Imaging Changes in Cross-Sectional Area of the Middle Cerebral Artery through the Cardiac Cycle at 7 Tesla
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 disease1 and vascular cognitive decline2. 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 geometry3. 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 protocol5. 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 mm3, voxel size = 0.3 mm3 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, Venc = 180 cm/s, TR/TE = 20/13 ms, voxel size = 0.5x0.5x5.0 mm3, 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 mm3, 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.

Figures

Figure 1. Left: Example of T­2-weighted slice perpendicular to the M1 segment of the MCA, located in the white square. The latter shown zoomed in on the right.

Figure 2. Group average results for the 4 different delay times. Data is normalized by dividing by the mean area. Error bars indicate standard error of the mean. *Significantly different (p < 0.01, paired t-test).



Proc. Intl. Soc. Mag. Reson. Med. 24 (2016)
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