Abstract 80: Early Intervention With High-Dose Statin Decreased the Plaque in Acute Stroke Patients With Intracranial Atherosclerosis: High-Resolution MR Wall Imaging Study

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Intracranial atherosclerosis (ICAS) is a common stroke etiology, especially in Asians. Current guidelines emphasize statin therapy with intensive lipid lowering effects for risk reduction in atherosclerotic strokes. High-dose statin therapy regress coronary, carotid and aortic atherosclerotic plaques. However the role of statin in patients with ICAS remains unknown. Thus we aimed to evaluate the impact of early intervention with rosuvastatin (20mg/day) on the symptomatic intracranial atherosclerotic plaque, using high-resolution (HR) wall MRI. Fiffteen patients with acute infarcts caused by ICAS were enrolled. All patients were given high-dose statin, rosuvastatin 20mg/day and performed serial HR MRI with 3-T scanner including proton density/T2-weighted axial/sagittal, T1 FLAIR pre- and post-contrast sagittal/axial and 3-dimensional volumetric isotropic turbo spin echo acquisition images. Serial HR wall MRI were taken before and after 3~6 months of treatment (interval, 141±45 days). Intracranial artery at the maximal stenosis on MRA was analyzed in terms of vascular remodeling (plaque burden) and wall enhancement (plaque activation). Normal vessels were also assessed for reference values. Intracranial atherosclerotic plaques were compared before and after statin treatment. Both intracranial atherosclerotic plaque burden and activation can be regressed by high-dose statin therapy (Figure). Wall area, a representative of plaque burden, was decreased (pre- vs. post-statin treatment, 5.74±2.63mm2 vs. 4.64±2.58mm2; p=0.027). Enhanced area within the wall, an indicator of plaque activation, was also lowered (pre- vs. post-statin treatment, 3.46±2.15mm2 vs. 2.32±1.81mm2; p=0.013). No patients stop rosuvastatin during follow-up period. Early intervention with high-dose rosuvastatin in acute stroke patients with ICAS enabled significant reduction of the symptomatic intracranial atherosclerotic plaque during 6 months.