endovascular management of carotid artery dissection

1280

AJNR Am J Neuroradiol 21:1280–1292, August 2000

Endovascular Management of Extracranial CarotidArtery Dissection Achieved Using Stent AngioplastyAdel M. Malek, Randall T. Higashida, Constantine C. Phatouros, Todd E. Lempert, Philip M. Meyers,

Wade S. Smith, Christopher F. Dowd, and Van V. Halbach

BACKGROUND AND PURPOSE: Dissection of the carotid artery can, in certain cases, leadto significant stenosis, occlusion, or pseudoaneurysm formation, with subsequent hemodynamicand embolic infarcts, despite anticoagulant therapy. We sought to determine the therapeuticvalue of stent-supported angioplasty retrospectively in this subset of patients who are poorcandidates for medical therapy.METHODS: Five men and five women (age range, 37–83 years; mean age, 51.2 years) with

dissection of the internal (n59) and common (n51) carotid artery were successfully treatedwith percutaneous endovascular balloon angioplasty and stent placement. The etiology wasspontaneous in five, iatrogenic in three, and traumatic in two. Seven of the treated lesions wereleft-sided and three were right-sided.RESULTS: The treatment significantly improved dissection-related stenosis from 7465.5%

to 5.562.8%. Two occlusive dissections were successfully recanalized using microcatheter tech-niques during the acute phase. Multiple overlapping stents were needed in four patients toeliminate the inflow zone and false lumen and establish an angiographically smooth outlinewithin the true lumen. There was one case of retroperitoneal hemorrhage, but there were noprocedural transient ischemic attacks (TIAs), minor or major strokes, or deaths (0%). Clinicaloutcome at latest follow-up (16.561.9 months) showed significant improvements compared withpretreatment modified Rankin score (0.760.3 vs 1.860.44) and Barthel index (99.560.5 vs80.568.9). One delayed stroke occurred in a treated patient with contralateral carotid occlusionfollowing a hypotensive uterine hemorrhage at 8 months; the remaining nine patients haveremained free of TIA or stroke.CONCLUSION: In select cases of carotid dissection associated with critical hemodynamic

insufficiency or thromboembolic events that occur despite medical therapy, endovascular stentplacement appears to be a safe and effective method of restoring vessel lumen integrity, withgood clinical outcome.

Dissection of the cervical carotid arteries occurswhen the integrity of the intima and media layersof the vessel wall is compromised, resulting inhemorrhage in the vessel wall and consequent com-promise of the native vessel lumen (1–4) (Fig 1).The formation of a false channel and associatedanatomic disruption of the endothelial monolayerresults in conditions favoring local thrombus for-

Received November 9, 1999; accepted after revision January24, 2000.From the Departments of Radiology (A.M.M., R.T.H.,

C.C.P. T.E.L., P.M.M., C.F.D., V.V. H.), Division of Inter-ventional Neurovascular Radiology, Neurosurgery (R.T.H.,C.F.D., V.V.H.), and Neurology (W.S.S.), University of Cali-fornia, San Francisco, 94143, USA.A.M.M. was supported by a grant from the Boston Neuro-

surgical Foundation.Address reprint requests to Adel M. Malek, M.D., Ph.D.,

Neurosurgery, Brigham and Women’s and Children’s Hospi-tals, 300 Longwood Avenue, Bader 3, Boston, MA 02115.

mation, which may then embolize distally, and re-sult in brain infarction (5). The accepted medicalstandard of therapy has consisted of systemic an-ticoagulation, and has been observed to lead to asignificant rate of subsequent resolution and heal-ing (6, 7). In a subset of patients, spontaneous heal-ing, with restoration of native vessel anatomy, failsto occur (1, 8–10). Instead, the arterial dissectionmay result in total occlusion of the true vessel lu-men by compression from the false lumen, createdby entry of pressurized blood in the dissected me-dial defect (2, 9). In another subset of patients, thedissection site may develop into a focal or exten-sive stenosis, with formation of an associated pseu-doaneurysm (1, 2, 8). In such cases, anticoagula-tion, although critical to prevent thromboembolicevents in the initial stages of the disease, may beinsufficient to overcome the flow-limiting nature ofthe dissecting lesion or may be contraindicated be-cause of risk of pseudoaneurysm rupture (3). En-

AJNR: 21, August 2000 CEREBRAL ISCHEMIA 1281

dovascular stents have been shown to be of benefitfor the treatment of coronary atherosclerosis (11),and have been considered for the treatment of ca-rotid atherosclerosis in certain high-risk patientsubgroups (12). Stents also have been used to treatintimal dissection resulting from balloon angio-plasty and trauma (13–16). By virtue of their de-sign, stents provide the necessary centrifugal forceto permit apposition of the dissected segment to thevessel wall to obliterate the false lumen and resolvethe stenosis (13, 17). Stents can also provide me-chanical support to serve as a scaffold for coil em-bolization of dissection-related wide-necked pseu-doaneurysms (18, 19) (Fig 1). In order to determinethe clinical and angiographic outcome of this formof therapy, we present our endovascular manage-ment of cervical carotid dissection, achieved usingpercutaneous stent angioplasty in a retrospectiveseries of 10 patients.

MethodsPatient Selection Criteria

During the 18-month period between October 1997 andMarch 1999, 10 consecutive patients underwent endovasculartreatment of carotid dissection performed using intraluminalstent placement. Informed consent was obtained from patientsor medical guardians. Patients were considered eligible forstent therapy of carotid dissection only if they had either failedoptimal medical therapy, were unable to undergo anticoagu-lation, or if they had no other therapeutic option of acceptablylow risk. The specific indications (Table 1) included the pres-ence of transient ischemic attacks (TIAs) despite anticoagulantor antiplatelet therapy (patients 4, 8, 10), contraindication toanticoagulation (patient 9), contralateral carotid occlusion orstenosis in a patient who was neurologically unstable or hadclinical evidence of hemodynamic insufficiency (patients 3, 5,5), documented poor collateral circulation (patient 1), need forelective occlusion of the contralateral internal carotid arteryfor aneurysm treatment (patient 2), and need to avoid flowincrease through the anterior communicating artery because ofthe presence of an aneurysm (patient 7). Patients who under-went stent placement for angioplasty-induced intimal dissec-tion during endovascular treatment of carotid atherosclerosiswere excluded from the study.

ProcedureAll patients underwent complete digital subtraction angi-

ography of both anterior and posterior cerebral circulations,including the external carotid arteries. Patients were adminis-tered intravenous heparin to achieve an activated clotting timeof greater than 250 seconds. A 7F or 9F guide catheter (BriteTip; Cordis Endovascular, Miami Lakes, FL) was placed in thecommon carotid artery via a femoral vascular sheath (Avanti;Cordis). A 2.3F microcatheter (Rapid Transit; Cordis) was usedcoaxially over a 0.014- to 0.016-in microguidewire (Instinct10; Cordis/Transend 14, Scimed, Maple Grove, MN) to enterthe true arterial lumen under real-time high-resolution digitalroadmap angiography (Toshiba, Tustin, CA). A 300-cm-longexchange microguidewire (Stabilizer; Cordis) was then passedthrough the microcatheter and used to exchange the latter forthe stent delivery catheter. Three types of stents were employedin this study: 1) a self-expanding stainless steel stent (Wal-lstent; Schneider, Plymouth, MN); 2) a premounted balloon-expandable stainless steel stent (GFX; Arterial Vascular En-gineering, Santa Rosa, CA); and 3) a Nitinol shape-memoryalloy self-expanding stent (S.M.A.R.T.; Cordis). After stent de-

ployment, the patients were administered ticlopidine (250 mgpo bid) or clopidogrel (75 mg po qd) for 6 weeks and aspirin(325 mg po qd) indefinitely. The vascular access sheath wasremoved on the day after the procedure, with the aid of anexternal femoral compression device (FemoStop; Radi, Upp-sala, Sweden).

Outcome AnalysisFollow-up was performed using both neurologic examina-

tion and telephone interview. The modified Rankin score andBarthel index were used, as previously described (20–22).Evaluation of stent patency was obtained by sonography orrepeat digital subtraction angiography.

StatisticsSeverity of stenosis was computed using the NASCET

method, with dimensions obtained either by using the relativefluorographic size of a reference object or the angiographicdigital computer system (Toshiba). Specifically, the diameterof maximal stenosis (DStenosis) was measured along with themost proximal diameter of the distal normal vessel (DNormal),and the degree of stenosis computed as Stenosis5[12(DStenosis/ DNormal)] 3100. The paired Student’s t test and analysis ofvariance were used in the comparison of numerical variables.For categorical analysis, a Pearson’s chi-square test was used.Statistical significance was assumed for P,.05.

Results

Patient Population and Lesion CharacteristicsThere were five male and five female patients,

ranging in age from 37 to 83 years (mean age,51.264.2 years) (Table 1). Seven (70%) of the 10patients suffered from coexisting hypertension andseven patients (70%) had suffered a stroke prior totreatment as a result of the initial arterial dissection.The location of dissections treated was as follows:one in the left common carotid artery, six in theleft internal carotid artery, and three in the rightinternal carotid artery. Two patients were treatedwithin 12 hours of the initial angiographic or symp-tomatic dissection, three patients were treated be-tween 3 and 10 days of symptomatic dissection,and the remaining five patients were treated forchronic dissection between 3 weeks and 10 yearsafter initial detection of their dissection.

Therapeutic InterventionsThe etiology of the carotid dissections encoun-

tered in this study was spontaneous, iatrogenic, ortraumatic. Five patients (50%) had spontaneousdissections, one of which was chronic (discovered10 years prior to admission), and three had iatro-genic dissections (30%) resulting during diagnosticangiography. Of these three patients, two under-went recanalization and stent angioplasty of a com-pletely occluded internal carotid artery, with com-plete restoration of flow (patients 1, 7). The third(patient 2) underwent stent angioplasty of a nar-rowed and dissected left internal carotid artery inorder to enable treatment of a contralateral giantcavernous carotid artery aneurysm that required

AJNR: 21, August 20001282 MALEK

FIG 1. Simplified schematic illustration ofthe pathophysiologic process of carotid ar-tery dissection proceeding from the acutestage to either spontaneous healing (1),formation of false lumen (2), residual ste-nosis of varying degree or complete occlu-sion (3), and formation of a pseudoaneu-rysm (4). A stent is used in cases that havenot responded to medical therapy either torelieve a hemodynamically significant ste-nosis, to occlude a false lumen, or to serveas a scaffold to enable coil embolization ofa wide-necked pseudoaneurysm.

balloon occlusion and carotid sacrifice. Two pa-tients (20%) presented with traumatic dissection,one as a result of manual strangulation by herspouse (patient 6), and the other after vehicularwhiplash (patient 10) (21) (Table 2). The angio-plasty and stent treatment improved dissection-in-duced stenosis significantly from 7465.5% to5.562.8% (P,.001).Two patients (patients 3 and 5) had bilateral in-

volvement of the internal carotid artery. These pa-tients suffered spontaneous dissection and had un-dergone diagnostic angiography at an outsidehospital 2 to 3 days prior to admission, whichshowed unilateral flow-limiting dissection on oneside and slight irregularity in the contralateral ca-rotid artery. After transfer, repeat angiography re-vealed progression of the disease to unilateral com-plete occlusion of the previously dissected internalcarotid artery and a severe flow-limiting lesion onthe contralateral side. Eight lesions were left-sidedand two were right-sided.In four patients, multiple stents were deployed

in an overlapping fashion in order to enable theelimination of the false lumen and to treat the re-

sidual stenosis. Two of these patients, with a severeform of bilateral dissection leading to unilateral oc-clusion at the time of treatment, required three tan-dem stents to reconstitute an angiographicallysmooth luminal outline (patients 3 and 5). In theother two patients, two tandem stents were used inboth cases to allow spanning the entire length ofthe dissection, which included the carotid bulb withits greater diameter compared with the proximalcommon carotid (patient 4) or the cervical internalcarotid artery (patient 9). In two patients (patients8 and 10), a stent was deployed to serve as a scaf-fold through which a wide-necked pseudoaneurysmwas subsequently treated using Guglielmi electro-lytically detachable coils, in a manner similar tothat reported on in previous reports (18, 19). Theseaneurysmal dilatations were located in the cervi-copetrous junction (patient 8) and in the petrocav-ernous segment (patient 10) of the internal carotidartery.

ComplicationsThere were no instances of postprocedural tran-

sient ischemic attacks (TIAs), new neurologic def-


TABLE1:Summaryoftheclinicalpresentation,coexistingmedicalproblems,durationofsymptomsuntiltreatment,presenceandlocationofanyinfarct,etiologyofthedissection,andindication

forendovasculartreatment

Pa-

tient

(No.)

Age

(yrs)/

Sex

PresentingSymptoms

Duration

between

Symptomsor

Dissection

and

Treatment

Infarct/Location

EtiologyofDissection

IndicationforTreatment

145/F

Lhemiparesisfollowingdiagnosticangio-

gram

12 hours

Rposteriorfrontalinfarct

Iatrogenic(angiography)

Restorationofflow,givenpoorcollaterals

246/F

Rptosis,CN

IIIpalsy,diplopiafrommass

effectofcavernousICAaneurysm

3 days

None


RestorationofLICA

flow,givenneedto

sacrificeRICA

351/M

SuddenlossofvisioninLeye10days

priortoadmission,headache,spontane-

ousbilateralICA

dissection

10 days

Bilateralinternalcapsule,L

occipitallobe

Spontaneous

RestorationofLICA

flow,givenoccluded

RICA

483/M

LhemisphericTIAs,aphasia,R

hemi-

paresis

3weeks

None

Spontaneous(extensionofaorticdissec-

tion)

Obliterationoffalse

channeltoeliminate

thrombusformation

551/M

Spontaneousdissection,aphasia,R

hemi-

paresis

10 days

Lperisylvian,insularandposteriorfrontal

infarct

Spontaneous

RestorationofRICA

flowgivenoccluded

LICA

637/F

Rhandandarmweakness,legnumbness,

anddysphasia

3months

Leftposteriorfrontalinfarct

Traumatic(strangulation)

ReductionofLICA

stenosisgivennar-

rowedandhypoplasticRICA

740/F

Asymptomatic,immediatedetectionofdis-

sectionduringfollow-upangiogramfor

Acommaneurysm

coiling

30 min-

utes

OldlacuneinposteriorlimbofRinternal

capsule


RestorationofLICA

flowtoavoidhigh

flow-mediatedAcommaneurysm

expan-

sion

864/M

Rsidehemiparesisandleftocularpain6

monthspriortoadmission.Diagnosed

withLICA

dissectionbutpersistentTIAs

despiteoralanticoagulanttherapy

6months

MulitpleinfarctsinLcapsule,basalgan-

glia,andfrontallobes

Spontaneous

Obliterationofpseudoaneurysm

andreduc-

tionofLICA

stenosistodecreasethrom-

busformation

951/M

Subarachnoidhemorrhage,intracranialva-

sospasm,headache

4weeks

None

Spontaneous

Obliterationoffalse

channelgivencontra-

indicationfororalanticoagulanttherapy

becauseofplannedabdominalsurgery

1044/F

Expressivedysphasia,R

armweaknessand

numbness

4months

LMCA

distribution

Traumatic(vehicularwhiplash)

RestorationofLICA

luminalintegrityand

caliber

Note.—L,left;R,right;ICA,internalcarotidartery;LICA,leftinternalcarotidartery;RICA,rightinternalcarotidartery;Acomm,anteriorcommunicatingartery;M

CA,middlecerebralartery.


TABLE2:Summaryoftheangiographiccharacteristicsofthelesion,includinglocation,presenceofcollaterals,methodoftreatment,stenosis,andcomplicationrelatedtotreatment

Patient

(No.)

LocationofLesion

EvidenceofAngiographic

Collaterals

Treatment

Pre/PostLuminal

Compromise

Complications

TreatmentComplication

1RICA

dissectionandocclu-

sion

AbsentAcomm,perfusion

fromRPcommandRop-

thalmicartery

1—Recanalizationoftrue

RICA

lumen

2—PlacementofSingleRICA

WallStent6

320(mm)

RICA 100%–.0%

Transientvasospasm

Resolvedspontaneously

upon

removalofguidecatheter

2LICA

dissectionandstenosis

PatentAcommandbilateral

Pcomm

1—PlacementofsingleLICA

WallStent7

320(mm)

2—Balloonocclusionof

RICA

3dayslater

LICA 80

%–.20%

None

N/A

3LICA

dissectionandocclusion

RICA


OccludedoriginLICA

1—Placementof3RICA

tan-

demstents:1WallStent6

320(mm)and2GFX

43

12(mm)inRICA

RICA 60

%–.15%

None

N/A

4LCCA

dissection

False

lumeninCCAshows

retrogradeflowbackdown

toaorticarch

1—AngioplastyofLCCA

ste-

nosis

2—Placementof2tandem

LCCA

WallStents8

340

and10

342(mm)

LCCA 60%–.20%

Persistentminimalfillingof

false

lumen

None

5LICA


RICA


PatentAcommandleft

Pcomm

1—Placementof3tandem

RICA

WallStents:6

345,7

320,and8

320(mm)

RICA 80

%–.0%

None

N/A

6LICA

chronicdissectionand

stenosis

PatentbilateralPcomm

1—PlacementofsingleLICA

WallStent6

320(mm)

LICA 85

%–.0%

Retroperitonealhematoma

Transfusionandsurgicalre-

pairofarteriotomy

7LICA


PatentAcomm

1—RecanalizationofLICA

2—Placementof1LICA

WallStent6

320(mm)

LICA 100–

.0%

TransienthighcervicalLICA

vasospasm

Percutaneousballoonangio-

plasty

8LICA


withpseudoaneurysm

for-

mation

None

1—Stentplacementof1

LICA

WallStent6

320

(mm)

2—GDCcoil-through-stentof

LICA

pseudoaneurysm

LICA 70

%–.0%

None

N/A

9LICA

dissectionatcarotid

bulb

None


tan-

demS.M.A.R.T.Stent8

340,10

320(mm)

LICA 40

%–.0%

None

N/A

10LICA

dissectionatcarotid

bulb

None


tan-

demS.M.A.R.T.Stent8

320(mm)

2—GDCcoil-through-stentof

LICA

pseudoaneurysm

LICA 75

%—

.0%

None

N/A

Note.—RICA,rightinternalcarotidartery;Acomm,anteriorcommunicatingartery;Pcomm,posteriorcommunicatingartery;CCA,commoncarotidartery.


icits, and no new minor or major strokes (0%) priorto patient discharge (Table 3). Two patients had in-traprocedural vasospasm of the high cervical ca-rotid artery; this vasospasm was severe enough tonecessitate angioplasty in one case (patient 7) andresolved spontaneously after removal of the micro-guidewire in the other (patient 1). One patient suf-fered a retroperitoneal hemorrhage after removal ofthe vascular sheath and placement of an externalcompression device (patient 6) on postoperativeday 1; this required blood transfusion (2 U) andwas surgically repaired without complication. Asingle, major, delayed complication occurred in pa-tient 2, who was referred with a left internal carotiddissection that occurred during angiographic work-up of a giant symptomatic cavernous aneurysm.The flow-limiting left internal carotid artery dis-section was treated successfully using stent deploy-ment. Three days later, permanent sacrifice of theright internal carotid artery was performed usingdetachable silicone balloons after the patient hadtolerated successful balloon test occlusion (30 min-utes with hypotensive challenge). The patient hadan uncomplicated postprocedural course and wasdischarged home. Eight months later, the patienthad a massive uterine hemorrhage with an associ-ated prolonged hypotensive episode, which led toan ischemic stroke of the right hemisphere (contra-lateral to stent, ipsilateral to balloon occlusion), re-sulting in left-arm weakness. The deficit has mostlyresolved at latest clinical follow-up (24 months).

OutcomeDuring the acute postprocedural period, no pa-

tients developed worsening of symptoms. Two pa-tients treated in the acute phase of dissectionshowed significant and rapid improvement insymptoms (patients 1 and 5). Clinical follow-upwas obtained from all patients at 16.561.9 months(range, 8–27 months) and angiographic or sono-graphic follow-up was available for seven patientsat 6.360.9 months (range, 3–10 months). Therewas no evidence of stent occlusion or stenosis inany of the follow-up radiographic studies (0%).Clinical outcome was evaluated using the modifiedRankin scale and was improved at latest follow-up(0.760.26) compared with pretreatment values(1.86.0.44) (P,.008). Similarly, the Barthel indexshowed improvement at latest follow-up (99.560.5)compared with pretreatment values (80.568.6). Ex-cept for patient 2 presented above, no other patientin this high-risk subset has suffered any delayedTIA or stroke since treatment at latest follow-up.

Illustrative Cases

Acute Symptomatic Occlusive Dissection Treatedwith Recanalization and Stent Placement

The patient (patient 1) is a 45-year-old womanwith a history of hypertension, lupus erythemato-

sus, and migraine headaches, who underwent di-agnostic angiography at an outside institution forevaluation of recurrent headaches with associatedleft-arm weakness and numbness. During the pro-cedure, the operator noted that an acute dissectionhad been induced by contrast injection in a spasticvessel. The procedure was halted and intravenousheparin was immediately administered, but the pa-tient developed hemiparesis 1 hour later. She wastransferred to our hospital, where emergent angi-ography revealed that the previously dissected leftinternal carotid artery now showed tapering to acomplete occlusion (Fig 2). Collateral evaluationrevealed no anterior communicating flow across themidline from the left internal carotid artery injec-tion, weak flow from the posterior circulation viathe posterior communicating artery, and retrogradeflow through the right ophthalmic artery from theright external carotid artery. A Rapid Transit mi-crocatheter was used in combination with an In-stinct-10 microguidewire to navigate through thetrue lumen carefully and to reestablish recanaliza-tion of the internal carotid artery, which was notedto harbor a tonsillar loop, a condition previouslydescribed to predispose to dissection (24). Evalu-ation of the major intracranial vessels by contrastinjection through the microcatheter revealed no ev-idence of a large thrombus, and showed that mostof the distal branches remained patent. A decisionwas thus made to treat the dissection flap by elim-ination of the inflow to the subintimal dissection.A single 8-mm 3 2-cm Wallstent was deployed atthe proximal inflow zone, after which control an-giography revealed that blood flow had resumed tonormal. The patient’s left hemiparesis improvedrapidly after the procedure, and she was discharged3 days later with a mild left pronator drift. Thepatient has had no further TIAs or stroke, and fol-low-up sonography at 6 months revealed the stentto be patent, with no abnormal flow characteristics.At latest neurologic follow-up (17 months), the pa-tient still complained of poor fine-finger movement,numbness of the left face, and subjective left-leghypesthesia, but is otherwise intact.

Bilateral, Subacute, Spontaneous CarotidDissection Progressing to Unilateral Occlusion

and Flow-limiting Contralateral StenosisThis patient (patient 5) is a 51-year-old man,

with no significant past medical history, who notedleft arm and hand numbness while chopping wood.Four days later, he was found lying in bed, aphasicand disoriented, with right hemiparesis. He was ad-mitted to an outside hospital, and imaging was per-formed. A head CT scan was unrevealing, but abrain MR scan showed a left posterior frontal in-farct, and carotid sonography showed little to noflow in the left internal carotid artery (Fig 3). Anangiogram obtained at an outside hospital showeda flow-limiting dissection of the left internal carotidartery and an irregular contour of a patent right


TABLE3:Outcomeoftreatedpatientsimmediatelyaftertheprocedureandatlatestfollow–up

Patient

(No.)

ImmediateOutcome

Long–termOutcome

AnatomicFollow–up

Clinical

Follow–up

(months)

Pre/PostmRankinandBarthelIndex

1RapidimprovementofLhemiparesis,CT

evidenceofRposterior/superiorfrontal

lobeinfarct

1—ResidualL

handweakness

6monthsU/Spatentstent

17mRankingPre/Post

54/1

BarthelPre/Post

545/100

2Nonewsymptoms,toleratedRICA

per-

manentballonocclusionforRCavern-

ousaneurysm

treatment

1—ImprovedRcavernousaneurysm

mass

effectsymptoms

2—Strokeat8monthsfollowingamas-

siveuterinehemorrhagewithassociated

prolongedhypotension

8monthsMRA

patentstent


24mRankinPre/Post

52/1

BarthelPre/Post

580/100

3Nonewsymptoms,noimprovementin

leftocularvision,persistentleftfrontal

headache

1—Persistentheadache

2—NofurtherTIAs


15mRankinPre/Post

52/1

BarthelPre/Post

580/100

4ResolutionofTIAs

Asymptomatic


16mRankinPre/Post

52/0

BarthelPre/Post

590/100

5Improvementofleg,arm,andfacehemi-

paresis,minimalimprovementinrecep-

tiveaphasia

Partialexpressiveaphasia,receptive

speechintact,normalmotorandsensory

exam


20mRankinPre/Post

54/2

BarthelPre/Post

520/100

6Nonewsymptoms

Asymptomatic

6monthsA/Gpatentstent

27mRankinPre/Post

51/0

BarthelPre/Post

5100/100

7Nonewsymptoms

Asymptomatic

N/A

13mRankinPre/Post

50/0

BarthelPre/Post

5100/100

8ResolutionofTIAs

Asymptomatic

6monthsA/Gpatentstent

17mRankinPre/Post

51/0

BarthelPre/Post

595/100

9Nonewsymptoms

Asymptomatic

N/A

8mRankinPre/Post

50/0

BarthelPre/Post

5100/100

10Nonewsymptoms

1—Persistentmildexpressivedysphasia

2—NofurtherTIAs

N/A

8mRankinPre/Post

52/2

BarthelPre/Post

595/95


internal carotid artery. Intravenous anticoagulationwith heparin was begun, and the patient was trans-ferred to our center. Examination disclosed that thepatient was aphasic and had a right upper motorfacial and right upper and lower extremity hemi-paresis, with no response to visual threat fromright-sided confrontation. A repeat diagnostic an-giogram was obtained 2 days after the previousstudy. The new angiogram revealed progression ofthe previously noted left internal carotid artery dis-section to complete occlusion. In addition, itshowed the previous contour abnormality of theright internal carotid artery had progressed to along-segment stenosis with an associated distalpseudoaneurysmal dilatation. Given the diseaseprogression in both internal carotid arteries despiteanticoagulation, a decision was made to proceedwith securing a patent luminal conduit to preventfurther progression of the right-sided dissection tocomplete occlusion. Recanalization of the left in-ternal carotid artery was not attempted, given theduration and extent of the established left middlecerebral artery distribution infarct. Microcatheteri-zation of the true lumen was performed with a Rap-id Transit microcatheter over an Instinct-10 micro-guidewire. A 6-mm 3 4.5-cm Wallstent wasdeployed over the Stabilizer exchange microgui-dewire at the proximal inflow zone to tack downthe dissection flap, followed by balloon angioplastyof the long- segment stenosis. An additional twoWallstents (7 mm 3 2 cm and 8 mm 3 2 cm) wereneeded to reconstruct the vascular channel to thesame size as the native vessel. After the procedure,the patient had progressive improvement of hisright-sided face and arm weakness and of his re-ceptive aphasia. Neurologic follow-up at 20 monthsrevealed persistent, moderate, expressive aphasiawith naming difficulty, normal comprehension,symmetric face, absent pronator drift, and intactsensation with normal gait. Sonography confirmedpersistent patency of the right internal carotid ar-tery and stents, with no abnormal flow character-istics within the deployed stents.

Treatment of a Symptomatic Carotid DissectionRelated to an Aortic Dissection

The patient (patient 4) is an 83-year-old right-handed man with previous type A aortic dissection(involving both the ascending and descending aorta)10 years prior to admission, which was surgicallyrepaired using a Dacron graft. Angiographic study ofthe arch after an episode of transient aphasia revealedextension of the repaired aortic dissection into the leftcommon carotid artery. The patient was begun onaspirin and Coumadin and had been neurologicallywithout symptoms until 3 weeks prior to admission.The patient began to have left hemispheric TIAs, re-sulting in episodes of right-hand weakness, with poorfine-finger movement, despite therapeutic oral anti-coagulant therapy. The patient was begun on intra-venous anticoagulation. Angiography of the aortic

arch revealed an extensive left common carotid arterydissection involving the origin of the common carotidartery, the cervical carotid bifurcation, and the prox-imal internal carotid artery to C3 (Fig 4). Flow wasantegrade in the true lumen of the left common ca-rotid artery and retrograde in the false lumen, whichexited at a poorly visualized area in the aortic arch.The retrograde flow back to the arch was the resultof a pressure gradient from a Venturi effect at thefalse lumen exit into the aorta. A 5F Simmons-1 cath-eter was used to catheterize the left common carotidartery selectively and was exchanged for a 9 F guidecatheter. Two Wallstent devices were deployed in anoverlapping fashion. The proximal stent measured 8mm 3 4 cm and was deployed in the common ca-rotid artery across the inflow zone. The second stentmeasured 10 mm 3 4.2 cm and was deployed dis-tally in the carotid bulb and into the origin of thecervical internal carotid artery. Postdeployment an-gioplasty was performed for each stent by using an8-mm then a 10-mm angioplasty balloon (Powerflex;Cordis) (Fig 4). Postprocedure angiography showednear-complete elimination of the false lumen and theretrograde flow component. The patient tolerated theprocedure well, without further symptoms, and wasmaintained on Coumadin until 1.5 months after dis-charge, when he underwent open prostatectomy with-out complication. Carotid sonography performed at 6months showed persistent patency of the stent, with-out evidence of retrograde flow in the previous falselumen. Neurologic follow-up at 16 months revealedno further TIAs.

DiscussionThe annual incidence of spontaneous carotid dis-

section has been reported to be 2.6 per 100 000(27), and has been estimated to account for up to20% of strokes in the younger population (28).Most infarcts associated with dissection have beenproposed to be embolic in nature, although a non-negligible proportion consists of hemodynamicflow-related infarcts (5, 6). Despite anticoagulation,a number of patients progress to have hemodynam-ically significant residual stenosis or develop pseu-doaneurysms (2), leading to a risk of hemodynam-ically significant stenosis or to a danger of delayeddistal embolization (10). Although the rate of re-peat embolization in unilateral spontaneous carotiddissection lesions is low (6, 29), and, as such, doesnot justify placement of an intravascular stent asprimary treatment, the patients presented in this se-ries underwent stent placement only after they hadfulfilled stringent criteria such as failure of medicaltherapy and absence of low-risk surgical options.Although surgery has been performed for direct re-pair of carotid dissection, it is difficult to identifythe inflow zone or repair the entire extent of thedissection (1). Consequently, surgery for carotiddissection is associated with a significantly greaterrisk than is carotid endarterectomy for atheroscle-rosis (1).


FIG 2. A 45-year-old woman (patient 1) noted to have developed left hemiparesis after diagnostic angiography at an outside hospital.Head CT scan shows evidence of a previous focal infarct as well as diffuse edema in the right posterior frontal lobe (A). Digital subtractionangiography of the right common carotid artery reveals tapering of the right internal carotid artery, to a complete occlusion, with ap-pearance consistent of dissection (B). Injection of the right external carotid artery (C) shows retrograde collateral flow through the rightophthalmic artery, with filling of the cavernous segment of the right ICA. Injection of the left internal carotid artery shows no significantflow across the anterior communicating artery (D).

Surgical options for the treatment of hemody-namic insufficiency as a result of carotid dissectionhave included an extracranial-to-intracranial bypassprocedure for patients with hemodynamic insuffi-ciency who have not responded to anticoagulanttherapy (29). The surgical treatment of dissection-induced cervical carotid aneurysm has includedbypass grafting (30) and ligation of the internal ca-rotid artery for pseudoaneurysm repair (29).

One of the drawbacks of conventional and stent-supported balloon angioplasty of the carotid arteryfor atherosclerosis has been the risk of distal em-bolization of atheromatous debris during the bal-loon dilatation phase of the procedure. We did notencounter in this series any cases of distal embo-lization, perioperative stroke, or new deficits attrib-utable to stent deployment despite performing an-gioplasty of the deployed stent in the majority of


Fig. 2 (continued). Treatment approach consisted of initial recanalization of the dissected right internal carotid artery achieved by enteringthe true lumen by using a Rapid Transit microcatheter and Instinct-10 microguidewire (arrowheads) (E), and advancing up to thecavernous portion of the right internal carotid artery (arrow) (F). Superselective injection shows a patent right middle and anterior cerebralartery (G). An 8-mm 3 2-cm Wallstent was then deployed at the dissection site over a Stabilizer exchange microguidewire at the C2level (H). The reconstitution of the lumen of the right internal carotid artery is shown by injection of the right common carotid artery (I),with resumption of intracranial perfusion (J).

cases. Unlike atherosclerotic stenoses, which re-quire higher-pressure angioplasty and necessitatefracturing the plaque, the stent deployment for dis-section is less traumatic and is performed at a lowerpressure because the lesions are more compliantand are not usually atheromatous or calcified.Additional advantages of endovascular therapy

of carotid dissection are that it enables the identi-fication of the true and false lumens by superselec-tive catheterization and angiography, and further al-

lows the recanalization of completely occludedvessels by use of microcatheter techniques, provid-ed the thrombus burden is not prohibitive (Fig 2).The availability of flexible stents that conform tothe contour of the artery enables the sequential re-construction of an angiographically smooth luminaloutline through the narrowed true lumen and oblit-eration of the false lumen (Fig 5). In addition, theendovascular approach circumvents the need forblood flow occlusion, which is required during di-


FIG 3. A 51-year-old man (patient 5) with a 10-day history of left-sided TIAs now presents with sudden onset of aphasia and righthemiparesis. Axial T1-weighted contrast-enhanced MR imaging shows a left frontal infarct (A). Digital subtraction angiography of theleft common carotid artery showed progression of a left internal carotid dissection from a partial stenosis, 2 days prior, to a completeocclusion despite systemic anticoagulation (B). Digital subtraction angiography of the right common carotid artery revealed a dissectionof the right internal carotid artery with an associated long-segment stenosis and an expansile pseudoaneurysm at the distal end (C). ARapid Transit microcatheter was used to navigate the patent lumen of the right internal carotid artery and to deploy three Wallstents (6mm 3 45 mm, 7 mm 3 20 mm, and 8 mm 3 20 mm) in a tandem overlapping fashion with postdeployment balloon angioplasty (D).The procedure resulted in reconstitution of the normal lumen of the right internal carotid artery (E).

FIG 4. An 83-year-old man (patient 4) with a history of aortic dissection, which was surgically repaired 10 years previously, presentswith left hemispheric TIAs and episodes of aphasia. Digital subtraction angiography of the left common carotid artery outlines a chronicextensive dissection, with antegrade flow through the true lumen and retrograde flow in the false lumen down to the aorta, by virtue ofthe Venturi effect at the aortic arch (A, early injection; B, late injection). Two stents were placed in tandem overlapping fashion, followedby postdeployment angioplasty, resulting in a near-complete elimination of the retrograde flow in the now-reduced false lumen (C, D).


FIG 5. A 51-year-old man (patient 3) developed sudden loss of vision in the left eye, a left Horner’s syndrome, and orthostatic light-headedness. Digital subtraction angiography with injection of the right common carotid artery shows intimal dissection of the right internalcarotid artery in the high cervical region, with delineation of the true and false lumen (A, B). Injection of the left common carotid artery,which had evidence of dissection but was shown to be patent on an angiogram obtained 4 days earlier, now reveals complete leftinternal carotid artery occlusion (arrowhead) despite systemic anticoagulation (C). A Rapid Transit microcatheter was used to catheterizethe true lumen, followed by deployment of a Wallstent (6 mm 3 20 mm) in the proximal portion of the dissected segment (D). Persistentfilling of the false lumen, however, required the tandem placement of two additional GFX stents (4 mm 3 12 mm) in the petrous segmentof the right internal carotid artery (E), with reconstitution of the normal luminal diameter (F).

rect surgical bypass procedures, a crucial factor thatmost patients in the current report would not havetolerated because of contralateral involvement orpoor collateral flow. Finally, the endovascular ap-proach enables the simultaneous treatment of anycoexistent pseudoaneurysmal dilatations by embo-lization using Guglielmi electrolytically detachablecoils, by the coil-through-stent technique, whichwas employed in two cases (patients 8 and 10) (Fig1). Although the current series is the largest re-ported to date, the number of patients treated re-

mains small. Nonetheless, the procedure has provedto be safe, because it was not associated with anyperiprocedural TIA or stroke. The success in re-ducing dissection-induced stenosis, the patency rateobtained at follow-up, and the lack of TIAs suggestthat stent angioplasty offers a viable alternative tocomplex surgical bypass procedures. The long-termefficacy and durability of stent placement for ca-rotid dissection remains to be determined. It is un-known whether intimal hyperplasia, which was notdetected during the anatomic follow-up periods de-


scribed herein, will become of concern in the dis-tant future.

ConclusionThe results of the intermediate-term follow-up

provided in this report suggest that treatment ofcarotid dissection is a useful technique for selecthigh-risk cases, such as when the lesion is hemo-dynamically significant from severe stenosis orcontralateral occlusion, or when anticoagulationhas failed to prevent TIAs or is contraindicated.Additional, extended, long-term angiographic andclinical follow-up will help define the potential im-portance and relative value of this technique for thetreatment of carotid dissection.

AcknowledgmentsWe would like to thank the assistance of Drs. Vineeta Singh,

Clay Johnston, and Daryl Gress.

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