Kelly Jarvis1, Alireza Vali1, Shyam Prabhakaran2, Jeremy D. Collins1, and Michael Markl1
1Radiology, Northwestern University, Chicago, IL, United States, 2Neurology, Northwestern University, Chicago, IL, United States
Synopsis
Reverse aortic flow causing
plaque embolization from the descending aorta (DAo) has been identified as a
new source of stroke but the underlying cause of flow reversal is unclear.
There is evidence that aortic stiffness can cause flow reversal but no study
has investigated this relationship in detail. This study used high-temporal
resolution 4D flow MRI to evaluate aortic stiffness and regional aortic flow
reversal in patients with cryptogenic stroke. Elevated PWV was associated with
reverse flow in areas of the aortic arch and DAo providing evidence for aortic
stiffness and flow reversal as a potential embolic mechanism.
Introduction
Even
after extensive evaluation, the cause of stroke remains undetermined (i.e.
cryptogenic) in 20-30% of patients leading to a high risk for recurrent stroke1,2. Atherosclerotic plaques
in the ascending aorta (AAo) have been associated with embolic stroke. Plaques
in the descending aorta (DAo) have not been previously considered because these
require reverse (upward) flow to reach the supra-aortic branches leading
directly to the brain. Recent evidence suggests stiffening of the aortic vessel
wall, which occurs with age and atherosclerosis, leads to aortic flow reversal3. However, no prior studies
provide a comprehensive assessment of both aortic stiffness (i.e. measured by
pulse wave velocity, PWV) and reverse flow. 4D flow MRI (3D time-resolved
3-directional velocity encoding) offers assessment of both aortic PWV4,5 and reverse flow6,7 along the entire aorta
based on a single scan. Prior 4D flow MRI studies have evaluated these
mechanisms separately and were additionally limited by temporal resolution and
pathline analysis. This study used optimized k-t accelerated 4D flow MRI with high-temporal
resolution coupled with multi-plane PWV assessment and regional
(voxel-by-voxel) visualization and quantification of reverse flow. We
hypothesized that elevated PWV would be associated with regions of reverse
aortic flow.Methods
Non-contrast free-breathing
4D flow MRI (spatial resolution=3-3.5 x 2.3-2.6 x 2.6-3 mm3,
temporal resolution=19.6 ms, venc=150 cm/s, k-t GRAPPA acceleration R=5, 1.5T
MAGNETOM Aera: Siemens Healthcare, Erlangen, Germany) was performed in 11 cryptogenic
stroke patients with DAo plaques and 16 age-matched controls. Cardiac function
was assessed using standard cine-MRI. Patients were evaluated for aortic
regurgitation by Doppler echo. The 4D flow MRI data analysis workflow is
illustrated in Figure 1. A 3D phase contrast MR angiogram (PC-MRA) was
generated from 4D flow MRI to depict vessels. Next, the aortic volume was
separated from the 3D PC-MRA by manual segmentation and used to mask the 4D
velocity data. For global aortic PWV quantification, a 3D aortic centerline was
calculated and analysis planes placed every 4 mm (Figure 1a). Flow waveforms
were generated for each location and linearly interpolated to 1 ms intervals. Global
aortic PWV was estimated using cross-correlation (Xcor)4,5,8 to determine the time-delay between
locations along the aorta (Figure 1b-c). For reverse flow analysis, the 4D
velocity data was regridded to isotropic 1 mm3 voxels using spline
interpolation. Each voxel in the aortic volume was analyzed to determine the
direction of forward and reverse flow as defined by the aortic centerline. For
every voxel inside the aorta segmentation, reverse and forward flow were summed
up over the cardiac cycle and reverse flow fraction, $$$RFF=(Reverse Flow)/(Forward Flow)$$$, was calculated9.
The lowest 1% of forward flow data was not included in the RFF calculation to reduce
RFF noise, followed by a 3D median 3-by-3-by-3 filter (also applied to forward
and reverse flow). To collapse the data into a 2D image, mean intensity projection
maps of forward flow, reverse flow, and RFF were generated (Figure 1d-f).
Regions of interest (n=6) were identified in the outer curvature (AAo1, aortic
arch: AArch1, DAo1) and inner curvature (AAo2, AArch2, DAo2) of the aorta and mean
forward flow, reverse flow and RFF were calculated.Results
Subject
demographics are shown (Table 1). Mild aortic regurgitation was reported for
one patient. Patients had elevated forward flow compared to controls in the
ascending aorta (AAo1: p=0.03) (Table 2). Results in 2 example patients and one
control are shown (Figure 2). For patients, age showed a trend with PWV (R2=0.33,
p=0.06) and was significantly correlated with RFF (AAo1: R2=0.65, p=<0.01;
AAo2: R2=0.58, p<0.01; AArch1: R2=0.38, p=0.04). For
controls, age was significantly associated with PWV (R2=0.66, p<0.001),
reverse flow (DAo1: R2=0.28, p=0.03) and RFF (DAo1: R2=0.31,
p=0.02; DAo2: R2=0.25, p<0.05). For patients, PWV was
significantly correlated with reverse flow (AArch1: R2=0.57,
p<0.01; DAo1: R2=0.40, p=0.04) (Figure 3) and RFF (AAo1: R2=0.61,
p<0.01; AAo2: R2=0.54, p=0.01; AArch1: R2=0.82, p<0.001; DAo1: R2=0.60, p<0.01)
(Figure 4). For controls, PWV was also significantly correlated with reverse
flow (DAo1: R2=0.34, p=0.02) and RFF (DAo1: R2=0.27, p=0.04).Conclusions
Associations
between PWV and reverse flow in
areas of the aortic arch and DAo support our hypothesis linking aortic
stiffness and aortic flow reversal as a potential thromboembolic mechanism in
cryptogenic stroke. This work suggests that medical de-stiffening therapies (e.g.
ACE-inhibitors) in a subset of stroke patients with plaques in the descending
thoracic aorta may be able to reduce the rate of recurrent stroke by reducing regional
flow reversal. Future work will focus on studying the progression of aortic
stiffness over time and associated changes in aortic flow and remodeling of the
vessel wall.Acknowledgements
Grant support by NIH, NHLBI T32
HL134633 and R21 HL132357References
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