Abstract MP42: Arterial Spin Labeling Imaging Assessment of Cerebrovascular Reactivity in Hypertensive Small Vessel Disease

Abstract

Objective: Cerebrovascular reactivity (CVR) represents the phenomenon that cerebral vessels dilate or constrict in response to vasoactive stimuli, and CVR impairment may contribute to the brain injury caused by cerebral small vessel disease (SVD). We aim to determine the CVR in hypertensive intracerebral hemorrhage (ICH) and to identify its vascular dysfunction. Methods: 21 patients with spontaneous hypertensive ICH (strictly deep or mixed deep and lobar hemorrhages, mean age 62.5 ± 11.3 years) and 10 control subjects (mean age 66.1 ± 6.0) were enrolled for CVR measurement. Each participant received a brain MRI study, and CVR was calculated as cerebral blood flow (CBF) change using arterial spin labeling (ASL) sequence at baseline and 10 minutes after intravenous dipyridamole injection (0.57mg/Kg). Traditional MRI markers for SVD including cerebral microbleed, white matter hyperintensity, lacune and MRI-visible enlarged perivascular space were also evaluated to determine the total small vessel disease score. Results: Hypertensive ICH patients showed reduced CVR in the basal ganglia (CBF change 22.4 ± 22.7% vs. 41.7 ± 18.3, p=0.026), the frontal (15.1 ± 11.9 vs. 26.6 ± 9.9, p=0.013) and the temporal lobes (14.7 ± 11.1 vs. 26.2 ± 10.0, p=0.010) compared to control subjects (Figure). These differences remained significant in multivariable models after adjusting for age, sex, hypertension, diabetes, and hyperlipidemia. Within ICH groups, the CBF change in basal ganglia was significantly correlated with total small vessel disease score (R=-0.58, p=0.006), but not with individual MRI markers. Conclusion: Patients with advanced HTN-SVD demonstrated impaired vasoconstriction after dipyridamole challenge in basal ganglia, frontal and temporal lobes. Our findings provide safe approaches for whole brain CVR mapping in small vessel disease, and identify the potential physiological basis of vascular dysfunction in HTN-SVD.