Stent Angioplasty For Intracranial Atherosclerosis

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Severe intracranial atherosclerotic disease accounts for an 8-12% yearly risk of stroke (8-10) and can be associated with recurrent neurological symptoms despite maximal medical therapy. These neurological events can result from either thromboembolism or hemodynamic insufficiency. Medical therapy with antiplatelet and anticoagulant therapy is only partially effective against throm-boembolic phenomena and largely futile in cases of insufficiency (9). Although surgical bypass grafting from the extracranial to intracranial circulation is technically feasible and effective in carefully selected cases, it was found to be not effective in the cooperative study for anterior circulation intracranial disease, possibly because of poor patient selection and study bias (11-14). In addition, a large proportion of intracranial posterior circulation stenoses are not suitable for bypass grafting because of lesion location in and around the brainstem or because of poor tolerance to temporary occlusion.

Intracranial atherosclerosis risk factors include age, hypertension, smoking, diabetes, and ethnic origin (8). Intracranial atherosclerotic lesions most commonly

From: Minimally Invasive Neurosurgery, edited by: M.R. Proctor and P.M. Black © Humana Press Inc., Totowa, NJ

involve the following locations: the distal V4 segment of the vertebral artery (VA), the basilar artery (BA), the petrous, cavernous, and paraclinoid segments of the intracranial internal carotid artery (ICA), and the M1 segment of the middle cerebral artery (MCA). Intracranial atherosclerotic lesions have a dynamic natural history showing progression and regression in certain cases (15). More distal lesions with poor collateral circulation are associated with a higher risk of stroke. Lesions of the MCA have a significantly higher risk of stroke compared with more proximal ICA lesions (16), and only one-third of patients with symptomatic intracranial ICA stenoses remained alive and free of strokes at 30 mo of follow-up (17) (Fig. 1). In the posterior circulation, the outcome of acute BA occlusion is almost invariably fatal (18-22), and a lesion in the BA has been shown to imply a 22% risk of a stroke over a 1-yr period (9). Although oral anticoagulation has been postulated to offer greater protection than antiplatelet therapy, the WASID trial will shortly yield outcome data comparing warfarin with aspirin in patients with intracranial atherosclerosis (23). However, patients remaining symptomatic despite warfarin or aspirin therapy have been increasingly treated with endovascular revascular-ization with an acceptable risk profile (5,7,24-26).

Percutaneous balloon angioplasty without stenting has been reported intracranially for the past two decades, but its efficacy has been hampered by a high incidence of iatrogenic intimal dissection, as well as vessel recoil (24-26). More recently long-term clinical follow-up of patients treated with primary balloon angioplasty (27) has shown encouraging results despite a relatively high residual stenosis. This can be partially attributed to the fact that resistance across a vessel is estimated to be inversely proportional to the fourth power of the radius according to Poiseuille's equation; accordingly, a small improvement in luminal caliber can significantly decrease resistance to flow. Technological advances and increased operator expertise have resulted in improved success rates and fewer complications over the last decade (27-30).

Rationale for Stent Angioplasty

The potential advantages of balloon angioplasty followed by stenting compared with angioplasty alone include a lower risk of intimal dissection with consequent thromboembolism or acute vessel closure and improved short-term patency rates. The main limiting factor for the use of stenting to treat intracra-nial lesions has been the lack of flexible low-profile stents that could be navigated into and deployed within the intracranial vasculature. The early attempts at intracranial stent deployment employed manually crimped Palmaz-Schatz coronary stents that were mounted on coronary balloon angioplasty micro-catheters (2). These hand-mounted stents had a high rate of slippage off the balloon microcatheter when the surgeon was navigating the sharp confines of intracranial vessels. A significant hurdle was overcome with the introduction of next-generation premounted coronary stents such as the GFX (Arterial Vascular Engineering, Santa Rosa, CA) in 1998; these coronary stents were significantly better suited for high cervical and intracranial navigation (31,32). More recent generations of coronary stents, including heparin-coated variants such as the Cordis Bx Velocity (Johnson & Johnson, New Brunswick, NJ) and lower pro-

Fig. 1. Stent angioplasty of a petrous internal carotid artery stenosis. A 69-yr-old man with coronary artery disease was noted to have postoperative blood pressure-dependent episodes of confusion and dysphasia. (A) MRI revealed a subacute infarct associated with a focal stenosis in the petrous segment of a dominant right internal carotid artery (arrow). (B) Angiography revealed a focal 80% stenosis with a poststenotic dilation (arrow). (C) A Medtronic-AVE S7 4 x 15-mm coronary stent was used to cross the stenosis primarily over a hydrophilic microwire whose tip is parked in the right M1 segment of the middle cerebral artery. (D) The stent was centered over the lesion and deployed successfully, but delayed angiography showed the de novo appearance of a postangioplasty dissection flap noted distal to the stent (arrowhead). (E) This was treated by traversing the first stent and positioning a second Medtronic-AVE S7 3.5 x 9-mm coronary stent in tandem fashion (arrows). (F) The final result shows a patent right petrous ICA with postprocedural resolution of the patient's symptoms.

Fig. 1. Stent angioplasty of a petrous internal carotid artery stenosis. A 69-yr-old man with coronary artery disease was noted to have postoperative blood pressure-dependent episodes of confusion and dysphasia. (A) MRI revealed a subacute infarct associated with a focal stenosis in the petrous segment of a dominant right internal carotid artery (arrow). (B) Angiography revealed a focal 80% stenosis with a poststenotic dilation (arrow). (C) A Medtronic-AVE S7 4 x 15-mm coronary stent was used to cross the stenosis primarily over a hydrophilic microwire whose tip is parked in the right M1 segment of the middle cerebral artery. (D) The stent was centered over the lesion and deployed successfully, but delayed angiography showed the de novo appearance of a postangioplasty dissection flap noted distal to the stent (arrowhead). (E) This was treated by traversing the first stent and positioning a second Medtronic-AVE S7 3.5 x 9-mm coronary stent in tandem fashion (arrows). (F) The final result shows a patent right petrous ICA with postprocedural resolution of the patient's symptoms.

file designs have been used. In addition, balloon-mounted stent designs have been developed specifically for use in the intracranial circulation such as the INX stent (Medtronic-AVE, Santa Rosa, CA) and the Neurolink (Guidant, Indianapolis, IN) (33); these designs feature easier tracking and more compliant balloons better suited to intracranial vascular characteristics.

The potential for endovascular therapy of a lesion reflects the heterogeneity of intracranial stenosis encountered in the workup of cerebrovascular disease. The treatment of lesions in the petrous and cavernous portions of the ICA at present represents a simple technical challenge compared with the ability to track the available stents beyond the carotid artery siphon into the paraclinoid portion of the carotid, or even into the MCA (34). Stenting of the intracranial portions of the vertebrobasilar system, namely, the V3 and V4 portions of the VA and the BA, has also been shown to be feasible and relatively safe (31,34-40), and this has proved to be an easier vascular territory to work in than the supr-aclinoid anterior circulation. The ability to reach the intracranial stenosis is highly dependent on the proximal cervical and great vessel anatomy, tortuosity, and degree of calcification. Although newer stents have better tracking and flexibility characteristics, they can be thwarted by tortuous vessel loops and sharp angulations.

Procedural and Technical Description

Patients are pretreated with aspirin (325 mg qd) and ticlopidine (150 mg bid) or clopidogrel (75 mg qd) for at least 3 d prior to the procedure. Although aspirin is rapidly absorbed, clopidogrel and ticlopidine require at least 3 d to achieve full effect; both antiplatelet regimens are continued indefinitely in cases of intracranial stenting for atherosclerosis. Most procedures are performed under general anesthesia in order to have the best possible imaging quality and to minimize motion artifact, given the small size of the target vessels. A complete four-vessel diagnostic angiogram is obtained (unless contraindicated) to assess the available collateral pathways in a dynamic fashion. Intravenous heparin is administered to achieve an activated clotting time between 250 and 300 s. The parent vessel is then accessed via a 6- or 7-Fr guiding catheter, which is positioned sufficiently distal in the cervical carotid or vertebral artery so as to form a stable delivery platform while maintaining flow downstream and avoiding iatrogenic vasospasm. The lesion can then be crossed either primarily using the stent delivery microcatheter over an exchange-length (260-300 cm) micro-wire (0.014 inch), or, in the case of more challenging and critically narrowed lesions by using a microcatheter as an intermediate step.

Once the stenosis has been traversed in a controlled fashion, the tip of the exchange wire is parked in a sufficiently distal location to allow tracking of the stent or balloon delivery. In cases of a proximal lesion of the VA or of the petrous segment of the ICA, the requirement for distal wire placement is less stringent than for a midbasilar or supraclinoid carotid stenosis, in which the tip of the wire is parked in a P2 (PCA) or M2 (MCA) branch, respectively. The microcatheter is then exchanged for the stent microcatheter catheter (for primary stent angioplasty) or a balloon microcatheter (in the case of secondary stent angioplasty). In cases of more proximal lesions of the petro-cavernous segment of the ICA or V4 segment of the VA, it may be possible and preferable to cross the lesion primarily with the stent or balloon delivery microcatheter to spare an exchange procedure. It is critical, however, to use exchange-length microwires in order to maintain access to the true lumen until after angioplasty and stent deployment have been performed successfully, to avoid the risk of irretrievable target vessel closure in the case of intimal dissection. Only after high-resolution control angiography has been performed with satisfactory results can the exchange wire be removed safely.

A number of obstacles can hinder successful intracranial stenting. The first impediment is the inability to obtain a secure platform using the guide catheter in the cervical region, either because of critical proximal stenosis or because of aortic arch or proximal vessel tortuosity. The former can often be solved by performing proximal angioplasty to allow passage of the guider; the latter can often be solved by opting for a larger bore guide catheter, by using a coaxial proximal long sheath-type shuttle to stiffen the assembly proximally, or by using a stabilizing wire (41). Alternatively, a nonfemoral percutaneous approach may be employed such as the radial or brachial artery (42), or in extreme cases direct carotid puncture, although the latter carries an associated higher risk of dissection or pseudoaneurysm (43).

Once a satisfactory proximal platform has been achieved, the next limiting factor will be the presence of any acute curvature or looping vascular segments of the proximal parent vessel, since these usually result in loss of distal microwire control, which will impede the ability to advance the microstent delivery catheter by compromising proximal guide catheter position. Great care needs to be taken to evaluate blood flow periodically in the parent vessel and detect any signs of proximal vasospasm and/or dissection that may result from the occasionally high frictional forces exerted on the intima by the guide catheteter or stent microcatheter in cases of difficult anatomy. When the lesion cannot be traversed by the balloon-mounted stent catheter, primary angioplasty can be performed using a miniature (1.5-mm-diameter) angioplasty balloon, which can then exchanged for a stent to be deployed in secondary fashion. In cases of acute thrombotic occlusion, the procedure is preceded or accompanied by intraarterial superselective infusion of a fibrinolytic agent (urokinase or tissue plasminogen activator). The emergence of contrast defect or haziness near the stent interstices after deployment is usually the result of exuberant platelet activation, which can proceed rapidly to complete vessel occlusion and formation of organized thrombus. Patients demonstrating de novo thrombus formation are administered a glycoprotein IIb/IIIa inhibitor intravenously, such as abciximab or eptifibatide, concomitantly.

The risks of deploying stents intracranially include vessel rupture during angioplasty, hemodynamically significant intimal dissection, and occlusion of target vessel perforating branches. The risk of vessel rupture can be decreased by a slight undersizing of the stent compared with the affected vessel and slow balloon inflation. Intimal dissection is a largely inevitable consequence of angioplasty and is tolerable unless a hemodynamically significant plaque develops, which can subsequently lead to thrombosis or vessel occlusion. Despite reports to the contrary, perforating vessel occlusion remains a risk of intracranial stent angioplasty and can lead to stroke (1,31,32,34-38,44-47). Postoperatively, patients are observed in the neurointensive care setting until they are deemed neurologically stable (Fig. 2).

Fig. 2. Stent angioplasty of a hemodynamically symptomatic basilar artery stenosis despite medical therapy. A 73-yr-old man presented with transient left-sided hemiplegia and hemianesthesia, episodes of lightheadedness, and vertical diplopia, which were persistent despite warfarin therapy. MRI revealed a severe midbasilar stenosis (A), which was confirmed to be greater than 85% with biplane digital subtraction angiography (B, anteroposterior; C, lateral). A Medtronic-AVE S670 3 x 9-mm stent was chosen, deliberately undersized to prevent angioplasty-induced intimal dissection or vessel rupture. It positioned across the stenosis and inflated. (D) The final result shows significant improvement in the basilar lumen (E,F); the patient has remained asymptomatic on antiplatelet therapy with aspirin and clopidogrel.

Fig. 2. Stent angioplasty of a hemodynamically symptomatic basilar artery stenosis despite medical therapy. A 73-yr-old man presented with transient left-sided hemiplegia and hemianesthesia, episodes of lightheadedness, and vertical diplopia, which were persistent despite warfarin therapy. MRI revealed a severe midbasilar stenosis (A), which was confirmed to be greater than 85% with biplane digital subtraction angiography (B, anteroposterior; C, lateral). A Medtronic-AVE S670 3 x 9-mm stent was chosen, deliberately undersized to prevent angioplasty-induced intimal dissection or vessel rupture. It positioned across the stenosis and inflated. (D) The final result shows significant improvement in the basilar lumen (E,F); the patient has remained asymptomatic on antiplatelet therapy with aspirin and clopidogrel.

Clinical Results and Patient Selection

Preliminary results of the University of California at San Francisco experience point to a statistically significant higher risk of postoperative intracranial and reperfusion hemorrhage in patients who were administered glycoprotein Ilb/IIIa inhibitors (48). In addition, symptomatic patients who underwent endovascular revascularization in the setting of a stroke or who were neuro-logically unstable had a significantly worse outcome compared with symptomatic patients treated in a preemptive fashion (48).

The intracranial stenting series in the literature have reported somewhat better results than those on primary unassisted balloon angioplasty despite the limitations inherent in stent navigation above the skull base (34,40,45,49). The rates of immediate postprocedure residual stenosis following stent angioplasty are between 0% and 18% (50), which compares favorably with 41-47% residual from angioplasty alone (24,27). Other reports demonstrate neurological complication rates of around 4.2-25% and mortality rates of 0-13% (24,27,49-51). More recent data, which included mostly neurologically unstable patients undergoing intracranial stenting emergently, showed a high rate of complication including postprocedural intracranial hemorrhage (17%) and stroke (11%) (4). Recent results from the Stenting of Symptomatic Atherosclerotic Lesions in the Vertebral or Intracranial Arteries (SSYLVIA) study indicated a 0% risk of death and a 6.6% risk of stroke in the 30-d periprocedural period. Angiographic follow-up indicated a 30% risk of more than 50% restenosis in the intracranial treatment subset at the 6-mo follow-up mark.

Angioplasty and stenting of selected atherosclerotic lesions should be considered as a treatment option when maximal medical management has failed because symptomatic intracranial stenosis carries a relatively high risk for stroke. Our current practice limits intracranial stent angioplasty to symptomatic patients who have already failed current optimal medical therapy consisting either of oral warfarin or of a combination of aspirin and clopidogrel. In this subset of patients, we recommend proceeding with stent angioplasty, and if the latter is not technically feasible, then unassisted angioplasty is indicated in an attempt to improve distal perfusion. A lower threshold for intervention is used in patients who clearly suffer from hemodynamic insufficiency rather than thromboembolism from an embologenic intracranial stenosis. The rate of technical complications and postprocedural stroke in intracranial stent angioplasty is undoubtedly higher than for extracranial carotid revascularization such as carotid endarterectomy or stenting. This is not surprising considering the size and fragile wall of the intracerebral vessel wall. Accordingly, this procedure should be reserved for cases of emergency or medically refractory ischemia and not used as a primary modality of treatment until a randomized trial can be performed comparing short- and long-term outcomes from best medical therapy and endovascular stenting (52-54).

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