Carotid angioplasty and stenting: Treatment of postcarotid endarterectomy restenosis is at least as safe as primary stenosis treatment

Article Outline

• Abstract
• Materials and methods
  • Patients
  • CAS procedure
  • TCD monitoring
  • Clinical outcome
  • Statistics
• Results
  • Clinical results
  • TCD data
  • Subgroup analyses
• Discussion
• Conclusion
• Author contributions
• Appendix (online only)
• References
• Copyright

Objectives

This study compared transcranial Doppler (TCD) imaging and outcomes of carotid angioplasty and stenting (CAS) in stenosis after carotid endarterectomy (CEA) vs primary atherosclerotic stenoses.

Methods

A prospectively accumulated database of 812 CAS procedures was analyzed retrospectively. Two groups were created. Group 1 had 72 restenoses at a mean of 71 months (range, 5-245 months) after initial CEA. Group 2 had 740 primary stenoses. Clinical end points were cerebral ischemic events and death. TCD end points were numbers of isolated microemboli and microembolic showers during five procedural phases.

Results

Groups 1 and 2 were evenly matched for demographic data: median age, 70 vs 71 years; 44 (61%) vs 525 men (71%); 14 (19%) vs 147 symptomatic (20%). Seven (0.9%) deaths and 10 major (1.2%) and 21 minor (2.6%) strokes occurred in group 2 (P = .049). Mean (standard deviation) numbers of isolated microemboli for groups 1 vs 2 were wiring, 37.0 (31.1) vs 50.4 (52.6); predilation, 14.8 (18.7) vs 21.7 (21.8); stent placement, 58.6 (31.1) vs 64.7 (38.8); postdilation, 20.4 (16.5) vs 27.2 (34.9), cerebral protection device (CPD) use, 44.2 (30.2) vs 37.5 (36.8); total, 134.8 (68.7) vs 175.3 (113.8). Microembolic showers: wiring, 1.7 (4.5) vs 2.2 (6.4); predilation, 2.1 (4.1) vs 3.3 (5.8); stent placement, 21.5 (22.0) vs 26.9 (25.1); postdilation, 5.3 (15.7) vs 5.0 (8.1); CPD use, 5.8 (6.9) vs 6.2 (8.9); total, 30.4 (36.0) vs 39.6 (35.0). TCD data for CPD use vs without for isolated emboli: wiring, 53.2 (45.1) vs 44.3 (51.7); predilation, 24.7 (20.2) vs 18.2 (22.5); stent placement, 77.5 (34.8) vs 53.5 (37.3); postdilation, 33.6 (36.6) vs 20.7 (21.8); CPD use, 38.3 (36.6) vs 0; total, 222.5 (113.8) vs 132.3 (89.1). Showers: wiring, 2.4 (6.6) vs 1.9 (5.8); predilation, 4.2 (6.4) vs 2.4 (5.0); stent placement, 38.9 (25.8) vs 16.2 (18.7); post-dilation, 7.0 (11.2) vs 3.4 (6.4); CPD use, 6.3 (8.9) vs 0; total, 58.4 (37.7) vs 23.3 (23.1). P = .01 for showers during wiring and P < .001 for all other variables. After correction for the difference in CPD use between groups 1 and 2 (17 out of 72 [24%] vs 369 out of 740 [50%]), no statistically significant differences remained in numbers of isolated emboli and embolic showers in the procedural phases or for the entire procedure. No statistically significant differences were found when TCD-detected microembolic load for early (<3 years between CEA and CAS) and late (>5 years) restenoses were compared.

Conclusions

CAS for restenosis after CEA has a complication rate lower than primary CAS. The time interval between CEA and CAS did not influence micro embolic load.

Because of the results of several large randomized trials, carotid endarterectomy (CEA) is currently the accepted standard treatment for patients with severe symptomatic and asymptomatic carotid artery stenosis.¹, ², ³, ⁴ Carotid angioplasty and stenting (CAS) has been evaluated as a potential alternative to CEA.⁵ Compared with the surgical approach, the endovascular procedure is associated with a significant cerebral embolic burden, as shown by transcranial Doppler (TCD) imaging of the ipsilateral middle cerebral artery⁶, ⁷ and magnetic resonance imaging (MRI) of the brain.⁸, ⁹

Postoperative restenosis after CEA, defined as a >50% diameter reduction, has been reported with incidences of 6% to 36%,¹⁰ partly depending on follow-up length. On account of scar tissue in the cervical region and the loss of tissue planes, redo operations are generally considered to be technically more challenging, and most reports cite a higher complication rate.¹¹ Because CAS is not hampered by previous neck dissection, it has been considered as an alternative to redo surgery in these patients, and encouraging results have been published within the last decade.¹², ¹³, ¹⁴, ¹⁵, ¹⁶

The main culprit in early restenosis after CEA is hypothesized to be myointimal hyperplasia (MIH), whereas late restenosis is generally considered to result from progression of the underlying atherosclerotic disease.¹⁷ Because MIH is supposed to be more stable and less embologenic,¹⁸ the procedural risk of emboli might be lower in CAS after prior ipsilateral CEA compared with primary CAS, especially in early restenoses.

We have previously reported our experience with TCD monitoring and its usefulness with regard to emboli detection and the prediction of early cerebral outcome in CAS.⁷, ¹⁹ In the present study, the TCD-detected embolic load and clinical outcome in patients who underwent stent placement for restenosis after prior ipsilateral CEA was compared with CAS performed for primary carotid artery stenosis. In addition, we stratified redo cases in early and late restenoses to establish any correlation between the time of onset of restenosis and the periprocedural embolic load.

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Materials and methods 

Written informed consent was obtained from all patients in accordance with institutional guidelines.

Patients 

Between December 1997 and June 2006, the 812 patients scheduled for CAS in our tertiary referral center for vascular disease were prospectively entered in a computerized database and included in this study. Median age was 71 years (interquartile range [IQR], 66-76 years), and 569 (70%) were men.

In a subgroup of 72 patients (group 1), CAS was performed for recurrent stenosis at a mean of 71 (SD 57) months (range, 5-245 months) after previous ipsilateral CEA. The median age in this subgroup was 70 years (IQR, 65-75 years) and 44 (61%) were men. In the 4 months preceding CAS, 14 (19%) had demonstrated symptoms of ipsilateral carotid artery stenosis, documented as transient ischemic attack (TIA), transient monocular blindness (TMB), or minor stroke. In four (29%), the symptoms occurred ≤36 months after the initial ipsilateral CEA. Most of the CEAs were performed in our institution.

The CAS procedures in the remaining 740 patients (group 2) were performed for primary carotid bifurcation stenosis. In this group, 525 (71%) were men, the median age was 71 years (IQR, 66-76 years), and 147 (20%) had recently been symptomatic. Baseline patient characteristics are summarized in Table I.

Table I. Patient characteristics

Characteristic	Group 1	Group 2	Total	Pa
Patients, No.	72	740	812
Male gender, No. (%)	44(61)	525(71)	569(70)	.08
Age median (IQR), y	70(65-75)	71(66-76)	71(66-76)	.28
Recent ipsilateral symptoms, No. (%)b	14(19)	147(20)	161(20)	.99
Side of stenting				.60
Left	38	391	429
Right	34	349	383
CPD use, No. (%)	17(24)	369(50)	386(48)	<.0001

CPD, Cerebral protection device; IQR, interquartile range.

In 588 patients (72%), CAS was performed before coronary artery bypass grafting, cardiac valve replacement, or reconstructive surgery of the thoracic aorta. These patients were treated to prevent perioperative complications,²⁰ and 505 (86%) had not presented with symptoms of ipsilateral carotid bifurcation stenosis.

Symptomatic patients were treated if the degree of stenosis at the carotid bifurcation was >70% according to the North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria.² For asymptomatic patients, the cutoff for treatment was a diameter reduction of 80%. The degree of stenosis was assessed by duplex ultrasound scanning and intra-arterial digital subtraction angiography before endovascular treatment.

CAS procedure 

In all patients, CAS was performed using a standard protocol described in detail previously.⁷, ¹⁹ All procedures were performed under local anesthesia from a groin approach. Several different types of appropriately sized self-expandable stents were used (Table II). Because we started performing CAS in our institution before cerebral protection devices (CPDs) had been developed, 426 patients (52%), mainly in the early part of our experience, were treated without these devices. The CPDs used are listed in Table III. To prevent hypotension and bradycardia resulting from carotid body compression, 0.5 mg of atropine sulphate was administered in the primary stenting cases. Because the ipsilateral carotid body generally is dysfunctional after prior CEA, atropine was not routinely administered in post-CEA restenosis cases. All procedures were performed by an experienced interventional cardiologist or an experienced interventional radiologist.

Table II. Types and numbers of stents used

Stent type	Manufacturer	No. (%)
Carotid Wallstent	Boston Scientific, Natick, Mass	355(54.1)
Acculink	Guidant, Indianapolis, Ind	210(25.9)
Precise	Cordis J&J, Miami Lakes, Fla	103(12.7)
Easy Wallstent	Boston Scientific, Natick, Mass	84(10.3)
Nex	Boston Scientific, Natick, Mass	15(1.8)
Carotid SE	Medtronic, Minneapolis, Minn	13(1.6)
Peripheral Wallstent	Boston Scientific, Natick, Mass	4(0.5)
Protegé	EV3, Plymouth, Minn	3(0.4)
Sinus Carotid	Optimed, Ettlingen, Germany	2(0.2)
Bridge	Medtronic, Minneapolis, Minn	1(0.1)
Not stented		22(2.7)
Total		812(100)

Table III. Types and numbers of protection devices used

Type	Manufacturer	No. (%)
Epifilter EZ	Boston Scientific, Natick, Mass	181(22.3)
Epifilter	Boston Scientific, Natick, Mass	98(12.1)
Spider filter	eV3, Plymouth, MN	28(3.4)
Angioguard XP	Cordis J&J, Miami Lakes, Fla	18(2.2)
Angioguard	Cordis J&J, Miami Lakes, Fla	14(1.7)
Accunet RX	Guidant, Indianapolis, Ind	12(1.5)
Trap filter	eV3, Plymouth, Minn	4(0.5)
Emboshield	Abbott, Santa Rosa, Calif	4(0.5)
Percusurge	Medtronic, Minneapolis, Minn	3(0.4)
Neuroshield	Abbott, Santa Rosa, Calif	1(0.1)
Interceptor	Medtronic, Minneapolis, Minn	1(0.1)
Failed protection		5(0.6)
No protection		421(51.8)
Not stented		22(2.7)
Total		812

TCD monitoring 

The technique of TCD monitoring during CAS has been described in detail in previous publications.⁷ During the various stages of the procedure, isolated microembolic signals were recorded according to the criteria described by the consensus committee.²¹ If the number of microembolic signals was too high to be counted separately, heartbeats with microemboli were counted as microembolic showers. Microembolic signals were stratified to five procedural stages: (1) wiring/passing of the stenosis, (2) predilation, (3) stent deployment, (4) postdilation, and (5), if applicable, placement and retrieval of a CPD.

Clinical outcome 

All patients were formally assessed before and after the procedure by a neurologist who was not involved in the intervention. During CAS, a different neurologist was present in the angiography suite. New cerebral deficits persisting for >24 hours were regarded as stroke, which was graded according to the modified Rankin scale.²² Major strokes exceeded 3 on the Rankin scale, whereas minor strokes did not. In patients with adverse cerebral outcome, computed tomography (CT) or magnetic resonance imaging (MRI), or both, of the brain were performed.

End points in the analyses were minor and major strokes (ischemic and hemorrhagic), death, TIA, and TMB during the procedure or ≤7 days after. Surrogate end points were the number of TCD-detected cerebral microemboli during the various stages of the procedure.

Statistics 

TCD data are presented with mean and SD and analyzed with the Mann-Whitney U test. For binomial data, the χ² test was used. To test interdependence of variables, the Mantel-Haenszel test was used for binomial data and univariate analysis for numeric variables. In all cases, P < .05 was regarded as statistically significant.

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Results 

Clinical results 

A filtering type distal CPD was used in 17 patients (24%) in group 1; CPDs were used in 369 (50%) in group 2, a difference that was statistically significant (P < .001).

No stent was placed in 22 of 812 arteries (2.7%) in the entire cohort. Two (2.8%) of these occurred in group 1, and neither procedure led to complications. In group 2, 20 procedures (2.7%) were terminated without placement of a stent. In two of these patients, a major stroke occurred during the initial angiography and the procedure was terminated; therefore, overall procedural success was achieved in 790 of 812 arteries (97.3%).

Clinical outcome is reported in Table IV. In 812 CAS procedures, seven patients (0.9%) died. A major stroke occurred in 10 additional patients (1.2%), including the two discontinued procedures, and a further 21 (2.6%) sustained a minor stroke. All strokes were confirmed by CT or MRI imaging. The combined stroke and death rate in the entire cohort was 38 of 812 (4.7%).

Table IV. Permanent cerebral deficits during CAS or ≤ 1 week

All fatalities and all strokes occurred in the primary CAS treatment group, giving a combined stroke and death rate in this group of 38 of 740 (5.1%). No strokes and no deaths occurred among the 72 patients who underwent CEA after CAS (P=.049). The Mantel-Haenszel test established that this difference was independent of CPD use.

Five TIAs occurred in group 1 versus 46 in group 2 (P = .8). TMB occurred in one patient in group 1 versus nine in group 2 (P = .9).

TCD data 

In 678 of 812 cases (83%), an adequate temporal window was available for TCD monitoring, comprising 65 of 72 (90%) in group 1 and 613 of 740 (83%) in group 2. Fewer isolated microemboli were documented in group 1 compared with group 2 in all phases of the procedure except the phase of CPD use (Table V). This difference was influenced, however, by the use of CPDs, which was much more prevalent in group 2. The influence of CPDs on the microembolic load is presented in Table VI. After correction for this difference using linear regression analysis, the difference was no longer statistically significant. The TCD data with correction for CPD use are summarized in Table VII, Table VIII, both for isolated emboli and for embolic showers, respectively.

Table V. Number of isolated emboli and embolic showers during the various stages of the procedure

Stage	Group 1,a mean (SD)				Group 2,b mean (SD)
	With CPD		Without CPD		With CPD		Without CPD
	Isolated emboli	Embolic showers	Isolated emboli	Embolic showers	Isolated emboli	Embolic showers	Isolated emboli	Embolic showers
Wiring	43.4(24.0)	3.0(4.6)	35.0(33.8)	1.4(4.5)	53.6(46.1)	2.3(6.7)	45.7(53.8)	2.0(6.0)
No.	16	16	47	47	280	280	310	310
Predilation	17.4(14.8)	4.1(6.3)	13.6(20.5)	1.2(2.5)	25.0(20.5)	4.2(6.4)	18.7(22.7)	2.5(5.1)
No.	12	12	28	28	251	251	2721	272
Stent placement	78.4(36.3)	30.8(28.4)	51.8(26.7)	18.4(19.1)	77.3(34.8)	39.4(25.6)	53.8(38.7)	15.9(18.7)
No.	16	16	47	47	280	280	310	310
Postdilation	25.4(14.3)	10.4(27.3)	18.6(17.1)	3.5(8.6)	33.9(43.6)	6.8(9.5)	21.0(22.5)	3.4(6.0)
No.	16	16	45	45	280	280	293	293
CPD use	44.2(31.2)	5.8(7.1)	NA	NA	37.9(36.9)	6.3(9.0)	NA	NA
No.	16	16			280	280
Total	203.9(68.8)	51.8(55.3)	111.3(51.8)	24.4(24.5)	216.1(95.1)	58.8(36.6)	135.5(93.2)	23.2(23.0)
No.	16	16	47	47	280	280	310	310

CPD, Cerebral protection device; NA, not applicable; SD, standard deviation.

Table VI. Mean (standard deviation) number of isolated microemboli and embolic showers during various phases of the procedure, comparing patients treated with and without filtering

Event	Isolated emboli, mean (SD)			Microembolic showers
	CPD	No CPD	Pa	CPD	No CPD	Pa
Wiring	53.2(45.1)	44.3(51.7)	<.0001	2.4(6.6)	1.9(5.8)	.01
No.	295	357		295	357
Predilation	24.7(20.2)	18.2(22.5)	<.0001	4.2(6.4)	2.4(5.0)	<.0001
No.	262	300		262	300
Stent placement	77.5(34.8)	53.5(37.3)	<.0001	38.9(25.8)	16.2(18.7)	<.0001
No.	295	357		295	357
Postdilation	33.6(42.5)	20.7(21.8)	<.0001	7.0(11.2)	3.4(6.4)	<.0001
No.	295	338		295	338
CPD use	38.3(36.6)	NA		6.3(8.9)	NA
No.	295			295
Total	222.5(113.8)	132.3(89.1)	<.0001	58.4(37.7)	23.3(23.1)	<.0001
No.	295	357		295	357

CPD, Cerebral protection device; NA, not applicable.

Table VII. Mean (standard deviation) of isolated microemboli stratified to procedural stage

Event	Gross number of microemboli			Correction for CPD usea
	Group 1b	Group 2c	P	Group 1b	Group 2c	P
Wiring	37.0(31.1)	50.5(52.6)	.017d	39.3(6.2)	49.8(2.0)	.11
No.	65	599		65	599
Predilation	14.8(18.7)	21.7(21.8)	<.001d	16.1(3.4)	21.9(0.9)	.1
No.	40	523		40	523
Stent placement	58.6(31.1)	64.7(38.8)	.119	64.3(4.6)	65.8(1.5)	.77
No.	64	592		64	592
Postdilation	20.4(16.5)	27.2(34.9)	.085	23.5(4.3)	27.6(1.4)	.36
No.	61	575		61	575
CPD	44.2(30.2)	37.5(36.9)	.218	43.4(12.4)	37.2(8.3)	.51
No.	16	282		16	282
Total	134.8(68.7)	175.4(113.8)	.004d	156.6(12.9)	180.3(4.2)	.08
No.	65	599		65	599

CPD, Cerebral protection device.

Table VIII. Mean (standard deviation) of microembolic showers stratified to procedural stage

Event	Gross number of embolic showers			Correction for CPD usea
	Group 1b	Group 2c	P	Group 1b	Group 2c	P
Wiring	1.7(4.5)	2.2(6.4)	.66	3.7(38.8)	14.5(12.6)	.66
No.	65	599		65	599
Predilation	2.0(4.1)	3.3(5.8)	.13	2.4(0.9)	3.4(0.248)	.32
No.	40	523		40	523
Stent placement	21.5(22.0)	26.9(25.2)	.25	26.9(2.9)	27.8(0.9)	.77
No.	64	593		63	593
Postdilation	5.3(15.7)	5.0(8.1)	.22	6.2(1.2)	5.1(0.4)	.37
No.	61	575		61	575
CPD	5.8(6.9)	6.2(9.0)	.82	9.2(3.0)	9.6(2.0)	.87
No.	16	282		16	282
Total	30.4(36.0)	39.6(35.1)	.028d	39.7(3.9)	41.3(1.3)	.71
No.	65	599		65	599

CPD, Cerebral protection device.

Subgroup analyses 

To establish any correlation between the rapidity of restenosis formation and the cerebral embolic load during CAS, an additional analysis was performed within group 1. Patients treated with CAS ≤36 months after CEA were compared with those treated >60 months after CEA. After the initial CEA procedure, 21 patients were treated ≤36 months and 35 after >60 months. TCD data of this comparison are presented in Table IX, Table X. There was no statistically significant difference in the TCD-detected cerebral embolic load between early and late restenoses in any of the phases.

Table IX. Mean(standard deviation) number of isolated microemboli in the various phases of the procedure in patients after carotid endarterectomy

Event	Early restenosesa	Late restenosesb	P
Wiring	29.5(12.0)	47.0(38.9)	.13
No.	20	30
Predilation	11.6(13.2)	19.6(23.0)	.36
No.	10	21
Stent placement	63.0(30.8)	59.6(25.2)	.59
No.	20	30
Postdilation	26.2(21.3)	17.5(12.2)	.31
No.	20	30
CPD use	40.0(16.5)	43.8(34.4)	.65
No.	4	11
Total	125.0(64.3)	152.6(67.1)	.26
No.	20	30

CPD, Cerebral protection device.

Table X. Mean(standard deviation) number of showers of microemboli in the various phases of the procedure in patients after carotid endarterectomy

Event	Early restenosesa	Late restenosesb	P
Wiring	0.7(1.4)	3.2(6.2)	0.28
No.	20	30
Predilation	2.0(2.8)	2.6(5.2)	0.88
No.	10	21
Stent placement	23.0(23.1)	24.8(23.5)	0.55
No.	20	30
Postdilation	5.1(11.7)	6.6(20.0)	0.73
No.	20	30
CPD use	4.8(3.3)	6.6(7.9)	0.9
No.	4	11
Total	29.1(32.7)	39.0(42.2)	0.22
No.	20	30

CPD, Cerebral protection device.

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Discussion 

In this study, we analyzed the results of CAS for treatment of restenosis after prior ipsilateral CEA compared with that of primary carotid stenosis. No strokes or deaths occurred in the post-CEA group compared with 38 strokes or deaths in the much larger group of primary CAS patients (P = .049). At first analysis, the TCD-detected cerebral microembolic load was significantly lower in post-CEA restenoses compared with primary cases. Multivariate regression analysis, however, showed that this difference was caused by a higher rate of CPD use in primary cases compared with restenosis cases. CPDs designed to protect the brain from clinically significant macroemboli have previously, paradoxically, been shown to be associated with an increase in TCD-detected cerebral microembolic load during CAS.²³, ²⁴

The low event rate establishes that CAS is a safe procedure for restenosis after prior CEA. In a subgroup analysis, we tried to determine whether the embolic load is affected by the rapidity of restenosis occurrence. No statistically significant differences were found between patients treated for early versus late restenosis.

Endarterectomy for restenosis after prior CEA is generally considered to be more challenging than primary CEA.¹¹ In 1989 the American Heart Association (AHA) issued guidelines for CEA.²⁵ These guidelines allow a <3% perioperative risk of complications during CEA for asymptomatic stenosis, <5% for patients with recent ipsilateral TIAs, <7% for recent ipsilateral stroke, and ≤10% periprocedural risk of complications for patients with recurrent stenosis after CEA. In several revisions of these guidelines, we have not been able to find a revocation of the last figure, and we therefore assume that the maximum of 10% complications during CEA for restenosis is still prevalent according to the AHA. In view of the results in this series as well as previous research by other authors, a revision is indicated. In our opinion, CAS in experienced hands should be considered the primary treatment option for restenosis after prior CEA.

Earlier series of CAS after CEA¹³, ¹⁴, ¹⁵, ¹⁶, ²⁶ have also shown a low periprocedural event rate comparable with our results. Only three previous studies²⁷, ²⁸, ²⁹ have specifically compared CAS for restenosis after CEA with CAS for primary stenosis. None of them used TCD to establish the periprocedural microembolic load, and neither did any study find a significant difference in outcome between groups for periprocedural stroke and death. Cuadra et al²⁸ concluded that CAS for restenosis should not be considered a low-risk procedure that is useful for training purposes. Although we did find a difference that was favorable for restenotic lesions, we agree that CAS should never be considered to be an easy procedure, but should always be performed by a highly experienced team. To our knowledge, our study is the first to compare TCD results in restenotic vs primary lesions. No difference in microembolic load was established, which underscores the fact that a significant embolic burden to the brain is present even in restenotic lesions.

Many authors have postulated an association between the time of onset of restenosis formation and the likelihood of cerebral sequelae, suggesting that early restenoses are less emboligenic than late restenoses¹⁷, ³⁰, ³¹; however, only one author actually reported a difference.¹¹

The cutoff point for early versus late restenosis after prior ipsilateral CEA varies among reports from 2 years¹⁷, ¹⁸, ³², ³³ to 3 years.³², ³⁴, ³⁵ To avoid any possible overlap in the mechanism of restenosis formation, we compared patients with an interval between CEA and CAS of <3 years, presumably MIH, with patients with an interval of >5 years, presumably renewed atherosclerotic lesions. No statistically significant difference in cerebral embolic load was found. This appears to imply that the risk of cerebral embolization during CAS for post-CEA restenosis is independent from the time interval.

This study has several limitations. The first is the nonrandomized design. One consequence of the nonrandomized design was that the primary stenting group contained significantly more patients with a CPD than the redo group. Univariate analysis and Mantel-Haenszel testing were used to correct for this difference in baseline data, and the difference in clinical outcome proved to be independent from CPD use.

The second limitation was the relatively limited number of patients in the restenosis group and, particularly, in the subgroups. We reported nonsignificant differences between the early and late restenosis groups and we acknowledge that such may be due to the sample size. Increasing the sample size lowers the probability of a type II error and of the magnitude of the difference detectable.

Third, the use of TCD as a surrogate end point has a number of limitations in monitoring cerebrovascular interventions, including that it cannot distinguish the size of microemboli. CPDs have pores of up to 100 μm to allow passage of blood while capturing potentially significantly larger particles. This may be one of the contributing factors to the paradoxic increase in microembolic load in CPD protected cases.

A further limitation was that clinical outcome is presented for the first week only compared with most other studies that report all cerebral events ≤30 days as the periprocedural event rate. In many patients in our series, the CAS was performed in the workup before major cardiothoracic surgery that was scheduled between 1 week and 1 month after the CAS procedure. The data of the second procedure might then have influenced the periprocedural data on the CAS procedure. Accordingly in this study, cerebral complications are represented for the first week only. Almost all cerebral sequelae after CAS occur during the procedure or within the first few hours after, so we do not believe this significantly influenced our results.

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Conclusion 

This study indicates that CAS for restenosis after CEA can be performed safely, with a complication rate and cerebral embolic load that is as least as good as primary CAS. The time interval between CEA and the occurrence of the restenosis does not appear to influence these results. We propose that CAS in experienced hands is an appropriate treatment for post CEA restenosis.

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Author contributions 

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Appendix (online only) 

Members of the Antonius Carotid Endarterectomy, Angioplasty, and Stenting Study Group:

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References 

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