Background and purpose Patients who undergo stent-assisted cerebral aneurysm coiling require long-term antiplatelet therapy (AT), and some studies have reported that cessation or modification of AT results in an increased risk of cerebral infarction due to delayed stent thrombosis. It is speculated that incomplete endothelialization due to poor stent wall apposition may be important causes of the delayed stent thrombosis. Recently LVIS stent has been available for cerebral aneurysm in Japan as new design braded stent have excellent wall apposition due to manipulation even if parent artery is tortuous like a carotid siphon. The aim of this study was to evaluate whether AT could be terminated without increasing the risk of ischemic event among patients who have undergone Lvis stent-assisted cerebral aneurysm coiling (LSAC).
Materials and methods Six consecutive patients with 6 unruptured aneurysms who underwent LSAC and were confirmed to have neointimal formation by follow-up angiography at 3 month were evaluated in this study. All aneurysms were located in internal carotid artery (Ophthalmic/paraophthalmic segment, n=5; petrous segment, n=1). Dual AT (aspirin 100 mg and clopidogrel 75 mg) was given for one month, and then one antiplatelet agent (clopidogrel) was given for 2 months until confirmation of neointimal formation. After confirmation of neointimal formation, AT was terminated. The incidence of ipsilateral ischemic events (transit ischemic attack, ischemic stroke, retinal ischemia) and stent occlusion, as evaluated by angiography or contrast-enhanced magnetic resonance angiography after termination of AT were prospectively assessed.
Results During follow-up, no ipsilateral ischemic events (mean, 92.5 days; range, 20–183 days) were occurred and no stent occlusion (mean, 66.7 days; range, 9-161 days) was observed in any cases.
Conclusion Termination of AT at 3 months postoperatively did not result in ischemic events among patients who underwent LSAC. Neointimal formation of Lvis stent may be a criterion for termination of AT without increasing the risk of ischemic event.
Disclosures: K. Takayama: None. K. Myouchin: None. T. Wada: None. S. Kurokawa: None. K. Kichikawa: None.
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