Abstract

Introduction: The precise interactions between collateral perfusion, hemodynamics, and infarct growth after large vessel occlusion (LVO) require further definition. This study examined whether patients with poor collateral circulation and rapid early infarct progression are more vulnerable to reductions in blood pressure (BP). Methods: We prospectively enrolled patients with LVO stroke who underwent thrombectomy. Volumes of arterial tissue delay and relative cerebral blood flow (CBF) were estimated with RAPID software; a poor collateral profile was defined by a hypoperfusion intensity ratio >0.4. Early infarct growth rate (EIGR) was defined as ischemic core volume (CBF<30%) divided by the time from symptom onset to imaging. A fast progressor profile was assigned to patients whose EIGR was >10 mL/h. The final infarct growth rate (FIGR) was the quotient of final infarct volume (FIV) and time from symptom onset to reperfusion. BP reduction was measured as the difference between admission mean arterial pressure (MAP) and lowest MAP before reperfusion. Results: Fifty-five patients (mean age 69 + 15, mean NIHSS 13) with successful reperfusion (TICI 2B/3) were included in the analysis. The median MAP reduction was 17 (IQR 9, 32). Poor collateral perfusion and EIGR were independent predictors of FIV after adjusting for age and admission NIHSS (mean FIV 70 vs. 31 mL, p=0.012 and 60 vs. 29 mL, p=0.01, respectively). A significant interaction was found between MAP reduction and both collateral status (p=0.04) and progressor profile (p=0.01). For every 10 mmHg MAP reduction, patients with poor collaterals experienced an average increase in FIGR of 3.6 mL/h (Fig. 1A). Above a critical MAP reduction threshold of 30 mmHg, mean FIV was significantly larger in patients with rapidly progressing infarcts (p<0.01, Fig. 1B). Conclusions: Patients with poor collaterals and rapid early infarct growth are at higher risk of accelerated infarct growth and larger FIV related to BP reductions.

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