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(Stroke. 2008;39:1770.)
© 2008 American Heart Association, Inc.
Original Contributions |
From the Division of Cerebrovascular and Endovascular Neurosurgery, Department of Neurosurgery (M.E.K., D.F.) and the University Hospitals Case Medical Center (A.J.F.), Cleveland, Ohio.
Correspondence to David Fiorella, MD, PhD, Division of Cerebrovascular and Endovascular Neurosurgery, Department of Neurosurgery, Cleveland Clinic, S80, Cleveland, OH, 44195. E-mail fioreld{at}ccf.org
| Abstract |
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Methods— A 55-year-old male presented with acute onset left hemiplegia (National Institutes of Health Stroke Score (NIHSS) of 20. Angiography showed an occluded right cervical internal carotid artery (ICA), a patent anterior communicating artery (ACOMM), and embolic occlusion of the right middle cerebral artery (MCA), M1 segment.
Results— Working through a 6F guide-catheter positioned in the left cervical ICA, an SL-10 microcatheter, and 0.014-inch Synchro-2 microwire were manipulated across the anterior communicating artery and into the right M1 segment occlusion. 5 mg of abciximab and 3 mg tPA were infused directly into the thrombus through the microcatheter. Mechanical thrombolysis using the microwire and microcatheter was ineffective in achieving any recanalization. An Enterprise stent (4x22 mm) was delivered across the occlusion site and partially unconstrained. The unconstrained portion of the stent expanded and acted as a temporary bypass, to circumferentially displace and structurally disrupt the M1 thrombus, producing immediate revascularization of the right territory MCA. After approximately 20 minutes, the Enterprise stent was reconstrained and removed. Final angiography demonstrated excellent filling of the right M1 and distal MCA branches. The patient improved to an NIHSS of 7, regaining movement of his left upper and lower extremities.
Conclusions— The temporary endovascular bypass technique yielded immediate and durable revascularization of an acutely occluded middle cerebral artery without the disadvantages associated with the placement of a permanent endovascular stent.
Key Words: acute stroke cerebral revascularization stent
| Introduction |
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Self-expanding intracranial stents, which are commercially available for the treatment of cerebral aneurysms and intracranial atherosclerotic disease, have been used off-label with high levels of success to recanalize occluded intracranial vessels.1–5 However, there are important disadvantages associated with the permanent implantation of self-expanding intracranial stents in the setting of acute ischemic stroke, including those associated with the need for long-term platelet inhibition and delayed in-stent stenosis.6,7 Furthermore, with embolic occlusion, the affected artery is structurally normal and does not require a permanently implanted stent.
We describe a novel technique in which a reconstrainable self-expanding intracranial microstent was successfully used to achieve the immediate recanalization of an occluded right MCA that was refractory to pharmacological thrombolysis with intravenous (IV) tissue plasminogen activator (tPA), intraarterial (IA) tPA, IA abciximab, and mechanical manipulation. This temporary endovascular bypass technique capitalizes on all of the advantages of stenting without the disadvantages associated with the placement of a permanent endovascular device.
| Materials and Methods |
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Intervention
The patient was immediately taken to the angiography suite and general endotracheal anesthesia was instituted. Diagnostic angiography was performed, confirming complete occlusion of the proximal right cervical ICA. Injection of the left vertebral artery showed minimal leptomeningeal collateral filling over the right hemisphere. A 6-French 90-cm Envoy guiding catheter (Cordis Neurovascular) was placed into the left cervical ICA at the C2 level. Angiography showed patency of the anterior communicating artery with filling of the right distal carotid terminus and proximal M1 segment of the right middle cerebral artery (Figure 1). A complete embolic occlusion of the M1 segment of the right MCA was present. (Figure 1, arrow).
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An SL-10 microcatheter (Boston Scientific) was manipulated over a Synchro-2 0.014 microwire (Boston Scientific) across the anterior communicating artery and into the right MCA under fluoroscopic roadmap control. IA abciximab (5 mg) and tPA (3 mg) were infused directly into the thrombus. Mechanical thrombolysis was performed with multiple passes of the microcatheter and microwire through the thrombus. These measures were ineffective in achieving recanalization over a 25-minute period.
The SL-10 was then exchanged for a Prowler Plus Select microcatheter (Cordis Neurovascular). A 4x22 mm Enterprise stent (Cordis Neurovascular) was introduced into the microcatheter and delivered across the site of occlusion (Figure 2). Approximately two-thirds of the stent was unconstrained across the M1 thrombus (Figure 3). The unconstrained portion of the stent expanded, acting as a temporary bypass to circumferentially displace and structurally disrupt the occlusive thrombus. This immediately restored robust flow across the anterior communicating artery, through the right M1 and into the distal right MCA circulation (Figure 4a through 4c) An additional 5 mg of abciximab was administered through the guiding catheter and the partially expanded Enterprise was left in position for 20 minutes. The Enterprise stent was then reconstrained and removed, and an additional 2 mg of abciximab and 2 mg of tPA were administered through the microcatheter.
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| Results |
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| Discussion |
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The available SES are unsheathed from their delivery microcatheters, opening distally to proximally. When positioned properly (distal to the leading edge of the occluding embolus) the stent opens to circumferentially displace the occluding clot, immediately reestablishing a channel of flow within the occluded vessel. Once flow is reestablished, the high local concentration of prothrombotic factors in the region of thrombus is immediately dissipated, creating a physiology favoring recanalization and thrombus dissolution. The SES also functions to trap the majority of the thromboembolic material against the wall of the parent vessel.4 This material (trapped between the SES and parent vessel wall) typically lyses over time (minutes) in response to the restoration of blood flow, the mechanical disruption produced by the outward radial force of the SES, and pharmacological thrombolysis with antiplatelet (typically IIb/IIIa inhibitors) and in some instances thrombolytic medications.
The application of SES in acute stroke appears to have several advantages compared to other interventional techniques. First, stenting has a very high reported rate of successful recanalization.4 Second, whereas other techniques often take hours to achieve recanalization, SES implantation typically produces immediate recanalization with robust reperfusion of the compromised territory. Third, SES deployment is less technically demanding and operator dependant than other revascularization strategies—particularly in comparison to thrombus retrieval devices such as the Merci retriever (Concentric Medical) and "The Alligator" (Chestnut Medical).
At the same time, there are important disadvantages to stenting in the setting of acute stroke. The implantation of a permanent intracranial SES requires immediate and prolonged therapy with multiple antiplatelet agents. Typically this consists of an intraprocedural IIb/IIIa inhibitor followed by immediate postprocedural loading with both aspirin and clopidogrel and prolonged dual antiplatelet therapy (for a minimum of 8 to 12 weeks).8–11 In the periprocedural period, the risk of clinically significant parenchymal hemorrhage, particularly when thrombolytic agents have been given, is likely increased by the addition of antiplatelet agents. In the postprocedural period, patients whose stroke is attributed to atrial fibrillation or a hypercoaguable state, may require long-term anticoagulation with warfarin. The combination of an anticoagulant (to prevent recurrent thromboembolism) with 1 or more antiplatelet agents (for stent prophylaxis) in a patient who has suffered cerebral ischemic injury is likely to be associated with a high risk of hemorrhage. The placement of any intracranial stent, either for aneurysm treatment or atherosclerotic disease, may induce in stent stenosis or restenosis.7,12–14 If symptomatic, in-stent stenosis may require more aggressive medical, surgical, or endovascular intervention. In acute embolic stroke to an otherwise normal intracranial vessel, with permanent stenting, we run the risk of exchanging one disease process (acute embolic occlusion) for another (intracranial in-stent stenosis).
The temporary endovascular bypass technique capitalizes on all of the advantages of permanent stenting while avoiding many of the disadvantages. Like stenting, the temporary bypass strategy has the potential to provide immediate robust recanalization. Unlike a fully deployed stent, the device may be reconstrained and repositioned if necessary to optimize flow restoration. If the vessel reoccludes after reconstrainment, the device can be redeployed to restore perfusion, and additional lytic agents can be administered as needed. Because the device is ultimately removed, there are no requirements for long-term antiplatelet medications (provided that the underlying artery is structurally normal). Finally, because no permanent stent is placed, there would be no risk of in-stent stenosis.
Summary
The temporary endovascular bypass technique using the Enterprise stent represents a novel strategy to achieve immediate recanalization of an occluded brain artery without the disadvantages and risks associated with permanent stent implantation.
| Acknowledgments |
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Dr Fiorella is a shareholder in Revasc Inc, and has received significant research support from Boston Scientific. The other authors report no conflicts of interest.
Received October 3, 2007; accepted November 14, 2007.
| References |
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2. Horowitz M, Jovin T, Levy E, Anderson W. Emergent basilar artery and bilateral posterior cerebral artery angioplasty, urokinase thrombolysis, and stenting for acute basilar artery occlusion secondary to diagnostic cardiac catheterization: Case presentation. J Neuroimaging. 2005; 15: 315–318.[CrossRef][Medline] [Order article via Infotrieve]
3. Levy EI, Ecker RD, Hanel RA, Sauvageau E, Wehman JC, Guterman LR, Hopkins LN. Acute m2 bifurcation stenting for cerebral infarction: Lessons learned from the heart: Technical case report. Neurosurgery. 2006; 58: E588; discussion E588.[Medline] [Order article via Infotrieve]
4. Levy EI, Ecker RD, Horowitz MB, Gupta R, Hanel RA, Sauvageau E, Jovin TG, Guterman LR, Hopkins LN. Stent-assisted intracranial recanalization for acute stroke: Early results. Neurosurgery. 2006; 58: 458–463;discussion 458–463.[Medline] [Order article via Infotrieve]
5. Sauvageau E, Levy EI. Self-expanding stent-assisted middle cerebral artery recanalization: Technical note. Neuroradiology. 2006; 48: 405–408.[CrossRef][Medline] [Order article via Infotrieve]
6. Levy EI, Turk AS, Albuquerque FC, Niemann DB, Aagaard-Kienitz B, Pride L, Purdy P, Welch B, Woo H, Rasmussen PA, Hopkins LN, Masaryk TJ, McDougall CG, Fiorella DJ. Wingspan in-stent restenosis and thrombosis: Incidence, clinical presentation, and management. Neurosurgery. 2007; 61: 644–651.[Medline] [Order article via Infotrieve]
7. Fiorella D, Albuquerque FC, Deshmukh VR, McDougall CG. In-stent stenosis as a delayed complication of neuroform stent-supported coil embolization of an incidental carotid terminus aneurysm. AJNR Am J Neuroradiol. 2004; 25: 1764–1767.[Medline] [Order article via Infotrieve]
8. Fiorella D, Thiabolt L, Albuquerque FC, Deshmukh VR, McDougall CG, Rasmussen PA. Antiplatelet therapy in neuroendovascular therapeutics. Neurosurg Clin N Am. 2005; 16: 517–540, vi[CrossRef][Medline] [Order article via Infotrieve]
9. Fiorella D, Albuquerque FC, Deshmukh VR, McDougall CG. Usefulness of the neuroform stent for the treatment of cerebral aneurysms: Results at initial (3-6-mo) follow-up. Neurosurgery. 2005; 56: 1191–1201;discussion 1201–1192.
10. Fiorella D, Albuquerque FC, Han P, McDougall CG. Preliminary experience using the neuroform stent for the treatment of cerebral aneurysms. Neurosurgery. 2004; 54: 6–16;discussion 16–17.
11. Fiorella D, Albuquerque FC, Woo H, Rasmussen PA, Masaryk TJ, McDougall CG. Neuroform in-stent stenosis: Incidence, natural history, and treatment strategies. Neurosurgery. 2006; 59: 34–42;discussion 34–42.[CrossRef][Medline] [Order article via Infotrieve]
12. Levy EI, Turk AS, Albuquerque FC, Niemann DB, Aagaard-Kienitz B, Pride L, Purdy P, Welch B, Woo H, Rasmussen PA, Hopkins LN, Masaryk TJ, McDougall CG, Fiorella DJ. Wingspan in-stent restenosis and thrombosis: Incidence, clinical presentation, and management. Neurosurgery. 2007; 61: 644–650;discussion 650–641.
13. Fiorella D, Levy EI, Turk AS, Albuquerque FC, Niemann DB, Aagaard-Kienitz B, Hanel RA, Woo H, Rasmussen PA, Hopkins LN, Masaryk TJ, McDougall CG. Us multicenter experience with the wingspan stent system for the treatment of intracranial atheromatous disease: Periprocedural results. Stroke. 2007; 38: 881–887.
14. Stenting of symptomatic atherosclerotic lesions in the vertebral or intracranial arteries (SSYLVIA): Study results. Stroke. 2004; 35: 1388–1392.
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