European Journal of Vascular & Endovascular Surgery
Volume 34, Issue 6 , Pages 655-662, December 2007

Carotid Artery Stenting in a Single Center: Are Six Years of Experience Enough to Achieve the Standard of Care?

Department of Surgery, Vascular and Endovascular Surgery Unit, University of Siena, Viale Bracci, I-53100 Siena, Italy

Accepted 13 July 2007. published online 21 September 2007.

Article Outline

Objectives

This study aims to determine safety, short and mid-term outcomes of Carotid Artery Stenting (CAS) and Endarterectomy (CEA) during the last 6 years in a single vascular surgery center.

Methods

We retrospectively reviewed 2624 consecutive carotid revascularizations performed between December 2000 and December 2006 in 2176 patients with severe carotid artery stenosis (symptomatic ≥70%, asymptomatic ≥80%), of which 1589 were CEA and 1035 CAS. Patients were followed up at 1, 3, 6 and 12 months after the procedure and then yearly.

Results

The percutaneous procedure was successful in 99.2% of the cases. No intra-procedural death occurred. The overall death and stroke rates at 30 days, 1 year and 3 years were 1.54%, 2.86%, 7.43% in the CAS group and 2.07%, 3.55%, 6.95% in the CEA group, respectively (p value not significant in any case).

Conclusions

At our vascular surgery centre the results of CEA and CAS are similar. CAS has become our standard of care in preventing strokes and is an effective alternative to CEA for low-risk patients as well.

Keywords: Carotid artery, Carotid stenosis, Angioplasty, Stent, Endarterectomy, Stroke, Mortality rate, Review

 

Back to Article Outline

Introduction 

In Western countries, stroke is the third leading cause of death and is the most common cause of permanent disability.1 A stenosis of the internal carotid artery may be responsible for 10% to 20% of all strokes or transient ischemic attacks (TIA). Carotid artery stenting (CAS) has emerged as a useful, potentially less-invasive alternative to carotid endarterectomy (CEA) but controversy presently surrounds this procedure.2 Part of the controversy arises from confusion regarding which physicians should treat carotid artery disease. Vascular surgeons, neurosurgeons, interventional cardiologists, neuroradiologists, radiologists, cardiac or general surgeons have openly embraced the treatment of carotid disease and in particular this new technology (CAS). At the same time, during the last decade there have been important innovations in the device, technical refinements and a better knowledge of patient selection. With the introduction of CAS, vascular surgeons have been challenged to change their point of view in managing severe carotid artery stenosis. The two most referenced trials in the current clinical decision-making process for carotid stenosis are the North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the Asymptomatic Carotid Atherosclerosis Study (ACAS). Both concluded there was a clear benefit to CEA in patients with symptomatic and asymptomatic carotid occlusive disease.3, 4 In current clinical practice, CAS has emerged as a viable alternative for patients who are deemed at high risk for surgery or poor candidates for CEA, which is considered the standard of care.5 Several trials have suggested equivalent results for CAS and CEA.6, 7, 8, 9

The purpose of this report was to review our experience with CAS in comparing to CEA over the last 6 years.

Back to Article Outline

Methods 

Between December 2000 and December 2006, 1027 successful CAS procedures (out of 1035 attempted procedures: procedural success 99.2%) were performed in our center of Vascular and Endovascular Surgery at the University of Siena, in 937 patients (98 treated with staged bilateral procedures). This represents 39.4% of all carotid lesions treated during the same period (CEA 1589 procedures in 1368 patients). Our indications for treatment were the presence of a symptomatic carotid-artery stenosis ≥70% or an asymptomatic stenosis of at least 80%. A large number of lesions were symptomatic (n=1238, 47.2%).

The demographic data and neurological history of the two study groups (CAS vs CEA) are summarized in Table 1. Demographic variables, clinical data, intraoperative and follow-up data were collected by the operative team in a special database. Written informed consent for intervention was obtained from all patients. Carotid stenting was carried out using self-expandable stents in all cases. Cerebral protection devices were also used in all cases, involving distal filter devices (91.1%), occlusive distal balloon (0.9%) or proximal balloon protection (8%). The majority of procedures were elective (CAS n=1002; CEA n=1527) while the remaining were urgent interventions (CAS n=33; CEA n=62). The reasons for urgent treatment were the same for both groups: amaurosis fugax, crescendo TIA or acute minor stroke within 14-28 days from the onset of symptoms (modified Rankin scale score <3).

Table 1. Demographic data and neurological history of the patient groups. CAS, carotid artery stenting; CEA, endarterectomy; COPD, Chronic Obstructive Pulmonary Disease; ASA, Score of the American Society of Anesthesiologists
CASCEAp-value
Clinical dataNo.%No.%
Procedures1035100.001589100.00–
Mean age74S.D. 365S.D. 6.4p<0.05
Over 80 years14113.65241.49p<0.001
Hypertension73671.11116473.29p=0.22
Smokers60558.583852.75p=0.004
Diabete mellitus32130.9852432.98p=0.30
Coronary artery disease45844.2270644.45p=0.93
Hypercolesterolemia28527.5241025.79p=0.34
Heart failure23122.3738123.97p=0.34
COPD32130.9845928.90p=0.25
Peripheral arterial disease22121.3233120.86p=0.76
Post-CEA restenosis13913.44130.84p<0.001
Post-attinic stenosis353.0430.19p<0.001
Previous radical surgery of the neck494.7270.45p<0.001
Significant medical comorbid conditions (ASA IV)46344.74583.69p<0.001
Carotid post-stenting restenosis181.74–––

Neurological historyNo.%No.%
Symptomatic lesions43842.3375747.63p=0.008
Asymptomatic lesions59657.6783252.37p=0.008

Data analysis included minor, major or fatal strokes and deaths (procedure-related and non-procedure-related), at discharge, at 30 days, at 1 and at 3 years and MI at 30 days. We also evaluated the overall death (procedure-related and non-procedure-related) and stroke rate at 30 days, 1 year and 3 years for CAS and CEA.

A transient ischemic attack (TIA) was defined as a focal, retinal or hemispheric event from which the patient made a complete recovery within 24 hours. A minor stroke was defined as a new neurological deficit that either resolved completely within 30 days or increased on the NIH (National Institutes of Health) Stroke Scale by ≤3. A major stroke was defined as a new neurological deficit that persisted >30 days and increased on the NIH Stroke Scale by ≥4. A fatal stroke was defined as death attributed to an ischemic stroke or intra-cerebral hemorrhagic stroke. MI was defined as new evidence of myocardial damage as indicated by elevation of either creatine kinase or CK-MB to more than 2 times the upper limit of normal and troponin T>0.1ng/mL, usually in the setting of chest pain or electrocardiogram changes. Table 2 shows baseline ultrasound lesion characteristics (Gray-Weale Classification10) between treatment arms.

Table 2. Baseline ultrasound lesion characteristics between treatment arms. CAS, carotid artery stenting; CEA, endarterectomy; PSV, Peak systolic velocity; EDV, End Diastolic Velocity
CAS=1035CEA=1589
PSV297±113cm/sec301±126cm/sec
EDV123±79cm/sec137±64cm/sec

Lesion characteristicsNo.%No.%
TYPE I23722.8970944.65p<0.01
TYPE II25224.3735922.62p=0.43
TYPE III23722.9030819.38p=0.08
TYPE IV30929.8421313.35p<0.01

Back to Article Outline

CAS Procedure 

Carotid stenting was carried out using self-expanding stents exclusively. Cerebral protection devices were used in all cases. All patients were pretreated with acetylsalicylic acid at a mean dosage of 125mg/d and with clopidogrel or ticlopidine at a mean dosage of 75mg/d or 500mg/d, respectively, for at least 4 to 5 days prior to admission. All the procedures were carried out percutaneously via puncture of the right and/or left femoral artery. Weight-adjusted (70 U/kg) heparin was administered and repeated as necessary to maintain an activated clotting time of 225 to 250 seconds throughout the procedure. Based on the experience with percutaneous coronary angioplasty and stenting, the common carotid artery (CCA) was selectively engaged directly by using an appropriate 8-F guiding catheter. When the use of a primary guide catheter was not possible due to the particular anatomy of the supra-aortic vessels, a stiff guidewire was placed into the external carotid artery to position a long sheath or a guiding catheter (coaxial technique) into the CCA. Atropine (0.5 to 1mg) was given intravenously to most patients just before the post-stenting dilation phase to reduce bradycardia and hypotension potentially associated with carotid dilation. Atropine was not administered in patients with tachycardia and uncontrolled systemic hypertension. All patients underwent an angiographic examination of the culprit carotid lesion in 2 projections and an angiographic examination of the intracranial circulation in anteroposterior and/or lateral projections. The same angiographic imaging was performed at the end of the procedure to determine whether there was any variation in the intracranial blood flow. Clopidogrel (75mg/d) or ticlopidine (500mg/d) was continued for at least 30 days after the interventional procedure (hemoglobin and white blood count were checked 7 to 10 days following the percutaneous intervention). Mono antiplatelet therapy (aspirin, clopidogrel, or ticlopidine) was continued indefinitely.11

Back to Article Outline

CEA Procedure 

Out of 1589 CEA procedures the majority (n=1502, 94.5%) were performed using local anesthesia (cervical block plus local infiltration). The remaining 87 cases received general anesthesia due to reduced compliance to local anesthesia of the patients (n=35) or to urgent cases (n=62). 1424 (89.6%) CEAs were performed using a standard medial approach and 165 (10.4%) using a retrojugular12 approach to the carotid bifurcation. In 1253 (78.8%) CEAs a longitudinal arteriotomy was used and in 336 (21.2%) an eversion endarterectomy was employed. The use of temporary shunting and patch closure was selectively done. Dacron patch angioplasty was used in 82.1% cases, including in 87.5% of the female patients. Pre-procedure medical treatment was to stop anti-platelet therapy 5-6 days before the procedure and to continue low-molecular-weight heparin, 4000IU SC a day until the day of procedure. Weight-adjusted (70 U/kg) heparin was administered during the procedure and repeated as necessary to maintain an activated clotting time of 225 to 250 seconds throughout the procedure. The day after the procedure, we started mono anti-platelet therapy (aspirin, clopidogrel or ticlopidine), which continued indefinitely.

Back to Article Outline

Follow-Up 

Echo-duplex and neurological examinations of all patients were carried out at 1, 3, 6 and 12 months after the procedure and then yearly. Patients were instructed to inform the vascular surgeon when any new symptoms occurred after hospital discharge.

Back to Article Outline

Statistical Analysis 

All results were analyzed using SPSS statistical software (SPSS, Chicago, IL). All values were expressed as mean±SD. The Fisher exact test was used to compare the rates between the two study groups (CEA vs. CAS) for categorical variables, and all probability values were two-tailed, with a value of p<0.05 considered as statistically significant. The Pearson χ2 test was used to evaluate the relationship between the categorical variables and the two study groups. Logistic regression was used to compare the stroke and death rate between the two study groups at 30 days, 1 year and 3 years. To evaluate the fate of the CAS and CEA patients, Kaplan-Meier survival analyses were generated for overall survival and freedom from neurological events.

Back to Article Outline

Results 

CAS was successfully performed in 1027/1035 cases (99.2%). The eight failed attempts were due to complex vessel access and underwent immediate intra-operative conversion to CEA. In these 8 patients we did not have any neurological complications at 30 days. The mean intervention time was 24±11 minutes (77±26 minutes for CEA).

The neurological and cardiac complications are described in Table 3. No intra-procedural death occurred.

Table 3. Overall neurological complications. CAS, carotid artery stenting; CEA, endarterectomy; TIA, Transient Ischemic Attack
Clinical outcome
CASCEA
Events during procedureNo.%No.%
Death (any cause)00.0000.00
Major stroke00.0020.12
Minor stroke20.1940.25
TIA60.58130.82
Myocardial Infarction00.0000.00
Cranial neuropathy––332.08

Postoperative Events, at dischargeNo.%No.%
Death (any cause) procedure related30.2970.44
Death (any causes) not procedure related00.0020.12
Major stroke30.2950.32
Minor stroke50.4890.56
TIA70.6840.25
Myocardial Infarction20.1970.44
All strokes and death at discharge131.26291.82p=0.34

Events between discharge and 30 daysNo.%No.%
Death (any cause) procedure related10.130.12
Death (any causes) not procedure related10.100.00
Major stroke00.0010.06
Minor stroke10.100.00
TIA30.2900.00
All TIAs at 30 days161.54171.07p=0.29
Myocardial Infarction at 30 days20.1970.44p=0.5
All stroke and death at 30 days161.54332.07p=0.37

Events between 30 days and 1 yearNo.%No.%
Death (any cause) procedure related10.1230.23
Death (any causes) not procedure related40.4850.39
Major stroke10.1220.15
Minor stroke20.2330.23
TIA50.5670.54
All TIAs at 1 year212.5141.08p=0.01
All stroke and death at 1 year242.86463.55p=0.45

Events between 1 and 3 yearsNo.%No.%
Death any cause51.0680.82
Major & Minor stroke61.27141.43
TIA112.33272.76
All TIAs at 3 years326.79414.19p=0.05
All stroke and death at 3 years357.43686.95p=0.74

Back to Article Outline

Thirty-Day Outcome 

We reported 2 deaths in the CAS group (one procedure-related death -congestive heart failure- and one non-procedure-related death at postoperative day 25 -acute pulmonary edema in dilative cardiomyopathy), 3 fatal strokes (2 intracranial hemorrhages, 1 severe cerebral embolization at postoperative day 1), 3 major strokes (1 acute in-stent thrombosis) and 8 minor strokes. All patients who experienced a major complication were neurologically symptomatic before CAS. In asymptomatic patients there were a number of transient ischemic attacks (13/596; 2.18%), with resolution of symptoms within 24 hours. We observed only 2 MIs.

In the subgroup of urgent CAS procedures, we observed a death/stroke rate of 6.06% at 30 days (no deaths, 2 minor strokes in patients already suffering from severe neurologic deficit before the procedure, and 1 TIA).

We observed 6 fatal strokes in the CEA group (5 intracranial hemorrhages, 1 massive ischemic lesion), 8 major strokes and 13 minor strokes. 65.7% of patients who had experienced a complication were neurologically symptomatic before CAS. Moreover we reported 4 procedure-related deaths (3 MIs at postoperative days 1, 3 and 7) and 2 non-procedure-related deaths at postoperative days 17 and 29 (road accident, re-activation of viral hepatitis). MI occurred in 7 patients.

In the subgroup of urgent CEA procedures, we observed a death/stroke rate of 6.45% at 30 days (1 death, 1 major stroke and 2 minor strokes).

The overall death and stroke rate at 30 days was 1.54% in the CAS group and 2.07% in the CEA group (p=0.37).

Back to Article Outline

Later Outcomes 

Between the 30-day and 1 year periods (patients with complete follow-ups at 1 year were 735/937, 78.4%, for the CAS group and 1276/1368, 93.3%, for the CEA group), the incidence of new strokes was 0.95% and 1.00% respectively for CAS and CEA (p=>1). At 1 year follow-up we observed 5 deaths (1 hemorrhagic stroke, 1 MI, 2 congestive heart failure, 1 acute lymphoma) in the CAS group and 8 deaths in the CEA group (3 hemorrhagic strokes, 3 MIs, 1 pneumonia, 1 gastric cancer), 3 major strokes (1 in the CAS group, 2 in the CEA group), 5 minor strokes (2 in the CAS group, 3 in the CEA group). The overall death and stroke rate at 1 year was 2.86% in the CAS group and 3.55% in the CEA group (p=0.45).

The overall death and stroke rate at 3 years (patients with complete follow-up at 3 years were 442/937, 47.1%, for the CAS group and 983/1368, 71.8%, for the CEA group) was 7.43% in the CAS group and 6.95% in the CEA group (p=0.74).

The cumulative freedom from neurological events and cumulative survival analysis are shown in Fig. 1, Fig. 2.

In-stent restenosis after CAS, at 1 year, occurred in 18 patients (2.45%) while restenosis after CEA occurred in 26 patients (2.04%) (p=0.63).

Back to Article Outline

Discussion 

The critical safety objective of carotid intervention is the avoidance of stroke, in particular, disabling stroke. On the basis of several trials,3, 4, 13, 14 CEA is generally considered the standard therapy for severe carotid artery disease. Recent trials have concentrated on investigating CAS, however there is no general agreement whether it should be accepted as an alternative therapy to CEA. This uncertainty is in part due to the lack of large randomized trials comparing endarterectomy to stenting and the fact that current trials have failed to establish a clear consensus.6, 15, 16, 17, 18, 19, 20, 21, 22, 23 The recent EVA 3-S22 trial found CEA to be superior to CAS. However, many of these trials have been heavily criticised 24, 25, 26, 27 making interpretation of their findings difficult.

We are aware of 5 ongoing randomized trials.28, 29, 30, 31, 32 The results of these trials will provide a more robust level of evidence regarding the risks and benefits of CAS. The experiences of the CAS Registries combined with those of single centers are currently supplying more data about long term results.33, 34, 35 Our experience with CAS started six years ago. Initially we carefully selected patients and focused endovascular treatment on patients with anatomically complex situations (hostile necks, deleterious neck surgery with tracheostomy, secondary interventions after endarterectomy, cervical radiotherapy, carotid stenosis after radiotherapy, large and short neck with high bifurcation, carotid bypass stenosis) or with poor clinical conditions where surgery offers worse results (contralateral occlusions, deficient Circle of Willis, severe coronary diseases, neurological deficit, heart failure or pending coronary revascularization, low life expectancy due to tumors, or old age) [High-risk patients]. Year after year of experience with CAS optimized our learning curve and the results obtained supported our conviction of offering CAS as the first choice to patients with severe carotid stenosis as shown in Table 4.

Table 4. Our management strategy for patients with carotid stenosis. MR, magnetic resonance; CT computed tomography; ICA, internal carotid artery; CCA, common carotid artery; CAS, carotid artery stenting; CEA, carotid endarterectomy; BMT, best medical treatment and ASA, Score of the American Society of Anesthesiologists

At the moment CAS is relatively contraindicated in our center to the following categories of patients: patients with floating thrombus in the internal carotid or common carotid arteries36 (some authors described a different approach to this open question37) or very young patients (≤ 50 years) if they are at standard risk for CEA (ASA≤2. Score of the American Society of Anesthesiologists).

During these six years we observed a drastic drop in the number of CEA procedures and on the contrary a rapid growth in the number of CAS procedures as shown in Fig. 3. The very infrequent periprocedural strokes seen in this review were presumably related to small emboli released during the manipulation of the arch, previous to catheter access into the common carotid artery, before embolic filter protection was in place and at the post-dilatation of the stent. Despite the fact that the immediate periprocedural and in-hospital results are encouraging, we are aware that embolic protection devices (in all their forms) allowed operators to protect the procedure.33, 38, 39

Long-term stroke prevention in our treated patients is the hallmark of successful carotid intervention. The 1 and 3 year rates of ipsilateral stroke for CAS in this review are 2.86 and 7.43%, respectively, similar to those of CEA (3.55% and 6.95%, p value not significant).

We believe that on the basis of the current evidence, CAS with cerebral protection, in the hands of experienced operators, can be considered equal if not superior to CEA in high-risk patients. On the basis of our results we demonstrate that if specific devices applied to specific lesions and/or anatomies are used (“tailored” CAS strategy),40 the endovascular procedure can be successful with a very low complications (Fig. 4). The “tailored” CAS strategy bases its rationale mostly on the complete knowledge of the patient's clinical status, vascular anatomy, carotid plaque characteristics and complexity. We believe that the pathological conditions have to be matched to the technical features of the materials at the disposition of the operator. Another important factor is that the best medical treatment has also dramatically improved compared to 20–25 years ago (the NASCET “era”). There are now many more medication to treat hypertension, dyslipidemia, coronary heart disease and diabetes. For example, there is convincing evidence that clopidogrel, a new generation of anti-platelet anti-aggregation drugs used widely for CAS in addition to aspirin, reduces the risk of myocardial infarction.41, 42

We strongly believe as well that the treatment of severe carotid stenosis must be successfully managed by skilled operators in high-volume centers. These must be performed by centers of vascular surgery, because the vascular surgeon is the operator most familiar with the pathology, the anatomy, hemodynamics and the correlation between Echo-duplex findings and lesion characteristics. These, combined with correct patient and lesion analyses, should indicate the right intervention for each individual patient (“tailored” procedure). A “tailored” procedure is possible only when the operator is completely familiar with both procedures.

Back to Article Outline

Conclusions 

We present our experience of CAS compared to CEA. We have developed an approach to use CAS as a first option, and we indicate CEA only for younger patients and those with particular hypoechoic lesions at duplex imaging. In our center, with our experience, we can now offer both CEA and CAS to the patient with the same awareness and confidence. For now, the literature lacks evidence to support our conclusions, and additional trials and registers will be necessary. At this time in Italy there is a simple, clear and updated evidence-based consensus document drawn up by an Italian multidisciplinary task force (neurologists, neuroradiologists, radiologists, cardiologists, vascular surgeons) for CAS and the prevention and treatment of carotid artery disease (Carotid Artery Stenting. First Consensus Document of the ICCS-SPREAD Joint Committee).43

Back to Article Outline

References 

  1. Heart Disease and Stroke Statistics–2006 Update. Dallas, Texas: American Heart Association; 2006;
  2. Rabe K, Sievert H. Carotid artery stenting: state of the art. J Interv Cardiol. 2004;17:417–426
  3. North American Symptomatic Carotid Endarterectomy Trial Collaborators . Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med. 1991;325:445–453
  4. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study . Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995;273:1421–1428
  5. Zarins CK. Carotid endarterectomy: the gold standard. J Endovasc Surg. 1996;3:10–15
  6. Yadav JS, Wholey MH, Kuntz RE, Fayad P, Katzen BT, Mishkel GJ, et al. Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med. 2004;351:1493–1501
  7. Gray WA, Hopkins LN, Yadav S, Davis T, Wholey M, Atkinson R, et al. Protected carotid stenting in high-surgical-risk patients: the ARCHeR results. J Vasc Surg. 2006 Aug;44:258–268
  8. Hobson RW. Carotid stenting: should it replace endarterectomy in higher-risk patients?. Semin Vasc Surg. 2006 Jun;19:83–86
  9. CaRESS Steering Committee . Carotid Revascularization Using Endarterectomy or Stenting Systems (CaRESS) phase I clinical trial: 1-year results. J Vasc Surg. 2005 Aug;42:213–219
  10. Gray-Weale AC, Graham JC, Burnett JR, Byrne K, Lusby RJ. Carotid artery atheroma: comparison of preoperative B-mode ultrasound appearance with carotid endarterectomy specimen. J Cardiovasc Surg. 1988;29:676–681
  11. Setacci C, de Donato G, Chisci E, Setacci F, Pieraccini M, Cappelli A, et al. Is carotid artery stenting in octogenarians really dangerous?. J Endovasc Ther. 2006 Jun;13:302–309
  12. Neri E, Giubbolini M, Setacci F, Baldi I, Setacci C. The retrojugular route: the ideal exposure for carotid endarterectomy performed under locoregional anesthesia. Eur J Vasc Endovasc Surg. 2003 Sep;26:250–255
  13. Barnett HJ, Taylor DW, Eliasziw M, Fox AJ, Ferguson GG, Haynes RB, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. North American Symptomatic Carotid endarterectomy Trial Collaborators. N Engl J Med. 1998;339:1415–1425
  14. Halliday A, Mansfield A, Marro J, Peto C, Peto R, Potter J, et al. MRC Asymptomatic Carotid Surgery Trial (ACST) Collaborative Group. Prevention of disabling and fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomised controlled trial. Lancet. 2004;363:1491–1502
  15. Coward LJ, Featherstone RL, Brown MM. Safety and efficacy of endovascular treatment of carotid artery stenosis compared with carotid endarterectomy: a Cochrane systematic review of the randomized evidence. Stroke. 2005 Apr;36:905–911
  16. CAVATAS Investigators . Endovascular versus surgical treatment in patients with carotid stenosis in the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS): a randomised trial. Lancet. 2001;357:1729–1737
  17. Brooks WH, McClure RR, Jones MR, Coleman TC, Breathitt L. Carotid angioplasty and stenting versus carotid endarterectomy: randomized trial in a community hospital. J Am Coll Cardiol. 2001;38:1589–1595
  18. Brooks WH, McClure RR, Jones MR, Coleman TL, Breathitt L. Carotid angioplasty and stenting versus carotid endarterectomy for treatment of asymptomatic carotid stenosis: a randomized trial in a community hospital. Neurosurgery. 2004;54:318–325
  19. Naylor RA, Bolia A, Abbott RJ, Pye IF, Smith J, Lennard N, et al. Randomized study of carotid angioplasty and stenting versus carotid endarterectomy: a stopped trial. J Vasc Surg. 1998;28:326–334
  20. Alberts MJ, McCann R, Smith TP, Stack R, Roubin G, Schneck M, et al. A randomized trial of carotid stenting versus endarterectomy in patients with symptomatic carotid stenosis: study design. J Neurovasc Dis. 1997;2:228–234
  21. Alberts MJ. WALLSTENT. Results of a multicenter prospective randomized trial of carotid artery stenting versus carotid endarterectomy. (abstract) Stroke. 2001;32:325
  22. SPACE Collaborators . Stent Protected Angioplasty versus Carotid Endarterectomy in symptomatic patients: 30 days results from the SPACE Trial. Lancet. 2006;368:1239–1247
  23. Mas JL, Chatellier G, Beyssen B, Branchereau A, Moulin T, Becquemin JP, et al. Endarterectomy versus stenting in patients with severe symptomatic stenosis. N Engl J Med. 2006;355:1660–1671
  24. Furlan AJ. Carotid-artery stenting–case open or closed?. N Engl J Med. 2006;19(355):1726–1729[Erratum in: N Engl J Med 2006;21(355):2712]
  25. Naylor AR. SPACE: not the final frontier. Lancet. 2006;368:1215–1216
  26. Setacci C, Cremonesi A. SPACE and EVA-3S trials: the need of standards for carotid stenting. Eur J Vasc Endovasc Surg. 2007;33:48–49
  27. Naylor AR. Where next after SPACE and EVA-3S: ‘the good, the bad and the ugly!’. Eur J Vasc Endovasc Surg. 2007;33:44–47
  28. Hobson RW, Howard VJ, Roubin GS, Brott TG, Ferguson RD, Popma JJ, et al. Carotid artery stenting is associated with increased complications in octogenarians: 30-day stroke and death rates in the CREST lead-in phase. J Vasc Surg. 2004;40:1106–1111
  29. The ACT I Trial (Asymptomatic Carotid Stenosis, Stenting Versus Endarterectomy Trial). Available at: http://www.strokecenter.org/trials/TrialDetail.aspx?tid=624 [Accessed Jan 15, 2007].
  30. The International Carotid Stenting Study – CAVATAS II (Endovascular versus surgical treatment in patients with carotid stenosis in the Carotid and Vertebral Artery Transluminal Angioplasty Study). Available at: http://www.strokecenter.org/trials/TrialDetail.aspx?tid=86 [Accessed Jan 15, 2007].
  31. Gaines PA, Randall MS. Carotid artery stenting for patients with asymptomatic carotid disease (and news on TACIT). Eur J Vasc Endovasc Surg. 2005;30:461–463
  32. The ACST II trial (Asymptomatic Carotid Surgery Trial). Available at: http://www.acst.org.uk/ [Accessed Jan 15, 2007].
  33. Wholey MH, Al-Mubarek N. Updated review of the global carotid artery stent registry. Catheter Cardiovasc Interv. 2003;60:259–266
  34. Roubin GS, New G, Iyer SS, Vitek JJ, Al-Mubarak N, Liu MW, et al. Immediate and late clinical outcomes of carotid artery stenting in patients with symptomatic and asymptomatic carotid artery stenosis: a 5-year prospective analysis. Circulation. 2001;103:532–537
  35. Bergeron P, Roux M, Khanoyan P, Douillez V, Bras J, Gay J. Long-term results of carotid stenting are competitive with surgery. J Vasc Surg. 2005;41:213–221
  36. Setacci C, de Donato G, Setacci F, Chisci E, Cappelli A, Pieraccini M, et al. Surgical management of acute carotid thrombosis after carotid stenting: a report of three cases. J Vasc Surg. 2005 Nov;42:993–996
  37. Parodi JC, Rubin BG, Azizzadeh A, Bartoli M, Sicard GA. Endovascular treatment of an internal carotid artery thrombus using reversal of flow: a case report. J Vasc Surg. 2005;41:146–150
  38. Kastrup A, Groschel K, Krapf H, Brehm BR, Dichgans J, Schulz JB. Early outcome of carotid angioplasty and stenting with and without cerebral protection devices: a systematic review of the literature. Stroke. 2003;34:813–819
  39. Cremonesi A, Manetti R, Setacci F, Setacci C, Castriota F. Protected carotid stenting: clinical advantages and complications of embolic protection devices in 442 consecutive patients. Stroke. 2003 Aug;34:1936–1941
  40. Cremonesi A, Setacci C, Manetti R, de Donato G, Setacci F, Balestra G, et al. Carotid angioplasty and stenting: lesion related treatment strategies. EuroIntervention. 2005;1:289–295
  41. Yusuf S, Zhao F, Mehta SR, Chrolavicius S, Tognoni G, Fox KK. Effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation. N Engl J Med. 2001;345:494–502[Erratum in: N Engl J Med 2001;345:1506, 1716]
  42. Fox KA, Mehta SR, Peters R, Zhao F, Lakkis N, Gersh BJ, et al. Benefits and risks of the combination of clopidogrel and aspirin in patients undergoing surgical revascularization for non-ST-elevation acute coronary syndrome: the Clopidogrel in Unstable angina to prevent Recurrent ischemic Events (CURE) trial. Circulation. 2004;110:1202–1208
  43. Cremonesi A, Setacci C, Bignamini A, Bolognese L, Briganti F, Di Sciascio G, et al. Carotid artery stenting. First Consensus Document of the ICCS-SPREAD Joint Committee. Stroke. 2006;37:2400–2409

PII: S1078-5884(07)00475-3

doi:10.1016/j.ejvs.2007.07.008

European Journal of Vascular & Endovascular Surgery
Volume 34, Issue 6 , Pages 655-662, December 2007

Article Tools

* Image Usage & Resolution