Annals of Vascular Surgery
Volume 24, Issue 2 , Pages 190-195, February 2010

Redo Surgery or Carotid Stenting for Restenosis after Carotid Endarterectomy: Results of Two Different Treatment Strategies

  • Nicolas Attigah

      Affiliations

    • Department of Vascular and Endovascular Surgery, University of Heidelberg, Heidelberg, Germany
    • Corresponding Author InformationCorrespondence to: Nicolas Attigah, MD, Department of Vascular and Endovascular Surgery, University of Heidelberg, Im Neuenheimer Feld 110, 69120 Heidelberg, Germany
    • ,
  • Sonja Külkens

      Affiliations

    • Department of Neurology, University of Heidelberg, Heidelberg, Germany
    • ,
  • Claudia Deyle

      Affiliations

    • Department of Vascular and Endovascular Surgery, University of Heidelberg, Heidelberg, Germany
    • ,
  • Peter Ringleb

      Affiliations

    • Department of Neurology, University of Heidelberg, Heidelberg, Germany
    • ,
  • Marius Hartmann

      Affiliations

    • Department of Neuroradiology, University of Heidelberg, Heidelberg, Germany
    • ,
  • Philipp Geisbüsch

      Affiliations

    • Department of Vascular and Endovascular Surgery, University of Heidelberg, Heidelberg, Germany
    • ,
  • Dittmar Böckler

      Affiliations

    • Department of Vascular and Endovascular Surgery, University of Heidelberg, Heidelberg, Germany

published online 14 September 2009.

Article Outline

Background

We evaluated retrospectively early and midterm results of conventional redo surgery and carotid stent–assisted angioplasty (CAS) in the treatment of carotis restenosis (CR) after carotid endarterectomy (CEA).

Methods

From January 1989 to April 2007, 79 consecutive patients (61 male, median age 65 years, range 51–82) were treated for CR. Seven patients were treated for bilateral CR, accounting for 86 reconstructions, 41 CEAs, and 45 CAS procedures. Fifty (58.1%) CRs were asymptomatic, and 36 (41.9%) CRs were symptomatic. Treatment for CR was recommended for any stenosis >70% based on duplex ultrasound imaging with a peak systolic flow of >200cm/sec.

Results

There was no difference in age in the two groups. The incidence of atherosclerotic risk factors and comorbidity was similar in the two groups. All patients received aspirin as basic medical treatment, and 53 patients (61.6%) were on statin therapy. The time period from primary CEA to reoperation or CAS was significantly shorter in the CAS group than in the CEA group (54.1 vs. 85.34 months, p=0.003). Correspondingly, the proportion of early CR was significantly higher in the CAS group as well (20 vs. 5, p=0.001). There was no perioperative mortality (30 days) in the two groups. In the CEA group, four neurological complications were seen versus one in the CAS group (p=0.13). Wound site and cardiac complication rates were significantly higher in the CEA group (p=0.029) with a median follow-up of 35 months (range 12–190). The overall actuarial survival after 60 months was 83% in the CEA group and 100% in the CAS group (p=0.87). Freedom from repeat intervention for re-recurrence was 89% in the CEA group and 95% in the CAS group (p=0.52).

Conclusion

CAS is feasible and safe in treating CR. Furthermore, midterm overall survival and need for treatment of re-recurrence is equal to CEA. However, reoperation is an established option and remains the treatment of choice when contraindications for CAS are evident.

 

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Introduction 

Since DeBakey performed the first thromboendarterectomy of the internal carotid artery (ICA), carotid endarterectomy (CEA) has become one of the most frequently performed vascular surgical procedures as secondary prophylaxis for carotid stenosis–associated stroke.1 Currently, in the United States an estimated 170,000 CEA procedures are performed each year.2 The role of CEA has been well documented in large randomized trials, whereas carotid artery stenting (CAS) has recently emerged as a less invasive treatment alternative, whose final role in carotid revascularization will be determined on the basis of ongoing randomized trials.3

However, in the case of carotid restenosis (CR) after CEA considerable controversy exists about clinical significance, natural history, threshold for management, and the appropriate choice of treatment. As reported in a consensus statement from the American Heart Association and the European Stroke Organization,4 CAS so far should be offered to a limited group of high-risk patients, such as patients with severe cardiopulmonary comorbidities, prior neck irradiation, inaccessible lesions above the C2 level, and post-CEA recurrent stenosis.5, 6 Despite early promising results of CAS, questions remained concerning the long-term durability of this endovascular treatment. Reports suggesting a low incidence of CAS-related in-stent restenosis (ISR) were largely derived from studies with small sample sizes and short follow-up periods. Other studies reported poor durability after stenting for recurrent artery stenosis, and still others reported good long-term results after CAS in high-risk patients.7, 8, 9, 10, 11, 12 The purpose of this study was to examine procedural indications, techniques, and midterm treatment outcomes of CEA and CAS for postendarterectomy stenosis in a single-center setting.

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Patients and Methods 

The records of patients treated for CR were systematically reviewed retrospectively concerning past medical history, symptoms at presentation, atherosclerotic risk factors, procedural details of carotid stenosis repair, duplex ultrasound scanning results, and intraprocedural and postprocedural complications. At 6 weeks, 6 months, and 1 year postoperatively all patients were invited for regular clinical and duplex ultrasound examinations of the extracranial carotid artery at our outpatient department; and the degree of stenosis, neurological symptoms, and survival data were obtained by an independent neurologist. In the further follow-up, duplex scans were obtained on a yearly basis.

Patient Selection Criteria 

Over an 18-year period (January 1989–April 2007) 79 consecutive patients were treated for CR in the Departments of Vascular and Endovascular Surgery, Neurology, and Interventional Neuroradiology of the University of Heidelberg. Seven patients were treated for bilateral CR, accounting in total for 86 reconstructions for CR. Redo surgery was undertaken 41 times, and in 45 cases CAS was performed. There were 61 men and 18 women treated, and there was no significant difference in gender distribution between the groups. The median age was 65 years at the time of reoperation or reintervention. Fifty (58.1%) CRs were asymptomatic, and 36 (41.9%) CRs were symptomatic. In the operation group 15 patients (17.44%) presented with a symptomatic CR vs. 21 (24.41%) in the stenting group. The difference was statistically not significant. In general, interventional treatment for CR was recommended for any stenosis >70% based on duplex ultrasound imaging with a peak systolic velocity (PSV) of >200cm/sec. All patients who underwent CAS received magnetic resonance imaging (MRI) angiography of the aortic arch in order to rule out anatomic contraindication for stenting. All patients who presented with a symptomatic carotid stenosis received a cerebral computed tomographic (CT) scan or MRI.

Operative Technique 

All patients with CR were operated by a board-certified vascular surgeon. Access was usually obtained over the old incision. The operation was done under general anesthesia by selective shunting according to somatosensory evoked potential monitoring and intraoperative transcranial Doppler measurement. In a total of 41 operations the repair technique consisted of four eversion CEAs (9.8%), 20 Dacron patch reconstructions (48.8%), seven greater saphenous vein patches (17.1%), seven Dacron grafts (17.1%), and three vein grafts (7.3%). Peri- and postoperatively, all patients received aspirin (100mg/day). Before carotid cross-clamping, a bolus of 3,000 IU heparin was administered.

CAS Technique 

All stenting procedures were done in an angio-suite by an interventional neuroradiologist under local anesthesia. Access was obtained through a 7-French guiding sheath (vista brite, Gateway®; Johnson & Johnson, Warren, NJ), which was placed usually into the right common femoral artery after transcutaneous puncture. Over a guiding catheter, a 0.014-inch guiding wire was passed distal to the stenosis (vista brite, Gateway, balanced middleweight guidewire; Abbott, Abbott Park, IL). Two types of stents were used (Carotid Wallstent® from Boston Scientific, Natick, MA [n=41] and Acculink® from Abbott [n=5]). After stent deployment, postdilatation percutaneous transluminal angioplasty (PTA) was performed selectively (Maverick®, Boston Scientific). For stenting of a recurrent stenosis, no cerebral protection device was used. No femoral closure device was used in the common femoral artery. All patients received aspirin (100mg/day) and 75mg clopidogrel at least 3 days prior to intervention. Aspirin was continued as a permanent treatment, whereas clopidogrel was given for 4 weeks after intervention (75mg/day).

Postoperative Follow-Up 

All surgical and CAS patients underwent intraoperative completion angiography and were evaluated on the next day by an experienced neurologist. Periprocedural ischemic complications were classified as transient ischemic attack (TIA) if the symptoms lasted less than 24hr or as stroke if symptom duration was longer. A stroke was called “minor” if the value on the National Institutes of Health Stroke Scale was ≤4. Patients were seen again in our outpatient departments for a routine physical examination, duplex scan of both carotid arteries, and examination by an independent neurologist 4-6 weeks after discharge from hospital, which was repeated after 6 months. After that, physical examinations and duplex scans were undertaken at least every 12 months. Survival data were obtained in cooperation with the general practitioners.

Statistical Analysis 

All patient data were collected in an electronic database (Excel; Microsoft, Redmond, WA), and data consistency checks were performed. In case of missing values or obvious entry mistakes, original patient files were again consulted to minimize incomplete data sets. For continuous variables, means and standard deviations were calculated. Where data were skewed, median values were determined. Overall acturial survival and incidence of re-restenosis were estimated according to the method of Kaplan-Meier and checked for statistical significance with the log rank test (with XLStat; Addinsoft, New York, NY). p≤0.05 was considered statistically significant.

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Results 

Patient Demographic Data 

There was no difference in age in the CEA group compared to the CAS group (mean ages 63.97 and 64.9 years, respectively). Incidence rates of atherosclerotic risk factors and comorbidity were similar in the groups (Table I). There were 39 right- and 47 left-sided CRs treated with similar distribution in the two groups. In 53 cases (61.6%) the patients were on statin therapy. Seventeen patients in the CEA group and 16 patients in the CAS group received no statin prior to diagnosis of CR; the difference was of no statistical significance. The time period from primary CEA to reoperation or CAS was significantly shorter in the CAS group than in the CEA group (54.1 vs. 85.34 months, p=0.003). Correspondingly, the proportion of early CR was significantly higher in the CAS group as well (n=20 vs. n=5, p=0.001) (Table II).

Table I. Patient demographics: comparison of atherosclerotic risk factors and comorbidity of the CEA and CAS groups.
CEA (n=38)CAS (n=41)
n%n%p
Hypertension3712.23844.10.42
Coronary artery disease2225.61517.50.57
Diabetes mellitus1618.6910.50.052
Hypercholesterolemia3237.23034.90.24
Tobacco abuse910.5910.50.9
Table II. Comparison of time period from primary CEA to reoperation or intervention.
CEA (n=41)CAS (n=45)
nnp
Early CR (≤18 months)5200.001
Late CR (>18 months)3625
Mean time to intervention (months)85.34 (±9.95)54.06 (±9.22)0.003

Early CR was defined as recurrent stenosis 3-18 months after CEA and late CR as recurrent stenosis occurring later than 18 months after CEA.

Periprocedural (30-Day) Morbidity 

There was no perioperative mortality in the two groups. In total, there were five postprocedural complications. Four neurological complications were seen in the CEA group (9.7%) and one in the CAS group (2.2%). In patients who were operated there were two TIAs and two minor strokes; in patients who underwent CAS for CR one TIA occurred after intervention (p=0.13).

Wound site and cardiac complication rates were significantly higher in the CEA group (p=0.029). In reoperated patients there was one case of unstable angina pectoris, one nonfatal respiratory failure, one hypertensive crisis, and three operation site hematomas, of which one had to be reoperated (14.6%). No cranial nerve injury was seen in the CEA group. In the CAS group there was one false aneurysm at the puncture site in the right groin and one hematoma (2.2%), which were treated conservatively.

Late Clinical Outcome 

The mean follow-up was 35 months (range 12-190); however, the follow-up period was significantly longer in the CEA group than in the CAS group (70.3 vs. 24.8 months, p=0.0001). The overall actuarial survival after 60 months was 83% in the CEA group and 100% in the CAS group (p=0.87) (Fig. 1). In the two groups no ipsilateral or contralateral strokes were encountered in the follow-up period. In the two groups, deaths were not disease-related. Patients died because of cardiovascular events or malignancy. In the redo CEA group four patients underwent redo CEA for re-recurrence (9.7%). In the CAS group one patient received PTA and placement of a second stent 5 months after initial CAS treatment (2.2%). Freedom from repeat intervention for re-recurrence was 89% in the CEA group and 95% in the CAS group (p=0.52) (Fig. 2).

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Discussion 

The treatment of CEA and CAS in the management of postendarterectomy CR is of current interest. Reliable data concerning the incidence of CR after CEA are derived from the Asymptomatic Carotid Atherosclerosis Study (ACAS) follow-up study. Moore et al.13 reported incidence rates of 7.6% for early CR (3-18 months) and 1.9% for late CR (18-60 months). The etiology of early and late CR might be of considerable difference. Whereas early CR is most likely secondary to myointimal hyperplasia, late CR displays features of de novo stenosis as a result of potentially ongoing atherosclerotic disease. This study showed a trend toward a lower procedure-related stroke rate with endovascular treatment of CR. However, in our study the number of early CR was significantly higher in patient who received CAS as treatment, which is certainly a bias. The complication rate in our study was significantly lower in the CAS group compared to the redo CEA group (14.6% and 2.2%, respectively). Overall survival was similar in the two groups (CEA 83% vs. CAS 100% after 60 months), as was the disease-free survival rate (89% and 95%, respectively). This late clinical outcome is comparable to the result of a recent study by Bowser et al.,14 who reported an overall survival rate of 92% in the two groups as well as an equivalent freedom of repeat treatment after CAS or redo CEA. In our series no cerebral protection device was used in the setting of CR, with satisfying results. However, in our patients the percentage of early restenosis was significantly higher in the CAS group, a condition where the necessity of protection devices might be questionable anyway. On the other hand, in the patients who were operated again the percentage of late restenosis was higher. According to current doctrine, one can assume that this type of stenosis is a de novo stenosis, whose plaque morphology is rather atherosclerotic than the homogeneous layer of myointimal hyperplasia in early recurrent stenosis. In our institution, concerning treatment strategies in CR, no standard protocol exists so far. Whereas patients who were diagnosed with CR up to 2004 were reoperated as the only available treatment option at that time, patients diagnosed with CR after 2004 increasingly underwent CAS, especially with growing experience in endovascular treatment of primary carotid stenosis. This explains the difference in the follow-up period and is certainly a flaw of our study. The high risk of cranial nerve damage for open CR repair is an often-cited argument in favor of CAS and is reported in the literature.15 However, cranial nerve injury was not observed in this study at all. This is consistent with data from larger series comparing primary and redo CEA.16 In our series, the examination by an independent neurologist included clinical investigation for cranial nerve damage. In our patients, diagnosis of recurrent carotid stenosis was based on duplex ultrasonography. Flow velocities correlated with the percentage of stenosis found in angiography in the unstented artery.17 However, ultrasonography velocity criteria have not been well-established in patients undergoing CAS. This could contribute to a potential bias because the stent enhances stiffness and reduces compliance.18 These altered biomechanical properties of a stented vessel could lead to increased velocity. For this reason, many authors suggest revised velocity criteria for diagnosing carotid restenosis after CAS. For example, Lal et al.19 compared duplex ultrasonographic measurements with luminal stenosis measurements by CT angiography. They suggested establishing the diagnosis of ≥80% ISR when PSV is >340cm/sec and the ICA/common carotid artery ratio is ≥4.15. In our series a patient was considered to have significant restenosis after CEA with a PSV of ≥200cm/sec; in the follow-up studies no different duplex criteria were used between patients who underwent reoperation or endovascular treatment of their postendarterectomy stenosis. This might be a potential flaw, but the latest evidence concerning this issue was not available when CAS was started at our institution. However, when favoring new velocity criteria in the stented ICA, one has to take into consideration that these might apply to some extent also to the previously operated artery. Another important but often neglected issue in terms of management of carotid restenosis is the pharmacological risk factor management. It is an important fact to recognize that the evidence used to develop international guidelines for the surgical or interventional treatment of atherosclerotic carotid artery disease was based upon trials that were conducted up to 20 years ago when the concept of “best medical therapy” was fairly rudimentary.20, 21 The two basic symptomatic carotid artery stenosis trials randomized patients throughout the 1980s and reported their results concerning the management of severe stenosis in 1991. The two big trials for patients with asymptomatic carotid stenosis (ACAS and the Asymptomatic Carotid Surgery Trial [ACST]) enrolled in the 1990s and reported in 1995 and 2004.22, 23 Statin therapy, maybe the most important single pharmacological advance in cardiovascular risk factor management, was not available when the European Carotid Surgery Trial (ECST), the North American Symptomatic Carotid Endarterectomy Trial (NASCET), and ACAS were recruiting.24 Even in the most recently published ACST trial only 30% of the patients were on statin therapy. Also, almost 40% of our patients did not have a statin on a regular basis. The exact mechanism of statin action on neointimal proliferation is not fully understood, but the effect of statins is evident independently from baseline cholesterol.25 These data show that medical risk factor management plays an important role, especially when dealing with CR, and is still underestimated. With the lack of prospective data at present, the choice of redo surgery or CAS in the treatment of CR remains to a great extent an individual one, taking the patient's comorbidities and possible contraindications for the two treatment modalities into consideration.

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Conclusion 

Our data show that CAS in the treatment of CR is feasible and safe. When CAS is contraindicated, CEA remains an alternative treatment option, with acceptable stroke risk. The risk of cranial nerve damage in reoperation might be overestimated.

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References 

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PII: S0890-5096(09)00161-7

doi:10.1016/j.avsg.2009.07.002

Annals of Vascular Surgery
Volume 24, Issue 2 , Pages 190-195, February 2010

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