Yang-Ha Hwang1, Yong-Won Kim1, Dong-Hun Kang1, Yong-Sun Kim1, David S Liebeskind2. 1. From the Department of Neurology (Y.-H.H., Y.-W.K.), Department of Neurosurgery (D.-H.K.), Department of Radiology (Y.-W.K., D.-H.K., Y.-S.K.), and Cerebrovascular Center (Y.-H.H., Y.-W.K., D.-H.K., Y.-S.K.), Kyungpook National University School of Medicine and Hospital, Daegu, South Korea; and UCLA Stroke Center (D.S.L.), University of California, Los Angeles. 2. From the Department of Neurology (Y.-H.H., Y.-W.K.), Department of Neurosurgery (D.-H.K.), Department of Radiology (Y.-W.K., D.-H.K., Y.-S.K.), and Cerebrovascular Center (Y.-H.H., Y.-W.K., D.-H.K., Y.-S.K.), Kyungpook National University School of Medicine and Hospital, Daegu, South Korea; and UCLA Stroke Center (D.S.L.), University of California, Los Angeles. davidliebeskind@yahoo.com.
Abstract
BACKGROUND AND PURPOSE: Acute intracranial occlusion can be associated with in situ thrombo-occlusion in relation to preexisting intracranial atherosclerotic disease. We aimed to assess residual stenosis at the site of a target arterial lesion (TAL) to determine whether residual stenosis at the TAL is associated with underlying intracranial atherosclerotic disease. METHODS: One hundred and sixty-three patients who underwent endovascular therapy for M1 middle cerebral artery occlusion and achieved angiographic reperfusion were selected for analysis. The presence of residual stenosis at the TAL was classified using the Arterial Occlusive Lesion (AOL) scale at postprocedural angiography, and the severity of stenosis was grouped into none, mild (<50%), moderate (50%-69%), severe (70%-99%), and occlusion on postprocedural and follow-up angiography. We also recorded the incidence of instant reocclusion occurring during the procedure and delayed reocclusion detected on follow-up angiography. RESULTS: Seventy-four patients (45.5%) showed target arterial residual stenosis (AOL 2). As to the TAL pathogenesis, 40 patients were classified into in situ thrombo-occlusion (54.1% of AOL 2 and 24.5% of M1 occlusion). The occurrence of instant or delayed reocclusion was independently associated with a low chance of favorable 3-month outcome. Furthermore, the occurrence of delayed reocclusion was associated with excellent pretreatment collateral flow and early neurological worsening, but not the severity of residual stenosis at the TAL. CONCLUSIONS: In population with a high prevalence of intracranial atherosclerotic disease, residual stenosis may be attributed to in situ thrombo-occlusion with underlying intracranial atherosclerotic disease in ≈25% of cases, hindering functional recovery via the occurrence of instant or delayed reocclusion.
BACKGROUND AND PURPOSE: Acute intracranial occlusion can be associated with in situ thrombo-occlusion in relation to preexisting intracranial atherosclerotic disease. We aimed to assess residual stenosis at the site of a target arterial lesion (TAL) to determine whether residual stenosis at the TAL is associated with underlying intracranial atherosclerotic disease. METHODS: One hundred and sixty-three patients who underwent endovascular therapy for M1 middle cerebral artery occlusion and achieved angiographic reperfusion were selected for analysis. The presence of residual stenosis at the TAL was classified using the Arterial Occlusive Lesion (AOL) scale at postprocedural angiography, and the severity of stenosis was grouped into none, mild (<50%), moderate (50%-69%), severe (70%-99%), and occlusion on postprocedural and follow-up angiography. We also recorded the incidence of instant reocclusion occurring during the procedure and delayed reocclusion detected on follow-up angiography. RESULTS: Seventy-four patients (45.5%) showed target arterial residual stenosis (AOL 2). As to the TAL pathogenesis, 40 patients were classified into in situ thrombo-occlusion (54.1% of AOL 2 and 24.5% of M1 occlusion). The occurrence of instant or delayed reocclusion was independently associated with a low chance of favorable 3-month outcome. Furthermore, the occurrence of delayed reocclusion was associated with excellent pretreatment collateral flow and early neurological worsening, but not the severity of residual stenosis at the TAL. CONCLUSIONS: In population with a high prevalence of intracranial atherosclerotic disease, residual stenosis may be attributed to in situ thrombo-occlusion with underlying intracranial atherosclerotic disease in ≈25% of cases, hindering functional recovery via the occurrence of instant or delayed reocclusion.
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