Hazar Benan Unal1, Shahriar Zeynali1, Fei Han2, Gregory J. Anthony3, Subha Raman4, Balaji Tamarappoo5, Rohan Dharmakumar1, and Behzad Sharif1
1Krannert Cardiovascular Research Center, Indiana University School of Medicine, Indianapolis, IN, United States, 2Siemens Medical Solutions, Inc., Los Angeles, CA, United States, 3Department of Radiology and Imaging Sciences, Indiana University, Indianapolis, IN, United States, 4Cardiovascular Medicine, IU Health/IU School of Medicine, Indianapolis, IN, United States, 5Indiana University Health, Indianapolis, IN, United States
Synopsis
Keywords: Myocardium, Ischemia, dobutamine
Myocardial T1
reactivity, defined as the relative T1 change from rest to stress, has been
proposed as a marker for detection of ischemic heart disease.
SASHA-based T1
mapping provides higher accuracy than MOLLI, but the scan time can be prohibitive under stress.
In this work, we
investigated the feasibility of accelerated SASHA T1 mapping for ferumoxytol-enhanced dobutamine-stress
T1 reactivity studies at 3T in a preclinical setting. We showed that a 2-fold accelerated SASHA T1 mapping can provide sufficiently accurate results compared to conventional SASHA.
Background
Myocardial T1
reactivity, defined as the relative T1 change from rest to stress, has been
proposed as a marker for detection and quantification of ischemic heart disease.
Among most commonly used myocardial T1 mapping techniques, SASHA-based T1
mapping provides higher accuracy than MOLLI, due to its robustness to heart
rate, T2 relaxation, and magnetization transfer (MT) effects.1-3 However, for T1 reactivity studies under
exercise or dobutamine stress, the scan time needed for SASHA can be
prohibitive. To mitigate this issue, recent work has shown the feasibility of
accelerating SASHA by using a reduced number of T1-weighted (T1w) images when
the SNR is boosted using denoising.4
An alternative to such approach can be to boost the signal by using low-dose
ferumoxytol-enhanced (FE) protocols given the desirable properties of
ferumoxytol for T1 reactivity studies.5
In this work, we investigated the feasibility of accelerated SASHA T1 mapping for
FE dobutamine-stress T1 reactivity studies at 3T in a preclinical setting.Methods
Based on prior work
by Kellman et al.,6 we used a
SASHA pulse sequence with optimized sampling scheme, i.e. fixed saturation
recovery time, with 2-parameter fitting. We
conducted phantom studies with ferumoxytol-doped agar (Fig 1a) with 6 vials with
T1 range of 900 ms-1700 ms to determine the optimum number, N, of T1w images to
use for accelerated SASHA mapping with acceptable precision. We compared the
precision of accelerated SASHA T1 maps for all feasible choices of N (i.e., all
possible combinations that use N T1-weighted images for T1 mapping). We used the coefficient of variation (CoV)
defined as “standard deviation over mean T1” as a measure of precision6 and determined the lowest N (i.e., highest
acceleration) that can achieve CoV < 1%. After that, we
conducted stress/rest FE studies in 6 healthy pigs under a wide range of
dobutamine-induced stress heart rates (to mimic exercise stress) and performed
T1 reactivity analysis (2 myocardial ROIs per animal) for conventional SASHA
and our proposed accelerated approach (with retrospective subsampling of
SASHA-acquired T1w images). We used the initial N T1w images for accelerated
SASHA T1 mapping. The ferumoxytol dose in each animal study was adjusted such that
the blood pool T1 was between 250-500 ms.Results
The FE phantom
experiments showed that, to achieve CoV < 1%, we need a minimum of N=5 (Fig
1b), implying a 2-fold acceleration compared to conventional SASHA (which uses
N=10). Fig 2 shows example SASHA T1 maps for native rest and FE rest/stress scans
in 2 representative animals. As highlighted with arrows, FE stress T1 values
are lower than FE rest indicating increased intravascular space (higher myocardial
blood volume) during dobutamine stress. Fig 3 compares the 2-fold accelerated
SASHA maps vs. conventional SASHA in terms of rest/stress T1 maps in (a) and T1
reactivities in (b). Both the error maps in Fig 3(a) and the correlation plot
in Fig 3(b) show excellent agreement: Average T1 reactivities for 2-fold
accelerated SASHA vs. conventional SASHA were -6.13% 2.57% vs. -6.34% 2.61%
with no significant difference and the correlation coefficient was R = 0.97
with p < 10^-4.Discussion
The phantom studies
demonstrated that the number of T1-weighted images needed for an accurate SASHA
T1 mapping can be reduced significantly by keeping the CoV within 1%. Although the
accelerated SASHA T1 maps under stress had higher error especially in bloodpool
borders (up to 5%), the resulting T1 reactivity agreement between conventional
SASHA and accelerated SASHA were less affected by this because of averaging pixel-wise
T1 reactivities inside myocardial ROIs. In addition, note that the T1 reactivities
had a wide range of values for both conventional SASHA and accelerated SASHA
techniques (Fig 3b). Although the diagnostic accuracy of accelerated SASHA T1
reactivity was beyond the scope of this work, future studies may better analyze
the effect of variation in T1 reactivity.Conclusion
In this work, we
showed the feasibility of accelerating SASHA T1 mapping in FE rest/stress T1
reactivity studies under dobutamine stress. Our initial results suggest that,
in FE stress studies, the scan time can be accelerated without a noticeable deterioration
in the accuracy of derived T1 maps or T1 reactivity values when compared to
conventional SASHA. A 2-fold acceleration has the potential to improve the
feasibility of SASHA-based T1 reactivity studies under dobutamine/exercise
stress in a clinical setting.Acknowledgements
No acknowledgement found.References
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