Impaired damping of cerebral blood flow velocity pulsatility is associated with the number of perivascular spaces as measured with 7T MRI

Author:

van den Kerkhof Marieke12,van der Thiel Merel M123,van Oostenbrugge Robert J245,Postma Alida A12,Kroon Abraham A56,Backes Walter H125,Jansen Jacobus FA127

Affiliation:

1. Department of Radiology & Nuclear Medicine, Maastricht University Medical Center, Maastricht, The Netherlands

2. School for Mental Health and Neuroscience, Maastricht University, Maastricht, The Netherlands

3. Department of Psychiatry & Neuropsychology, Maastricht University, Maastricht, The Netherlands

4. Department of Neurology, Maastricht University Medical Center, Maastricht, The Netherlands

5. Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands

6. Department of Internal Medicine, Maastricht University Medical Center, Maastricht, The Netherlands

7. Department of Electrical Engineering, Eindhoven University of Technology, Eindhoven, The Netherlands

Abstract

Arterial walls stiffen with age, cardiovascular risk factors, and various vascular diseases, which may lead to less damping of the arterial blood flow pulse, subsequent microvascular damage, and enlarged perivascular spaces (PVS). However, the exact interplay between these processes is unclear. This study aimed to investigate the relation between blood flow velocity pulsatility in the small lenticulostriate arteries and their supplying middle cerebral artery and the respective damping factor (DF), with the number of MRI-visible PVS in elderly subjects. Blood flow velocity waveforms were obtained in 45 subjects (median age [range]: 64 [48–81] years, 47% male) using 7T MRI. PVS were scored in the basal ganglia (BG) and centrum semiovale (CSO). Spearman correlation analyses were used to determine associations of the blood flow pulsatility and the DF, with PVS score, adjusted for age and sex. We found a significant association between a lower DF and a higher number of PVS in the BG ( rs = −0.352, P = 0.021), but not in the CSO. This finding supports the supposed pathophysiological mechanism in which excessive kinetic energy deposition leads to damage of small perforating arteries and contributes to the enlargement of PVS at the level of the BG, but possible other pathways might also be of influence.

Publisher

SAGE Publications

Subject

Cardiology and Cardiovascular Medicine,Neurology (clinical),Neurology

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