Emilie Bollache1, Kristopher Knott2, Redha Boubertakh2, Ryan Scott Dolan1, Claudia Camaioni2, Saadullah Ahmed-Villiers2, Thomas Treibel2, James C Carr1, Pim van Ooij3, Jeremy D Collins1, Julia Geiger4, James Moon2, Alex J Barker1, Steffen E Petersen2, and Michael Markl1,5
1Department of Radiology, Northwestern University, Chicago, IL, United States, 2Barts Heart Centre, London, United Kingdom, 3Department of Radiology, Academic Medical Center, Amsterdam, Netherlands, 4University Children's Hospital, Zurich, Switzerland, 5Department of Biomedical Engineering, Northwestern University, Chicago, IL, United States
Synopsis
Our aims were to study the feasibility at two centers of a newly developed
k-t accelerated non-navigator gated 2-minute aortic 4D flow MRI sequence and
to evaluate its wall shear stress (WSS) estimates. Eleven and 14 healthy
volunteers, as well as 10 and 6 patients were scanned at Northwestern University
and Barts Heart Centre, respectively. Despite an underestimation of distal
aortic WSS in patients when compared to conventional 4D flow, our measurements
were sensitive to expected aging and disease-related variations. We confirmed that
aortic 4D flow MRI in 2 minutes is feasible and provides consistent WSS
measurements.
Introduction
4D flow MRI possesses great potential to investigate aortopathy or
valvular dysfunction; however, its clinical use is hindered by long scan times
and complex preparation, such as respiration control. We recently developed a rapid
4D flow sequence for the assessment of 3D aortic blood flow in 2 minutes by
combining high k-t acceleration, free breathing with no respiratory navigator, and optimized Cartesian ky-kz-space sampling1.
In a pilot feasibility study, we demonstrated its ability to provide
velocity and flow indices in agreement with conventional 4D flow MRI1.
The aims of this study are to 1) expand the feasibility study to a second
center, and 2) investigate the performance of the 2-minute 4D flow sequence for the quantification of 3D aortic wall
shear stress (WSS), which has been shown to play an important role in the
regulation of endothelial cellular function and remodeling2.Methods
Healthy volunteers (HV) and patients were prospectively recruited at Northwestern
University (NU, Chicago, USA) and Barts Heart Centre (London, UK). NU subjects underwent
conventional respiration-controlled 4D flow MRI acquired according to current
consensus3 and free breathing k-t accelerated 4D flow MRI1
(Table 1). Subjects at Barts underwent k-t accelerated 4D flow MRI only. All
scans were acquired on 1.5T scanners (Siemens, Germany) using prospective ECG gating.
Gd-contrast agent was intravenously administered in NU patients (Gadavist,
Bayer) and in all Barts subjects (Dotarem, Guerbet). As illustrated in Figure 1,
after standard analysis of each 4D flow MRI dataset4, 3D WSS was
computed using a previously described method5. Peak systolic maximal
WSS, averaged over the 2% highest values, was then quantified along the entire
wall surface of the ascending (AA) and descending (DA) aorta, as well as the
aortic arch. Differences between NU conventional and k-t accelerated 4D flow,
as well as between NU and Barts, were tested using Wilcoxon signed rank and Wilcoxon
rank sum tests, respectively.Results
A total of 41 subjects (Table 2) were scanned
between NU (n=11 HV, n=10 patients) and Barts (n=14 HV, n=6 patients), confirming
scan times around 2 minutes for k-t accelerated 4D flow MRI (NU: 2:00±0.31min; Barts:
2:02±0.27min, p=0.33). HV included significantly more women and were
significantly younger at Barts than at NU. NU patients had various aortic
diseases, while most Barts patients had aortic valve stenosis (AS). NU data
additionally included conventional 4D flow MRI in the 21 subjects (scan time:
12:16±2:16min). Figure 2.a-b provides peak systolic aortic WSS 3D distribution
in representative cases. Overall small biases and differences around 10% were
found between NU k-t accelerated and reference 4D flow (Figure 3). Differences
were significant only distally in the aortic arch (p=0.03) and DA (p=0.006) of
patients. However, as expected, pooled NU and Barts data in HV demonstrated
significant inverse correlations between age and WSS normalized by aortic
diameter (Figure 2.c). Moreover, after subdividing patients (Figure 2.d), we observed
expected disease-related tendencies in proximal aortic WSS, such as increase in
patients with AS and decrease in patients with a dilated aorta and no AS or
hypertension. Of note, WSS was highly variable in the post-surgery subgroup,
which might be due to heterogeneous diseases and procedures.Discussion
k-t accelerated 4D flow-derived WSS was
significantly underestimated in the distal aorta of patients when compared to
standard respiration-controlled 4D flow MRI. However, agreement was obtained in
the proximal AA, the most important region affected by disease, as well as in
HV at all locations. Despite this underestimation, our WSS measurements were
sensitive to expected aging and disease-related alterations. We observed a
significant decrease in WSS with age, which was more pronounced distally in the
aorta with strong correlations, as previously demonstrated in healthy
volunteers6. Furthermore, in agreement with previous studies7,
WSS was found to be reduced in patients with a dilated aorta and no AS, while
it was higher in AS patients. Finally, WSS was also decreased in the single
patient with hypertension8. Our study was limited by the small
sample size and heterogeneity of subjects. However, the good agreement between
our findings and literature suggests the consistency of our WSS measurements.
We are currently recruiting more subjects and expanding our study to additional
centers.Conclusion
We demonstrated the feasibility of our 2-minute
k-t accelerated aortic 4D flow sequence at 2 centers and its ability to provide
consistent WSS measurements. Such efforts are crucial to promote the use of 4D
flow MRI in routine clinical use, as well as to allow longitudinal
and larger studies needed to investigate the ability of WSS to non-invasively predict
future events, such as aneurysm progression, dissection or rupture.Acknowledgements
This work was supported by the National Institutes of Health grants
R01HL115828 and K25HL119608 as well as the American Heart Association Midwest
Affiliate grant 16POST27250158.References
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