Neuroradiology (2004) 46: 81–84 DOI 10.1007/s00234-002-0895-7
E. Janssens X. Leclerc C. Gautier O. Godefroy M. Koussa H. He´non C. Lucas D. Leys J.P. Pruvo
Published online: 4 December 2003 Ó Springer-Verlag 2003 E. Janssens (&) Æ O. Godefroy H. He´non Æ C. Lucas Æ D. Leys Department of Neurology, Stroke Unit, Hoˆpital Salengro, CHRU Lille, 59037 Lille cedex France E-mail:
[email protected] Tel.: +33-0320-446814 Fax: +33-0320-446028 X. Leclerc Æ C. Gautier Æ J.P. Pruvo Department of Neuroradiology, Hoˆpital Salengro, CHRU Lille, 59037 Lille cedex, France C. Gautier Department of Cardiac and Neurological Sonography, Hoˆpital Salengro, CHRU Lille, 59037 Lille cedex, France M. Koussa Department of Vascular Surgery, Hoˆpital Cardiologique, CHRU Lille, 59037 Lille cedex, France
INTERVENTIONAL NEURORADIOLOGY
Percutaneous transluminal angioplasty of proximal vertebral artery stenosis: long-term clinical follow-up of 16 consecutive patients
Abstract We report long-term (average 30 months) clinical and radiological follow-up of 16 consecutive patients with uni- or bilateral proximal vertebral artery stenosis who underwent percutaneous transluminal angioplasty (PTA), without stenting, between 1995 and 1998. Assessment was performed by an independent neurologist. All patients but one remained asymptomatic during follow-up; moderate restenosis was observed in four. PTA of the proximal vertebral artery is safe but in the absence of knowledge of the natural history of atherosclerotic vertebral artery stenosis, whether it is beneficial or not remains unproven. The decision as to whether to perform this procedure is individual.
Introduction Clinicians face the question of whether percutaneous transluminal angioplasty (PTA) for vertebral artery stenosis is beneficial and has acceptable risks. The results in small, open series have shown that it is feasible, but the long-term outcome is unknown in most cases. We report a long-term clinical and radiological follow-up of 16 consecutive patients with uni- or bilateral proximal vertebral artery stenosis who underwent PTA without stenting
Patients and methods Over the 4-year period January 1995–August 1998, 16 patients (12 men, four women), mean age 53.5 years (range 38–70 years),
Keywords Percutaneous transluminal angioplasty Æ Vertebral artery stenosis Æ Outcome
underwent PTA without stenting for 19 atherosclerotic stenoses of the vertebral arteries. The main vascular risk factors were arterial hypertension (in seven), current (9), or former (2) cigarette smoking and hypercholesterolaemia (15); two patients had ischaemic heart disease, four were thought to have chronic alcohol abuse, four concomitant peripheral artery disease, one was diabetic and one had chronic atrial fibrillation. No patient was a migraineur. None of the women was on oral contraceptives and only one had postmenopausal hormonal replacement therapy. Of the 16 patients, five had had an ischaemic stroke and three a transient ischaemic attack (TIA) in the vertebrobasilar territory; six had had an ischaemic stroke in the carotid territory, two of whom also had TIAs in the carotid territory. One patient had only a TIA in the carotid territory. All these ischaemic events were presumed to be thromboembolic. One patient was asymptomatic. Initial assessment before angioplasty included a Rankin scale score, CT of the brain, ultrasonography of the cervical arteries, conventional angiography and in some cases MRI or MR
None None None None None None None None None None None TIA None None Thrombosed 70 – Hypoplastic Hypoplastic 10 – 0 40 – 50 Hypoplastic 20 0 50 0 0 60 40 60 Thrombosed 10 0 40 Hypoplastic 40 20 0 0 30 – Hypoplastic Hypoplastic 10 – 0 40 + dissection – 50 Hypoplastic 20 0 40
Thrombosed 0
>90 0 80 90 70 60 95 90 50 90 Hypoplastic 80 70 >90 Occluded 3 2 2 2 0 3 0 1 0 2 1 0 0 3 6
0 >90 –a Hypoplastic Hypoplastic 70 – 0 80 – 90 Hypoplastic 70 0 80
90 1
Occlude
Dissection and thrombus 0 0 0 20 20 + dissection Unchanged Unchanged 10 0 40 Hypoplastic 40 20 Dissection Occluded
Thrombosed
angiography (MRA). Rankin scores before angioplasty were 0 in five patients, 1 in one, 2 in seven and 3 in three (Table 1). CT and/ or MRI showed 25 infarcts, 12 in the carotid and 13 in the vertebrobasilar territory. Angiography and in some cases MRA showed 21 vertebral stenoses presumed due to atheroma, of which 19, all on the proximal part of the vertebral artery, were treated by PTA. The mean degree of stenosis in the treated group was 80% (range 50%–90%). We also saw nine arterial thromboses (seven internal carotid and two vertebral arteries and found six stenotic lesions in addition to those dilated (four in internal carotid arteries and two in the contralateral vertebral artery). There were five hypoplastic vertebral arteries. All patients were treated by antiplatelet therapy and optimal correction of risk factors for stroke. The decision to proceed to angioplasty was taken by consensus of a stroke neurologist, a vascular surgeon and an interventional radiologist. They concluded in each individual patient that there was a possible benefit of proximal uni-or bilateral vertebral angioplasty. We performed angioplasties only in short, uncalcified, severe ostial stenoses. The vertebral artery had to be intact apart from the ostial stenosis and the circle of Willis had to function well. A clear, extensive explanation was given to the patient and PTA was performed only after informed consent. All procedures were performed via the femoral approach. After an aortogram including two oblique views, the subclavian artery was selectively catheterised to confirm the stenosis and to detect significant distal lesions. Angioplasty was carried out using a percutaneous catheter. We did not use any endovascular device for protecting the brain. The angioplasty catheter was chosen so that the diameter of the balloon did not exceed the estimated normal arterial diameter. The balloons ranged from 20 to 30 mm in length and from 3 to 4 mm in diameter. They were inflated by hand, at most three times, with maximum duration of 30 s. The aim of dilatation was not to obtain a normal diameter but to ‘‘underdilate’’ slightly to avoid intimal dissection. We gave a bolus of 5000 units heparin just before starting the angioplasty and adjusted the dose of heparin over 48 h after the procedure to maintain the activating clotting time at about 120 s (doses ranging from 120 to 150 mg/12 h). In all cases antiplatelet treatment (aspirin 150 or 300 mg or ticlopidine 500 mg/day) was restarted 48 h after the angioplasty. All patients were clinically reassessed between April and September 1999, with an average observation time of 30 months, by the same neurologist (E.J.), independently of both the interventional radiology team and the neurology ward on which they were treated. Rankin scores were established and new vascular events registered. Then they had a radiological assessment consisting of Doppler sonography and contrast-enhanced MRA of the cervical arteries in April 1999–September 2000. Conventional angiography was performed after this only in patients who would possibly be dilated again or undergo endarterectomy.
not assessed a
60, M 63, F 70, M 45, M 38, M 57, M 57, M 52, M 48, M 49, M 47, M 55, F 55, F 42, F 68, M 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16
3 3 3 3 0 3 0 2 0 2 1 0 0 3 2
50, M
2
Results
1
Left Left Left
Right
Residual Before After Before
Stenosis (%) Rankin score Age (years), sex Patient
Table 1 Results of percutaneous transluminal angioplasty (PTA). TIA transient ischaemic attack
Right
Follow-up
Right
None
Further ischaemic episodes
82
Clinical details are provided in Table 1. All patients attended the clinical and radiological follow-up visits, apart from one who was too handicapped to be mobilised. However, in this case, we had clinical and radiological data from the referring neurologist. Rankin scores remained unchanged in 13 patients and improved by one point in two; one died in a car crash 1 year after angioplasty, but had a antemortem Rankin score of 0. One patient had three TIAs in the vertebrobasilar territory, one 14 and two 26 months
83
after PTA, probably of atherothrombotic origin. The radiological studies of that patient showed a residual stenosis of 40%; we decided to modify our medical treatment by giving clopidogrel instead of aspirin. No patient had an ischaemic stroke within the follow-up period. Very few adverse events were seen during and after angioplasty: in three patients we saw an intimal flap and in one an intraplaque dissection, but all of these were asymptomatic. Transient headache was reported by two patients. Local complications consisted of one haematoma and one bilateral dissection of the iliac artery with temporary ischaemia of the left leg. No embolic cerebral events, cranial nerve palsy or arteriovenous fistula was reported. Angiography at the end of the PTA showed no residual stenosis in three lesions, 10% of residual stenosis in two, 20% in four, 30% in one, 40% in three and 50% in one. Signs of dissection were present in four lesions, together with a thrombus in one; because of this, it was impossible to quantify residual stenosis in two cases. No significant change was observed after angioplasty in two cases because the stenoses could not be crossed by the balloon. Duplex sonography and MRA showed the following on follow-up: 11 of the 19 dilated arteries were normal or unchanged; there was moderate (40, 50, 60 and 70%) restenosis of four. As the latter patients were asymptomatic, we decided not to investigate them further. Both arteries with signs of dissection immediately after angioplasty, where it was difficult to quantify residual stenosis, were subsequently of normal calibre. In the other two cases the signs of dissection also disappeared. One of the two lesions unchanged angioplasty, one remained unchanged, while the other progressed to occlusion, although both patients remained asymptomatic. Atherosclerosis of the other extracranial arteries was stable in only six patients; the other nine developed more or less severe stenosis of the subclavian or internal carotid arteries. Some underwent angiography and endarterectomy. MRA and duplex sonography showed concordant results in all cases.
Discussion Our study confirms that PTA without stenting of the proximal part of the vertebral artery is feasible and seems to be safe, as suggested previously [1, 2, 3, 4, 5, 6]. Very little is known about the natural history of vertebral artery atherosclerosis and if these lesions are generate emboli [7, 8, 9, 10]. Stenoses occur primarily at the origin of the vertebral artery [7] and the plaques are usually small, not ulcerated and harder than carotid artery plaques [7, 8], which probably makes PTA easier and safer, as the risk of embolism is smaller. Several
centres have reported excellent results [1, 2, 3, 4, 5, 6] (Table 2). We can not compare description the patients in these reports, as in some information is given for the whole group of patients including those with further stenoses at other sites [1, 4, 6]. In other studies very little data was given for the [2, 3, 5]. In all these studies follow-up was by the medical team which performed the angioplasty, which may have influenced the results. We tried to provide neutrality by choosing an independent neurologist for clinical follow-up. Thus, we can not compare our results with those of previous studies. We did not consider studies with angioplasty plus stenting: only a few patients also had stenting in our centre and we wished to review a homogeneous group of patients. Now we do use stenting and our antithrombotic therapy after PTA consists of clopidogrel and aspirin, taking note of the results of the CLASSICS trial [11]. We started stenting because it is said that long-term radiological results in the carotid and the coronary arteries are better, with a lower rate of restenosis. We also found that without a stent that we did not obtain a normal diameter vessel by angioplasty alone. We had only local problems at the puncture site and only one patient had a TIA during follow-up. This excellent clinical result was obtained even though we slightly ‘‘underdilated’’ in most cases. The patient who did have a TIA had moderate (40%) residual stenosis. Moderate restenosis was found in another four patients, all of whom were asymptomatic; we did not investigate them further. In two cases, the degree of stenosis was similar after angioplasty, a finding which has been reported previously [5, 6]; as in our experience, this was due in one report to tortuosity of the subclavian arteries [6 ] or to Z-shaped elongation of the proximal vertebral artery [5]. Given data on the natural history of vertebrobasilar arteriosclerosis, angioplasty series and this study, things are rather confusing. No clear guidelines for selection criteria can be defined with the current knowledge. Several groups have suggested vertebral angioplasty is indicated only when collateral blood flow is compromised [1, 4, 5, 6], because then the impaired haemodynamics are likely to be the cause of vertebrobasilar ischaemia. However, the risk of this approach is to have a more or less significant failure rate: other mechanisms can lead to vertebrobasilar ischaemia. Embolisation from a plaque seems less frequent than in the carotid artery system is thought possible by some workers [9, 10, 12]. Caplan [10] suggested that at the moment of and just after occlusion of the vertebral artery distal embolisation from the tail of the thrombus may cause of vertebrobasilar ischaemia, this suggestion being supported by a post-mortem study [12]. Patients with severe, unilateral ostial stenosis with well functioning collateral circulation might thus also be eligible for angioplasty. However,
84
Table 2 Review of published studies of vertebral artery PTA Reference, date
Patients
Clinical follow-up Duration (months)
1, 1993
34
0–12
2, 3, 4, 5,
1984 1982 1993 1986
2 5 25 13
0–4 months 1–18 3–148 3–25
6, 1996
35
Up to 60
Radiological follow-up Results One TIA, two arterial spasms immediately post-PTA; two patients symptomatic, at 2 and 3 months; one death (aneurysm) Both asymptomatic All asymptomatic All asymptomatic Eight asymptomatic; three with TIAs, one stroke; one death (myocardial infarct) One TIA immediately post-PTA (many patients lost to follow-up)
faced with a patient with symptoms and/or radiological signs of vertebrobasilar ischaemia and a severe stenosis of a vertebral artery, the ischaemia may still be cardioembolic, or due to vertebrobasilar small-vessel disease. In conclusion, if selection criteria are too restrictive, some patients, who could conceivably benefit from angioplasty may be excluded; however, with current
Duration (months)
Results
0–12
Restenosis (severe?) at 2,3 and 5 months, two symptomatic and retreated
4 – 3–148 3–25
One occlusion One patient no result from PTA No restenosis One severe restenosis, one occlusion, both asymptomatic
?
94% success; no restenosis (many patients lost to follow-up)
technology we cannot eliminate with certainty the patients whose ischaemia has a cause other than vertebral artery narrowing. Large studies on the natural history of vertebrobasilar arteriosclerosis from the clinical and radiological points of view might resolve these questions.
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