Abstract

Backgrounds: Penumbral perfusion dynamically changes with alterations of collateral flow and systemic blood pressure. We investigated the association between acute changes of systolic blood pressures and infarct growth within penumbral area. Method: We included ischemic stroke patients <24h after onset from Jan 2015 to Mar 2018 with the following criteria; initial NIHSS score ≥ 6-point, internal carotid or middle cerebral artery occlusion, no recanalization treatment, baseline penumbral volume >15 mL, and mismatch ratio >1.8. Perfusion quantification, 3D voxel-registration and image segmentation were done by Olea 3.0 and Analyze 12.0. Penumbra was defined as Tmax >6s lesion without infarct. Infarct growth within penumbra was defined by the infarct volume at a follow-up image. Hypoperfusion intensity ratio (HIR) was defined by the proportion of Tmax >10s within penumbra. Blood pressure change integral (BPCI) was defined by an integration of SBP initial - SBP trajectory over 24 h (Figure A). BP dropmax was defined by a maximum decrease of SBP between successive measurements. Results: Among 25 patients included (age, 71.3±13.5; male, 56%), median baseline NIHSS score was 13 (interquartile range [IQR], 8-18). Median volume of initial infarct within Tmax >6s was 16 mL (IQR, 6-58), penumbra was 80 mL (IQR, 29-138), HIR was 46% (IQR, 31-63), and infarct growth within penumbra was 26% (IQR, 11-48). Median BPCI was 157.4 mmHg·h (IQR, -76.8-566.2) and BP dropmax was 34 mmHg (IQR, 25-43). Median infarct growth was linearly associated with BPCI (β=0.022; p -value=0.03; Figure B), BP dropmax (β=0.77; p -value=0.048; Figure C), and HIR (β=0.69; p -value<0.01). High dichotomized BPCI and BP dropmax increased infarct growth rate (Figure D). Conclusions: Acute decline of systemic blood pressure may aggravates penumbral perfusion and thus increase infarct growth within penumbral tissue in emergent large vessel occlusion patients without recanalization.

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