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* Date : 06-08-2009 - 07:12 PM (5407 days ago),
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Recurrent Intracranial Stenosis Induced by the Wingspan Stent: Comparison with Balloon Angioplasty alone in a Single Patient.
SUMMARY: We present a case in which angioplasty alone and stent-assisted angioplasty were performed in the same patient to treat medically refractory intracranial stenoses. This elderly patient with presumed intracranial atherosclerotic disease underwent angioplasty alone for his anterior cerebral artery stenosis. Stent-assisted angioplasty was used for treatment of his ipsilateral middle cerebral artery stenosis. Follow-up angiography at 4 months documented severe recurrent stenosis confined only to the stented portion of the middle cerebral artery.
We present this case because the patient's anatomy offers a fortuitous chance to compare, in a single subject, the results of angioplasty alone with the results of stent-assisted angioplasty. Both the M1 and A1 segments initially presented with high-grade stenoses. However, we noted marked neointimal hyperplasia in the stent-bearing M1 segment compared with nearly absent neointimal hyperplasia in the nonstent-bearing A1 segment. This finding implies that the stent itself may elicit neointimal hyperplasia beyond that produced by angioplasty alone. In light of the recent upsurge in enthusiasm for stent placement for ICAD, this case gives us pause concerning what we actually know about the fundamental biology of intracranial vessels in response to stent placement.
There are currently no data from a controlled study comparing angioplasty alone with stent-assisted angioplasty in a large cohort of patients. However, there have been recent reports suggesting high rates of restenosis in stent-assisted angioplasty cases.4-6 Subgroup analysis of the same cohort implicated stenoses in young patients in the supraclinoid ICA as those most prone to restenosis.6 Given that particular subgroups display a higher propensity to restenosis, it seems that not all stenotic intracranial lesions are alike in their response to stent implantation. Our single case offers some potential advantage over these previous reports, because the nonstented A1 segment acted as an internal control for the stented M1 segment. Of significant note, the patient reported herein was not young, and his restenotic lesion was not in the supraclinoid ICA. This suggests to us that the stent itself may be the primary factor in the development of restenosis. Indeed, a previous series of intracranial angioplasty alone has reported restenosis rates apparently lower than that seen with stent placement.3
We readily admit that a single case report can prove nothing definitively. It is true that restenosis is a documented event after angioplasty alone in ICAD. This case and the recent reports of stent-associated restenosis illustrate the critical need for a randomized trial comparing angioplasty alone with stent-assisted angioplasty in patients with ICAD who have failed maximum medical therapy.7
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