Emergency Rescue Primary Stenting for Atherosclerotic Basilar Artery Occlusion with Acute Thrombosis

Summary

We demonstrate endovascular stent deployment for the treatment of atherosclerotic basilar artery occlusion with acute thrombosis. Application of a microstent without previous balloon dilatation resulted in vessel reopening and good clinical improvement. Emergency primary stent application can be technically feasible and improve the outcome in acute basilar artery occlusion and clinical status.

Introduction

Patients with vertebrobasilar occlusive disease are at risk for stroke that open leads to fatality or disabling neurologic symptoms. Although an unfavorable clinical outcome is found in as many as 60% of patients with vertebrobasilar ischemic stroke, technically successful thrombolysis of vertebrobasilar artery occlusion is associated with beneficial clinical outcome¹.

The vertebrobasilar junction and proximal basilar artery are sites of predilection for atherosclerotic narrowing². In cases of basilar artery occlusion resulting from superimposed thrombus, attempted recanalization with thrombolytic therapy may be unsuccessful unless primary treatment of the stricture is undertaken. Several authors have reported of stent use in the intracranial atherosclerotic stenosis^3-5, and there are a few case reports on stenting as emergency therapy in acute occlusion of the basilar artery^6,7.

We report a case with acute basilar artery occlusion superimposed on severe atherosclerotic basilar stenosis. Application of a stent without previous dilatation resulted in marked angiographic, haemodynamic and clinical improvement.

Case Report

A 61-year-old man was admitted to the neurological intensive care unit with aphasia, hemiparesis on the right and intermittent disturbances of the consciousness (NIH stroke scale: 15). The patient had longstanding arterial hypertension with a history of cerebral ischemia. The initial CT excluded a haemorrhage and revealed an old lacunar infarct in the right putamen. Diffusion weighted images demonstrated multiple dotted high signal lesions at the cerebellar hemisphere, pons and bilateral occipital cortex, suggesting acute embolic infarctions (figure 1).

Figure 1.

Diffusion-weighted image (TR/TE 6000,90 b=1000) revealed hyperintense lesions in the pons and scattered in the cerebellum and occipital lobe (not shown).

The T2-weighted MR images revealed a small old lacunar infarct in the pons and intraluminal high signal lesion of the basilar artery. Contrast enhanced three-dimensional time-of-flight (TOF) MR angiography showed a lack of arterial flow in the region of the basilar artery (figure 2). The patient showed a progressive deterioration in consciousness as time went on. Intra-arterial angiography was performed four hours after symptom aggravation. The vertebral arteries were codominant, of good caliber,and free of significant atherosclerotic disease in their extracranial portions. Left vertebral arteriography revealed complete occlusion in the proximal basilar artery (figure 3). Heparin (5,000 U) was administered intravenously to avoid thrombus formation during the procedure, a microcatheter (Prowler, Cordis, Miami,FL) was inserted coaxially into the left vertebral artery through a 6F guiding catheter (Envoy, Cordis, Miami, FL). Local intra-arterial fibrinolysis was performed at different catheter positions within and proximal to the thrombus. Intra-arterial Urokinase (UK) was given via the pulse-spray technique (total amount of 300,000 units) and mechanical thrombus disruption using microguide-wire (Agility, Cordis, Miami, FL) manipulation was also performed. After thrombolysis, angiography demonstrated severe irregular atherosclerotic stenosis at proximal and mid basilar artery including proximal segment of bilateral anterior inferior cerebellar artery (AICA) (figure 4).

Figure 2.

Coronal contrast-enhanced 3-D TOF MR angiography revealed subtle flow signal in the basilar artery.

Figure 3.

Left vertebral angiogram revealed complete occlusion of the basilar artery and contrast refluxes across the basilar artery into the distal right vertebral artery.

Figure 4.

After thrombolysis using local infusion of 300,000 units of UK, residual underlying severe proximal and mid basilar artery stenosis including proximal segments of bilateral anterior inferior cerebellar artery (AICA) revealed.

The proximal segment of right AICA was markedly affected by atherosclerosis. Concerning the refractory nature of atherosclerotic plaque and the strong likelihood of rethrombosis if narrowing were not relieved, we decided on endovascular treatment using a balloon-mounted coronary stent. Because the patient was not premedicated, additional bolus dose of heparin (5,000 U) was administrated intravenously. Under the guidance of digital road-map fluoroscopy, we crossed the lesion with a 0.014-inch hydrophilic guidewire (Transend, Scimed, Maple Grove, MN). The wire tip was anchored in the right posterior cerebral artery to facilitate tracking of the stent. A Jostent Flexmaster (Abbott vascular devices, Redwood city, CA), with a nominal diameter of 3 mm and a length of 23 mm, was slowly and carefully advanced along the guidewire and positioned across the stenotic lesion. To reduce the serious risk of vessel rupture and dissection, the balloon was inflated from a pressure of 4 to 10 atmospheres (recommended pressure) with the slow oscillating inflation technique⁸. The pressure elevation was performed by one atmosphere in each step.

The inflated balloon remained for no longer than 20 seconds in each step, uneventful and satisfactory stent deployment was achieved (figure 5). The balloon was carefully withdrawn, taking care not to dislodge the stent. The final angiography demonstrated patent lumen and good flow of a basilar artery with mild flow reduction of right AICA (figures 6,7). To prevent the ensuing thromboembolic complication, intravenous heparin treatment was continued for five days, maintaining the activated partial thromboplastin time between 50 and 80 seconds. Two days after the endovascular treatment of stenotic proximal basilar artery, the patient showed restoration of mental function. Neurologic examination results were normal except for dysarthria and right hemiparesis. After discharge from hospital, the patient received a combination of aspirin (100mg/d) and clopidogrel (75mg/d) for secondary prophylaxis. Within the first seven months after intervention, the patient had no new ischemic symptoms in the treated vascular territory and presented mild dysarthria and moderate spastic hemiparesis of the right side (modified Rankin Scale 3).

Figure 5.

After stent deployment, normal vessel lumen is regained.

Figure 6.

Early-arterial phase image of left vertebral arteriogram after stenting showed sufficient dilatation of the lesion and no residual stenosis.

Figure 7.

Mid-arterial phase image of left vertebral arteriogram revealed mild flow reduction of the right AICA.

Discussion

The prognosis for patients with basilar artery atherothrombotic occlusion is poor, with a greater than 70% mortality rate if untreated. Even with local intra-arterial fibrinolytic treatment, death is still a probable outcome for these patients ¹. In contrast to acute occlusions of the distal third of the basilar artery, which are predominantly embolic in origin, occlusions of the proximal and middle third of the basilar artery in the majority of cases are caused by thrombus formation on pre-existing atherosclerotic stenoses ².

Percutaneous transluminal angioplasty (PTA) of the basilar artery has been performed successfully by several groups ^9,10. However, PTA is compromised by the risk of vasospasm, dissection, thrombosis, thromboembolism, and occlusion of perforators and has only minor effects on the luminal diameter of intracranial stenosis. The recent advent of new-generation, flexible stents has enabled reliable and less traumatic percutaneous access of the intracranial vasculature.

Several cases have been reported of endovascular stent treatment in the atherosclerotic stenosis of vertebrobasilar artery ^3-5. But, there are only few reports of stent application as rescue therapy in acute basilar artery occlusion. Phatouros et Al ⁶ reported a single case of endovascular stenting of a basilar artery. The patient presented with acute basilar artery thrombotic occlusion requiring thrombolysis. Once patency was established, balloon angioplasty of an underlying stenosis was unsuccessful in establishing an acceptable luminal diameter, probably due to underlying severe atherosclerotic change. Percutaneous endovascular deployment of a Gianturco-Roubin-2 coronary stent of 4-mm diameter was subsequently performed, with excellent angiographic results. Like this case report, angioplasty alone is ineffective in maintaining the patency of the vessel in many instances, because of recoil of plaque. Mori et Al⁷ described a case of primary angioplasty with stenting of an acutely thrombosed intracranial vertebral artery without using initial thrombolytic therapy. Total occlusion of a long segment of the vertebrobasilar artery was completely recanalized by implanting two flexible, balloon-expandable coronary stents. The patient's clinical outcome 30 days later was favorable.

In our patient, there was underlying severe stenosis of the proximal basilar artery and strong likelihood of rethrombosis if narrowing was not relieved. We decided to apply the stent without previous dilatation to decrease the risk of intimal dissection and distal embolism by plaque fracture. This procedure was able to reduce the time until successful reperfusion and increase the possibility of patient's neurological recovery. Balloon overdilatation may be especially dangerous in the basilar artery, because of the insubstantial muscularis and adventitial layers of the arterial wall. Therefore, different reports advocated underdilatation to reduce subsequent elevated risk of perforation¹¹. Dilatation of the basilar artery with or without stent application inevitably carries the risk of occluding small pontine perforators. For stenting, the risk of impairing small perforating vessels is probably not higher than with angioplasty because of the wide interstices and thin strut. Masuo et Al ¹² showed that the small lumbar artery branch of the abdominal aorta of rabbits were patent even when stent struts crossed the ostium. Thus, intracranial stenting may not pose a risk of occluding perforating arteries of the same diameter of the lumbar artery even if stent struts cover the ostium. In view of the devastating prognosis of acute basilar thrombosis the risk of occlusion of perforators seems to be acceptable.

In our case, final angiography after stenting revealed patent basilar artery with mild flow reduction through the right AICA. We speculated that this flow reduction of the right AICA was caused by flow alterations at the inflow zone. The lower margin of the stent in our case at least partially covered the origin of the right AICA.We cannot rule out the possibility of mechanical disruption of atherosclerotic plaque and dislodgement of a thrombus into the adjacent right AICA at the time of stent placement. These haemodynamic alterations may promote acute thrombosis within the right AICA.

With continued development of flexible balloon and stent systems, primary stenting of basilar artery stenosis will become more common and help to reduce the problems associated with intracranial occlusions and stenoses. Several studies showed good follow-up clinical outcome after endovascular stent treatment for atherosclerotic cerebral artery stenosis for at least six months^3,4. However, its impact on longterm stroke prevention and its durability are unknown and will require further study.

In conclusion, emergency primary stent application of the atherosclerotic basilar artery stenosis can be technically feasible and effective in patients with acutely thrombosed basilar artery.