Abstract 372: Precision Reperfusion in Acute Ischemic Stroke: Angiography and Reperfusion after Successful Thrombectomy

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Introduction Angiographically occult microcirculatory “no‐reflow” has been hypothesized to play a role in suboptimal outcomes after endovascular thrombectomy (EVT) for acute ischemic stroke. In the present study, we sought to evaluate the presence of perfusion asymmetry within infarctions present on MRI imaging following TICI 3 recanalization. Methods Consecutive patients treated between 8/2020 ‐ 7/2023 with EVT at a single institution for complete occlusions of the anterior circulation with core lab‐confirmed TICI 3 recanalization who subsequently underwent MR‐based perfusion imaging within 96 hours of EVT were evaluated for qualitative perfusion asymmetry on Tmax, CBV, and CBF, or TTP if images were not processed through RAPID. Strict exclusion criteria were employed, including ≥70% ipsilateral ICA stenosis, chronic contralateral intracranial occlusions, angioplasty/stenting during EVT or patients with prior intracranial stents, dissection, ICH (≥HI‐2, more than trace SAH), re‐occlusion during the hospitalization, or poor quality perfusion scans. Results Nineteen patients met inclusion criteria with MR‐based perfusion imaging after EVT. Occlusion locations included the cervical ICA (2), intracranial ICA (2), M1 (8), M2 (6), and M3 (1). Median NIHSS was 10. Six patients had pre‐morbid mRS≥3. MRIs were obtained at two time points: Early, median of 4.7 hours (1.5 ‐ 15.4), and Late, median of 30.0 hours (20.4 ‐ 74.4). Three of 19 patients demonstrated no infarct on any MRI in the affected territory. Of 16 patients with evidence of ischemia on MRI, 6 had punctate foci of ischemia <1.5cm within which perfusion could not be accurately assessed. Of the remaining 10 with clearly demarcated territories of stroke, 7 had evidence of at least mild hyperperfusion within the infarct bed on Tmax, CBV, and CBF. Two patients did not show any clear perfusion asymmetries within the area of infarct. No patients demonstrated sustained hypoperfusion within the infarct bed. However, one patient had initial Tmax hypoperfusion on Early MRI prior to infarct development (at 4.8hrs) followed by hyperpefusion on the Late scan (57.7 hrs) when infarct developed. Otherwise, perfusion remained consistent in all other cases between Early and Late scans. In terms of outcomes, 14/20 (70%) patients had discharge mRS 0‐2 or equivalent to baseline if pre‐morbid mRS ≥3. Of the 6 with outcomes mRS >2, three had pre‐morbid mRS≥3. Of those with no pre‐morbid disability, one improved to mRS ≤2 at 90 days. No clear association noted between poor outcome and perfusion pattern on MRI, however the single patient in whom hypoperfusion was noted on initial MRI subsequently had poor outcome (mRS 4). Conclusions In our retrospective series of highly selected patients with core‐lab confirmed TICI 3 recanalization, variable patterns of abnormal perfusion were evident on post‐EVT imaging. Hypoperfusion within ischemic tissue suggestive of microvascular no‐reflow was not frequently observed. On the contrary, most patients demonstrated hyperperfusion patterns. However, normal perfusion was also noted in a minority of cases. The precise reperfusion pattern seen after TICI 3 recanalization is likely variable and may depend on an interplay of other factors, such as imaging timing or pattern of stroke, which should be explored more in the future.