Brain Sciences, Vol. 16, Pages 160: Vascular Steal in White Matter of Non-Flow-Limited Cerebral Hemispheres Following Acetazolamide Challenge Using Arterial Spin Labeling Magnetic Resonance Imaging

Brain Sciences doi: 10.3390/brainsci16020160

Authors:
Rahim Ismail
Denes Szekeres
Stephen Smith
Giovanni Schifitto
Timothy Hoang
Evan McConnell
Matthew Bender
Henry Wang

Background: Vascular disease is a known risk factor for the development of leukoaraiosis. Assessment of cerebral blood flow (CBF) was performed at baseline and after acetazolamide (AZM) challenge to evaluate for vascular reserve and steal within the brain. Little has been reported on the physiological reserve in the non-flow-limited hemispheres. This study attempts to evaluate for vascular steal in areas commonly involved in leukoaraiosis, in the setting of pharmaceutically induced states of increased CBF. Methods: Patients who underwent AZM challenge MRI from 2014 to 2021 and a cerebral angiogram within one year were included. Patients with bilateral disease or non-diagnostic imaging artifacts were excluded. MRIs were obtained after 1 g of AZM was administered 5 and 10 min prior to acquisition. Augmentation and steal maps were generated. Regression analysis, Pearson correlation coefficient, two-sample t-test, Spearman and Mann–Whitney U analyses were utilized for statistical evaluation. Results: A total of 38 patients with unilateral cerebral vaso-occlusive disease underwent the AZM challenge. Vascular steal and T2 hyperintensities were assessed in non-flow-limited hemispheres (NFLH) and flow-limited hemispheres (FLH). A moderate correlation was demonstrated between NFLH steal and NFLH T2 hyperintensities (rs = 0.48, p = 0.0020). A weak correlation without statistical significance was demonstrated between ipsilateral T2 and contralateral T2 hyperintensities (rs = 0.27, p = 0.10). Conclusions: The vascular steal phenomenon was demonstrated in the distal cerebral vasculature of cerebral white matter even in the absence of upstream flow-limiting stenosis, suggesting an inherent vulnerability of these structures to hemodynamic fluctuations and possiblly contributing etiology to leukoaraiosis.

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Rahim Ismail www.mdpi.com