Michael James Rose1, Kelly Jarvis2,3, Susanne Schnell2, James D Thomas4, Joshua D Robinson1,5,6, Cynthia K Rigsby1,2, Michael Markl2,3, and Alex J Barker2
1Medical Imaging, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, IL, United States, 2Department of Radiology, Feinberg School of Medicine, Northwestern University, 3Department of Biomedical Engineering, McCormick School of Engineering, Northwestern University, 4Division of Cardiology, Feinberg School of Medicine, Northwestern University, 5Division of Pediatric Cardiology, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, IL, United States, 6Department of Pediatrics, Feinberg School of Medicine, Northwestern University
Synopsis
Mean and peak pressure gradients are an important measure of
aortic stenosis severity. In this study, we present a novel method for measuring
mean pressure gradients using 4D flow MRI. 4D flow MRI peak and mean pressure
gradients were measured in 23 pediatric BAV patients and compared to Doppler
echocardiography (echo). There was no significant difference between 4D flow
MRI and echo in peak or mean pressure gradients. 4D flow MRI mean pressure
gradients correlated better with echo than peak pressure gradients (R2=
0.78 vs. R2=0.27), suggesting 4D flow to be better suited for
measuring mean pressure gradients.
Purpose
The
accurate estimation of aortic valve stenosis (AS) severity is necessary to
effectively manage therapy and intervention in patients1. Among the various
markers of severity, the transvalvular pressure gradient is an important metric
informing AS severity. Combining noninvasive imaging and the simplified
Bernoulli equation, the peak pressure gradient is often estimated from a
singular peak systolic velocity value, while the mean pressure gradient is
computed from the time-averaged pressure gradient over the systolic phase. The
findings from peak and mean pressure gradients can be used to corroborate each
other as well as other AS severity measures, such as valve orifice size. Currently,
the non-invasive gold standard for pressure gradient determination is Doppler echocardiography
(echo). 2D PCMRI and time resolved 3D PCMRI (4D flow) have been shown to be
reliable alternatives to echo for measuring peak pressure gradients. However,
prior studies have not employed MRI to measure the mean pressure gradient. In
particular, 4D flow is advantageous since the vena contracta can be localized
and followed over the cardiac cycle. Therefore, the aim of this study is to test
the ability to measure mean pressure gradient with 4D flow MRI. We hypothesize
that 4D flow will produce pressure gradients comparable to echocardiography and
that mean pressure gradients from 4D flow will agree better with
echocardiography than peak pressure gradients.Methods
23 pediatric patients (age = 14 ± 5 (min: 3 max:
22) years, male:female = 16:7) with diagnosed bicuspid aortic valve (BAV) received
4D flow MRI included in a physician-ordered cardiac MR assessment as part of
this IRB-approved study. MRI scans were performed at 1.5 T (Avanto or Aera, Siemens, Germany) with spatial resolution = 1.9-3.5 x 1.6-2.5 x
1.9-4.0 mm3, temporal resolution 37.6-40.8 ms, TE/TR/FA = 2.3-2.6ms/4.7-5.1ms/15°
and velocity sensitivity = 150–400 cm/s. 4D flow data were preprocessed to
reduce noise and artifacts caused by velocity aliasing and phase offset errors (Maxwell terms, eddy currents). 3D
PC-MR angiograms were computed from 4D flow data as described previously2 and used to obtain a 3D segmentation of the aorta (Mimics, Materialise, Belgium), which was then used to mask the 4D flow velocity
field. The time-resolved aorta velocity field was used to generate a velocity maximum intensity projection (MIP) as described
previously3, from which the peak velocity in the ascending aorta (AAo) was
extracted. A velocity-time curve was plotted for the location of peak velocity
and each of its nearest neighbor voxels (27 voxels total, Figure 1D). If the
location of the peak velocity was not in the vena contracta, it was selected using
the velocity MIP. Peak pressure gradients were calculated from the peak
velocity and simplified Bernoulli equation (P=4v2) as previously
described by Rose et al3. The mean pressure gradient was determined by tracing the velocity-time curve plots from the beginning till the end of systole and then taking the mean of the
trace (Figure 1B). A temporal filter was used to exclude any noisy voxels from
the trace. The peak and mean pressure gradients of each patient were then
compared to a recent echocardiogram (<6 months).Results
Doppler and 4D flow velocity-time curve plots are shown in
Figure 1. The mean time difference
between echo and 4D flow studies was 2.4 months. 4D flow and echo showed
no significant difference in either peak (24.2 ± 19.5 vs. 25.1 ± 25.1 mmHg, p=0.35)
or mean pressure gradient (11.7 ± 9.2 vs. 11.9 ± 9.8 mmHg, p=0.98).
Bland-Altman (Figure 2) analysis illustrates the bias between 4D flow and echo
for both peak and mean pressure gradients (0.93 and 0.25 mmHg) and limits of
agreement (±37.14 and ±8.68 mmHg). However, the slope and correlation between 4D
flow and Doppler improved when comparing peak (b=0.74, r2=0.27) to mean
pressure gradient (b=0.93, r2= 0.78, Figure 2).
Discussion and Conclusion
The
relatively large limits of agreement suggest some disagreement between 4D flow
and echo, which may be associated with time between exams, differences in
anesthesia levels, or measurement error; however, this error is seemingly not
systematic (as seen with the low bias). Nonetheless, an apparent
underestimation occurs in the regression analysis of the peak pressure gradient
(Figure 2 B) between 4D flow and echocardiography. 4D flow mean pressure
gradients correlated better with echo, suggesting this approach may help close
the gap between MRI and echo when measuring transvalvular pressure gradients.
This study is limited by its small cohort and differences in scan dates between
echo and MRI. Future studies investigating this approach can benefit from
concurrent intermodality measurements.
Acknowledgements
Grant support was provided by NIH R01HL115828 and K25HL119608
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