Abstract
Objective: Cerebrovascular reactivity (CVR) represents the phenomenon where cerebral vessels dilate or constrict in response to vasoactive stimuli. CVR impairment may contribute to brain injury due to cerebral small vessel disease (SVD). We aimed to determine the CVR in hypertensive intracerebral hemorrhage (ICH) and to identify its vascular dysfunction.Methods: A total of 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 years) were enrolled for CVR measurement at least 3 months after the symptomatic ICH event. Each participant underwent a brain MRI study, and CVR was calculated as the cerebral blood flow (CBF) reduction using arterial spin labeling (ASL) between baseline and 10 min after an intravenous dipyridamole injection (0.57 mg/kg). Traditional MRI markers for SVD were also evaluated, including cerebral microbleed, white matter hyperintensity, lacune, and MRI-visible enlarged perivascular space, which were used to determine the total small vessel disease score.Results: Compared to control subjects, hypertensive ICH patients showed reduced CVR in the basal ganglia (CBF reduction 22.4 ± 22.7% vs. 41.7 ± 18.3, p = 0.026), the frontal lobe (15.1 ± 11.9 vs. 26.6 ± 9.9, p = 0.013), and the temporal lobe (14.7 ± 11.1 vs. 26.2 ± 10.0, p = 0.010). These differences remained significant in multivariable models after adjusting for age and sex. Within ICH groups, the CBF reduction in the basal ganglia was significantly correlated with the total small vessel disease score (R = 0.58, p = 0.006), but not with individual MRI markers.Conclusion: Patients with advanced hypertensive SVD demonstrated impaired vasoconstriction after dipyridamole challenge in the basal ganglia and the frontal and temporal lobes. Our findings provide safe approaches for whole-brain CVR mapping in SVD and identify a potential physiological basis for vascular dysfunction in hypertensive SVD.
Highlights
Hypertensive small vessel disease (SVD) is the most common etiology of non-traumatic spontaneous intracerebral hemorrhage (ICH) and has significant morbidity and mortality around the globe [1, 2]
Hypertensive ICH was significantly associated with conventional image markers of hypertensive SVD, including deep cerebral microbleeds (CMBs) (76.2% vs. 0%, p < 0.001) and higher volume of white matter hyperintensities (WMH) (7.0 ± 5.6 vs. 2.6 ± 2.0 mL, p = 0.007)
There was no significant difference in cerebral blood flow (CBF) reduction in the cerebral white matter, parietal or occipital lobes between the ICH group and healthy controls
Summary
Hypertensive small vessel disease (SVD) is the most common etiology of non-traumatic spontaneous intracerebral hemorrhage (ICH) and has significant morbidity and mortality around the globe [1, 2]. In addition to symptomatic ICH, hypertensive SVD can result in the occurrence of cerebral microbleeds (CMBs) and other non-hemorrhagic presentations, including deep lacunar infarcts and white matter hyperintensities (WMH), which typically can be detected in conventional MRI [4]. Most of the studies on hypertensive SVD are still focusing on analyzing conventional MRI markers, including the distribution and number of CMBs, lacune, WMH, and MRI-visible enlarged perivascular space. These markers could only reflect the end-stage parenchymal change from damaged small vessels
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