Mihaela Rata1,2, Nina Tunariu1,2, Yun Jiang3, Julie Hughes1, Georgina Hopkinson1, Erica Scurr1, Jessica M Winfield1,2, Vikas Gulani3, Dow-Mu Koh1,2, and Matthew R Orton1,2
1Radiology/MRI Unit, Royal Marsden NHS Foundation Trust, Sutton/London, United Kingdom, 2Division of Radiotherapy and Imaging, Institute of Cancer Research, Sutton/London, United Kingdom, 3Radiology, University of Michigan, Ann Arbor, MI, United States
Synopsis
Magnetic
resonance fingerprinting (MRF) generates fast, co-registered quantitative maps from
a single acquisition. This prospective study evaluates MRF-derived measures of
treatment-induced T1 and T2 changes in prostate cancer
patients with metastatic bone disease, by comparison with existing quantitative T1
and T2 measurements. This study demonstrated a good correlation of
MRF-derived T1 and T2 changes with existing quantitative methods,
supporting the use of MRF for faster measurements in bone lesions.
Introduction
Magnetic
resonance fingerprinting (MRF) generates co-registered quantitative maps from a
single acquisition1. These acquisitions are faster than typical quantitative MR measurements and may re-open the way to using T1
and T2 measurements for assessment of tumours and normal tissues.Aim
This prospective
study evaluates MRF-derived measures of treatment-induced T1 and T2
changes in prostate cancer patients with metastatic bone disease, by comparison
with existing quantitative T1 and T2 measurements.Patient cohort
A
cohort of 13 patients with metastatic prostate cancer (mean age: 68 years,
range: 57-76) with focal active pelvic bone lesions were recruited according to
an ethics and research board approved protocol and were scanned before and
after the start of a new line of treatment. The follow-up scan was usually performed
after an average of 3.3 months (range: 2-6 months). Methods
All
imaging was performed on a 1.5T MAGNETOM Aera scanner (Siemens Healthcare,
Erlangen, Germany) using a prototype MRF Fast Imaging with Steady State
Precession (FISP) sequence2 with Gadgetron reconstruction3
which yields maps of T1 and T2 relaxation times, and
proton density M0. Established sequences were utilised as comparative
techniques for T1 (inversion recovery turbo spin echo, IR-TSE) and T2
(double spin echo, DSE) measurements. These sequences were validated against the ISMRM/NIST MRI system phantom
(CaliberMRI, Inc, Boulder, CO), and were accurate to within 9% (T1) and
12% (T2) over the T1 and T2 ranges observed in the patients in this
study. The MR parameters of MRF and standard quantitative T1 and T2 sequences were matched as best as
possible, see Table 1. To limit the
total acquisition time to 15 minutes, the T1 (5
inversion times) and T2 measurements (2 echo times) were acquired
from a single axial slice covering the biggest active lesion in the pelvis. The
MRF sequence covered 3 slices, with its central slice having matched location
and field-of-view to the other measurements slice.
The MRF,
IR-TSE and DSE added 15 minutes to the end of routine clinical scans that
included diffusion-weighted imaging (DWI) and T1-weighted Dixon sequences. DWI
and Dixon sequences were used to identify the active target lesion (high signal
on b=900 s/mm2 images, low signal on apparent diffusion coefficient
map, and low signal on post-processed fat-fraction Dixon images). No contrast
agent was administrated during the scanning session.
Regions
of interest (ROIs) drawn on the MRF M0 image (using the DWI and
Dixon images as a visual guide) were copied to MRF T1 and T2
images, as well as to the other T1 and T2 maps, which were calculated using an in-house software
(MATLAB R2019a, The MathWorks, Inc.). Lesion ROIs were drawn for each patient, at
each visit, using Horos software (Horosproject.org) and saved to DICOM-RT using
a pyOsiriX plugin4. ROI-derived statistics (median and standard
deviation values) for each map and Spearman correlation tests were obtained
using MATLAB. Spearman correlation coefficients were considered according to
the following scale: weak (0.0-0.39), moderate (0.4-0.59), strong (0.6-0.79)
and very strong (0.8-1).Results
Figure 1 shows example
MRF- and IR-TSE T1 and DSE T2 maps acquired on the
same patient before (first row) and after treatment (second row) with overlaid contours
delineating the selected active lesion.
Cohort
summary results (mean and standard deviation values) are plotted in Figure 2, showing no significant
statistical differences between IR-TSE and MRF T1 measurements at both time-points, while T2
measurements showed significant differences at both time-points.
Figure
3
compares the treatment-related
changes induced in pelvic bone metastases observed using the MRF and existing quatitative methods, where a very strong correlation was found for T1
relative changes (Spearman R=0.84) and a moderate correlation for T2
relative changes (R=0.46). In addition,
9/13 patients had relative MRF T1 changes outside the limits of
agreement (LoA) values previously obtained using this imaging sequence5,
while 4/13 patients with significant changes were detected with MRF T2.Discussion
This
cohort included patients with a high burden disease who had exhausted several lines
of treatment, and so a variety of T1 and T2 treatment
responses (magnitude and trend) were expected in this group. Nevertheless, the
same trend of increased T1 and T2 values post-therapy was
observed with both standard and MRF methods across the cohort (Figure 2). Whilst the range of relative changes in T1
and T2 measures were similar (0.87 – 1.2 for T1; 0.84 – 1.3
for T2), the tighter limits of agreement on the T1
measures (relative repeatability coefficient: 6.2% for T1, 28.4% for
T2) meant that more patients had significant changes detected with T1
than with T2. This is consistent with previous evaluations of
the repeatability of T1 and T2 measures obtained with MRF
in other tissue types6. Conclusion
This
study demonstrated a good correlation of MRF-derived T1 and T2
measurements with existing quantitative methods, supporting the use of MRF for faster measurements in bone lesions.Acknowledgements
We acknowledge the support of NHS funding to the
NIHR Biomedical Research Centre and NIHR Royal Marsden Clinical Research
Facility. This report is independent research funded partially by the National
Institute for Health Research. The views expressed in this publication are
those of the author(s) and not necessarily those of the NHS, the National
Institute for Health Research or the Department of Health.References
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