RCB

CCI

Oapsw�Cs1th6hid

D

A

0d

ecurrent Carotid Stenosis afterEA and CAS: Diagnosis and Management

rajesh K. Lal, MD

Carotid endarterectomy (CEA) is the preferred method for cerebral revascularization inpatients with symptomatic and asymptomatic high-grade extracranial carotid artery steno-sis. Carotid artery stenting (CAS) has recently emerged as a less invasive alternative toendarterectomy. Carotid stenting has been demonstrated to be technically feasible andsafe in high-risk patients. It has been approved as an acceptable method for revascular-ization in circumstances where CEA yields suboptimal results. While the final role of CASin carotid revascularization will be determined on the basis of ongoing randomized trials, itis clear that stenting will continue to be performed in subgroups of patients with carotidstenosis. Therefore, it is anticipated that there will be a corresponding increase in thenumber of in-stent restenosis cases. Considerable controversy exists regarding the clinicalsignificance, natural history, threshold for management, and appropriate intervention ofrecurrent carotid stenosis after endarterectomy and after stenting. This review analyzescurrent information on this important clinical problem and presents evidence-based rec-ommendations for the diagnosis and management of recurrent carotid stenosis.Semin Vasc Surg 20:259-266 © 2007 Elsevier Inc. All rights reserved.

itorddftr

STtdCtimaCossmt

arotid Restenosis afterarotid Endarterectomy

ncidenceVER 150,000 CAROTID ENDARTERECTOMIES (CEA)are performed annually in the United States.1 The most

ccurate assessment of carotid restenosis (CR) incidence isrovided in the prospective Asymptomatic Carotid Athero-clerosis Study (ACAS) follow-up data.2 In this report, CRas defined as Doppler-determined diameter reductions of60%. From 3 to 18 months after operation, the incidence ofR was 7.6%. This early development of CR is probably

econdary to myointimal hyperplasia. The incidence of CR8 to 60 months after operation was 1.9%; potentially relatedo progression of atherosclerotic disease. Although studiesave documented absolute rates of CR (�50%) to occur in% to 14% of patients, accompanying neurological eventsave been reported in only 1% to 5% of these patients.3-5 The

ncidence of CR is variable and is, in part, dependent on theefinition of restenosis and the technique used to calculate its

ivision of Vascular Surgery, UMDNJ-New Jersey Medical School, Newark,NJ and Department of Biomedical Engineering, Stevens Institute ofTechnology, Hoboken, NJ.

ddress reprint requests to Brajesh K. Lal, Division of Vascular Surgery,UMDNJ-New Jersey Medical School, 185 South Orange Avenue, MSB-

eH570, Newark, NJ 07103. E-mail: lalbk@umdnj.edu

895-7967/07/$-see front matter © 2007 Elsevier Inc. All rights reserved.oi:10.1053/j.semvascsurg.2007.10.009

ncidence. DeGroote and associates6 emphasized the impor-ance of using life-table methods to determine the incidencef restenosis. Calculation of an absolute CR rate (arteries withestenotic lesions/total carotid procedures) will generally un-erestimate the incidence of restenosis because it is indepen-ent of the duration, frequency, and completeness of clinicalollow-up. However, with life-table methods, the probabili-ies of developing CR (�50%) 7 years after CEA have beeneported as 31% to 32%.5,6

urveillance and Diagnosishe ACAS data on recurrent stenosis after CEA2 emphasize

he value of serial noninvasive testing after CEA, particularlyuring the first few years postoperatively. Although risk ofR was highest during the first few years after CEA and low

hereafter, the recommended frequency of noninvasive test-ng after CEA remains controversial.5,7 However, we recom-

end noninvasive duplex ultrasonography testing of patientst 6-month to 12-month intervals during the first 3 years afterEA. Thereafter, follow-up testing is based on developmentf cervical bruits and nonspecific or lateralizing neurologicalymptoms, rather than routine screening. Patients withymptomatic or high-grade (�80%) asymptomatic stenosisay then be referred for management. Importantly though,

he heterogeneity of published results on restenosis and op-

rative complications7 suggests that much better data are

259

np

wd(swnm

NIRdrffiuma

eItu0Bpamttpc

ahrstsiltws

OOapwrssw

pcppcsse

barpioor

dospittc

EEncawnmTwcpp

aitoes(soTtssc

260 B.K. Lal

eeded if we are to arrive at reliable estimates of these com-lications and recommendations on follow-up frequency.The ACAS2 also demonstrated that CR in patients closed

ith patch angioplasty was 4.5% compared with an inci-ence of 16.9% in patients who underwent primary closureP � .001). None of the other risk factors analyzed (cigarettemoking, hypercholesterolemia, age, and female gender)ere found to have a statistically significant effect on reste-osis. Therefore, patients closed without a patch warrantore frequent and longer follow-ups.

atural History andndications for Retreatmentestenosis is generally attributed to neointimal hyperplasiauring the early postoperative period (within 24 months) orecurrent atherosclerosis thereafter.4,8,9 Exact mechanismsor development of neointimal hyperplasia are still being de-ned. The lesion, on gross as well as angiographic or duplexltrasonography interrogation, is generally smooth and ho-ogeneous in appearance. Late CR lesions are indistinguish-

ble from primary atherosclerosis.The clinical significance of CR is still debated. Consensus

xists regarding the need for treatment for symptomatic CR.n asymptomatic CR, however, authors have acknowledgedhat the risk of stroke or progression to total occlusion4,5 isncommon. The incidence of symptomatic CR ranges from% to 8.2%, while asymptomatic CR occurs in 1.3% to 37%.3

ased on the low incidence of symptoms in this cohort ofatients, these authors have proposed careful surveillancelone for asymptomatic patients. This recommendation wasade in the absence of randomized trial data, with the belief

hat neointimal hyperplasia carries a low risk for emboliza-ion, and with the knowledge that reoperation has been re-orted to carry an increased risk of perioperative neurologi-al events and cranial nerve palsies.

Conversely, most surgeons have taken a more aggressivepproach toward asymptomatic CR, and elect to operate onigh-grade (�80%) asymptomatic lesions. In O’Hara et al’seport10 of 206 redo CEAs only 43% had symptoms. Man-our et al11 operated on 82 CRs, of which 66% were symp-omatic, and the remaining had high-grade asymptomatictenoses �80%. The rationale for such an approach is that its extremely difficult to predict which preocclusive (�80%)esions will remain asymptomatic. Our group subscribes tohis view, and we have reported our low complication rateith redo CEAs for asymptomatic high-grade (�80%) and

ymptomatic (�50%) carotid restenosis.12

perative Managementperative management for CR was first outlined by Stoney

nd String in 1976.13 They reported on the treatment of 29atients with CR with various combinations of second CEAith/without a vein patch, vein patches alone, and vein graft

eplacement. One postoperative death (3.4%) because oftroke was the only complication in their series. An expandederies of 116 reoperations for CR from the same institution

as reported by Bartlett et al.9 This experience was accom- c

anied by a 4.3% stroke morbidity, with two deaths (1.7%)aused by stroke. Transient cranial nerve palsies were re-orted in 23 cases (19.8%). Das et al14 reported the use ofatch angioplasty in 59 of 62 reoperations for CR, with aombined stroke-death rate of 4.6% and an incidence of tran-ient cranial nerve palsy of 9.2%. Similar reports of successfulurgical revascularization of CR have been reported by sev-ral groups.10,11,15-18

The long-term durability of reoperations for CR has noteen extensively studied, because the number of cases is lownd the follow-up has been nonuniform. Rockman et al19

eported a late recurrent stenosis rate of 19.5% (8 of 41atients) in an early series of patients who underwent primar-

ly redo CEA with patch angioplasty for CR. In a later reportf 72 patients managed with a combination of patched CEAr vein interposition grafts, they noted a recurrent stenosisate of 11%.

Hill et al20 have documented no complications of stroke oreath in their experience with 40 restenosis cases treated byperative management. Despite near perfect results fromome institutions, it is generally accepted that reentering areviously operated field may be associated with a higher

ncidence of cranial nerve injuries, as well as wound hema-omas. In addition, some of the restenoses may occur beyondhe original endarterectomy site, making the dissection tolear them more difficult and hazardous.

ndovascular Managementndovascular management for CR was proposed as an alter-ative to reoperation in the late 1990s.12,21Consideration forarotid artery stenting in the management of CR was encour-ged based on several rationales. First, CR, when observedithin the first 2 years after CEA, is usually due to a smootheointimal hyperplastic lesion. Second, reoperations may beore difficult and the lesion may be surgically inaccessible.hird, reoperations for CR have been associated with a some-hat higher complication rate than operation for primary

arotid stenosis. Fourth, there was an inherent appeal of re-lacing an open operation with a less-invasive catheter-basedrocedure.In 1999, we reported our initial experience with carotid

rtery stenting (CAS) for recurrent carotid stenosis after CEAn 17 patients.12 These patients underwent CAS with Walls-ents (Boston Scientific, Natick, MA) and, despite the absencef antiembolic protection in this early phase of our experi-nce, we observed no periprocedural strokes or deaths. Weubsequently reviewed our results for 210 CAS procedures116 procedures for CR and 94 for primary carotid steno-is).22 Neurological event rates were determined on the basisf examinations performed by an independent neurologist.hirty-day outcomes were not significantly different between

he CR and primary carotid stenosis groups. The rate oftroke was 2.6% in the CR group versus 3.2% in the primarytenosis group (P � .56). However, the neurological compli-ation rate (stroke � transient ischemic attack) was signifi-

antly lower in patients that were treated for early CR (�24

mC

macn

RaIClgsHeIoiCsffodtslstnwastob

SDcapaoHwrprorra

pgpwo(actr�v

F(iMsaeos

Recurrent carotid stenosis after CEA and CAS 261

onths post-CEA) compared to late CR (�24 months post-EA) (1.5% v 10.2%, P � .048).Carotid artery stenting is now considered an option for theanagement of symptomatic and asymptomatic restenosis

fter prior CEA. Based on a consensus conference,23 clini-ians agreed that CR currently constitutes one of the limitedumbers of indications for CAS.

ecurrent Stenosisfter Carotid Artery Stenting

ncidenceoronary stenting has been associated with significantly

ower rates of angiographic and clinical restenosis than an-ioplasty alone.24 This salutary effect may be due to thetent’s ability to provide predictably larger arterial lumens.owever, myointimal hyperplasia accompanies virtually ev-

ry stent placement in the coronary, iliac, or carotid system.24

ntimal hyperplastic recurrence has been observed after cor-nary stenting in 16% to 59% of cases and after iliac stentingn 13% to 39% of reported series.25 A valid concern was thatAS could be associated with equivalent rates of recurrent

tenosis within the stent (in-stent restenosis [ISR]) duringollow-up. We used life-table analysis to provide specific in-ormation on ISR after CAS26 (Fig 1). Over a follow-up periodf 1 to 74 months (mean 18.8 � 10), 22 of 122 patientsemonstrated ISR � 40%. All 22 ISR patients were asymp-omatic on presentation and were diagnosed by duplex ultra-onography during routine follow-up. Although restenoticesions ranged from 40% to 99%, only five patients demon-trated high-grade ISR (�80%), while the remaining fell inhe following ranges: 40% to 59%, n � 11 and 60% to 79%,� 6. The projected 5-year recurrence rate for ISR �80%as 6.4%. Cumulative 4-year rate of ISR � 60% was 16.4%,

nd of ISR � 40% was 42.7%. These observations were sub-equently confirmed by others.27 While ISR does not appearo occur at the high rates associated with bare metal stentingf the coronary arteries; a substantial number of patients cane anticipated to progress to moderate and high-grade ISR.

urveillance and Diagnosisuplex ultrasonography is the standard technique to followarotid stenosis patients treated with CEA or medical therapylone. Ultrasonography velocities correlate with angiographicercent stenosis in the native unstented carotid artery and theppropriate threshold velocities, signifying different degreesf stenoses have been intensively analyzed and identified.28-30

owever, ultrasonography velocity criteria have not beenell-established for patients undergoing CAS. In 2004, we

eported that placement of a stent altered the biomechanicalroperties of the carotid territory, such that compliance waseduced31 (Fig 2). We speculated that the enhanced stiffnessf the stent-arterial wall complex renders the flow-pressureelationship of the carotid artery closer to those observed in aigid tube,32 so that the energy normally applied to dilate the

rtery results in an increased velocity. In this report, we com- h

ared post-CAS ultrasonography velocities with angio-raphically measured residual in-stent stenosis after 90 CASrocedures. Mean angiographic residual stenosis after CASas 5.4%, while corresponding peak systolic velocity (PSV)n ultrasonography was 120.4 cm/s; end diastolic velocityEDV), 41.4 cm/s; PSV/EDV ratio, 3.3; and internal carotidrtery to common carotid artery (ICA/CCA) ratio, 1.6. Re-eiver operating characteristic (ROC) analysis demonstratedhat a combined threshold of PSV � 150 cm/s and ICA/CCAatio � 2.16 were optimal for detecting residual stenosis20%. Based on these observations, we concluded that re-

ised velocity criteria would need to be developed to identify

igure 1 Incidence of in-stent restenosis after carotid artery stenting.A) Kaplan-Meier cumulative event rates for clinically significantn-stent-restenosis (ISR) � 80% after carotid artery stenting. (B) Kaplan-

eier cumulative event rates for ISR � 60% after carotid arterytenting. (C) Kaplan-Meier cumulative event rates for ISR � 40%fter carotid artery stenting. Number of patients at the beginning ofach time interval and standard error are indicated below the X axisf each graph. CAS, carotid artery stenting; N, number at risk; SE,tandard error. Adapted with permission from Lal et al.26

igher grades of ISR in stented carotid arteries.

tusnaampd75aiaCrtwnmahs

ugsasdp

velrptuCpnipr0.do12�flcgcpt

NTct1tswabtplmdlmPw

Fo(sf

262 B.K. Lal

These observations were followed by at least four studieshat have addressed this hypothesis. Peterson et al33 analyzedltrasonography velocity and angiographic measurements oftenosis in three patients with high-grade ISR and proposedew criteria defining ISR � 70% (PSV � 170, EDV � 120,nd velocity increase �50% over baseline). Stanziale et al34

nalyzed velocity/angiography observations obtained pri-arily from procedural angiography and selected angiogra-hy performed in patients with suspected high-grade ISRuring follow-up. They proposed new criteria defining ISR �0% (PSV � 350 and ICA/CCA ratio � 4.75), and ISR �0% (PSV � 225 and ICA/CCA ratio � 2.5). Chi et al35

nalyzed 13 pairs of ultrasound and angiogram observationsn CAS patients with suspected high-grade ISR. They offeredlternate criteria to define ISR � 70% (PSV � 450, or ICA/CA ratio � 4.3) and ISR � 50% (PSV � 240 or ICA/CCA

atio � 2.45). Chahwan et al36 analyzed six pairs of observa-ions from patients with high-grade ISR on follow-up, alongith procedural angiograms (n � 71). They concluded that aormal ultrasound after CAS is reliable in identifying a nor-al artery, but larger studies would be required to determine

ppropriate threshold criteria. These studies confirm thatigher grades of restenosis are also overestimated in the

igure 2 Carotid artery stenting alters the biomechanical propertiesf the stent-arterial complex. Measurement of elastic modulusA) and compliance (B) of the native internal carotid artery versustented internal carotid artery. CAS, carotid artery stenting. Adaptedrom Lal et al.31

tented artery when velocity criteria for native arteries are p

tilized. However, procedural risks precluded routine angio-raphic follow-up, thereby limiting the number of compari-ons that were made between velocity measurements andngiographic stenosis in these studies. Therefore, compari-ons could not be performed across the full spectrum ofegrees of restenosis. This explains why each report pro-osed different threshold velocity criteria for ISR.In a recent report,37 we compared duplex ultrasonography

elocity measurements with luminal stenosis measured byither angiography or CT angiography (CTA) during fol-ow-up of all our CAS patients (n � 310 observations). Ca-otid angiograms performed at completion of CAS were com-ared with duplex ultrasounds performed immediately afterhe procedure. Patients were followed with annual duplexltrasonography and underwent both ultrasonography andTA at their most recent follow-up visit. Patients with sus-ected high-grade ISR on ultrasonography underwent diag-ostic carotid angiography. The ultrasonography protocol

ncluded PSV and EDV measurements in the native CCA,roximal stent, mid stent, distal stent, and distal ICA. Accu-acy of CTA versus carotid angiography was confirmed (r2 �.88) in a subset of patients (n � 19). Post-CAS PSV (r2 �

85) and ICA/CCA ratios (r2 � .76) correlated most with theegree of stenosis. ROC analysis demonstrated the followingptimal threshold criteria: residual stenosis �20% (PSV �50 cm/s and ICA/CCA ratio � 2.15), ISR � 50% (PSV �20 cm/s and ICA/CCA ratio � 2.7), and ISR � 80% (PSV

340 cm/s and ICA/CCA ratio � 4.15) (Fig 3). We, there-ore, proposed revised velocity criteria37 to serve as guide-ines for other vascular laboratories when studying stentedarotid arteries (Table 1). While our results can be used asuidelines, individual laboratories must develop thresholdriteria that are accurate for their own environment. Theseroposed criteria can form the basis for additional prospec-ive validation studies.

atural Historyhe majority of restenoses �40% in our series of CAS pro-edures occurred within 18 months (13 of 22 [60%]), andhe majority of high-grade restenoses �80% occurred within5 months (3 of 5 [60%]), of their intervention26 (Fig 4). We,herefore, recommend more frequent follow-up duplex ultra-onography evaluations early after CAS. In our own practice,e evaluate patients every 6 months for the first 2 years, and

nnually thereafter. We also recommend early registration ofaseline velocity measurements after CAS, against which fu-ure results should be compared. We recommend that allatients undergoing CAS must be placed in a regular fol-

ow-up protocol. The first follow-up duplex ultrasonographyust occur as soon after the procedure as possible, preferablyuring the same admission. B-mode imaging of the arterial

umen and spectral waveform analysis must be used to supple-ent and enhance the accuracy of velocity criteria. Elevations in

SV and/or ICA/CCA ratios are indicative of developing ISR,hich must then undergo angiographic evaluation when appro-

riate thresholds are reached.

airop(smoi

mgittbtT(pTwt(.t4faohdf

Fmiwidfel

TA

0258

A

A

Fdtcmp

Recurrent carotid stenosis after CEA and CAS 263

As stated previously, predictors for neointimal hyperplasiare the subject of continued investigation. There is limitednformation on what factors constitute risks for ISR. Ourecent report attempts to address this question. We devel-ped a novel protocol to assess and classify the morphologicatterns of ISR occurring in patients after CAS38 into type Ifocal �10 mm end-stent lesions), II (focal �10 mm, intra-tent), III (diffuse � 10 mm, intra-stent), IV (diffuse � 10m proliferative, extending outside the stent), and V (total

cclusion) (Fig 5). We then entered potential risk factors,ncluding morphologic pattern of ISR, into a multivariate

igure 3 Receiver operating characteristic (ROC) analysis to deter-ine accuracy parameters of threshold velocities appropriate for the

dentification of high-grade in-stent restenosis � 80%. ROC curvesere developed for peak systolic velocity (PSV) (bold black line),

nternal carotid artery/common carotid artery ratios (red line), endiastolic velocity (EDV) (green line), and PSV/EDV ratios (blue line)

or each threshold stenosis. Adapted with permission from Lalt al.37 (For interpretation of the references to color in this figureegend, the reader is referred to the web version of this article.)

able 1 Suggested Velocity Criteria Defining Stenoses in the Srtery Utilized at our Institution

Stented Carotid Artery

–19% PSV < 150 cm/s and ICA/CCA ratio <2.150–49% PSV 150–219 cm/s0–79% PSV 220–339 cm/s and ICA/CCA ratio >2.70–99% PSV > 340 cm/s and ICA/CCA ratio >4.15

bbreviations: CCA, common carotid artery; EDV, end diastolic velomeasurements for stented carotid arteries are performed within

dapted with permssion from Lal et al.37

odel to determine independent predictors of future high-rade ISR and need for reintervention. Risk factors studiedncluded age, gender, hypercholesterolemia, diabetes, hyper-ension, coronary artery disease, etiology of stenosis, symp-omatic status, prior history of ISR, type of stent used, num-er of stents used, and residual stenosis after CAS. We foundhat 85 ISR lesions developed after 255 CAS procedures.heir percent distribution was 40, 25.9, 12.9, 20 and 1.2types I through V, respectively). Accuracy of ultrasonogra-hy classification was confirmed by angiography (r2 � 0.82).hirteen lesions were �80% diameter reducing, and under-ent endovascular reintervention. On univariate analysis,

he need for reintervention was highest in type IV lesions0%, 0%, 27.3%, and 58.8%; types I to IV, respectively; P �001). A history of prior ISR (2.9%, 0%, 0%, and 41.2%;ypes I to IV; P � .003) and of diabetes (20.6%, 22.7%,5.5%, and 52.9%; types I to IV; P � 0.02) occurred morerequently with type IV ISR lesions (Table 2). On multivariatenalysis, only the type of ISR (odds ratio � 5.1) and a historyf diabetes (odds ratio � 9.7) were independent predictors ofigh-grade recurrent ISR and reintervention.38 Follow-upuplex ultrasonography evaluations after CAS must, there-ore, include an assessment of the morphologic pattern of ISR

d Carotid Artery Compared to Criteria for the Native Carotid

Native Carotid Artery

0–19% PSV < 130 cm/s20–49% PSV 130–189 cm/s50–79% PSV 190–249 cm/s and EDV < 120 cm/s80–99% PSV > 250 cm/s and EDV > 120 cm/s,

or ICA/CCA ratio >3.2

A, internal carotid artery; PSV, peak systolic velocity; PSV and EDVnted segments.

igure 4 Distribution of in-stent restenosis cases based on time ofiagnosis from initial carotid artery stenting procedure. Note thathe majority of restenoses occurred within 18 months of the initialarotid artery stenting procedure. Dotted line identifies the 18-onth postprocedure mark. ISR, in-stent restenosis. Adapted withermission from Lal et al.26

tente

city; ICthe ste

silit

EIipri(wtfitIaddE

ebvorItlgIepctc

SRbTwsbsssopaoe

CWwswcp

Fslss

T

IDB

P

AA*

264 B.K. Lal

o that patients with type IV lesions can be placed on a morentensive monitoring program (perhaps every 6 months forife). Additional data must be acquired to validate these find-ngs in prospectively implemented studies at multiple cen-ers.

ndovascular Managementn our program, patients developing �80% diameter-reduc-ng ISR undergo angiographic confirmation of the lesion andreferential endovascular treatment.25,26,39 In our most recenteport,38 endovascular retreatment was required in 3 of 11nstances of type III ISR, and 10 of 17 instances of type IV ISRTable 1). The mean interval between CAS and reinterventionas 18.2 months. We observed a significant increase in rein-

ervention in association with increasing levels of ISR classi-cation (0%, 0%, 27.3% and 58.8% for types I to IV, respec-ively; �2 trend � 29.4, P � .001). Modalities used to treatSR included balloon angioplasty, stenting, cutting balloonngioplasty alone, or in conjunction with stenting. Proce-ural success was achieved in all these cases, without evi-ence of any abrupt arterial closure or neurological events.ndovascular treatment of ISR afforded similar percent diam-

igure 5 Classification of the morphologic patterns of carotid in-tent restenosis. Classification is based on the length and geographicocation of the neointimal hyperplastic lesion with respect to thetent. The shaded area represents the stent. CAS, carotid arterytenting. Adapted with permission from Lal et al.38

able 2 Details of Endovascular Reinterventions Performed fo

FocalEnd-Stent I

(n � 34)

ncidence of TLR* 0evices used for treatment of ISR (n)alloon angioplasty 0Stent 0Cutting balloon 0Cutting balloon � stent 0

osttreatment result, % residual stenosis NA

bbreviations: ISR, in-stent-restenosis; NA, not applicable; TLR, tardapted with permission from Lal et al.38

P � .001.

ter residual stenoses in all instances and was not influencedy ISR class. Three of the patients have required repeat inter-entions. One patient has required two repeat interventionsver a follow-up period of 3 years. Other investigators haveeported similar success with endovascular management ofSR. Zhou et al40 have recently reported on the successfulreatment of seven ISR lesions and Setacci et al41 on 15 suchesions. They utilized angioplasty alone, cutting balloon an-ioplasty alone or repeat stenting as their modes of therapy.ncreasing experience with the treatment of these lesions willnable formulation of standardized approaches and establishotential limitations of repeated treatments. However, weurrently recommend angioplasty as the primary approach tohese intimal hyperplastic lesions with restenting in thoseases with suboptimal results.

urgical Treatmentecurrent ISR after endovascular management of ISR haseen reported in our series as well as those by others.25,26,40,41

hey tend to occur in a small percentage of cases and respondell to repeat angioplasty and/or stenting. Individual in-

tances of stent explantation and repeat endarterectomy haveeen reported by our group39 and others.42,43 They are re-erved for heavily calcified lesions with suboptimal primarytenting results,39 for preocclusive lesions no longer respon-ive or approachable by angioplasty,42,43 for technical failuref stent material,44 or for primary stent thrombosis.45 As ex-erience with endovascular approaches to recurrent lesions,nd technological advances in catheters/guide wires/stentsccur, we anticipate a decreasing need for explantation op-rations.

onclusionse have restricted the majority of our clinical experienceith CAS to post-CEA restenoses, surgically inaccessible le-

ions, radiation-induced stenoses and patients presentingith prohibitively high medical risks. Results from our series

onfirm that CAS is safe and effective for CR and that itseriprocedural complications are comparable with operative

tent Restenosis after Carotid Artery Stenting

Patterns of ISR (%)

FocalIntra-Stent II

(n � 22)

DiffuseIntra-Stent III

(n � 11)

DiffuseProliferative IV

(n � 17)

0 27.3 58.8

0 1 30 1 50 0 10 1 1

NA 10.4 � 6.9 11.9 � 6.1

ion revascularization.

r In-s

get les

irrdplt

ASs

R

1

1

1

1

1

1

1

1

1

1

2

2

2

2

2

2

2

2

2

2

3

3

3

3

3

3

3

3

3

3

4

4

Recurrent carotid stenosis after CEA and CAS 265

ntervention with the additional advantage of eliminating theisk of cranial nerve injuries. It appears that the recurrent ISRates are low and subsequent interventions by means of en-ovascular methods are not associated with additional com-lications. If this experience is confirmed on further fol-

ow-up and in larger studies, CAS may become the preferredreatment of post-CEA restenosis.

cknowledgmentupported, in part, by a grant from the American Heart As-ociation.

eferences1. Cronenwett JL (ed): Carotid artery disease, in The Dartmouth Atlas of

Vascular Health Care, Chicago, IL, AHA Press, Division of Health Fo-rum Inc., 2001, pp 41-64

2. Moore WS, Kempczinski RF, Nelson JJ, Toole JF: Recurrent carotidstenosis: results of the asymptomatic carotid atherosclerosis study.Stroke 29:2018-2025, 1998

3. Beebe HG: Scientific evidence demonstrating the safety of carotid an-gioplasty and stenting: do we have enough to draw conclusions yet?J Vasc Surg 27:788-790, 1998

4. Lattimer CR, Burnand KG: Recurrent carotid stenosis after carotid end-arterectomy. Br J Surg 84:1206-1219, 1997

5. Healy DA, Zierler RE, Nicholls SC, et al: Long-term follow-up andclinical outcome of carotid restenosis. J Vasc Surg 10:662-668; discus-sion 668-669, 1989

6. DeGroote RD, Lynch TG, Jamil Z, Hobson RW 2nd: Carotid restenosis:long-term noninvasive follow-up after carotid endarterectomy. Stroke18:1031-1036, 1987

7. Frericks H, Kievit J, van Baalen JM, van Bockel JH: Carotid recurrentstenosis and risk of ipsilateral stroke: a systematic review of the litera-ture. Stroke 29:244-250, 1998

8. Sterpetti AV, Schultz RD, Feldhaus RJ, et al: Natural history of recurrentcarotid artery disease. Surg Gynecol Obstet 168:217-223, 1989

9. Bartlett FF, Rapp JH, Goldstone J, Ehrenfeld WK, Stoney RJ: Recurrentcarotid stenosis: operative strategy and late results. J Vasc Surg 5:452-456, 1987

0. O’Hara PJ, Hertzer NR, Karafa MT, Mascha EJ, Krajewski LP, Beven EG:Reoperation for recurrent carotid stenosis: early results and late out-come in 199 patients. J Vasc Surg 34:5-12, 2001

1. Mansour MA, Kang SS, Baker WH, et al: Carotid endarterectomy forrecurrent stenosis. J Vasc Surg 25:877-883, 1997

2. Hobson RW 2nd, Goldstein JE, Jamil Z, et al: Carotid restenosis: oper-ative and endovascular management. J Vasc Surg 29:228-235; discus-sion 235-228, 1999

3. Stoney RJ, String ST: Recurrent carotid stenosis. Surgery 80:705-710,1976

4. Das MB, Hertzer NR, Ratliff NB, O’Hara PJ, Beven EG: Recurrent ca-rotid stenosis. A five-year series of 65 reoperations. Ann Surg 202:28-35, 1985

5. Gagne PJ, Riles TS, Imparato AM, Lamparello PJ, Giangola G, LandisRM: Redo endarterectomy for recurrent carotid artery stenosis. EurJ Vasc Surg 5:135-140, 1991

6. Gagne PJ, Riles TS, Jacobowitz GR, et al: Long-term follow-up of pa-tients undergoing reoperation for recurrent carotid artery disease.J Vasc Surg 18:991-998; discussion 999-1001, 1993

7. Mansour MA, Webb KM, Kang SS, et al: Decreased recurrent carotidstenosis by routine patching and intraoperative scanning. Am Surg67:328-332; discussion 332-323, 2001

8. Treiman GS, Jenkins JM, Edwards WH, Sr, et al: The evolving surgicalmanagement of recurrent carotid stenosis. J Vasc Surg 16:354-362;discussion 362-353, 1992

9. Rockman CB, Riles TS, Landis R, et al: Redo carotid surgery: an analysis

of materials and configurations used in carotid reoperations and their

influence on perioperative stroke and subsequent recurrent stenosis. JVasc Surg 29:72-80; discussion 80-71, 1999

0. Hill BB, Olcott CT, Dalman RL, Harris EJ Jr, Zarins CK: Reoperation forcarotid stenosis is as safe as primary carotid endarterectomy. J VascSurg 30:26-35, 1999

1. Yadav JS, Roubin GS, King P, Iyer S, Vitek J: Angioplasty and stentingfor restenosis after carotid endarterectomy. Initial experience. Stroke27:2075-2079, 1996

2. Lal B, Hobson R, Cuadra S, et al: Carotid artery stenting: does theoutcome depend on the indication? Presented at Vascular 2005, An-nual Conference of the Society for Vascular Surgery, Chicago, IL, 2005

3. Veith FJ, Amor M, Ohki T, et al: Current status of carotid bifurcationangioplasty and stenting based on a consensus of opinion leaders.J Vasc Surg 33:S111-S116, 2001 (suppl)

4. Tepe G, Schmehl J, Claussen CD, Ernemann U, Pereira P, Duda SH:Drug coated stents for carotid intervention. J Cardiovasc Surg (Torino)46:249-259, 2005

5. Chakhtoura EY, Hobson RW 2nd, Goldstein J, et al: In-stent restenosisafter carotid angioplasty-stenting: incidence and management. J VascSurg 33:220-225; discussion 225-226, 2001

6. Lal BK, Hobson RW 2nd, Goldstein J, et al: In-stent recurrent stenosisafter carotid artery stenting: life table analysis and clinical relevance.J Vasc Surg 38:1162-1168; discussion 1169, 2003

7. Bosiers M, Peeters P, Deloose K, et al: Does carotid artery stenting workon the long run: 5-year results in high-volume centers (ELOCAS Reg-istry). J Cardiovasc Surg (Torino) 46:241-247, 2005

8. Faught WE, Mattos MA, van Bemmelen PS, et al: Color-flow duplexscanning of carotid arteries: new velocity criteria based on receiveroperator characteristic analysis for threshold stenoses used in thesymptomatic and asymptomatic carotid trials. J Vasc Surg 19:818-827;discussion 827-818, 1994

9. Lal BK, Hobson IR: Carotid artery occlusive disease. Curr Treat OptionsCardiovasc Med 2:243-254, 2000

0. Mintz BL, Hobson RW 2nd: Diagnosis and treatment of carotid arterystenosis. J Am Osteopath Assoc 100:S22-26, 2000 (suppl)

1. Lal BK, Hobson RW 2nd, Goldstein J, Chakhtoura EY, Duran WN:Carotid artery stenting: is there a need to revise ultrasound velocitycriteria? J Vasc Surg 39:58-66, 2004

2. Green JF: Mechanical concepts in cardiovascular and pulmonary phys-iology. Philadelphia, Lea & Febiger Publishers, 1977, pp 47-53

3. Peterson BG, Longo GM, Kibbe MR, et al: Duplex ultrasound remains areliable test even after carotid stenting. Ann Vasc Surg 19:793-797,2005

4. Stanziale SF, Wholey MH, Boules TN, Selzer F, Makaroun MS: Deter-mining in-stent stenosis of carotid arteries by duplex ultrasound crite-ria. J Endovasc Ther 12:346-353, 2005

5. Chi YW, White CJ, Woods TC, Goldman CK: Ultrasound velocitycriteria for carotid in-stent restenosis. Catheter Cardiovasc Interv 69:349-354, 2007

6. Chahwan S, Miller MT, Pigott JP, Whalen RC, Jones L, Comerota AJ:Carotid artery velocity characteristics after carotid artery angioplastyand stenting. J Vasc Surg 45:523-526, 2007

7. Lal BK, Hobson RW, Tofighi B, Kapadia I, Cuadra S, Jamil Z: Duplexultrasound velocity criteria for the stented carotid artery. J Vasc Surg. Inpress

8. Lal BK, Kaperonis EA, Cuadra S, Kapadia I, Hobson RW: Patterns ofin-stent restenosis after carotid artery stenting: classification and impli-cations for long-term outcome. J Vasc Surg 46:833-840, 2007

9. Choi HM, Hobson RW, Goldstein J, et al: Technical challenges in aprogram of carotid artery stenting. J Vasc Surg 40:746-751; discussion751, 2004

0. Zhou W, Lin PH, Bush RL, et al: Management of in-sent restenosis aftercarotid artery stenting in high-risk patients. J Vasc Surg 43:305-312,2006

1. Setacci C, de Donato G, Setacci F, et al: In-stent restenosis after carotidangioplasty and stenting: a challenge for the vascular surgeon. Eur J

Vasc Endovasc Surg 29:601-607, 2005

4

4

4

4

266 B.K. Lal

2. Akin E, Knobloch K, Pichlmaier M, Haverich A: Instent restenosis aftercarotid stenting necessitating open carotid surgical repair. Eur J Car-diothorac Surg 26:442-443, 2004

3. Gray WA, White HJ Jr, Barrett DM, Chandran G, Turner R, Reisman M:Carotid stenting and endarterectomy: a clinical and cost comparison of

revascularization strategies. Stroke 33:1063-1070, 2002

4. de Vries JP, Meijer RW, van den Berg JC, Meijer JM, van de PavoordtED: Stent fracture after endoluminal repair of a carotid artery pseudo-aneurysm. J Endovasc Ther 12:612-615, 2005

5. Setacci C, de Donato G, Setacci F, et al: Surgical management of acutecarotid thrombosis after carotid stenting: a report of three cases. J Vasc

Surg 42:993-996, 2005