Abstract

Background: We hypothesized that cerebral perfusion deficits are more severe in acute stroke patients with poor collaterals and that the severity would increase over time if reperfusion does not occur. Methods: This is a substudy of DEFUSE 2. Collaterals were assessed on conventional angiography and dichotomized as poor vs. good flow. DWI and PWI were performed before and within 12 hrs after endovascular therapy; PWI lesion volumes were determined using a Tmax>6sec threshold. The hypoperfusion ratio (HR) was calculated by determining the proportion of the PWI lesion that had severe Tmax delay (>10sec). Acute lesion growth was defined as the difference between the baseline and follow-up DWI volume. Part 1: In patients with an ICA or M1 occlusion we compared the HR to the collateral score. An ROC curve assessed whether the HR predicts the collateral score. Part 2: Among patients who did not experience early reperfusion, the difference between the baseline and follow-up HR was assessed and correlated with early infarct growth. Results: Part 1: Fifty six patients were eligible. Poor collateral flow was associated with larger baseline PWI lesion volume, p=0.012 and a higher HR compared to patients with good flow [median HR 45% (IQR: 35-52%) vs. 34% (IQR 14-41), p=0.003]. A HR > 41% predicted poor collateral flow with an AUC=0.73 (sensitivity 65%, specificity 78%, p=0.003). Part 2: Thirty two patients who did not achieve reperfusion were included; PWI Tmax >6sec lesions volumes at baseline and follow-up were similar (median volume 75 mL at both time points). The median HR at follow-up was significantly higher than baseline [46% IQR (34-65) vs. 40% (24-48), p=0.007; median difference = 13% (IQR: 3.5-17)]. Patients who had worsening of their HR between baseline and follow-up were more likely to experience early ischemic lesion growth (R=0.53, p=0.002). Conclusion: The size and severity of Tmax lesions are associated with angiographic collateral scores. Patients who have a high percentage of their PWI lesion comprised of severe Tmax delays are likely to have poor collaterals. When early reperfusion is not achieved, the severity of hypoperfusion progresses and this progression is associated with early infarct growth.

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