Abstract

Background and Purpose: Inter-individual variability of fast to slow progression of early infarct growth in anterior circulation large vessel occlusion (ACLVO) stroke has been previously well quantified. However, the underlying pathophysiology of these clinical phenotypes remains poorly understood. We aimed to determine clinical and radiographic variables associated with fast or slow progressor phenotypes of ACLVO stroke. Methods: Single-center retrospective study of all patients with intracranial ICA or MCA occlusion, with or without tandem cervical ICA occlusion, who underwent baseline advanced imaging including CTP or MRI within 24 hours of stroke onset. Fast progressors (ischemic core > 70 ml, < 6 hours of stroke onset) and slow progressors (ischemic core ≤ 30 ml, > 6 to 24 hours of stroke onset) were identified. Demographics, co-morbidities, admission NIHSS and ACLVO type were tested in univariate and multivariate analysis for association with fast or slow progressor status. Results: A total of 185 patients were included with mean age 71 ± 15 and NIHSS 17 ± 7; 60% were female. Patients had occlusion of the MCA in 72% or the intracranial ICA in 28% of cases. Of these, 20% had a tandem cervical ICA occlusion. In the early epoch, there were no significant differences in age, sex, NIHSS, co-morbidities or ACLVO type between fast progressors (n=19) versus controls (n=56). In the delayed epoch, the mean NIHSS was 14±6 in slow progressors (n=61) versus 19±7 in controls (n=49). Slow progressors had MCA occlusion in 80% versus 63% (p < 0.05) and tandem occlusion in 10% versus 35% of controls (p < 0.01). In multivariate logistic regression modeling, age (OR 1.04, 95% CI 1.01-1.07) and NIHSS (OR 0.87, 95% CI 0.81-0.93) but not ACLVO types were independently associated with slow progressor status. Conclusions: Although greater frequency of MCA occlusion and absence of tandem cervical ICA occlusion were prevalent amongst slow progressors, only age and NIHSS were independent predictors. Future studies are needed to better characterize the underlying clinical substrates for fast versus slow progression of ACLVO stroke.

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