Abstract TP190: Higher Pre-Hospital Blood Pressure is Associated With Lower Mismatch Volume and Poorer Collateral Status in Patients With Acute Ischemic Stroke Due to Large Vessel Occlusions

Abstract

Introduction: Immediately after AIS onset, blood pressure variability (BPV) arises as the result of a complex interplay between brain and systemic physiological hemodynamic responses. In this study, we examined the effect of BPV on early infarct growth in patients with large vessel occlusions (LVO) during their prehospital transfer. Methods: We included consecutive patients with AIS-LVO from 2 large comprehensive stroke centers. We collected the BP values from emergency medical services arrival to hospital admission. Patients with <3 BP recordings were excluded. BPV was assessed using the standard deviation (SD) of the systolic (SBPv), diastolic (DBPv), and mean BP (MBPv). Initial infarct volume (IIV) was defined as rCBF <30%, penumbra area as time to maximum concentration (Tmax) >6s, and mismatch volume as the difference between these two volumes (Tmax 6 - rCBF<30%). Collateral status was evaluated using the hypoperfusion intensity ratio (HIR), defined as the Tmax>10s/Tmax>6s ratio. We used linear regression to investigate associations between these variables, using log-transformation to achieve normality, and final exponentiation for a better interpretability of the results. Results: We included 171 patients, mean age was 70.9± 13.7, 51.5% female, 88.3% white, median NIHSS was 15. Mean BP: SBP=12.37 + 6.8, DBP=10.2 + 7.1, and MBP=8.9 + 5.9. CTP values: rCBF >30% (5 [IQR 0.001 - 22]), Tmax >6s (103 [60.5 - 158.5]), and HIR (0.38 [0.17 - 0.54]). Higher SBP variability was significantly associated with lower mismatch volumes. Furthermore, higher SBP tertiles were associated with worse collaterals (high HIR) (Figure) . Conclusion: Pre-hospital BPV is associated with lower mismatch volume, likely mediated by the effect of BP on collateral status. Our findings are consistent with previous studies; the association between higher pre-treatment blood pressure and poorer collaterals might be due to an imbalance in the need of increasing perfusion to the ischemic tissue.