Nilesh R. Ghugre1,2,3, Venkat Ramanan1, Jing Yang1, Idan Roifman3, Mohammad I Zia3, Bradley H Strauss3, Kim A Connelly4, and Graham A Wright1,2,3
1Physical Sciences Platform, Sunnybrook Research Institute, Toronto, ON, Canada, 2Department of Medical Biophysics, University of Toronto, Toronto, ON, Canada, 3Schulich Heart Research Program, Sunnybrook Health Sciences Centre, Toronto, ON, Canada, 4Cardiology, St. Michaels Hospital, Toronto, ON, Canada
Synopsis
T1 and T2 relaxation parameters have been instrumental
in quantifying both edema and hemorrhage in acute myocardial infarction (AMI). Unlike
T2, the combined effect of edema and hemorrhage on T1 has not been well
described. Our study assessed and compared the
impact of microvascular obstruction (MVO) and hemorrhage on the sensitivity of
T1 and T2 in the quantification of edema. Our study indicated that the capacity
of T1 to detect edema is affected by the counteracting influence from
hemorrhage. Furthermore, T2 may be more sensitive to edema than T1 in AMI,
particularly in the presence of MVO and hemorrhage.Background
Ischemia-reperfusion injury (IRI) is an undesirable sequela
following successful reperfusion in acute myocardial infarction (AMI). The
lethal form of IRI can result in aggravated edema, microvascular obstruction
(MVO) and injury and myocardial hemorrhage (1). Hemorrhage in
association with MVO is also considered to be independent predictor of adverse
outcomes (2). In this respect, T1
and T2 relaxation parameters have been instrumental in quantitatively
characterising both edema and hemorrhage in AMI (3–5). It is well known that
T2 is affected by counteracting influences from edema and hemorrhage, when simultaneously
present in the tissue, resulting in an underestimation of edematous content.
However this confounding effect has been neglected when evaluating the
performance of T1 mapping techniques; this could be an important consideration
when evaluating clinical outcomes.
Purpose
The
objective of our study was to access and compare the impact of MVO and
hemorrhage on the sensitivity of T1 and T2 relaxation parameters in the
quantification of infarct zone edema following AMI.
Methods
18
patients with ST-segment elevation myocardial infarction (STEMI) underwent a MRI
exam on a 1.5T scanner (GE MR450w) at 48 hrs post
percutaneous-coronary-intervention (PCI). T2 was quantified using a previously
validated cardiac-gated free-breathing T2-prepared spiral imaging sequence:
TE=2.9-184ms, 12 spiral interleaves, 4096 points (16.4 ms duration) (6). T1 was quantified using a
Modified Look-Locker Inversion recovery (MOLLI) sequence acquired with two
inversion schedules in a 3-5 pattern with 3 pausing heart-beats resulting in 8
images in 11 heart-beats. T2* was utilized as a reference for the
identification of hemorrhage; the sequence was a multi-echo gradient-echo acquisition with 8 echos, TE=1.4-12.7ms and TR=14.6
ms. Finally, gadolinium-DTPA (Magnevist, 0.2 mmol/kg) was administered to
identify regions of MVO and infarction with early- and late gadolinium
enhancement (EGE, LGE) imaging initiated at 1 min and 8 min post injection,
respectively. Patients were divided into two groups: a) with MVO (MVO+) and b)
without MVO (MVO-). Relaxation parameters were then measured in infarcted, core
MVO and remote myocardial territories based on contrast-enhanced images.
Results
MVO
was identified on EGE and LGE images in 8 of the 18 patients (44%). In the MVO+
group, low T2* values in the MVO region (26.1±6.3 vs. 34.7±3.2 ms remote)
confirmed the presence of hemorrhage (see Fig. 1); the MVO- group was
non-hemorrhagic. T2 values were significantly higher in the infarcted tissue in
both MVO+ (55.4±6.9 vs. 37.6±1.6 ms remote) and MVO- (50.7±5.2 vs. 37.6±1.5 ms remote)
groups, indicative of edematous development. As expected, T2 in the core MVO
region was significantly depressed compared to that in the infarct zone
(44.9±6.3 ms, p=0.0004) due to interaction with hemorrhage; this value was
still higher than remote tissue (p<0.007) given the simultaneous influence
from edema (see Fig 2). Interestingly, T1 also demonstrated an identical
behaviour. T1 in the infarct zone was driven up by edema in both MVO+ (1156.4±50.8
vs. 996.8±33.7 ms remote) and MVO- (1112.2±80.6 vs. 979.6±35.8 ms remote)
groups. However, T1 in the core MVO region was significantly lower than the
infarct value (1088.1±71.2, p=0.002) as a result of hemorrhagic byproducts
while still being higher than that in remote myocardium due to an effect from edema
(see Fig. 3). Figure 4 demonstrates the effect of hemorrhage on T1 maps in a representative
patient with MVO. Overall in the MVO+ group, T2 values were 48% and 20% higher
while T1 values were 16% and 9% higher in the infarct and MVO regions,
respectively, when compared with remote values; this highlights the influence
of hemorrhage in the presence of edema.
Conclusion
T1 and T2 relaxation parameters are
sensitive to both edema and hemorrhage in clinical AMI. Similar to T2, the
capacity of T1 to detect edema is also affected by the counteracting influence from
hemorrhage. Our findings suggest that T2 may be more sensitive to edema than T1
in AMI, particularly in the presence of MVO and hemorrhage. The effects of the
underlying pathophysiology need to be carefully taken under consideration when
interpreting relaxation parameters with respect to their role in predicting clinical
outcomes and therapeutic response in AMI.
Acknowledgements
We would like to acknowledge funding support from the Ontario Research Fund, the Canadian
Institutes of Health Research and GE Healthcare.References
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