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Background and Purpose: Patients with intracranial atherosclerotic disease (ICAD) are believed to have enhanced collateral flow. We have anecdotally perceived that large vessel occlusion acute strokes (LVOS) patients due to ICAD have more benign automated CT perfusion (CTP) defect profiles, potentially reflecting improved collateralization in comparison to embolic LVOS.Methods: Retrospective review of a prospectively collected interventional stroke database from Sep 2010-Mar 2015. Patients were dichotomized into ICAD vs. other etiology. Patients with a technically adequate CTP and an intracranial ICA, MCA M1 or M2 occlusion were included. Tandem extracranial carotid occlusions were excluded due to the known effects on bolus dispersion and delay of bolus passage. Ischemic core (relative CBF<30%) and perfusion defects were estimated by RAPID automated CTP. The primary endpoint was to compare the ratio of CTP Tmax>4s (“benign oligemia”) / Tmax>6s (“territory at risk”) between the two groups.Results: A total of 250 patients fit inclusion criteria, of whom 21 (8%) were classified as ICAD and 229 had other stroke etiologie. Baseline characteristics were similar between the two groups, except for higher hemoglobin A1c levels (p<0.01), higher baseline systolic blood pressure (p<0.01); and lower rates of atrial fibrillation (p<0.01) in the ICAD group. There were no differences in ischemic core (p=0.51), perfusion defect Tmax>4s (p=0.86), Tmax>6s (p=0.57) and Tmax>10s (p=0.17). ICAD patients had a median ratio of Tmax>4s/ Tmax>6s of 2. A Tmax>4s/ Tmax>6s ratio≥2 showed a specificity of 83% and a sensitivity of 52%, and was more common in the ICAD group (p=0.1). Multivariate logistic regression analysis revealed that higher rates of Tmax>4s/ Tmax>6s ratio≥2 (OR 3.36 95% CI 1.05-10.71, p=0.04), lower rates of atrial fibrillation(OR 0.17 95% CI 0.04-0.86, p=0.03), and higher systolic pressure (OR 1.03 95% CI 1.01-1.05, p=0.002) were independently associated with ICAD.Conclusion: A RAPID CTP Tmax>4s/ Tmax>6s ratio≥2 profile is an independent and highly specific indicator of underlying ICAD LVOS etiology.