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. 2023 Jun;43(6):856-868.
doi: 10.1177/0271678X231155222. Epub 2023 Feb 7.

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

Affiliations

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

Marie Luby et al. J Cereb Blood Flow Metab. 2023 Jun.

Abstract

A substantial proportion of acute stroke patients fail to recover following successful endovascular therapy (EVT) and injury to the brain and vasculature secondary to reperfusion may be a contributor. Acute stroke patients were included with: i) large vessel occlusion of the anterior circulation, ii) successful recanalization, and iii) evaluable MRI early after EVT. Presence of hyperemia on MRI perfusion was assessed by consensus using a modified ASPECTS. Three different approaches were used to quantify relative cerebral blood flow (rCBF). Sixty-seven patients with median age of 66 [59-76], 57% female, met inclusion criteria. Hyperemia was present in 35/67 (52%) patients early post-EVT, in 32/65 (49%) patients at 24 hours, and in 19/48 (40%) patients at 5 days. There were no differences in incomplete reperfusion, HT, PH-2, HARM, severe HARM or symptomatic ICH rates between those with and without early post-EVT hyperemia. A strong association (R2 = 0.81, p < 0.001) was found between early post-EVT hyperemia (p = 0.027) and DWI volume at 24 hours after adjusting for DWI volume at 2 hours (p < 0.001) and incomplete reperfusion at 24 hours (p = 0.001). Early hyperemia is a potential marker for cerebrovascular injury and may help select patients for adjunctive therapy to prevent edema, reperfusion injury, and lesion growth.

Keywords: Hyperemia; cerebrovascular autoregulation; hyperperfusion; luxury perfusion; reperfusion injury.

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Conflict of interest statement

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Figures

Figure 1.
Figure 1.
(a) Patient with successful recanalization and early hyperemia that resolved at 24 hours and remained so at 5 days with HI-2 on FLAIR. Serial rCBF (from left to right: early—24hr—5d) in top panel with corresponding MTT (from left to right: early—24hr—5d) in bottom panel illustrating the elevated rCBF and decreased MTT on early post-EVT, normalized rCBF and MTT at 24 hours, and normalized rCBF and MTT at 5 days with FLAIR (right image) and (b) Patient with successful recanalization and MR angiographic “blush” seen at 24 hours (left image), persistent hyperemia at 5 days demonstrated by elevated rCBF (left middle image), low ADC (right middle image), and lesion growth and edema on FLAIR (right image). Note – HI: hemorrhagic infarction; FLAIR: fluid attenuated inversion recovery; rCBF: relative cerebral blood flow; MTT: mean transit time; MR: magnetic resonance; ADC: apparent diffusion coefficient.
Figure 2.
Figure 2.
(a) Comparison of rCBF signal intensity ratios on early post-EVT for visually guided hyperemic VOIs vs. ipsilateral control VOIs and (b) DWI-based and MCA-guided M2 region VOI on early post-EVT for successfully recanalized patients with vs without hyperemia. Note – EVT: endovascular therapy; rCBF: relative cerebral blood flow; DWI: diffusion-weighted imaging; VOI: volume of interest.
Figure 3.
Figure 3.
(a) Patient with successful recanalization, early hyperemia (circled with short-dashed lines), and incomplete reperfusion (circled with long-dashed lines). Early DWI in top panel with corresponding MTT and rCBF illustrating the elevated rCBF and decreased MTT on early post-EVT and (b) Same patient in bottom panel at 24 hours with DWI lesion growth (circled with dashed lines), persistent hyperemia and incomplete reperfusion with corresponding MTT and rCBF. Note – DWI: diffusion-weighted imaging; MTT: mean transit time; rCBF: relative cerebral blood flow.
Figure 4.
Figure 4.
Mechanisms of post-EVT hyperemia. (a) Mean arterial pressure and cerebral blood flow before and after recanalization demonstrating the loss of arterial tone and associated hypermetabolism due to loss of cerebral autoregulation. (b) Patient example of large vessel occlusion with associated ischemic core and surrounding penumbra before recanalization indicated on the CBF with consistent hypoperfusion on MTT and lesion on DWI and (c) Patient examples after recanalization of hypermetabolism visualized as an increase in CBF, decrease in MTT, and associated DWI lesions. Note – CBF: cerebral blood flow; MTT: mean transit time; DWI: diffusion-weighted imaging.

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