Anke Wouters1, Patrick Dupont2, Soren Christensen2, Bo Norrving2, Rico Laage2, Götz Thomalla2, Greg Albers2, Vincent Thijs2, Robin Lemmens2. 1. From the Department of Neurosciences, Experimental Neurology and Leuven Research Institute for Neuroscience and Disease (LIND), KU Leuven-University of Leuven, Leuven, Belgium (A.W., R.L.); Laboratory of Neurobiology, VIB, Vesalius Research Center, Leuven, Belgium (A.W., R.L.); Department of Neurology, University Hospitals Leuven, Leuven, Belgium (A.W., R.L.); Laboratory for Cognitive Neurology, KU Leuven, Leuven, Belgium (P.D.); Department of Neurology, Stroke Center, Stanford University, Palo Alto, CA (S.C., G.A.); Section of Neurology, Department of Clinical Sciences, Lund University, Lund, Sweden (B.N.); Guided Development GmbH, Heidelberg, Germany (R.L.); Uinversitätsklinikum Hamburg-Eppendorf, Klinik und Poliklinik für Neurologie, Kopf-und Neurozentrum, Hamburg, Germany (G.T.); and Department of Neurology Austin Health, Melbourne Brain Center, Florey Institute of Neuroscience and Mental Health, Heidelberg, Australia (V.T.). anke.wouters@med.kuleuven.be. 2. From the Department of Neurosciences, Experimental Neurology and Leuven Research Institute for Neuroscience and Disease (LIND), KU Leuven-University of Leuven, Leuven, Belgium (A.W., R.L.); Laboratory of Neurobiology, VIB, Vesalius Research Center, Leuven, Belgium (A.W., R.L.); Department of Neurology, University Hospitals Leuven, Leuven, Belgium (A.W., R.L.); Laboratory for Cognitive Neurology, KU Leuven, Leuven, Belgium (P.D.); Department of Neurology, Stroke Center, Stanford University, Palo Alto, CA (S.C., G.A.); Section of Neurology, Department of Clinical Sciences, Lund University, Lund, Sweden (B.N.); Guided Development GmbH, Heidelberg, Germany (R.L.); Uinversitätsklinikum Hamburg-Eppendorf, Klinik und Poliklinik für Neurologie, Kopf-und Neurozentrum, Hamburg, Germany (G.T.); and Department of Neurology Austin Health, Melbourne Brain Center, Florey Institute of Neuroscience and Mental Health, Heidelberg, Australia (V.T.).
Abstract
BACKGROUND AND PURPOSE: In patients with acute stroke, the intensity of a fluid-attenuated inversion recovery (FLAIR) lesion in the region of diffusion restriction is associated with time from symptom onset. We hypothesized that collateral status as assessed by the hypoperfusion intensity ratio could modify the association between time from stroke onset and FLAIR lesion intensity. METHODS: From the AX200 for ischemic stroke trial, 141 patients had appropriate FLAIR, diffusion-weighted imaging, and perfusion-weighted imaging. In the region of nonreperfused core, we calculated voxel-based relative FLAIR (rFLAIR) signal intensity. The hypoperfusion intensity ratio was defined as the ratio of the Tmax >10 s lesion over the Tmax >6 s lesion volume. A hypoperfusion intensity ratio threshold of ≤0.4 was used to dichotomize good versus poor collaterals. We studied the interaction between collateral status on the association between time from symptom onset and FLAIR intensity. RESULTS: Time from symptom onset was associated with the rFLAIR intensity in the region of nonreperfused core (B=1.05; 95% confidence interval, 1.0-1.1). We identified an interaction between this association and collateral status; an association was present between time and rFLAIR intensity in patients with poor collaterals (r=0.53), but absent in patients with good collaterals (r=0.17; P=0.04). CONCLUSIONS: Our findings show that the relationship between time from symptom onset and rFLAIR lesion intensity depends on collateral status. In patients with good collaterals, the development of an rFLAIR-positive lesion is less dependent on time from symptom onset compared with patients with poor collaterals.
RCT Entities:
BACKGROUND AND PURPOSE: In patients with acute stroke, the intensity of a fluid-attenuated inversion recovery (FLAIR) lesion in the region of diffusion restriction is associated with time from symptom onset. We hypothesized that collateral status as assessed by the hypoperfusion intensity ratio could modify the association between time from stroke onset and FLAIR lesion intensity. METHODS: From the AX200 for ischemic stroke trial, 141 patients had appropriate FLAIR, diffusion-weighted imaging, and perfusion-weighted imaging. In the region of nonreperfused core, we calculated voxel-based relative FLAIR (rFLAIR) signal intensity. The hypoperfusion intensity ratio was defined as the ratio of the Tmax >10 s lesion over the Tmax >6 s lesion volume. A hypoperfusion intensity ratio threshold of ≤0.4 was used to dichotomize good versus poor collaterals. We studied the interaction between collateral status on the association between time from symptom onset and FLAIR intensity. RESULTS: Time from symptom onset was associated with the rFLAIR intensity in the region of nonreperfused core (B=1.05; 95% confidence interval, 1.0-1.1). We identified an interaction between this association and collateral status; an association was present between time and rFLAIR intensity in patients with poor collaterals (r=0.53), but absent in patients with good collaterals (r=0.17; P=0.04). CONCLUSIONS: Our findings show that the relationship between time from symptom onset and rFLAIR lesion intensity depends on collateral status. In patients with good collaterals, the development of an rFLAIR-positive lesion is less dependent on time from symptom onset compared with patients with poor collaterals.
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