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Malignant cerebral edema is the leading cause of death in acute ischemic stroke (AIS), and in patients with large vessel occlusion, malignant cerebral edema occurs in more than 20% of patients despite successful recanalization
.
In contrast, little is known about the contributing factors after the initial hyperacute phase of 24 to 72 hours, when edema is actively developing
stroke vessel
Microvascular dysfunction may be involved in the pathogenesis of AIS complications
.
Disruption of the blood-brain barrier (BBB) in AIS has been shown to be a key mechanism of hemorrhagic transformation (HT)
thrombus
Hyperperfusion after thrombolysis and thrombectomy is also associated with hypertension and is considered to be a dysfunction of cerebrovascular autoregulation
.
Likewise, cerebral hyperperfusion syndrome characterized by headache, neurological dysfunction, and vasogenic edema has been recognized following recanalization of chronic stenotic carotid arteries
They performed a pooled analysis of patients with pre-treatment circulation large vessel occlusion in the EXTEND-IA TNK and EXTEND-IA TNK Part II trials who underwent dynamic susceptibility contrast-enhanced perfusion-weighted MRI imaging 24 hours after treatment
.
We then explored the relationship between BBB disruption and intra-infarct cerebral blood flow and assessed cerebral edema using 2 metrics: first, midline shift (MLS), which was classified as negligible (<1 mm), mild (≥1 to <5 mm) or severe (≥5 mm), followed by relative hemisphere volume (rHV), defined as the ratio of the 3-dimensional volume of the ischemic hemisphere relative to the contralateral hemisphere
.
Of the 238 patients analyzed, 133 (55.
9%) had negligible, 93 (39.
1%) mild, and 12 (5.
0%) severe MLS within 24 hours
Increased BBB permeability was independently associated with more edema after adjusting for age, occlusion location, reperfusion, parenchymal hematoma, and thrombolytic used (MLS cOR, 1.
12 [95% CI, 1.
03-1.
20], P=0.
005; rHV beta, 0.
39 [95% CI, 0.
24-0.
55], P<0.
0001), decreased cerebral blood flow (MLS cOR, 0.
25 [95% CI, 0.
10-0.
58], P=0.
001; rHV beta, - 2.
95 [95% CI, -4.
61 to -11.
29], P=0.
0006)
.
In a subgroup analysis of patients with successful reperfusion (extended cerebral ischemia therapy 2b-3, n=200), decreased cerebral blood flow remained significantly associated with edema (MLS cOR, 0.
37 [95% CI, 0.
14-0.
98], P =0.
045; rHV beta, -2.
59 [95% CI, -4.
32 to -0.
86], P=0.
004)
.
The significance of this study is the finding that BBB disruption and persistent hypoperfusion in the infarcted area after reperfusion therapy are associated with space-occupying brain edema
.
Further studies are warranted to evaluate microvascular dysfunction after the hyperacute phase as a biomarker and potential therapeutic target for post-stroke edema
BBB disruption and persistent hypoperfusion in the infarcted area after reperfusion therapy are associated with space-occupying brain edema
Original source:
[Ng FC, Churilov L, Yassi N, et al.
Microvascular Dysfunction in Blood-Brain Barrier Disruption and Hypoperfusion Within the Infarct Posttreatment Are Associated With Cerebral Edema .
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