European Journal of Vascular & Endovascular Surgery
Volume 40, Issue 3 , Pages 312-319, September 2010

An Update of the Role of Endovascular Repair in Blunt Carotid Artery Trauma

  • K.G. Moulakakis

      Affiliations

    • Department of Vascular Surgery, Athens University Medical School, Attikon University Hospital, Athens, Greece
    • Corresponding Author InformationCorresponding author at: Department of Vascular Surgery, Athens University Medical School, Attikon University Hospital, 1 Rimini Street, GR 12462 Haidari, Greece. Tel.: +30 6937357508.
    • ,
  • S. Mylonas

      Affiliations

    • 1st Department of Surgery, ‘Hellenic Red Cross Hospital’, Athens, Greece
    • ,
  • E. Avgerinos

      Affiliations

    • Department of Vascular Surgery, Athens University Medical School, Attikon University Hospital, Athens, Greece
    • ,
  • T. Kotsis

      Affiliations

    • Vascular Surgical Unit, 2nd Surgical Department, Aretaieion Hospital, Medical School, University of Athens, Greece
    • ,
  • C.D. Liapis

      Affiliations

    • Department of Vascular Surgery, Athens University Medical School, Attikon University Hospital, Athens, Greece

Received 10 February 2010; accepted 11 May 2010. published online 23 June 2010.

Article Outline

Abstract 

Blunt carotid injury (BCAI) is an increasingly recognised entity in trauma patients. Without a prompt diagnosis and a proper treatment, they can result in devastating consequences with cerebral ischaemia rate of 40–80% and mortality rate of 25–60%. Several applied screening protocols and continuously improving diagnostic modalities have been developed to identify patients with BCAI. The appropriate treatment of BCAI still remains controversial and strictly individualised. Besides anti-thrombotic/anticoagulation therapy and surgical intervention, continuously evolving endovascular techniques emerge as an additional treatment option for patients with BCAI. We provide an update on blunt carotid trauma, emphasising the role of endovascular approaches.

Keywords: Blunt injury, Carotid trauma, Endovascular, Stent

 

Traumatic carotid injuries can be divided into three main categories: penetrating, blunt from contusion with an obvious neck trauma and those vessel injuries accompanied by the absence of any physical contact in the neck area. Bleeding is a serious complication in penetrating injury needing immediate management, but in all three categories, the main concern is cerebral blood supply derangement.1, 2, 3 The first report on blunt carotid injury (BCAI) was published by Verniuel in 1872.4 Almost a century passed since Yamada reported a patient with carotid artery occlusion after a non-penetrating injury.5 In the modern era, BCAI is still considered to be quite rare, occurring in nearly 1–2% of blunt trauma patients.6, 7, 8 Without a prompt diagnosis and a proper treatment, however, they can result in devastating consequences with a cerebral ischaemia rate of 40–80% and mortality rate of 25–60%.9, 10, 11, 12, 13, 14

The purpose of this article is to review the current literature emphasising the management of BCAI and focussing on the role of endovascular approach.

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Mechanisms of Blunt Carotid Trauma 

The mechanisms by which carotid artery damage is produced in closed traumas have been determined in detail.10 Carotid injuries include injury to the intrapetrous or cevernous portion of the carotid artery during basal skull fracture, injury to the internal carotid artery in the neck due to direct contusion or from a straight stretching or shearing effect. Further, a direct blow to the neck or trauma to the paratonsillar area by a foreign object carried in the mouth has been described as a potential mechanism.15 Furthermore, BCAI after strangulation and choking has been described.16 Moar,17 in 1987, reported after 200 consecutive autopsies on victims of motor vehicle accidents that in nearly one-third of subjects there was some degree of arterial disruption; dual- or even triple-vessel involvement in both ipsilateral and contralateral distribution occurred in 38.6% of the 57 subjects in whom traumatic arterial lesions were found; compound intima–medial tears occurred in almost two-thirds (63.2%) of the 57 subjects; and adventitial contusions were found in 70.2% of the 57 subjects.

Bilateral injury of the carotid artery ranges from 20.9% to 37.5% of carotid traumas in the reported series.18

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Clinical Presentation and Diagnosis of BCAI 

Onset of symptoms due to closed carotid trauma may occur immediately, but a relevant percentage of patients exhibit a latent period, ranging from 1h to several weeks.7, 19, 20, 21 In this undefined period, the initial subfailure, which usually occurs after blunt vessel injuries, cascades to catastrophic vessel failure.22 The asymptomatic phase is clinically important as it implies the Willy’s circle completeness, the autoregulation ability of the brain circulation and the severity of carotid artery damage. Berne et al. found a median time to diagnosis of 12.5h for survivors of BCAI and 19.5h for non-survivors23 emphasising the need for accurate identification of the patients at great risk of BCAI. Associated injuries in blunt carotid trauma are common and range from 48% to 93%.8, 24, 25, 26 Several authors have proposed signs, symptoms or injury patterns that should raise the suspicion to the physicians for BCAI. Parikh et al. reported that a combination of head and chest trauma was found to be associated with a 14-fold increase in the likelihood of carotid injury.27 With the screening protocol suggested by the Denver Health Medical Center12, 28 the authors reported an overall blunt cardiovascular injury (BCVI) incidence of 0.86%; 4.8% of all trauma patients were screened and 18% of screened patients were found to have a BCAI. Miller et al.,11following the ‘Memphis criteria’ (cervical spine fracture, Horner’s syndrome, Le Fort II or III facial fracture, skull-base fracture involving the foramen lacerum and neck soft-tissue injury), found an incidence of 1.03%; 3.5% of all blunt trauma patients were screened, and 29% of screened patients were found to have BCAI. Extracranial BCAI were more commonly asymptomatic, predicted by a Glasgow Coma Scale (GCS) of <8 and thoracic injury. Intracranial injuries, on the other hand, were frequently detected on initial investigations and were associated with GCS<8 and facial injuries.25 The ‘seat belt’ sign has also been used as a trigger for screening.21, 29, 30 More liberal screening for BCAI has been proposed by Kerwin et al. who suggest expanding the criteria for screening to include all patients with basilar skull fractures and all patients with unstable cervical spine fractures.31 In a recent study by Berne et al., it is suggested that high-risk mechanism and a low GCS, high injury-severity score, mandible fracture, basilar skull fracture or cervical spine injury are independent predictors for BCAI.32 Moreover, Hwang suggested that patients with cervical spine fractures, especially of the upper C-spine, are at much higher risk of BCVI than those without such injuries.33 Despite the widely applied resource-consuming screening programmes of BCAI, an improvement in outcome is uncertain as the natural history of these lesions are not well defined, and the available diagnostic and treatment options are ambiguous.11, 34, 35

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Screening/Diagnostic Modalities 

Digital subtraction arteriography (DSA) remains the gold standard for the diagnosis of BCAI. Although it is an invasive method associated to a low risk of stroke, DSA can not only depict the extent and the severity of the vessel injury, but also provide information about the integrity of the cerebral circulation.6 Based on the hypothesis that different injury grades might have distinct implications in terms of response to therapy and ultimate neurologic outcome, Biffl and associates have proposed an arteriographic grading scale for BCAI (Table 1).24 In fact, Biffl demonstrated an improved outcome and a decreased rate for stroke in relation to the gravity of carotid lesion; Edwards et al. showed an increased rate of healing for grade I and II lesions comparing diagnostic arteriograms with follow-up arteriograms.26

Table 1. Denver “grading scale for blunt carotid injury” proposed by Biff and associates.22.
Grade IArteriographic appearance of irregularity of the vessel wall or a dissection/intramural hematoma with less than 25% luminal stenosis
Grade IIIntraluminal thrombus or raised intimal flap is visualized, or dissection/intramural hematoma with 25% or more luminal narrowing
Grade IIIPseudoaneurysm
Grade IVVessel occlusion
Grade VTransection with free extravasation

The adequacy of helical computed tomographic angiography (CTA) in BCAI diagnosis is controversial. Several authors underline the effectiveness of 16-channel, multislice CTA in diagnosis of BCAI34, 36 while others believe that CTA is not as reliable and accurate as DSA; it has a significant false-negative rate and underestimates the severity of the injury.37, 38

Magnetic resonance angiography (MRA) is another safe, non-invasive depicting technique that can provide data concerning the vessel morphology and blood flow and permit the early identification of a cerebral ischaemic infarction.39 A recent review demonstrates that MRA is equal to CTA in the diagnosis of carotid and vertebral dissection.40 Despite new developments (gadolinium infusion, dedicated head/neck coils and novel acquisition sequences), limitations relative to the required time for the examination and the high cost still reduce MRA applicability in patients with suspected BCAI.

Duplex ultrasound (DU) has a limited usefulness to identify patients with BCAI.39 The main limitation of the technique is the inability to directly evaluate the distal internal carotid artery above the angle of the mandible (zone III) and the more proximal segment under the clavicle (zone I).41 In addition, cervical stabilisation modalities, which are obligatory in high-energy trauma patients, may be another impediment for DU application.42 However, DU can be useful in the follow-up of these patients.43

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Treatment of BCAI 

Controversy exists about BCAI therapy, as the correlation of trauma mechanism and the concurrent injuries with the risk of brain hypoperfusion due to dissection or occlusion or embolism cannot be predicted; occasionally, management swings between a thrombosed carotid and thrombo-embolised brain. A retrospective study from a single institution published in 2008, in which 25.8% of untreated patients developed a stroke and only 3.9% (p=0.0003) of treated patients, underline the need to promptly identify and rapidly treat these injuries.8 Grade I lesions, according to Denver scale, have a better outcome and midterm healing and could be treated conservatively with anti-thrombotic therapy. A direct aggressive surgical repair of accessible grade II, III, IV and V lesions, according to the Denver Scale, should be individualised and considered on decision making, although its role has fallen out of practice due to inaccessibility of lesions, and due to recent promising results using anti-thrombotic therapy. In the small subset of patients with bilateral BCAI, some authors suggest conservative anti-thrombotic therapy while late reports propose the option of early carotid artery stenting.18, 44 Superior cervical sympathectomy and cervical sympathetic block, used in the past, have been abandoned due to controversial results and poor outcomes.45

Accumulated data based on level III evidence have shown a beneficial effect of anti-thrombotic therapy in preventing cerebral infarction.12, 20, 26, 43, 46 Edwards et al., in a study of 110 patients with blunt carotid injury, demonstrated that anti-thrombotic therapy prevents cerebral infarction while anti-platelet therapy (clopidogrel 75mg daily and/or aspirin 325mg daily) and anticoagulation (INR 2–3) are equally effective.26 In addition, Cothren and Biffl recommend heparinisation as first-line therapy for BCAI, reserving anti-platelet agents for patients not deemed to be candidates for anticoagulation.12, 20, 34 However, recent studies confirm the safety of the rational use of anti-thrombotic regimens in trauma patients.47, 48 Further investigation is mandatory to assess the safety of these agents in patients with ‘traditional’ contraindications such as spinal cord injury or solid abdominal organ injury.

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Search Strategy 

A multiple electronic health database search was performed, including Medline, Embase, Ovid and the Cochrane Database, on all articles published between January 1997 and April 2010, referring to BCAI. These databases were searched with an unrestricted search strategy, using exploded MeSH (Medical Subject Heading) terms (‘carotid’, ‘injury’, ‘blunt injury’, ‘cerebrovascular injury’, ‘endovascular’, ‘stent-graft’ and ‘endograft’). Twenty-nine studies with a total of 160 patients were included in the present review.

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BCAI and Endovascular Treatment 

The era of endovascular treatment of carotid artery injuries began in the mid-1990s after reports of successful interventions of coronary artery rupture.49, 50 The use of stents, coils or even stent grafts, theoretically can protect both against vessel-lumen, and vessel-wall complications, such as dissection, thrombosis, pseudo-aneurysm and haemorrhage. Furthermore, endovascular techniques offer potential benefit in cases of distal internal carotid artery injury, where surgical exposure is complicated by the need for extensive dissection or mandible subluxation to gain exposure.51 Surgical repair of these patients has been associated with 9% perioperative stroke rate.52 A recent retrospective study by Li53 comparing treatment options for patients with BCAI failed to demonstrate improved outcomes with endovascular approaches. However, a literature review by DuBose on stenting for the treatment of carotid injuries – either penetrating or blunt – revealed a follow-up patency of 79.6% and no stent-related mortalities while new neurologic deficits after stent placement occurred in 3.5%.54

The most recent advantages in carotid artery stenting have been developed from extensive experience in the field of atherosclerotic carotid disease. These stents are self-expanding with small (closed cells) or larger interstices (open cells), and the deployment promotes laminal flow through the lumen.55 Three to 6 weeks after placement, the stent is covered completely with endothelium.56 An additional benefit of endovascular techniques is the exclusion of the pseudo-aneurysm with use of a bare (uncovered) stent and catheter-directed coil (with/without thrombogetic agents) delivery through the interstices of the stent. The stent acts as a barrier, confining the coils to the pseudo-aneurysm, ensuring its adequate embolism and preventing the outflow of these materials into the vital carotid artery.50, 57 Indications for stenting in the setting of carotid injury include contraindication to coagulation, enlarging pseudo-aneurysm, progressive dissection and high inaccessible operatively lesions.

Sporadic case reports are followed by controversial case series in the literature (Table 2). One of the promising early reports describing endovascular therapy for the treatment of pseudo-aneurysms came from the Denver group, who demonstrated good results in 14 treated patients.58 In a mean 6-month follow-up with angiography, they noted patent carotid arteries. However, more recently, the same group reported a 45% carotid occlusion in 23 patients who had been treated with stents.59 In this study,59 46 patients were diagnosed with carotid blunt injury and pseudo-aneurysm during an 8.5-year period. Twenty-three patients were treated with stents and 23 with anti-thrombotic therapy, anticoagulation or anti-platelets. Most of the patients (42) were asymptomatic at the time of diagnosis. Eight patients in the stent group (45%), and only one in the anti-thrombotic group, developed carotid artery occlusion on follow-up angiography. Cothren et al. concluded that carotid stenting cannot be considered a safe alternative to anti-thrombotic-alone therapy.

Table 2. Endovascular treatment of blunt carotid injury in reported series. Avg:average.
YearAuthor/StudyPatients (n)Type of InjuryGenderAgeOutcome/Follow-up
1997Duke et al. J Neurosurg6Transection (3) Pseudoaneurysm (3)M(3) F(3)Avg 26UNEVENTFUL
1997Matsuura et al. J Endovasc Surg1PseudoaneurysmF20UNEVENTFUL 12-month follow-up (U/S)
1997Parez-Cruet et al. Neurosurgery1PseodoaneurysmM20UNEVENTFUL 20-month follow-up
1997Bernstein et al. J Vasc Intervent Radiol1PseudoaneurysmF20UNEVENTFUL 3-month follow-up (DSA)
1999Shames et al. J Trauma1PseudoaneurysmM29UNEVENTFUL Immediate No follow-up
1999Liu et al. Neurosurgery2Dissection (1) Pseudoaneurysm (1)M(1) F(1)Avg 151 ICA occlusion 3 months after
2000Coldwell et al. J Trauma14PseudoaneurysmM(7) F(7)Avg 27UNEVENTFUL 16-month mean follow-up (DSA)
2000Kerby et al. J Trauma1Initmal flapF37UNEVENTFUL 6-month follow-up (DSA)
2000Malek et al. J Neurosurg2DissectionFAvg34UNEVENTFUL Immediate No follow-up
2000Malek et al. Am J Neuroradiol2DissectionFAvg41UNEVENTFUL 6-month follow-up (DSA or U/S)
2001Brandt et al. J Trauma2Transection(1) Pseudoaneurysm(1)FAvg44UNEVENTFUL
2001Redekop et al. J Neurosurg2FistulaMAvg19UNEVENTFUL 9-month follow-up (DSA or CTA)
2001Scavee et al. Cardiovasc Intervent Radiol1PseudoaneurysmM53UNEVENTFUL 6-month follow-up (CT)
2002Duane et al. J Trauma1PseudoaneurysmF31Stent and ICA occlusion at 3 months
2004Lee et al. J Neurosurg1FistulaM19UNEVENTFUL 7-month follow-up (DSA)
2004Fusonie et al. Ann Vasc Surg1PseudoaneurysmM37UNEVENTFUL 3-months follow-up (U/S)
2005Fateri et al. Ann Vasc Surg1DissectionM52UNEVENTFUL 24-months follow-up (CTA)
2005Cothren et al. Arch Surg23PseudoaneurysmM(15) F(8)Avg 32IMMEDIATE: 3 strokes, 1 subclavian dissection, 2.4-months follow-up (DSA): 8 patients stent occlusion
2005Joo et al. Ann Vasc Surg9Fistula (3) Pseudoaneurysm (5)M(8) F(1)Avg371 coil migration to ICA – ICA thrombosis
2005Cohen et al. Neurol Res12Dissection–Avg41UNEVENTFUL Mean 9.2-month follow-up (U/S)
2005Szopinski et al. Eur J Vasc Endovasc Surg2Dissection (1) Pseudoaneurysm (1)M(1) F(1)Avg46UNEVENTFUL
2007Archondakis et al. Am J Neuroradiol8FistulaM(5) F(3)14–701 ICA occlusion at 6-month follow-up
2007Edwards et al. J Am Coll Surg18Dissection (4) Pseudoaneurysm (14)–Avg 37In-Hospital: 1 stroke and death on 5th post operative day, 1 death due to pulmonary failure, After Discharge: 1 death AIDS related. 14-months follow-up (DSA)
2007Nakagawa et al. Minim Invasive Neurosurg1FistulaF48UNEVENTFUL 6-years follow-up
2008Cohen et al. J Neurol Sci1DissectionM43UNEVENTFUL 1-year follow-up (DSA)
2008Berne et al. J Trauma11PseudoaneurysmM(8) F(3)Avg27Immediate: 1 death from brain injury, 1 death from stroke Follow-up: 1 stenosis 50% at 6-months
2008Chaer et al. Ann Vasc Surg1PseudoaneurysmF19UNEVENTFUL 2-years follow-up (U/S)
2009Stein et al. J Trauma33Pseudoaneurysm–Avg422 Strokes
2010Testerman South Med J1Bilateral dissectionF35UNEVENTFUL 6-months follow-up (CTA)

However, there were some limitations in this report. First, there were no selection criteria for the selection of one treatment over another and the decision to stent the lesion or to leave the patient in the conservative therapy was made by the surgeon in charge. This could represent a selection bias for stenting in more difficult cases.50 Second, the patients were treated between 1996 and 2001 during which time the lack of dual anti-platelet administration could be responsible for the high rate of in-stent thrombosis. Finally, there is little data in the study concerning follow-up. There are numerous reports of patients treated with anti-thrombotic therapy and presenting weeks to a year later with life-threatening haemorrhage or Horner’s syndrome from untreated pseudo-aneurysms.50, 51, 60, 61, 62 This may suggest that anti-thrombotic therapy alone may not be the best treatment for blunt carotid injury and pseudo-aneurysm.

Berne et al.50 published a study designed to compare early anticoagulation alone versus stenting combined with anti-platelets for Grade III carotid artery injuries and pseudo-aneurysms (Table 1). The authors chose Grade III lesions to treat with stent because of their suitability for endovascular treatment, as the majority of these lesions are located at the skull base just below or within the carotid canal of the petrous bone. A total of 11 patients were treated with stents during a 5.5-year period from 2000 to 2005. All patients were put into dual anti-platelet regimens (clopidogrel 75mg and aspirin 81mg, daily). Two, out of 11, patients died due to cerebral oedema; these patients suffered also from severe closed head injuries. From the remaining nine survivors, seven were available for the follow-up. The authors followed the patients for up to 4 years with DSA and DU. No in-stent thrombosis was observed. The study concluded that early anticoagulation therapy, followed by carotid artery stenting, is a safe and effective alternative therapy for non-occlusive injuries and pseudo-aneurysms.

The results of Berne et al.50 contradict the ones by Cothren et al.59. However, it should be emphasised that the study by Berne et al. covers a later time period when stent technology, procedural expertise and pharmacologic agents have probably reduced the short- and long-term morbidity associated with carotid stenting.

Duane et al.63 and Parodi et al.64 each describe a patient who developed stent graft occlusion, while Biffl et al.24 describe occlusion of two stents out of the 18 treated patients. Both occlusions occurred on cessation of anticoagulation. In another study by Edwards et al.,26 18 patients were treated by endovascular means. Fourteen of them were available for a mean follow-up of 29.7 months. Angiographic follow-up revealed that all patients had patent stents. Joo et al.65 treated 10 patients with stent-assisted coil embolisation of the fistula or the pseudo-aneurysm. In one patient, a stent graft was inserted to exclude the aneurysm. They observed one internal carotid artery thrombosis due to coil migration. At a mean follow-up of 20.3 months, no delayed neurological or vascular complications were reported. However, the follow-up was made by telephonic interviews or by reviewing the most recent office notes, and not by imaging techniques. The authors concluded that endovascular treatment of carotid injury is feasible and safe.

In another optimistic case series, Cohen et al66 reported their experience with the endovascular treatment of 10 patients with traumatic dissection of the carotid artery. They used a total of 22 stents as seven patients needed multiple stents to treat dissection. No peri-procedural complication was observed. Stenting reduced mean dissection stenosis from 69% to 8%. At sonographic follow-up up to 28 months, no in-stent thrombosis was noted. All patients were under dual anti-platelet therapy for 3 months. The authors concluded that endovascular stenting seems a rationale and effective way to restore the artery lumen in selected patients.

Our literature search yielded 160 patients (60% males, average 34.8 years) with BCAI treated with endovascular techniques. Four of them (2.5%) suffered a post-procedural stroke while in an average follow-up of 8.5 months, 12 ICAs occluded. In the absence of level I evidence, treatment of BCAI is debatable and surveillance with anticoagulation or anti-platelet regimens remains the first management approach in preventing cerebral infarction (Fig. 1). It seems that in selected patients, especially in the ones with carotid injuries Grade III, the endovascular techniques could have a beneficial role. Highly experienced vascular specialists versed in carotid stenting techniques are of great importance for good peri-procedural results. The appropriate post-stenting anti-thrombotic therapy remains also ambiguous; the risk of anti-platelet regimens administration in trauma patients and, on the other hand, the risk of an early stent occlusion should be considered. Many authors advocate dual anti-platelet therapy (clopidogrel 75mg and aspirin 80mg, daily) at least for 3 months44, 50, 66while others suggest solid anti-platelet therapy lifelong.26 Recent guidelines of the European Society for Vascular Surgery (ESVS) for carotid artery stenting in atherosclerotic disease prescribe the use of dual anti-platelet treatment.67 Thus, Hershberger et al.68 suggest that protocols for long-term follow-up should be developed before routine use of stents for the treatment of carotid artery trauma, while Biffl et al.28 emphasise that careful risk–benefit analysis must be performed before placing stents in the acutely injured carotid artery.

The timing of stenting is also controversial in literature. Some authors suggest delay of carotid stenting, thus decreasing the risk of thrombotic and embolic adverse events related to catheter manipulation in the acutely injured artery, while others recommend delaying carotid stenting until approximately 1 week.34, 68 The long-term follow-up of patients with BCAI also appears very confusing in literature. The optimal radiologic follow-up for these lesions has not been determined and will require further studies.50 DU is cheap, simple and easily repeatable, but it may miss traumatic lesions within the bone canal at the base of the skull. Angiography may represent the optimal imaging technique at the moment; however, it is not an examination of choice for follow-up due to its invasive nature. CTA may be the technique of choice in the follow-up of these patients, but concern for the effects of radiation may not justify the benefit.50

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Prognosis 

The prognosis seems to be correlated with certain parameters such as: presence of associated injuries in the brain or other organs, presence of injury in both carotid vessels and/or vertebral arteries, period of onset of symptoms and gravity of neurological picture, imaging findings of brain parenchymal damage, arteriographic appearance of the lesions, indicating the gravity of the damage in the arterial wall and the potential induced mechanisms of hypoperfusion or embolism in the brain.69 Although diagnosis of BCAI has been increased and the treatment modalities have been enriched by endovascular techniques, BCAI still results in more severe functional disability at discharge than penetrating CAI.70

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Conclusions 

Haemodynamic stability, neurological picture, presence of active haemorrhage and type of arterial injury should be evaluated before decision making. Although the appropriate treatment of BCAI still remains controversial and strictly individualised, close surveillance with anticoagulation or anti-platelet should be the first line of treatment in case of neurologically stable patients. If neurological worsening continues despite adequate anticoagulation or contraindication exists for anti-thrombotic therapy, endovascular reconstruction can be attempted in arterial lesions suitable for endovascular repair. Important issues concerning the optimum time after injury for endovascular intervention and the duration of post-procedural anti-thrombotic therapy have to be addressed through large clinical trials.

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Conflict of Interest/Funding 

None.

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References 

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PII: S1078-5884(10)00318-7

doi:10.1016/j.ejvs.2010.05.003

European Journal of Vascular & Endovascular Surgery
Volume 40, Issue 3 , Pages 312-319, September 2010

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