Esther AH Warnert1, Jasper Verbree2, Richard G Wise1, and Matthias JP van Osch2
1Cardiff University Brain Research Imaging Centre, Cardiff University, Cardiff, United Kingdom, 2Radiology, Leiden University Medical Center, Leiden, Netherlands
Synopsis
Arterial stiffness is an important marker for cerebrovascular
health, as increased stiffness can lead to a range of cerebrovascular
pathologies. A non-invasive assessment of cerebral arterial stiffness could therefore
be an important imaging marker for cerebrovascular health. Here we show the
feasibility of using high field MRI to non-invasively assess cerebral arterial
stiffness by measuring the changes in cross-sectional area of the middle
cerebral artery throughout the cardiac cycle. Introduction
Cerebral arterial stiffness is an important
marker for cerebrovascular health: increased arterial stiffness may lead to
severe pathology including cerebral small vessel disease
1
and vascular cognitive decline
2. With
increased arterial stiffness arteries become less pulsatile, i.e. the volume
changes occurring over the cardiac cycle decrease. The current standard of assessing
cerebral arterial stiffness is by assessing blood flow velocity profiles
through the skull with transcranial Doppler ultrasound (TCD), which relies on
assumptions of geometry
3. It
is also possible to assess volume changes of cerebral arteries with computed
tomography (CT)
4,
which use is limited in longitudinal studies due to the accompanying radiation
dose. Here, we aim to assess cerebral arterial stiffness non-invasively by
measuring the change in cross-sectional area of the middle cerebral artery
(MCA) with high field magnetic resonance imaging (MRI).
Methods
Ten healthy participants were recruited for this
experiment (average age 30.2 ± 10.3 years; 6 females, non-smoking). MRI scans
were performed at 7 Tesla (whole body Philips Achieva system, Philips
Healthcare, Best, The Netherlands) and similar to a previously described
protocol
5. A
3-dimensional time-of-flight angiogram was performed to identify the MCA (TR/TE
= 12.5/3.7 ms, flip angle = 20°, field of view = 180x170x50 mm
3, voxel
size = 0.3 mm
3 isotropic). Peak-diastole and systole were determined
from a quantitative flow scan, planned perpendicular to the M1 segment of the
MCA (phase contrast MRA, retrospective triggering via pulse oximetry, V
enc
= 180 cm/s, TR/TE = 20/13 ms, voxel size = 0.5x0.5x5.0 mm
3, 18
reconstructed cardiac phases). Per participant, 8 T2-weighted images
at 4 delay times were acquired in pseudo-random order: 200 and 100ms preceding
peak-diastole, and 50 ms before and 50 ms after peak-systole. Two repetitions per
delay time were acquired. Acquisition parameters were: prospective triggering, TR/TE
= 2 heartbeats/116 ms, acquisition matrix = 1,200x900, voxel size = 0.2x0.2x5
mm
3, turbo spin echo factor = 12 (+ 4 start-up echoes), read-out
duration per block = 130 ms, acquisition duration = 2.5 min. Two observers,
blinded to participant and cardiac phase of the images, manually drew
elliptical regions of interests to determine the MCA surface area. Each
observer repeated this process at minimum 24 hours after the first session. The
reported MCA area per delay time is the average of 8 observations (4
observations and 2 repetitions per delay time). The intraclass correlation
coefficient for consistency between observers was 0.84.
Results and Discussion
There was a significant increase in MCA area
between diastole and systole of 2.58% [min-max range: 0.08% – 6.48%] (paired
t-test, p < 0.01), see Figure 2. This increase is in line with previously
reported volume changes over the cardiac cycle in cerebral arteries assessed by
computed tomography (approximately 5%)
4. The
slightly lower values found here may be explained by prospective gating of the
image acquisition, which likely underestimates the volume changes due to
heart rate variability. This study illustrates the use of high field MRI for
non-invasive assessment of cerebral arterial stiffness.
Acknowledgements
No acknowledgement found.References
1. O’Rourke MF et al.
Hypertension. 2005;46:200–4. 2.Zlokovic B V. Nature Reviews Neuroscience. 2011.
3. Flück D et al. Front Physiol. 2014;5:49. 4. Kuroda J et al. Stroke. 2012. p.
61–6. 5. Verbree J et al. J Appl Physiol. 2014;117:1084–9.