Abstract

BACKGROUND:

Carotid and vertebral artery dissections are a leading cause of stroke in young individuals.

OBJECTIVE:

To examine the published safety and efficacy of endovascular stenting for extracranial artery dissection.

METHODS:

We conducted a systematic review of the literature to identify all cases of endovascular management of extracranial carotid and vertebral artery dissections.

RESULTS:

For carotid dissections, our review yielded 31 published reports including 140 patients (153 vessels). Reported etiologies were traumatic (48%, n = 64), spontaneous (37%, n = 49), and iatrogenic (16%, n = 21). The technical success rate of stenting was 99%, and the procedural complication rate was 1.3%. Mean angiographic follow-up was 12.8 months (range, 2-72 months) and revealed in-stent stenosis or occlusion in 2% of patients. Mean clinical follow-up was 17.7 months (range, 1-72 months), and neurological events were seen in 1.4% of patients. For vertebral artery dissections, our review revealed 8 reports including 10 patients (12 vessels). Etiologies were traumatic (60%, n = 6), spontaneous (20%, n = 2), and iatrogenic (20%, n = 2). There was a 100% technical success rate. The mean angiographic follow-up period was 7.5 months (range, 2-12 months). No new neurological events were reported during a mean clinical follow-up period of 26.4 months (range, 3-55 months).

CONCLUSION:

Endovascular management of extracranial arterial dissection continues to evolve. Current experience shows that this treatment option is safe and technically feasible. Prospective randomized trials compared with medical management are needed to further elucidate the role of stenting.

Carotid and vertebral artery dissections are a leading cause of stroke in young people.14 Spontaneous carotid artery dissection occurs in about 2.6 per 100 000 and is thought to be mostly idiopathic, although fibromuscular dysplasia has been reported in approximately 12% of these patients.57 The annual incidence of spontaneous vertebral arterial dissections has been estimated at 1 to 1.5 per 100 000.8 These lesions typically arise from a tear in the intimal layer of the artery, which allows subsequent hemorrhage into the vessel wall. Dissections through the subadventitial layer may result in pseudoaneurysms.9

Determining optimal therapy for patients with extracranial carotid and vertebral artery dissections is empirical because no randomized controlled trials have compared one treatment with another. Although up to 85% of spontaneous carotid dissections improve on antithrombotic therapy, medical management may be contraindicated in certain conditions or may be insufficient to prevent thromboembolic complications in others such as bleeding diatheses and many congenital thrombophilic states.7,1012 When extracranial dissections warrant surgical intervention, endovascular techniques are generally considered before surgical ligation or bypass.1315 Endovascular methods are associated with lower complication rates and allow reconstitution of the vessel lumen with immediate reestablishment of blood flow.16 They also provide the opportunity to treat any associated pseudoaneurysms.1719

In this article, we review 31 case series of endovascular treatment of carotid dissection and 8 studies of endovascular therapy of vertebral dissections to summarize the experience to date in the medical literature.

METHODS

We conducted a systematic review of the English medical literature reported through PubMed (from 1967 to September 3, 2009) to find all studies involving endovascular management of extracranial arterial dissections. Initial literature was found using the search terms “carotid” or “vertebral,” “dissection,” “stent”, “extracranial,” “extradural,” and “pseudoaneurysm,” and references were further examined for additional relevant studies pertaining to this review. We excluded any study that included intracranial extension of a dissection, did not provide outcome data, or used a combined open technique. Articles describing endovascular repair of an extracranial carotid or vertebral dissection were then analyzed for the following parameters: number of patients, age, sex, location of dissection, injury mechanism, clinical presentation, indication for stenting, technical success, procedural complications, number of pseudoaneurysms, resolution of pseudoaneurysms, type of endovascular stents used, stent patency, medical therapy after stenting, neurological events on follow-up, and mortality. We defined neurological events on clinical follow-up as any neurological symptom, transient or permanent, related to stent deployment. Symptoms were related to stent deployment if they occurred ipsilateral to the side of the stented vessel during the clinical follow-up period after the procedure.

RESULTS

Carotid Dissections

Thirty-one published studies describing endovascular stenting of extracranial carotid artery dissections in a total of 140 patients and 153 arteries were identified (Table 1).10,13,16,1947 The patients' mean age was 49.1 years (range, 12-83 years). Male patients made up 56.6% of the subjects, and there was a left-to-right vessel ratio of 1:1. Sixty-one of these patients had pseudoaneurysms that were stented and/or coiled. Reported etiologies for the dissections included traumatic (48%, n = 64), spontaneous (37%, n = 49), and iatrogenic (16%, n = 21). Traumatic dissections were defined as any temporally related traumatic event that may have had a causative relationship to the lesion. Spontaneous dissections were defined as any lesion without any objective history of trauma. The mean angiographic follow-up was 12.8 months (range, 2-72 months) with a mean clinical follow-up of 17.7 months (range, 1-72 months). Indications for stenting were available for 25 studies and are listed in Table 2. Failure of medical management was the most common indication (56%), followed by acute stroke (28%) and contraindications to anticoagulation (24%). In the literature, medical treatment was considered a failure if the patient had a new ischemic event, experienced a progression of initial symptoms, or demonstrated an enlarging pseudoaneurysm despite adequate anticoagulation or antiplatelet treatment.

TABLE 1.

Clinical Characteristics of Patients With Extracranial Carotid Dissectionsa

TABLE 2.

Indications for Endovascular Management of Extracranial Carotid Artery Dissections

Technical Success and Anticoagulation Regimens

The technical success rate of endovascular management was 99%. There were 2 reported procedural complications in which 1 procedure was then terminated with no intervention (Table 3).23,29 Kadkhodayan et al29 reported halting a procedure when a new intimal flap was created before stent deployment; this patient remained asymptomatic. Lavallee et al23 described a patient who developed an embolic infarct in the territory of the anterior cerebral artery during the procedure. Despite this infarct, this patient improved from a baseline National Institutes of Health Stroke Scale score of 17 to 5 at 24 hours and 0 at 3 months, with a modified Rankin Scale score of 0 at 3 months. No stent-related deaths were reported in any study, as defined by mortalities occurring after stent deployment and unrelated to comorbid conditions.

TABLE 3.

Pooled Clinical and Angiographic Outcome of All Carotid Patients Treated Endovascularly

Table 4 lists studies \that reported types of stents used.10,16,1921,23,24,2631,3347 Of the 28 studies, Wallstents (Boston Scientific, Natick, Massachusetts; Schneider, Minneapolis, Minnesota) were most commonly deployed in 15 studies (54% of the studies). SMART stents (Cordis, Bridgewater, New Jersey) were the next most common in 5 studies (18% of the studies).

TABLE 4.

Stent Types Used Across Various Reporting Carotid Studiesa

Twenty-three studies reported poststenting anticoagulation regimens (Table 5).10,16,1921,2325,27,29,30,3335,37,38,40,4247 A combination of clopidogrel and aspirin therapy was most commonly used (in 57% of the studies), followed by combination ticlopidine and aspirin therapy (in 26% of the studies). One study used aspirin monotherapy.

TABLE 5.

Poststent Anticoagulation Regimen Used Across Various Reporting Carotid Studiesa

No distal protection device filters were used in any study.

Angiographic Follow-up

Of 140 patients, 137 (98%) had follow-up imaging at least 2 months after stenting with an overall mean angiographic follow-up of 12.8 months (range, 2-72 months). Most studies presented their data with mean follow-up periods, so median follow-up could not be determined.

Three stents were noted to have developed in-stent stenosis or occlusion (Table 3).19,23,29 Schulte et al19 observed asymptomatic carotid restenosis (< 30%) 23 months after stenting and treated this patient conservatively with atorvastatin. No further information was available regarding the choice of statins as a treatment method and this patient's repeat imaging. Kadkhodayan et al29 reported 2 occlusions of stented carotid arteries, 1 at 3.4 months and 1 at 22 days. These patients remained asymptomatic. Although Lavallee et al23 described the development of an asymptomatic acute in-stent thrombus postprocedurally despite antithrombotic therapy, this was not considered true in-stent de novo thrombosis. This thrombus also did not progress or cause symptoms over a mean follow-up of 15 months while the patient was on clopidogrel 75 mg for 12 weeks and acetylsalicylic acid indefinitely.

Clinical Follow-up

In our study, 138 of 140 patients had clinical follow-up of at least 1 month for an overall mean clinical follow-up period of 17.7 months (range, 1-72 months). Median follow-up could not be determined because these studies reported their follow-up as means.

Two patients experienced ipsilateral transient ischemic attacks during follow-up at 2.7 months and 12 months after the procedure.29 Both patients had repeat diagnostic angiograms that showed no stent stenoses or new vascular lesions. All other studies described no further transient or permanent neurological events during clinical follow-up. Patients had stable neurological deficits from the dissection, interval neurological improvement, or complete resolution of presenting symptoms.

Pseudoaneurysms

In patients presenting with dissections associated with pseudoaneurysm, 98.4% were successfully occluded with stents and/or coils (Table 3). Most studies, however, did not distinguish between whether the pseudoaneurysms resolved in the immediate postprocedural period or during angiographic follow-up. The 1 patient (1.6%) whose pseudoaneurysm persisted had nearly complete obliteration of the lesion after the coiling procedure. The authors decided to stop at that time because only trivial filling at the base of the pseudoaneurysm remained. They elected to proceed with close angiographic follow-up for the neck remnant.34

Vertebral Artery Dissections

Eight published reports describing endovascular stenting of extracranial vertebral artery dissections for a total of 10 patients and 12 arteries were identified (Table 6).4855 The mean age was 37.9 years (range, 16-52 years). The male-to-female ratio was 1:1. Of these patients, 70% had associated pseudoaneurysms and 20% had bilateral lesions. Etiologies included traumatic (60%), spontaneous (20%), and iatrogenic (20%).

TABLE 6.

Clinical Characteristics of Patients With Extracranial Vertebral Dissectionsa

Technical Success and Anticoagulation Regimens

Table 7 describes the endovascular management of these extracranial vertebral artery dissections. Indications for stenting were failure of medical management (40%), contraindication to anticoagulation (20%), and severity of dissection hemodynamics (70%). Similar to carotid dissections, medical treatment of vertebral dissections was considered a failure if the patient had a new ischemic event, experienced a progression of initial symptoms, or demonstrated an enlarging pseudoaneurysm despite adequate anticoagulation or antiplatelet treatment.

TABLE 7.

Endovascular Treatment of Extracranial Vertebral Dissectionsa

Stent-assisted coiling of a ruptured pseudoaneurysm was performed in 1 patient54; another patient, who had bilateral dissections, also had the contralateral vertebral artery occluded with coils because it was a nondominant artery and contained intraluminal thrombus.49 Adjuvant antithrombotic therapy after stent placement was used in 80% of patients. Antiplatelet agents were most commonly used (70% of cases), although warfarin was also given in 10% of patients. The type of anticoagulation could not be determined in 1 study accounting for 10% of the total number of patients and was not given in 1 study (10% of patients) because of patient death.

No stent-related complications or mortalities were reported in any study. However, there was 1 case of a dissection-related death. The stenting was technically successful, but the patient succumbed to irreversible brainstem infarction relating to his initial dissection. There was also 1 case of in-stent thrombosis without any clinical correlation (Table 8).

TABLE 8.

Pooled Clinical and Angiographic Outcome of All Vertebral Patients Treated Endovascularly

Angiographic and Clinical Follow-up

After stent placement, 60% of patients underwent angiographic follow-up with the use of digital subtraction angiography (Table 9). The mean follow-up period was 7.5 months (range, 2-12 months) and demonstrated stent patency in 88%; in the remaining 12%, stent occlusion was due to in-stent thrombosis. Of vessels amenable to follow-up, there was 1 case of in-stent stenosis during which the patient remained asymptomatic and exhibited no new or recurrent symptoms.54 There was also clinical follow-up for 50% of patients over a period ranging from 3 to 55 months. No new neurological events were reported during this follow-up.

TABLE 9.

Studies With Clinical and Angiographic Outcome of Extracranial Vertebral Dissections Treated Endovascularlya

Pseudoaneurysms

In patients presenting with dissections associated with pseudoaneurysm, 90% were successfully occluded, with the remaining 10% showing decreased flow. All surviving patients demonstrated improvement or complete resolution of presenting symptoms. No patient with documented clinical follow-up displayed any new neurological deficits.

DISCUSSION

Extracranial arterial dissection accounts for 5% to 22% of strokes in young patients and is the leading cause of stroke in patients < 45 years of age. The incidence of carotid dissection is about 2 to 3 occurrences per 100 000 per year, and the recurrence rate of stroke in this condition ranges from < 1% to 4%.56,57 Doppler studies have demonstrated a high frequency of intracranial microemboli, which supports the idea that the majority of infarcts caused by dissection are thromboembolic rather than hemodynamic in nature.58 The current treatment for most of these carotid lesions is anticoagulation with warfarin or antiplatelet therapy.10,25 Medical therapy, however, is not without its pitfalls. Patients who undergo antiplatelet therapy still have a 1.8% to 3.8% risk for a first or recurrent stroke; patients undergoing anticoagulation have a 1.2% risk for a first or recurrent stroke and a 0.5% risk of intracranial hemorrhage.56,57

Endovascular therapy should be considered in patients who fail medical therapy. Our review found that most authors defined failure of medical therapy as a new ischemic event, a progression of neurological symptoms, or an enlarging pseudoaneurysm despite adequate anticoagulation or antiplatelet treatment. We agree with these criteria with the exception of pseudoaneurysm enlargement. We are not convinced that this alone constitutes an indication for stenting. In light of the safety and feasibility of endovascular management, we recommend that surgeons consider stent therapy if either of the following findings are noted despite adequate medical therapy: new ipsilateral ischemic event, whether embolic or hemodynamic in nature, or the absence of collateral flow to the affected territory with a flow-limiting stenosis.

Endovascular therapy should also be considered in patients with contraindications to antithrombotic agents of any kind.16,39,43,59 Relative contraindications to anticoagulation include increased propensities for hemorrhage such as significant peripheral trauma, gastrointestinal bleeding, severe liver disease, known bleeding disorders, or hemorrhagic conversion of ischemic infarcts. Thromboembolic complications have also been shown to occur twice as often in persistently stenotic or nonhealing dissections.11 With a potentially analogous benefit seen in carotid atherosclerosis trials of surgery over medical management in patients with high-grade carotid stenosis, some authors have advocated earlier intervention for carotid dissections as well.29,60,61 The fact that some studies report a higher incidence of stroke within 30 days of dissection (21%-41%) also makes early vessel reconstruction a reasonable consideration.11,54,62,63

As for the technical aspect of stenting, it is important to pass a microcatheter atraumatically over a microwire beyond the dissected segment. A microcatheter angiogram should then be performed to ensure that the catheter is in the “true lumen.” If this is confirmed, an exchange length wire should be left beyond the dissected segment. Ideally, wire access should not be lost until satisfactory stenting is completed. For extracranial dissections, we typically do not use more than 1 stent unless the dissected segment is longer than the longest available and appropriate stent. Overlapping stents can be useful in certain cases with long dissected segments.

Surgical repair can be challenging for extracranial arterial dissection.6 Hence, endovascular options are typically preferred as a first-line option when revascularization is deemed necessary.16,43 Endovascular repair offers the ability to reconstruct the lumen without compromising cerebral blood flow.10,31,39,64 By reapposing the intimal flap, stent placement can reconstruct the true lumen of a vessel and limit the occurrence of hemodynamic and embolic complications.16,18 Our review of 140 patients treated endovascularly for extracranial carotid artery dissection demonstrated a periprocedural complication rate of 1.3%, all of which were asymptomatic and discovered on standard-of-care follow-up imaging. During clinical follow-up, transient symptoms developed in 1.4% of our study population, and there were no cases of permanent neurological events. In-stent stenosis occurred at a rate of 2%, and these patients similarly remained clinically asymptomatic. These results are in stark contrast, however, to the Cothren et al65 study on stenting for blunt carotid injury. They reported an occlusion rate of 45% in 23 patients with stents over a mean follow-up period of 72 days. Patients had been instructed to continue their warfarin (18 patients) or combination aspirin and clopidogrel therapy (2 patients) for 6 months. Three patients with stenting received no poststenting anticoagulation therapy. This study was not included in our review because we could not determine which carotid lesions were extracranial.

Balloon-expandable stents have been used to promote spontaneous healing of dissecting aneurysms with their greater metal matrix and radial force.54,6671 These stents, however, are relatively inflexible and may not be ideal for extracranial artery dissections. Cohen et al49 suggested that the ideal stent for these vessels would be flexible and self-expanding. The lower pressure required for deployment is thought to reduce the risk of further trauma in potentially fragile vasculature and possible pseudoaneurysm rupture. Self-expandable stents are also more flexible, adapt better to arterial walls, and resist compression after placement.19 In our review, 15 of 28 studies reported using the self-expandable Wallstent, and another 4 used the self-expandable SMART stent with excellent results (Table 4). Wallstents were used most commonly, likely because of the greater metal density of this stent.

Persistent pseudoaneurysms may constitute a long-term risk for distal embolic stroke.47,7274 Treatment of these lesions, however, remains controversial. Touze et al75 reported no evidence of embolic events or rupture for untreated pseudoaneurysms over a follow-up period of 14 months. On the other hand, El-Sabrout and Cooley76 demonstrated a combined major stroke and death rate of 21% for patients with pseudoaneurysms treated nonoperatively and followed up over 5.9 years. Endovascular stenting may promote spontaneous thrombosis of pseudoaneurysms associated with the dissection.54,77,78 Direct coil embolization through the interstices of a stent scaffold is a technique that can also be used for large pseudoaneurysms.16,29,34,43,47,67,79 One study described the use of covered stents in the treatment of pseudoaneurysms.80 There were 61 associated pseudoaneurysms in this review, 60 of which were successfully occluded with stents and/or coils for a success rate of 98.4%.

All studies reviewed did not use distal protection device filters. It is generally agreed that the risk of worsening the dissection or creating a new intimal flap with these devices outweighs any potential for protection against embolization, especially if there is no associated atherosclerotic plaque underlying the stenosis.10,19,20 Proximal protection devices have been introduced to protect the brain from emboli without the need for advancing the catheter through the stenotic lesion. These may prove useful in this population.81 In general, however, stenting for dissection does not require angioplasty, which is probably the cause of most emboli in the treatment of atherosclerotic stenoses.

Although rare, extracranial vertebral artery dissection deserves a special mention with regard to its clinical presentation, etiology, and treatment paradigms. Posterior neck pain and occipital headache are common clinical manifestations of spontaneous vertebral artery dissections.82 Unilateral pain or arm weakness as a result of either cervical root involvement or spinal epidural hematomas has also been reported in the literature.83 Up to 25% of spontaneous vertebral artery dissections are due to connective tissue disorders such as Ehlers-Danlos syndrome type IV, Marfan syndrome, autosomal-dominant polycystic kidney disease, and osteogenesis imperfecta type I.8,8486 In young adults, however, trauma is the major cause of vertebral artery dissection and can occur as a result of excessive rotation, distraction, or flexion-extension injuries.87,88 The extracranial components of the vertebral arteries have a higher likelihood of dissecting because of their contact with the cervical vertebrae and their mobility within the soft tissue of the neck.8991 Although the vertebral artery is freely mobile at its proximal and distal segments, it is fixed at its origin, within the cervical transverse foramina, and at its entry into the dura. This results in the distal segment at C1-C2 being a common area for extracranial dissection, as well as the proximal segment just before its entry into the transverse foramina.89,90,92 Up to 10% of extracranial vertebral artery dissections extend intracranially, especially those associated with pseudoaneurysms. Those that do extend can be associated with subarachnoid hemorrhage and a much poorer outcome.93,94

We report here 31 studies describing the endovascular management of 140 patients with 153 extracranial carotid artery dissections, as well as 8 studies describing the endovascular management of 10 patients with 12 extracranial vertebral artery dissections. To the best of our knowledge, this is the largest review of stenting for these lesions to date. Nearly all stents (164 of 165) were deployed successfully in the extracranial carotid and vertebral vasculature, with only a 1.3% procedural complication rate in the carotid arteries and 0% in the vertebral arteries. Of patients presenting with associated pseudoaneurysms, 98.4% carotid and 88% vertebral pseudoaneurysms showed complete occlusion at discharge or on subsequent follow-up imaging. There were 3 cases of carotid in-stent stenosis or occlusion that occurred from 22 days to 23 months after stenting and 1 case of vertebral in-stent stenosis at 12 months after stenting. These 4 patients all remained asymptomatic. All other vessels with at least 1 month of follow-up were otherwise reported to be patent on follow-up angiography.

This review lends itself to several limitations. Our literature data come mostly from case series that often had a small population of patients who were not randomized. Surgical case series also inherently have a referral bias because less complicated cases are often treated conservatively and may not ever be seen by a surgeon for inclusion in studies. Bias may also be introduced by the retrospective nature of this literature. Nevertheless, all reports indicate that stenting for extracranial dissection was safe and associated with a stable to improved neurological outcome.

In light of the lack of Level I evidence, a randomized controlled trial for the management of extracranial vertebral and carotid artery dissections would be timely and appropriate. There are almost no data on the outcome of patients who stay on medical management despite “failing” it. Two different trials could be envisioned: (1) stenting plus medical management vs medical management after acute spontaneous dissection and (2) stenting plus medical management vs continued medical management for patients who fail medical management for acute spontaneous extracranial dissection

CONCLUSIONS

Level I data are currently lacking for the treatment of extracranial artery dissections. Antiplatelet therapy and anticoagulation therapy are generally considered first line95 but are contraindicated or ineffective in some patients. Improvements in stent technology may expand the population that may be eligible for endovascular treatment. This review suggests the safety and feasibility of endovascularly managing both extracranial carotid and vertebral artery dissections. Randomized trials are needed to further validate the treatment of this disease.

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COMMENT

This article addresses the issue of endovascular stenting of extracranial carotid and vertebral artery dissections, presenting a complete review of the available literature. It is my impression that stenting supraaortic dissections has become a routine procedure in most neuro-catheterization laboratories, and I am surprised by the small number of patients that this complete review gathered, considering the fact that advanced carotid stenting has been performed for more than a decade. The most accepted therapy for supraaortic dissections is formal anticoagulant therapy. The indications for stenting are currently limited and should be based on contraindication for anticoagulation, proven failed anticoagulation (refractory to medical therapy), or impending stroke according to clinical and neuroradiological examinations.

A significant proportion of the reviewed patients sustained traumatic dissections. Most dissections occur spontaneously after minor precipitating factors. It is curious how infrequently stenting is performed in the setting of symptomatic spontaneous acute dissections. The procedural risks are low and the technical success is high. Stenting is a continuously evolving field with a definite place in the management of supraaortic dissections.

Jose E. Cohen

Jerusalem, Israel