Association of Multiple Passes during Mechanical Thrombectomy with Incomplete Reperfusion and Lesion Growth

Abstract

<b><i>Introduction:</i></b> Despite complete recanalization by mechanical thrombectomy, abnormal perfusion can be detected on MRI obtained post-endovascular therapy (EVT). The presence of residual perfusion abnormalities post-EVT may be associated with blood-brain barrier breakdown in response to mechanical disruption of the endothelium from multiple-pass thrombectomy. We hypothesize that multiple-pass versus single-pass thrombectomy is associated with a higher rate of residual hypoperfusion and increased lesion growth at 24 h. <b><i>Materials and Methods:</i></b> For this analysis, we included patients presenting to one of two stroke centers between January 2015 and February 2018 with an acute ischemic stroke within 12 h from symptom onset if they had a large vessel occlusion of the anterior circulation documented on magnetic resonance angiography or CTA, baseline MRI pre-EVT with imaging evidence of hypoperfusion, underwent EVT, and had a post-EVT MRI with qualitatively interpretable perfusion-weighted imaging data at 24 h. MRI <i>T</i><sub>max</sub> maps using a time delay threshold of >6 s were used to quantitate hypoperfusion volumes. Residual hypoperfusion at 24 h was solely defined as <i>T</i><sub>max</sub> volume >10 mL with >6 s delay. Complete recanalization was defined as modified treatment in cerebral infarction visualized on angiography at EVT completion. Hyperintense acute reperfusion injury marker was assessed on post-EVT pre-contrast fluid-attenuated inversion recovery at 24 h. Major early neurological improvement was defined as a reduction of the admission National Institutes of Health Stroke Scale by ≥8 points or a score of 0–1 at 24 h. Good functional outcome was defined as 0–2 on the modified Rankin Scale on day 30 or 90. <b><i>Results:</i></b> Fifty-five patients were included with median age 67 years, 58% female, 45% Black/African American, 36% White/Caucasian, median admission National Institutes of Health Stroke Scale 19, large vessel occlusion locations: 71% M1, 14.5% iICA, 14.5% M2, 69% treated with intravenous recombinant tissue plasminogen activator. Of these, 58% had multiple-pass thrombectomy, 39% had residual perfusion abnormalities at 24 h, and 64% had severe hyperintense acute reperfusion injury marker at 24 h. After adjusting for complete recanalization, only multiple-pass thrombectomy (odds ratio, 4.3 95% CI, 1.07–17.2; <i>p</i> = 0.04) was an independent predictor of residual hypoperfusion at 24 h. Patients with residual hypoperfusion had larger lesion growth on diffusion-weighted imaging (59 mL vs. 8 mL, <i>p</i> < 0.001), lower rate of major early neurological improvement (24% vs. 70%, <i>p</i> = 0.002) at 24 h, and worse long-term outcome based on the modified Rankin Scale at 30 or 90 days, 5 versus 2 (<i>p</i> < 0.001). <b><i>Conclusions:</i></b> Our findings suggest that incomplete reperfusion on post-EVT MRI is present even in some patients with successful recanalization at the time of EVT and is associated with multiple-pass thrombectomy, lesion growth, and worse outcome. Future studies are needed to investigate whether patients with residual hypoperfusion may benefit from immediate adjunctive therapy to limit lesion growth and improve clinical outcome.

Post-ischemic hyperemia following endovascular therapy for acute stroke is associated with lesion growth

“…The rate of severe HARM at 24 hours found in this study, 57%, is within the reported range, 54–64%, of prior studies from the same centers involving different patients with similar inclusion criteria. 5,8 The rate of any HT at 24 hours, 48%, was also within the reported range of these same studies, 45–51%. 5,8 Though we expected patients with hyperemia would be more likely to have blood-brain barrier disruption or hemorrhage, there were no significant differences in the rates of HARM, severe HARM or HT between patients with and without early post-EVT hyperemia.…”

“…5,8 The rate of any HT at 24 hours, 48%, was also within the reported range of these same studies, 45–51%. 5,8 Though we expected patients with hyperemia would be more likely to have blood-brain barrier disruption or hemorrhage, there were no significant differences in the rates of HARM, severe HARM or HT between patients with and without early post-EVT hyperemia. Other studies have also reported an unclear association between hyperemia and HT, perhaps significant for severe HT only.…”

“…Ischemic core volumes using an apparent diffusion coefficient threshold ≤620 µm 2 /s were calculated using the early post-EVT DWI and apparent diffusion coefficient images using a fully automated novel NIH tool in Mipav (v10, Center for Information Technology, NIH). 8 Core at 24 hours was not calculated due to the prominent presence of areas of both hemorrhagic transformation and associated heterogeneous signal, making a meaningful measure of ischemic core technically difficult. DWI lesion volumes were calculated by two trained raters (ML and RD) on early post-EVT and 24 hours, and FLAIR volumes at 5 days.…”

“…One relatively unexplored mediator of clinical outcome is injury to the vasculature and brain following recanalization, secondary to the index ischemic event. [4][5][6][7][8] Reperfusion injury has been long recognized as a contributor to secondary injury in pre-clinical models, but has not been widely considered a main contributor to clinical outcome in large vessel occlusion stroke patients. Frequent, early, and abrupt recanalization brought on by modern EVT may have altered that balance.…”

Advances in differential diagnosis of cerebrovascular diseases in magnetic resonance imaging: a narrative review

“…With a clear history and careful physical exam, a stroke and its cerebral location can be identified. Although occlusion at different segments of the cerebral vessels can exhibit different symptoms and signs, the infarct areas present basically the same pathologic alterations (51,52), which form the basis of neuroimaging diagnosis of ischemic stroke (Figure 1C, Figure 2A).…”