Caroline M. Colbert1,2, Anna Le3, Jiaxin Shao1, Jesse Currier3, Peng Hu1, and Kim-Lien Nguyen1,2,3
1Department of Radiological Sciences, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, 2Physics and Biology in Medicine Graduate Program, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States, 3Division of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States
Synopsis
T1
reactivity can be used as a marker for myocardial perfusion reserve in the
setting of ischemia or hypoperfusion. We hypothesize that ferumoxytol, as a
pure intravascular agent with high r1 relaxivity, sensitizes T1 reactivity for assessment
of myocardial perfusion. We selectively induced acute myocardial hypoperfusion
in twelve healthy male Yorkshire swine. We then performed native and ferumoxytol-enhanced
adenosine stress testing with the MOLLI sequence at 3.0T. Ferumoxytol increased
absolute T1 reactivity in remote regions by 4.62-fold. The normalized
difference in T1 was 4.5-fold greater in FE images compared to native T1.
Introduction
In ischemic heart disease (IHD), narrowing of the
epicardial coronary arteries leads to myocardial hypoperfusion. Moderate to
severe coronary narrowing can lead to a blunted myocardial perfusion reserve in
the setting of exercise- or pharmacologic-induced stress. In cardiac magnetic
resonance imaging (MRI), T1 reactivity [1] [2], which reflects the relative difference in tissue
T1 between rest and vasodilator stress, can be used as a marker for reduced
perfusion reserve in the setting of ischemia or hypoperfusion. Previous work
shows that native T1 reactivity can be used effectively to distinguish between
remote and ischemic myocardium [3]. As an ultrasmall superparamagnetic iron oxide
ion, ferumoxytol can be used off-label as an MR contrast agent [4] to
sensitize myocardial T1 to vasodilator-induced stress [5]. We hypothesize that in addition to sensitizing
myocardial T1 to vasodilator stress, ferumoxytol increases the normalized
relative difference in T1 reactivity between remote and ischemic myocardial
regions, thereby increasing the conspicuity of ischemic defects. Our aim is to
determine the relative difference in T1 reactivity of remote and ischemic myocardium
using native and ferumoxytol-enhanced (FE) stress T1 mapping in swine models of
acute myocardial hypoperfusion.Methods
We selectively induced acute myocardial hypoperfusion in twelve healthy
male Yorkshire swine using either a partially inflated coronary angioplasty
balloon in the LAD (n=3) or a 3D printed intracoronary stenosis implant in the
LAD (n=8) or LCX (n=1). We then performed native and ferumoxytol-enhanced
adenosine stress testing (Figure 1).
A left ventricular short-axis stack of T1 maps (base, mid, apex) was acquired
at rest and at peak pharmacologic stress (adenosine, 300 µg/kg/min, 4 min
infusion) using the 5(3)3 MOLLI sequence in all swine (n=12) [FOV = 741 x 1522
mm, matrix size = 384 x 308, TR = 349 ms, TE = 1.08 ms, slice thickness = 8 mm,
pixel bandwidth = 1085, flip angle = 35˚]. We used the Instantaneous Signal
Loss simulation (InSiL) algorithm for T1 fitting of MOLLI images in order to
minimize T1 error at high heart rates (>80 bpm) [6]. We contoured a single region of ischemic
myocardium and a corresponding remote region in the contralateral myocardial
segment in each subject. Statistical analyses were performed in MedCalc version
19.0.5 (MedCalc Software, Ostend, Belgium). The D’Agostino-Pearson test was
used to assess normality of the data. T1 reactivity was compared using either
the student’s t test or Wilcoxon signed-rank test according to normality.Results
No ferumoxytol-related adverse events
occurred. At baseline, subjects showed an average heart rate of 88.3±12.5 bpm
(beats per minute), systolic blood pressure of 101±10 mmHg and diastolic blood
pressure of 61.4±9.1 mmHg. At peak adenosine infusion, subjects showed an
average heart rate of 86.3±14.1 bpm, systolic blood pressure of 76±12 mmHg, and
diastolic blood pressure of 40±7 mmHg. Ferumoxytol increased absolute T1 reactivity in
remote regions by a factor of 4.62 (p<0.0001). FE T1 reactivity in ischemic
regions remained blunted as expected. Both native and FE T1 reactivity were
significantly different between ischemic and remote regions. Native T1
reactivity values in ischemic and remote regions were 1.6±1.0% vs 3.1±1.7% (p=0.0008),
respectively. FE T1 reactivity values in ischemic and remote regions were -4.5±5.0%
and ‑11.1±7.0% (p<0.0001), respectively. Relative to remote regions, absolute
FE T1 reactivity was blunted in ischemic regions. The normalized difference in
T1 reactivity, defined as (ReactivityRemote – ReactivityIschemic)
/ ReactivityIschemic, was 4.5-fold greater in FE images (FE:
401±589% vs native: 89±235%, p=0.0038.)Discussion
Myocardial T1-mapping is used to diagnose a range of cardiovascular
pathologies. This study investigated the effect of ferumoxytol on T1
reactivity, which reflects the relative increase or decrease in T1 caused by vasodilator-induced
stress. Adenosine induced vasodilation typically causes an increase in native
myocardial T1, presumably due to expansion in the vascular compartment. Ferumoxytol
shortens the T1 with adenosine-induced vasodilation. Our results demonstrate
that native and FE T1 mapping can both distinguish between remote and ischemic
myocardial regions in swine models of acute myocardial hypoperfusion. However,
ferumoxytol increases the dynamic range of T1 reactivity as a measure of
vasodilator response, causing a significant increase in absolute T1 reactivity
in remote myocardium. As a result, ferumoxytol also increases the normalized
difference in T1-reactivity between remote and ischemic myocardial regions. This
increased contrast in T1-reactivity between remote and ischemic myocardium may
enhance the visual conspicuity of ischemic defects, potentially making
ferumoxytol-enhanced stress T1 mapping a more sensitive diagnostic tool. Conclusion
Ferumoxytol
contrast increases the dynamic range of T1 reactivity as a measure of
myocardial vasodilator response. Ferumoxytol also increases the normalized
difference between remote and ischemic myocardium, increasing the visual conspicuity
of ischemic defects.Acknowledgements
This work was supported by American Heart Association Transformational
Award 18TPA34170049, and pilot funding from the UCLA Department of Medicine. We
thank the UCLA Lux Lab for providing 3D printing services. References
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