as vertigo, Symptoms: Commonly manifested as vertigo,

visual disturbances, progressive neuro deficitvisual disturbances, progressive neuro deficit Mechanisms:Mechanisms:

Microembolization: from heart or more proximal Microembolization: from heart or more proximal arteries. Less common.arteries. Less common.

innominate, prox subclavian, and vertebralsinnominate, prox subclavian, and vertebrals– Low-flow: lack appropriate inflow from the Low-flow: lack appropriate inflow from the

vertebral artery and have inadequate compensation vertebral artery and have inadequate compensation from the carotid.from the carotid.

More frequentMore frequent Stenosis/occlusion of vert, also extrinsic compressionStenosis/occlusion of vert, also extrinsic compression Orthostatic hypotension, antihypertensive meds, Orthostatic hypotension, antihypertensive meds,

arrythmias, CHF, pacemaker malfunction, anemiaarrythmias, CHF, pacemaker malfunction, anemia

Page 25: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Evaluation of PatientsEvaluation of Patients

Dizziness, vertebral artery stenosis are Dizziness, vertebral artery stenosis are common complaints/findingscommon complaints/findings

Imaging brain to r/o tumor, investigate for Imaging brain to r/o tumor, investigate for infarctionsinfarctions

Check bilateral arm BP’s to r/o subclavian Check bilateral arm BP’s to r/o subclavian steal syndromesteal syndrome– Document reversal of flow by duplexDocument reversal of flow by duplex

Extrinsic compression by osteophytesExtrinsic compression by osteophytes– Turning head side to side, slowly, then briskly to Turning head side to side, slowly, then briskly to

differentiate from BPVdifferentiate from BPV– Confirm with angiogramConfirm with angiogram

Page 26: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Global ischemiaGlobal ischemia

““Drop attacks” comprise roughly 30% of Drop attacks” comprise roughly 30% of presentationspresentations

One or both internal carotid arteries One or both internal carotid arteries occluded or with severe siphon stenosis.occluded or with severe siphon stenosis.

Vertebral arteries important pathways Vertebral arteries important pathways for cerebral revascularization when they for cerebral revascularization when they are critically stenosed or occluded.are critically stenosed or occluded.– Minimal anatomic req to justify vert Minimal anatomic req to justify vert

reconstruction is >60% stenosis in dominant reconstruction is >60% stenosis in dominant if contra is hypoplastic, or >60% in both.if contra is hypoplastic, or >60% in both.

Page 27: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Angiography Angiography

Most common athersclerotic Most common athersclerotic lesion is stenosis of its originlesion is stenosis of its origin– Presence of post-stenotic Presence of post-stenotic

dilation proximally is dilation proximally is suggestive of hidden suggestive of hidden stenosisstenosis

Extrinsic compression seen Extrinsic compression seen at V2—multiple at V2—multiple views/manipulation views/manipulation necessarynecessary

V2-V3 segments: site of V2-V3 segments: site of traumatic injury from traumatic injury from periosteum/adventitia periosteum/adventitia fixationfixation

V3 usually area of V3 usually area of reconstitution secondary to reconstitution secondary to collaterals from occipital collaterals from occipital arteryartery

Page 28: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

AngiographyAngiography

Page 29: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

TreatmentTreatment

AnticoagulationAnticoagulation– Trial of medical therapy prior to Trial of medical therapy prior to

pursuing any surgical interventionpursuing any surgical intervention– Most effective for lesions that cause Most effective for lesions that cause

symptoms through embolization or symptoms through embolization or thrombosis of small arteriesthrombosis of small arteries

If definite clinical syndrome, MRI documenting If definite clinical syndrome, MRI documenting absence of alternate pathology, arteriography absence of alternate pathology, arteriography with structural lesion, and persistent symptoms with structural lesion, and persistent symptoms on anticoagulationon anticoagulationsurgerysurgery

Page 30: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Surgical OptionsSurgical Options

Transposition of Vertebral Artery into the Transposition of Vertebral Artery into the Common Carotid ArteryCommon Carotid Artery– Origin stenosisOrigin stenosis– Supraclavicular at level of C6Supraclavicular at level of C6– Patency 90-97%, stroke risk 2%, Patency 90-97%, stroke risk 2%,

mortality risk <1%mortality risk <1%– Complications: Horner’s, lymphoceleComplications: Horner’s, lymphocele

Distal Vertebral Artery ReconstructionDistal Vertebral Artery Reconstruction– GSVGSV– Level of C2Level of C2

Endovascular interventions?Endovascular interventions?

Page 31: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Subclavian DiseaseSubclavian Disease

Atherosclerotic disease left>rightAtherosclerotic disease left>right Asymptomatic lesions even with Asymptomatic lesions even with

asymptomatic stealasymptomatic stealtreatment treatment deferreddeferred

Subclavian steal: Subclavian steal: – Retrograde blood flow associated Retrograde blood flow associated

with proximal subclavian stenosis or with proximal subclavian stenosis or occlusionocclusion

– Upper extremity ischemia (71%), VBI Upper extremity ischemia (71%), VBI (44%), Hemispheric TIA (29%)(44%), Hemispheric TIA (29%)

Page 32: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Subclavian Steal Subclavian Steal SyndromeSyndrome Physical examPhysical exam

– Blood pressure differential >=20mmHgBlood pressure differential >=20mmHg 2-3x more common on the left2-3x more common on the left

– Embolic phenoma to handsEmbolic phenoma to hands Duplex ultrasonographyDuplex ultrasonography

– Reversal blood flow within vertebralReversal blood flow within vertebral– Monophasic waveforms in subclavian a.Monophasic waveforms in subclavian a.– High-frequency blood flow patternHigh-frequency blood flow pattern

Arch aortography with selected viewsArch aortography with selected views

Page 33: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

TreatmentTreatment

Treat ICA lesion first!Treat ICA lesion first! If symptoms persistIf symptoms persist

– Transposition of subclavian artery onto the common Transposition of subclavian artery onto the common carotidcarotid

Approx 100% patency rate at followupApprox 100% patency rate at followup– Carotid-Subclavian bypassCarotid-Subclavian bypass

Approx 94% patency at 10 yearsApprox 94% patency at 10 years– Axilloaxillary bypassAxilloaxillary bypass

Setting of previous extensive neck surgery or Setting of previous extensive neck surgery or radiationradiation

Long-term durability inferiorLong-term durability inferior– Subclavian artery stenting/angioplastySubclavian artery stenting/angioplasty

Page 34: Carotid, Subclavian, and Vertebrobasilar Disease Kelley Hodgkiss-Harlow 9/30/2009

Any Questions?Any Questions?