Back to Search Start Over

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

Authors :
Marieke van den Kerkhof
Merel M van der Thiel
Robert J van Oostenbrugge
Alida A Postma
Abraham A Kroon
Walter H Backes
Jacobus FA Jansen
RS: MHeNs - R1 - Cognitive Neuropsychiatry and Clinical Neuroscience
Beeldvorming
Klinische Neurowetenschappen
MUMC+: MA Neurologie (3)
RS: Carim - B05 Cerebral small vessel disease
MUMC+: Hersen en Zenuw Centrum (3)
MUMC+: DA BV Medisch Specialisten Radiologie (9)
MUMC+: DA BV AIOS Nucleaire Geneeskunde (8)
MUMC+: DA BV AIOS Radiologie (8)
Interne Geneeskunde
MUMC+: MA Alg Interne Geneeskunde (9)
RS: Carim - V02 Hypertension and target organ damage
MUMC+: DA BV Klinisch Fysicus (9)
MUMC+: DA BV Research (9)
Source :
Journal of Cerebral Blood Flow and Metabolism, 43(6), 937-946. SAGE Publications Inc.
Publication Year :
2023
Publisher :
SAGE Publications, 2023.

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.

Details

ISSN :
15597016 and 0271678X
Volume :
43
Database :
OpenAIRE
Journal :
Journal of Cerebral Blood Flow & Metabolism
Accession number :
edsair.doi.dedup.....64f8b1d0fae1192cee9a7cc5defa67e3