Percutaneous Transluminal Cerebral Angioplasty and Stenting in Acute Vertebrobasilar Ischemic Stroke

Summary

Reports of cerebral transluminal angioplasty and stenting in patients with vertebrobasilar ischemic stroke are scanty. Herein we report on the use of “monorail” coronary balloon angioplasty and stent balloon mounted catheters in two patients with acute vertebrobasilar ischemic stroke, focussing on the differences and possible advantages of the “monorail” technique in comparison with the “over-the-wire” technique. In both patients, the clinical picture was characterized by progressive brainstem symptoms followed by acute loss of consciousness related to an atherothrombotic occlusion and subocclusion of the dominant intracranial vertebral artery, respectively. In one patient, superselective thrombolytic therapy and balloon angioplasty resulted in a dissection flap at the vertebrobasilar junction. The latter was treated by successful deployment of a coronary stent. In the other patient, the subocclusive lesion was directly treated by angioplasty and stenting without thrombolytic therapy. The clinical outcome was poor for one patient (“locked in” syndrome) while the other had a complete clinical recovery.

In acute atherothrombotic vertebrobasilar stroke transluminal cerebral angioplasty and stenting may be successfully performed allowing vessel recanalization.

Introduction

The stroke rates in patients with symptomatic vertebrobasilar atherosclerosis are high and acute vessel occlusion represents a life-threatening condition with a mortality of 80% to 90%^1,2. In patients with basilar artery embolic occlusion, superselective thrombolytic therapy may achieve recanalization and reduce mortality².

However, stenosis or occlusion of the intracranial vertebral artery is commonly caused by lumen thrombosis on a pre-existing atherosclerotic plaque and rarely by embolic occlusion. This may explain the therapeutic failures of isolated locoregional fibrinolysis and stenting for adjunctive therapeutic options^3-7.

Herein we report on two patients with acute atherothrombotic occlusion and subocclusion of the vertebrobasilar system treated with percutaneous transluminal cerebral angioplasty (PTCA) and stenting.

Case Reports

Case 1

A 61-year-old man with a history of hypertension was admitted to an outlying hospital for intermittent episodes of disorientation, vomiting and ataxia. Soon after admission he rapidly shifted into a comatose state (Glasgow Coma Scale score: 7) with spontaneous breathing.

An nonenhanced computed tomography (CT) examination of the head did not show evidence of ischemic lesions or intracranial hemorrhage and acute vertebrobasilar ischemia was suggested. The patient arrived in the angiographic suite at our institution ten hours after the onset of symptomatology. General anesthesia was administered and a 6 Fr groin sheath was inserted into the right common femoral artery. A four vessel cerebral digital subtraction angiography (DSA) revealed an occlusion of the right vertebral artery (VA) proximal to theorigin of the posterior inferior cerebellar artery (PICA) (figure 1A) associated with controlateral VA hypoplasia ending in the PICA. Right internal carotid artery angiograms showed a collateral circulation through the posterior communicating artery with a faint retrograde filling of the basilar artery (figure 1B). An intravenous loading bolus of 5000 IU of heparin followed by infusion of 1000 IU/h was administered. A 6 Fr guiding catheter (Envoy - Cordis Endovascular System - Miami - FL) was placed in the right VA and a microcatheter (Tracker 18 - Boston Scientific - Fremont - CA) primed with a 0.014 inch guidewire (Transed EX 14 - Boston Scientific Fremont - CA) was subsequently advanced proximal to the occlusion.

Figure 1.

Lateral views of the right VA (A) and the right internal carotid artery (B) angiogram shows VA occlusion proximal to the origin of the PICA (A) and retrograde filling of the basilar artery through the right posterior communicating artery (B). C) Anteroposterior view of the right VA angiogram after 700.000 units of UK shows the restoration of antigrade basilar artery flow with the presence of a subocclusive atherosclerotic lesion of the distal vertebral artery associated with an irregular stenosis of the vertebrobasilar junction. Post PTCA oblique (D) and anteroposterior view (E) of the right VA angiogram shows the reconstitution of VA lumen to an almost normal distal caliber. Note the persistence of the vertebrobasilar stenosis with a small dissection flap (arrow). F) Post stenting angiogram reveals restoration of vessel lumen with regular wall profile in the absence of residual stenosis at the vertebrobasilar junction.

Local infusion of urokinase (UK) and mechanical manipolation of the thrombus with the guidewire was started. After 700.000 units of UK, antigrade basilar artery filling was restored revealing a concentric subocclusive lesion of distal VA proximal to the PICA origin and an irregular, severe stenosis of the vertebrobasilar junction (figure 1C). The microcatheter was withdrawn and the guidewire was advanced directly beyond the P2 segment of the right posterior cerebral artery with a 3 × 12 mm monorail coronary balloon angioplasty catheter (Searider - Nycomed Amersham-Paris - France). The balloon was then positioned across the proximal stenosis and four consecutive brief (20 s) and gradual dilatations to pressures of 6 atm corresponding to 3 mm balloon diameter were performed with a good result (figure 1D).

The same balloon was used to dilate the distal stenosis; after one 20 s dilatation to the same pressure an intervening angiographic run showed the persistence of an irregular stenosis at the vertebrobasilar junction with a dissection flap (figures 1D-E). In view of the unstable nature of the latter finding a stenting procedure of the lesion was subsequently undertaken with a 3 × 12 mm monorail balloon mounted coronary stent (Seaquence - Nycomed Amersham - Paris - France). The stent was straddled across the lesion over the same guidewire and inflated to a pressure of 8 atm resulting in a satisfactory and uncomplicated stent deployment. Post-stenting angiograms showed a restoration of the vertebrobasilar junction lumen to an almost normal caliber (figure 1F). The right femoral sheath was left in place and intravenous heparin infusion was continued for 48 hours maintaining activated partial thromboplastin time between 70 and 80s. Antiplatelet treatment with aspirin (325 mg daily) and ticlopidine (250 mg twice daily) was also started. In the following days the patient progressed into a “locked-in” state and a cerebral CT scan showed a midsagittal pontine ischemic lesion. A follow-up CT-angiography and DSA of the vertebrobasilar system 15 days later confirmed both the stent patency and the pontine infarction. Three months later his neurologic condition was unchanged.

Case 2

A 57-year-old man with a two month history of intermittent episodes of gait ataxia and dizziness was admitted to hospital because of sudden onset dysarthria, left side paresthesias, dizziness and dysphagia.

His medical history was characterized by surgical clipping of an anterior communicating artery aneurysm. Following admission, he gradually became stuporous (Glasgow Coma Scale score: 12) and was transferred to our institution. Neither ischemic nor hemorrhagic lesions were detected on an unenhanced CT scan of the head. A diagnostic cerebral DSA four hours after the onset of symptomatology yielded a subocclusion of the left VA proximal to the origin of the PICA associated with controlateral VA hypoplasia ending in PICA (figure 2A).

Figure 2.

A) Lateral view of the left VA angiogram shows a preocclusive concentric lesion of the intradural VA proximal to the PICA origin. B) Post PTCA and stenting angiogram reveals a restoration of the distal VA lumen with no residual stenosis.

No significant collateral circulation from either posterior communicating artery was demonstrated. General anesthesia was administered and a 6 Fr guiding catheter (Envoy - Cordis Endovascular System - Miami - FL) was advanced in the left VA after a intravenous bolus of 10.000 IU heparin and 250 mg of acetyl-salicylic acid. The lesion was crossed with a 0.014 inch guidewire (Transed EX 14 - Boston Scientific - Fremont - CA) advanced directly with a 2.5 × 15 mm monorail coronary balloon angioplastic catheter (Searider - Nycomed Amersham - Paris - France). The balloon was slowly inflated for 30 s to a pressure of 6 atm (corresponding to a 2.5 mm balloon diameter). After PTCA a control angiogram revealed a partial reconstitution of the vessel lumen caliber with an irregular profile. A 3 × 8 mm monorail balloon mounted coronary stent (Seaquence - Nycomed Amersham - Paris - France) was straddled across the lesion and inflated to a pressure of 8 atm resulting in stent deployment.

Post-stenting angiograms showed restoration of the distal VA caliber (figure 2B). Post-procedural pharmacological management was the same as in case 1. The patient's outcome was excellent and he was discharged ten days later with a minimal residual dysarthria that completely regressed at follow-up one month later. A CT angiography three months later confirmed the stent patency.

Discussion

The most remarkable features in our cases are twofold. First, intracranial vertebrobasilar PTCA and stenting were performed in the acute stage in patients harbouring an anatomical variant of the posterior circulation. Second, a “monorail” technique instead of the “over-the-wire” technique was employed. In both patients a dominant VA almost entirely sustaining the posterior circulation represented an unfavorable prognostic factor. Its occlusion/subocclusion was decisive in the onset of the acute stroke, the latter being heralded by transient ischemic attacks probably related to hemodynamic phenomena.

In the first case, the presence of a significant collateral flow from the anterior circulation prompted the treatment despite a ten hour time lag. In both our cases, the patients'age as well as the site and the angiographic appearance of the vessel stenosis supported an atherothrombotic etiology of the lesions. Since vessel recanalization in patients with acute vertebrobasilar occlusion is associated with a significant increase in survival rates ², an aggressive therapeutic option aimed at the treatment of primary vascular stenosis appeared appropriate in our patients ^3,4,6-8.

Although cerebral PTCA has been reported to be suitable in the treatment of symptomatic short (5 mm or less in length) cerebral atherosclerotic lesions ⁹, its role is still debated. The anatomic characteristics of the cerebral sub-arachnoid arteries (thin muscularis and adventitia layers) result in an increased risk of complications during PTCA in comparison with extracranial arteries. Furthermore, complications including vessel perforation, thrombo-embolism or acute occlusion from elastic recoil, in situ thrombosis or dissection can have disastrous consequences expecially in the vertebrobasilar system. Therefore underdilatations to a less than optimal size are advocated in vertebrobasilar stenosis even if they rarely result in normalization of vessel diameter especially with long or totally occluded lesions^3,7.

The use of a stent can prevent some complications of PTCA, in particular elastic recoil and vessel dissection^4-7,10-12.

Data on intracranial vertebrobasilar stenting for the treatment of atherosclerotic lesions are sparse and mainly regard symptomatic basilar artery stenosis refractory to medical therapy^4,7,8,11 or iatrogenic dissection¹². Only two reports addressed vertebrobasilar PTCA and stenting in the treatment of acute stroke. Mori et Al⁵ treated a patient with an occluded vertebrobasilar artery using PTCA and stenting with a favorable clinical outcome. Phatourous et Al⁶ reported successful superselective thrombolytic therapy, PTCA and stenting of acute basilar artery atherotrombotic occlusion in an 83-year-old man who died as result of systemic complications. The inability of the stent-delivery catheter to track through the tortuous and small caliber intracranial arteries without damaging them has been regarded as a major drawback. Introduction of highly flexible coronary stents with a small diameter delivery system has facilitated both navigation and appropriate placement in intracranial vessels ¹⁰.

In our cases, the use of “monorail” balloon angioplasty and stent-mounted catheters simplified the procedure and was less time consuming than the “over-the-wire” technique. In “over-the-wire” technique, the lesion is first crossed with the microcatheter/microguidewire unit. The standard microguidewire is then withdrawn and an exchange guidewire is placed distally through the microcatheter. The stenosis is usually not crossed directly with the exchange guidewire because of its stiffness that may be traumatic in small intracranial atherosclerotic vessels causing intraprocedural vasospasm³. In “monorail” balloon and stent-mounted delivery catheters, the distal shaft comprises two lumens, one is used for inflation of the balloonand the other allows the exit of the guidewire through a notch located at variable distance proximal to the distal tip (approximately 25 cm in the catheters employed by us). This rapid exchange delivery system can be primed over a standard microguidewire avoiding the use of the exchange guidewire. On the other hand, the monorail system does not allow drugs delivery through the catheter lumen as with the “over-the-wire” technique once the guide is removed. This, however, did not represent a major drawback in our experience.

Using the monorail tecnique we were able to negotiate the stenosis directly with the angioplastic balloon and stent without difficulties notwithstanding the lower stiffness of the standard microguidewire. In both our patients, the length of the stents employed was relatively short, thus facilitating their progression. Longer stents are more difficult to navigate through the proximal turns of the extracranial vertebral artery.

In the first patient, we decided to dilate the vertebrobasilar stenosis in addition to the proximal lesion in view of its angiographic appearance (severe and irregular stenosis) with strong chance of rethrombosis. The ineffectiveness of PTCA with the appearance of a dissection flap at this level after the first inflation of the balloon induced us to perform stent placement. Although the recanalization was successful and stable he developed a permanent “locked-in” syndrome related to a pontine ischemic lesion. This represents a distal vascular territory with respect to the site of endovascular procedures and it may be related to long-term hypoperfusion in the deep territories of the basilar artery. Experimental work in dogs and experience in humans have demonstrated that small side branches and perforating arteries remain patent after stent placement ^{6, 7, 10, 11}. Furthermore, neither patient showed any evidence of infarction in distal VA and PICA perforator branch territories.

Both our patients were treated in the acute phase and were not pretreated with antiplatelet drugs as is usually the case with scheduled procedures. This somewhat influenced intra and postprocedural therapy.

The major factor of acute and subacute thrombosis after angioplasty and stent placement is local platelet deposition and activation on stent struts and damaged intima/media ^{10, 13}. The combination of aspirin (325 mg daily) and ticlopidine (500 mg daily) seems to have a synergistic effect on platelet aggregation and adhesion but adequate inhibition required two to three days after the initiation of therapy. For this reason, in both our cases heparin infusion was continued for 48 hours after the end of the procedure mantaining an activated partial thromboplastin time of 1.5 to 2.5 times the control values to avoid acute stent thrombosis ¹⁴.

For patients treated with PTCA and stenting who cannot be given antiplatelet agents orally, a novel approach involves the use of intravenous glycoprotein IIb/IIIa inhibitors (abciximab). Abciximab inhibits the binding of fibrinogen to platelet and thus platelet aggregations. Intravenously administered abciximab is a short acting agent with a half-life of ten minutes but its effects on platelets last for almost 12 hours. Recently, administration of an intravenous abciximab bolus (0,25 mg/Kg) followed by infusion (10 μg/min) for a period ranging from 12 to 24 hours has been shown to reduce the frequency of neurological events in high risk patients undergoing carotid or vertebrobasilar angioplasty with or without stent placement¹⁵.

The use of local UK in the setting of angioplasty and stenting is controversial. The aim of UK infusion is to dissolve any clots from the plaque when the wire and balloon/stent catheter are advanced across the stenosis and possibly to increase the available vessel lumen. However, it is well known that local UK infusion can increase the risk of hemorrhagic events in patients under heparin and/or antiplatelet drugs infusion ¹⁰. Furthermore, UK is reported to show procoagulant properties mediated by platelet activation and/or release of clot-bound thrombin¹⁰. In our first patient, local UK infusion and mechanical manipulation of the thrombus induced recanalization of the vessel lumen without hemorrhagic complications.

In conclusion, PTCA and stent placement represent a feasible therapeutic option in patients with acute atherothrombotic vertebrobasilar stroke. In particular, stent placement seems to yield better radiological results than PTCA alone, decreasing the risk of complications due to vessel dissection. Further studies are required to assess the long term patency of intracranial stent.