Abstract TMP11: Leptomeningeal Collaterals Predict Infarct Growth And 90 Day Clinical Outcome In Acute Ischemic Strokes Given Intra Arterial Therapy.

Abstract

Introduction: We tried to explore the role of lepto meningeal collaterals, baseline imaging to recanalization time in predicting infarct growth and final clinical outcome in acute ischemic strokes. Methods: Data is from a prospective study of consecutive acute stroke patients (2005-2009) from Keimyung University, Daegu,South Korea analysed at University of Calgary. Only patients with M1 MCA+/- intracranial ICA on baseline CT-angio, known stroke onset time with MR DWI at baseline and follow-up were included for analyses. Baseline infarct volume on DWI was calculated using Quantomo, a validated in house software. Infarct growth was calculated as difference in DWI volume between 24 hrs and baseline. Lepto meningeal collaterals at baseline CT-angio assesed using a previously published scale. Results: Of the 264 patients analysed 84 patients were eligible for the study. Of 84 patients [mean age 65.2 +/- 13 yrs, 52.4% male, median NIHSS 14 IQR=8.5, median time from onset of stroke symptom to baseline MR 164 mins, IQR 100.5) in the study, 59.5% achieved TIMI 2-3 recanalization and 35.7% good clinical outcome (mRS 0-2). Median baseline DWI volume was 31.6 ml (IQR 75); median infarct growth 29.8 ml (IQR 64.1). We noted significant correlation (spearman’s r=-0.68, p<0.001) between baseline DWI volume and collateral status and between infarct growth and collateral status (r=-0.38, p<0.01). No correlation (r=0.1, p=0.34) was noted between infarct growth and baseline MR to recanalization time. In patients with baseline DWI volume <=18 ml (group 1), 61.3% of patients achieved good clinical outcome when compared to 26.7% in patients with volume 18-80 ml (group 2) and 13% with volume >80 ml (group 3). Median infarct growth was lowest in group 1 (5.9 ml, IQR 52.7) followed by group 2 (30.5 ml, IQR 70.6) and group 3 (63 ml, IQR 108.1). Conclusion: Leptomeningeal collateral status determines baseline infarct volume and the extent of infarct growth until recanalization is achieved