Intracranial arteriosclerosis and cerebrovascular function in the general aging population - A 7T MRI Study

Structured AbstractO_ST_ABSBackground and ObjectivesC_ST_ABSIntracranial arteriosclerosis is a prevalent condition linked to serious health outcomes, such as stroke and dementia. It is hypothesized that intracranial arteriosclerosis compromises brain health by disrupting the functioning of adjacent vessels, including the middle cerebral artery (MCA) and the perforating small arteries downstream. Using 7T MRI, this study aims to assess the association between intracranial arteriosclerosis and cerebrovascular function in the MCA and in the downstream small perforating arteries. MethodsThis study is based on 195 participants (43.6% female, average age 70.8 years ({+/-} 4.52 years)) from the population-based Rotterdam Study who previously underwent a non-enhanced low-dose CT on which we measured intracranial carotid artery calcification (ICAC) and vertebral artery calcification (VAC) bilaterally as hallmark of intracranial arteriosclerosis. Participants underwent a 7T brain MRI to assess blood flow velocity and pulsatility in the MCA and small perforating arteries as well as whole-brain cerebrovascular reactivity (CVR). We assessed the relationship of left and right intracranial arteriosclerosis presence, burden, and subtypes with vessel function using linear regression and linear mixed models with a random intercept. Analyses were adjusted for age, sex and cardiovascular risk factors. ResultsThe prevalence of ICAC was 77.4%. VAC prevalence was notably lower, at 10.3%. ICAC and VAC presence and burden were associated with higher pulsatility but not blood flow velocity in the MCA (e.g. {beta}ICAC presence: 0.07 [95% Confidence interval: 0.02, 0.13]). There was no association with pulsatility or blood flow velocity in the small perforating arteries. Neither ICAC nor VAC were associated with CVR. ConclusionsIntracranial arteriosclerosis influences pulsatility but not blood flow velocity in the MCA. This finding, combined with the absence of an effect between intracranial arteriosclerosis and cerebrovascular function further downstream, indicates that its impact is limited to cerebrovascular hemodynamics in adjacent vessels.