Guan Wang1,2, Hsin-Jung Yang1, Ivan Cokic1, Avinash Kali1, Richard Tang1, Joseph Francis3, Songbai Li2, and Rohan Dharmakumar1,4
1Pacific Theatres Suite 400. 8700 Bevely Boulevard, Cedars-Sinai Medical Center BIRI, Los angeles, CA, United States, 2Dept of Radiology, The First Affiliated Hospital of China Medical University, Shenyang, China, 3Dept of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, Baton Rouge, LA, United States, 4David Geffen School of Medicine, University of California, Los angeles, CA, United States
Synopsis
Cardiac
MRI (CMR) based staging of myocardial infarction (MI) with or without contrast
agents relies on the resolution of edema in the chronic phase, which is
typically determined on the basis of T2-based MRI. However, whether T2 CMR is sufficient for
staging all MI types has not been studied. We investigated this using animal
models with and without hemorrhagic MIs. Our results show that non-hemorrhagic
MIs can be staged based on T2 changes in the MI territory. However, the
incomplete resolution of T2 elevations in the peripheral layers of hemorrhagic
MI territories can confound staging of hemorrhagic MIs.
Introduction
Cardiac MRI based staging
of myocardial infarction (MI) with or without contrast agents relies on the
resolution of edema in the chronic phase, which is typically determined on the
basis of T2-based imaging. However, whether T2 CMR is sufficient for
staging all MI types has not been studied. We hypothesized that prolonged
inflammation associated with chronic iron deposits following hemorrhagic MIs
promote incomplete resolution of edema in the chronic phase which limit the
capability of T2 imaging to stage hemorrhagic MIs. Methods
Hemorrhagic (n=15) and non-hemorrhagic (n=9)
MIs were created in dogs following a period of prolonged ischemia followed by
reperfusion. Multi-parametric non-contrast mapping (T1, T2 and T2*) and LGE
were performed at 1.5T and 3.0T at 5 days (acute) and 8 weeks (chronic) post
MI. MR relaxation values and LGE intensities of hemorrhagic, peri-hemorrhagic,
non-hemorrhagic and remote territories were measured. Histopathology was
performed to elucidate cardiac MRI findings.Results
T2 of non-hemorrhagic MIs was significantly elevated in the acute phase
relative to remote territories (39.8±12.8%(1.5T) and 27.9±16.5%(3.0T), p<0.0001 for both) but resolved
to remote values by week 8 (-0.0±3.2%(1.5T,
p=0.678) and -0.5±5.9%(3.0T, p=0.601)). In
hemorrhagic MI, T2 of hemorrhage core was significantly elevated in the acute
phase (17.7±10.0%(1.5T) and 8.6±8.2%(3.0T),
p<0.0001 for both) but decreased below remote values by week 8 (-8.2±3.9%(1.5T)
and -5.6±6.0%(3.0T), p<0.0001 for
both). In contrast, T2 of the periphery of hemorrhage within MI zone was
significantly elevated in the acute phase relative to remote territories (35.0±16.1%(1.5T)
and 24.2±10.4%(3.0T), p<0.0001
for both) and remained elevated at 8 weeks post MI (8.6±5.1%(1.5T)
and 6.0±3.3%(3.0T), p<0.0001 for
both). The observed elevation in T2 in the peri-hemorrhagic zone of MIs and
absence of T2 elevation in the non-hemorrhagic MI were consistent with ongoing
or absence of histological evidence of inflammation, respectively.Conclusions
Non-hemorrhagic
MIs can be staged based on T2 changes in the MI territory. However, the
incomplete resolution of T2 elevations in the periphery of hemorrhage
associated with ongoing inflammation, well after scar formation, requires
additional consideration of the spatial localization of sustained T2 elevations
for staging hemorrhagic infarctions. Acknowledgements
This work was supported in
part by a grant from NIH ( R01-HL133407)
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