(Circulation. 2000;102:1678.)
© 2000 American Heart Association, Inc.
Basic Science Reports |
Early Assessment of Myocardial Salvage by Contrast-Enhanced Magnetic Resonance Imaging
From the Northwestern University Medical School Feinberg Cardiovascular Research Institute (H.B.H, R.J.K., M.A.P., D.S.F., R.M.J.), Departments of Medicine (R.J.K., M.A.P., R.M.J.), and Biomedical Engineering (R.M.J.), Chicago, Ill.
Correspondence to Robert M. Judd, PhD, Feinberg Cardiovascular Research Institute, Northwestern University Medical School, 303 East Chicago Ave, Tarry 12–723, Chicago, IL 60611-3008. E-mail rjudd{at}nwu.edu
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Abstract |
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Background—Myocardial salvage after acute myocardial infarction is defined clinically by early restoration of flow and long-term improvement in contractile function. We hypothesized that contrast-enhanced magnetic resonance imaging (MRI), performed early after myocardial infarction, indexes myocardial salvage. We studied the relationship between the transmural extent of hyperenhancement by contrast-enhanced MRI, restoration of flow, and recovery of function.
Methods and Results—The left anterior descending coronary artery was occluded in dogs (n=15) for either 45 minutes, 90 minutes, or permanently. Cine and contrast-enhanced MRI were performed 3 days after the procedure; cine MRI was also done 10 and 28 days after the procedure. The transmural extent of hyperenhancement and wall thickening were determined using a 60-segment model. The mean transmural extent of hyperenhancement for the 45-minute occlusion group was 22% of the 90-minute group and 18% of the permanent occlusion group (P<0.05 for both). The transmural extent of hyperenhancement on day 3 was related to future improvement in both wall thickening score and absolute wall thickening at 10 and 28 days (P<0.0001 for each). For example, of the 415 segments on day 3 that were dysfunctional and had <25% transmural hyperenhancement, 362 (87%) improved by day 28. Conversely, no segments (0 of 9) with 100% hyperenhancement improved. The transmural extent of hyperenhancement on day 3 was a better predictor of improvement in contractile function than occlusion time (P<0.0001).
Conclusions—A reduction in the transmural extent of hyperenhancement by contrast-enhanced MRI early after myocardial infarction is associated with an early restoration of flow and future improvement in contractile function.
Key Words: magnetic resonance imaging • contrast media • myocardial infarction • salvage therapy
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Myocardial salvage is the hallmark of successful reperfusion therapy. The assessment of myocardial salvage is important clinically because significant salvage results in the long-term reestablishment of myocardial contractile function and is associated with improved prognosis and outcome.1 2 3 4 5 6
Ventricular wall motion at rest cannot be used to quantify myocardial salvage early after myocardial infarction because both necrotic and stunned myocardium will have impaired contractile function.7 8 9 Wall motion during exercise or pharmacological stress may be used to distinguish between infarcted and stunned myocardium,10 but this approach can be problematic if residual stenosis is present in the infarct-related artery.11 It would be advantageous to index myocardial salvage within regions exhibiting acute contractile dysfunction.
In previous studies, we found that contrast-enhanced magnetic resonance imaging (ce-MRI) can distinguish between reversible and irreversible ischemic injury within the region at risk,12 independent of wall motion.13 Specifically, we found that nonviable myocardium was hyperenhanced, whereas viable myocardium was not. Because irreversible ischemic injury begins in the subendocardium and progresses as a "wavefront" of necrosis moving toward the epicardium,14 we hypothesized that the transmural extent of hyperenhancement can be used to index myocardial salvage early after infarction.
In this study, we produced a full range of salvage and necrosis by subjecting animals to 45 minutes, 90 minutes, and permanent coronary artery occlusion.1 We tested the hypothesis that ce-MRI can index myocardial salvage by relating the transmural extent of hyperenhancement observed early after injury to early restoration of flow and future improvement in contractile function.
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Methods |
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Experimental Preparation
A total of 15 purpose-bred dogs weighing 20 kg were studied. The care and treatment of all animals was in accordance with the Position of the American Heart Association on Research Animal Use, which was adopted November 15, 1984. The animals were premedicated with 1 mL of intramuscular Innovar-Vet (0.4 mg/mL fentanyl and 20 mg/mL droperidol) followed by 11 mg/kg IV Brevital (methohexital); they were then intubated and ventilated with gas anesthesia (isoflurane and nitrous oxide). Using a sterile technique, a lateral thoracotomy was performed at the fourth left intercostal space to expose the heart, and the pericardium was opened. The proximal left anterior descending coronary artery was carefully dissected distal to the first major diagonal. In groups 1 (n=5) and 2 (n=5), the artery was occluded for 45 and 90 minutes, respectively, using a removable soft occluder, and then reperfusion was restored. In group 3 (n=5), the artery was permanently occluded with a snare ligature. The chest was then sutured closed and the animals were allowed to recover.
MRI and Experimental Protocol
All animals were studied 3 days after the procedure by cine and
ce-MRI; cine MRI studies were also performed 10 and 28 days after the
procedure. MRI was performed using a 1.5 Tesla clinical scanner
(Siemens Sonata) using a flexible radiofrequency receiver coil.
Each study day, the animals were tranquilized with 1 mL of
Innovar and transported to the MRI facility. There, they
were anesthetized with methohexital (11 mg/kg IV), intubated,
ventilated under gas anesthesia (isoflurane), and placed in
the right lateral decubitus position in the scanner.
MRI
MRIs were ECG-gated, and all images, which were prescribed as
short-axis views of the heart, were acquired during repeated
breathholds. Both cine and ce-MRIs were prescribed every 5 mm from
base to apex (12 to 15 cine short-axis views and 12 to 15 corresponding
contrast-enhanced views per heart). Cine-MRI was performed using a
retrogated true-FISP (fast imaging with steady-state precession)
sequence, which yielded 32 image frames throughout one RR cycle, with a
heart rate–dependent temporal resolution of between 20 and 30 ms. All
cine images were acquired before the administration of the contrast
agent. Typical imaging parameters were the following:
repetition time, 3.0 ms; echo time, 1.5 ms; flip angle, 50°; in-plane
resolution, 1x1 mm; slice thickness, 5 mm. Ce-MRI was
performed 
20 minutes after the intravenous
administration of 0.3 mmol/kg Gd-HP-D03A (Prohance,
Bracco Pharmaceuticals). T1-weighting was achieved using a segmented
inversion-recovery fast low-angle shot (IR-FLASH) pulse sequence, which
has been described in detail elsewhere.15 Typical
parameters were as follows: repetition time, 8 ms; echo
time, 4 ms; in-plane resolution, 1x1 mm; slice thickness, 5
mm; "typical inversion delay," 250 ms; and k-space data segmented
over 4 cardiac cycles (23 lines/cycle) with data acquired every other
cardiac cycle. Ce-MR images were ECG-gated to
end-diastole.
Data Analysis
Image Registration
Figure 1
summarizes the
registration procedure. On the basis of the 12 to 15 short-axis cine
views taken at 3 days, a single view was chosen in which the papillary
muscles were most prominent (Figure 1). The angle required to
rotate this view such that the anterior insertion of the right
ventricle was located at 12 o’clock was recorded. Next, every
other view (10 mm apart) moving apically from this view and distal
to the occlusion site was selected for further analysis. This
yielded 5 short-axis views per animal distal to the site of
occlusion. One additional view at the base of the heart was located
proximal to the occlusion and was excluded from the analysis.
Each of these 5 cine views located distal to the site of occlusion and
the corresponding contrast-enhanced views were rotated by the
prerecorded angle. For each pair of cine and ce-MRI views, the
center point of the heart was defined, and the myocardium
was divided into 12 circumferential segments; this nominally yielded 60
segments per animal (12 segments/view x 5 views).
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Registration of the cine views on days 10 and 28 with the views from day 3 was accomplished by a choice from the total of 12 to 15 views by a consensus of 3 observers using anatomical landmarks. The views at 10 and 28 days were rotated using the same procedure as that at 3 days. Using this approach, the registration between cine and contrast-enhanced views at 3 days would be precise because both were acquired in the same imaging session and that between cine images at 3 days and cine images at 10 and 28 days would be within 50% of the 5-mm slice thickness and 5-mm interslice separation.
Delayed MRI Contrast Enhancement
Ce-MRIs acquired at 3 days were analyzed by defining
hyperenhancement as >3 SD above remote. On the basis of this
definition, binary images were produced in which regions with image
intensities >3 SD were white (hyperenhanced) and regions with image
intensities 
3 SD were black (non-hyperenhanced). Within each
segment, the hyperenhanced area (HEA) and normal enhanced area (NEA)
were outlined by hand in magnified views. The transmural extent of
hyperenhancement within each segment was calculated as a percentage of
the total segment area: HEA(%)=(HEAx 100)/(HEA+NEA). For each study
group, the mean transmural extent of hyperenhancement was calculated by
averaging the HEA for all dysfunctional segments at 3 days.
Wall Thickening
Wall thickening was analyzed qualitatively and
quantitatively. For both analyses, cine MR images on days 3,
10, and 28 were randomized and presented to observers who were
blinded to animal group and the ce-MRI results. For the qualitative
analysis, each myocardial segment was scored independently by 2
observers using the following system: 0, normal thickening; 1, mild to
moderate hypokinesis; 2, severe hypokinesis; and 3, akinesis or
dyskinesis. Wall thickening was first scored by the observers
individually and then by consensus to resolve cases of disagreement.
Remaining discrepancies were resolved by a third observer who was also
blinded to animal group and the ce-MRI results. For dysfunctional
segments on day 3, improvement was defined as normal thickening or a
reduction in score of 
2 levels by days 10 and 28. For the
quantitative analysis, wall thickening was determined by the
modified centerline method and expressed as a percent of
end-diastolic wall thickness. For this analysis,
dysfunction at 3 days was defined as any segment with wall thickening
<2 SD below the mean of wall thickening in segments in the half of the
heart opposite the wall motion abnormality.
Statistical Analysis
Continuous data are expressed as mean±SEM. Between-group
comparisons in continuous data were made using ANOVA. The
2 test for trend was used to assess the
relationship between segmental hyperenhancement on day 3 and follow-up
wall thickening. The data were also analyzed using a linear
mixed effects model with a separate parameter for "dog"
to eliminate the problem of nonindependence of segments.
Receiver-operating characteristic (ROC) curves were generated for the
prediction of wall thickening improvement based on day 3
hyperenhancement and occlusion time according to the method described
by Metz.16 ROC curves were compared using the CORROC2
program of Metz. The Bonferroni method was used when making multiple
between-group comparisons. All statistical tests were 2-tailed;
P<0.05 was regarded as statistically significant.
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Results |
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A total of 75 short-axis views (5 levels x 15 animals) were analyzed for contrast enhancement at 3 days and wall thickening at 3 days, 10 days, and 28 days. Four of the 75 short-axis views were excluded by the observers because they were located too apical to allow for accurate wall thickness determination (2 views in group 1 and 1 view in groups 2 and 3), thus yielding a total of 71 views (x12 circumferential segments) and 852 segments.
Transmural Extent of Hyperenhancement
Figure 2 shows one
representative contrast-enhanced short-axis view from
each of the 15 dogs on day 3. Hyperenhanced regions were small and
subendocardial in the 45-minute occlusion group. After 90 minutes of
occlusion, hyperenhanced regions were larger and comprised 50% of
wall thickness. Hyperenhanced regions were even larger in animals with
permanent occlusion and, in 3 of the 5 animals, the hyperenhanced
region extended to the epicardial border. The mean transmural extent of
hyperenhancement for the 45-minute group was 22% of the 90-minute
group and 18% of the permanent occlusion group
(P<0.05 for both; Figure 3).
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Relationship Between the Transmural Extent of Hyperenhancement on
Day 3 and Recovery of Function
A total of 201 of the 852 segments (24%) were hyperenhanced. For
the qualitative analysis, 567 of the 852 segments (67%) were
dysfunctional on day 3. By day 10, contractile function had improved in
347 segments (61%) and by day 28, contractile function had improved in
440 (78%). For the quantitative analysis, dysfunction at 3
days was defined as wall thickening <12±4% (<2 SD below remote; see
Methods). Using this criterion, 357 of the 852 segments (42%) were
dysfunctional on day 3. Whether they improved is reflected by absolute
wall thickening in these same segments at 10 and 28 days.
Figure 4 shows 3 examples of how the
contrast enhancement observed on day 3 predicted long-term improvement.
Each row in the figure shows a different dog, with contrast enhancement
in the first column and the corresponding end-diastolic and
end-systolic still frames on days 3 and 28 in the remaining
four columns. For all 3 dogs, a severe impairment in wall thickening
was observed in the cine images at day 3. Contrast enhancement on day
3, however, reveals essentially transmural hyperenhancement in the
first dog, hyperenhancement extending to 50% of wall thickness in
the second dog, and no hyperenhancement in the third dog. On day 28,
wall thickening minimally improved in the first dog, partially improved
in the second dog, and significantly improved in the third dog.
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Figure 5A shows the percentage of
improved segments by days 10 and 28 on the basis of qualitative wall
thickening as a function of the transmural extent of hyperenhancement
on day 3. The percentage of improved segments decreased with increasing
transmural extent of hyperenhancement at both 10 and 28 days
(P<0.0001 for both). For instance, 321 of 368 segments
(87%) without any hyperenhancement and 362 of 415 segments (87%) with
<25% transmural extent of hyperenhancement on day 3 improved by day
28. Conversely, only 2 of 17 segments (12%) with 76% to 100%
hyperenhancement and 0 of 9 segments (0%) with 100% hyperenhancement
improved. Concordance between the 2 observers for improvement in
contractile function was 83% from 3 days to 10 days and 88% from 3
days to 28 days.
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Figure 5B
shows quantitative wall thickening at 3, 10, and 28
days for the 357 dysfunctional segments at 3 days. Wall thickening at 3
days was <10% on average for all categories of hyperenhancement. By
10 and 28 days, however, segments with little or no hyperenhancement
improved wall thickening to >30%. Conversely, segments with
increasingly large regions of hyperenhancement showed significantly
less improvement by 10 and 28 days (P<0.0001 for both).
Analysis of the wall thickening data by dog as opposed to by
segment revealed a similarly strong dependence on the transmural extent
of hyperenhancement (P<0.0001).
Predictive Value of Hyperenhancement Compared With Occlusion
Time
Figure 6 shows ROC curves for the
prediction of wall-thickening improvement by day 28 as a function of
both occlusion time and transmural extent of hyperenhancement on day 3.
Ce-MRI was a stronger predictor of wall thickening improvement than was
occlusion time (P<0.0001).
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Discussion |
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The data from this study demonstrate that the transmural extent of hyperenhancement by ce-MRI performed early after infarction is inversely related to the early restoration of flow and future improvement in contractile function. The relationships between ce-MRI and these clinical indices of myocardial salvage have not been previously shown.
Study Limitations
The extent to which the data from this article relate to the
clinical setting in humans is unknown. The contrast dosage used in the
present study (0.3 mmol/kg) is higher than that used
clinically (0.1 to 0.2 mmol/kg), and the images were acquired
20 minutes after contrast to improve the distinction between
subendocardial hyperenhancement and blood in the left
ventricular cavity. In addition, the extent to which
partial volume effects may have caused the spatial extent of
hyperenhancement to appear greater than true infarct size was not
evaluated.
Hyperenhancement and Occlusion Time
In previous studies, we found that delayed hyperenhancement by
ce-MRI was exclusively associated with irreversible ischemic
injury, as defined histologically.12 13
Assuming that hyperenhancement indicates infarction, the increase in
the transmural extent of hyperenhancement with increasing duration of
coronary occlusion observed in the current study (Figure 3) could be explained by the "wavefront phenomenon" of
infarct progression beginning in the endocardium and growing toward the
epicardium.14
Interestingly, however, considerable animal-to-animal variations in the
transmural extent of hyperenhancement were also observed, even for
those with identical occlusion times (Figure 2). Again, assuming
that hyperenhancement indicates infarction, these animal-to-animal
variations might be explained by additional factors that influence
infarct progression, such as the degree of collateral
flow.17 The assumption that hyperenhancement indicates
infarction would suggest that the transmural extent of hyperenhancement
would be a better predictor than occlusion time of future improvement
in contractile function because it would represent a direct
measure of the transmural extent of necrosis. The ROC curves shown in
Figure 6 demonstrate that hyperenhancement was indeed a better
predictor than occlusion time of future improvement in contractile
function.
Hyperenhancement and Recovery of Function
We found that segments for which the transmural extent of
hyperenhancement at 3 days was >75% were unlikely to exhibit improved
wall thickening at 10 and 28 days (Figure 5). This finding would
be expected on the basis of the interpretation that hyperenhancement
indicates myocardial infarction.
Conversely, 87% of segments for which the transmural extent of
hyperenhancement was <25% at 3 days exhibited improved thickening by
28 days (Figure 5). This finding could be explained on the basis
of the data from our previous article, in which we found that
hyperenhancement did not occur in regions subjected to severe but
reversible ischemic injury, despite a persistent wall motion
abnormality.13 The lack of hyperenhancement after the
severe but reversible injury observed in our previous
study,13 combined with our current finding that these
regions eventually recover contractile function (Figure 5),
strongly suggests that dysfunctional regions without hyperenhancement
observed in the setting of acute ischemic injury
represent stunned myocardium.
In addition to regions with nearly transmural hyperenhancement
(>75%) and nearly absent hyperenhancement (<25%), however, a
significant number of segments exhibited a transmural extent of
hyperenhancement between 25% and 75% and were associated with
intermediate likelihoods for contractile improvement (Figure 5).
The presence of these segments underscores the fact that segmental
viability defined by contrast MRI is not an "all-or-none"
phenomenon; instead, the intrinsically high spatial resolution of the
technique seems to allow direct visualization of the transmural extent
of infarction and of residual viable tissue.
Our finding that 87% of segments with <25% hyperenhancement
improved raises the question as to why the remaining 13% did not
improve. It has been shown that wall motion recovery after myocardial
infarction may last for several weeks or even months.18
Thus, improvement in additional segments may have been found if the
animals had been imaged beyond 28 days. At the other end of the
hyperenhancement range, we found that 2 of 17 segments (12%) with 76%
to 100% hyperenhancement improved by day 28 (Figure 5). When
these segments were reexamined, we found that they did indeed exhibit
wall thickening but that these segments were located exactly at the
border between hyperenhanced and non-hyperenhanced
myocardium. One possible explanation for this finding would
be tethering7 19 between actively contracting regions and
scar. Another possible explanation relates to infarct shrinkage. In a
previous study, we found that the spatial extent of hyperenhancement
decreased between 3 days and 8 weeks as the acutely necrotic zone was
replaced by collagenous scar.13 Infarct shrinkage may have
caused misregistration of contrast-enhanced segments at 3 days and cine
segments at 28 days for regions at the infarct border.
Mechanism of Hyperenhancement
The mechanism responsible for the hyperenhancement of acutely
necrotic myocardium has not been established.
Gadolinium-DTPA and Gd-HP-DO3A, with molecular weights of 800
daltons, are thought to be biologically inert and to passively diffuse
throughout the extracellular space. Loss of sarcomere membrane
integrity after acute cellular injury may allow the Gd chelate to enter
the intracellular space, thereby increasing the myocardial
concentration of Gd and resulting in hyperenhancement.
Clinical Implications
The data from the current study indicate that ce-MRI can be used
to index myocardial salvage acutely within regions of contractile
dysfunction. In addition, the technique does not require exercise or
pharmacological stress testing, which may be of practical utility in
the acute setting. Of potentially greater importance, however, is the
observation that ce-MRI can be used to directly visualize nontransmural
infarction, which is not possible using any other existing technique.
Further investigation will be required to determine whether this
physiological information is of additional clinical
importance.
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Acknowledgments |
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This work was supported by NIH-NHLBI grants R29-HL53411 and R01-HL63268 (R.M.J.). The authors thank Francis J. Klocke, MD, for helpful discussions and Kathleen R. Harris, BS, for guidance concerning the surgical preparation.
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Footnotes |
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An animated version of Figure 4
can be found at http://www.circulationaha.org This article originally appeared Online on August 31, 2000.
Received July 28, 2000; revision received August 18, 2000; accepted August 18, 2000.
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H. P. Kuhl, T. S. Papavasiliu, A. M. Beek, M. B. M. Hofman, N. S. Heusen, and A. C. van Rossum Myocardial Viability: Rapid Assessment with Delayed Contrast-enhanced MR Imaging with Three-dimensional Inversion-Recovery Prepared Pulse Sequence Radiology, February 1, 2004; 230(2): 576 - 582. [Abstract] [Full Text] [PDF]
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 L. Van Hoe and M. Vanderheyden Ischemic Cardiomyopathy: Value of Different MRI Techniques for Prediction of Functional Recovery After Revascularization Am. J. Roentgenol., January 1, 2004; 182(1): 95 - 100. [Abstract] [Full Text] [PDF]
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A. M. Beek, H. P. Kuhl, O. Bondarenko, J. W. R. Twisk, M. B. M. Hofman, W. G. van Dockum, C. A. Visser, and A. C. van Rossum Delayed contrast-enhanced magnetic resonance imaging for the prediction of regional functional improvement after acute myocardial infarction J. Am. Coll. Cardiol., September 3, 2003; 42(5): 895 - 901. [Abstract] [Full Text] [PDF]
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P. R. Knuesel, D. Nanz, C. Wyss, M. Buechi, P. A. Kaufmann, G. K. von Schulthess, T. F. Luscher, and J. Schwitter Characterization of Dysfunctional Myocardium by Positron Emission Tomography and Magnetic Resonance: Relation to Functional Outcome After Revascularization Circulation, September 2, 2003; 108(9): 1095 - 1100. [Abstract] [Full Text] [PDF]
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H. Mahrholdt, A. Wagner, M. Parker, M. Regenfus, D. S. Fieno, R. O. Bonow, R. J. Kim, and R. M. Judd Relationship of contractile function to transmural extent of infarction in patients with chronic coronary artery disease J. Am. Coll. Cardiol., August 6, 2003; 42(3): 505 - 512. [Abstract] [Full Text] [PDF]
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J. Schulz-Menger, M. Gross, D. Messroghli, F. Uhlich, R. Dietz, and M. G. Friedrich Cardiovascular magnetic resonance ofacute myocardial infarction at a very early stage J. Am. Coll. Cardiol., August 6, 2003; 42(3): 513 - 518. [Abstract] [Full Text] [PDF]
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H. P. Kuhl, A. M. Beek, A. P. van der Weerdt, M. B. M. Hofman, C. A. Visser, A. A. Lammertsma, N. Heussen, F. C. Visser, and A. C. van Rossum Myocardial viability inchronic ischemic heart disease: Comparison of contrast-enhanced magnetic resonance imaging with 18F-fluorodeoxyglucose positron emission tomography J. Am. Coll. Cardiol., April 16, 2003; 41(8): 1341 - 1348. [Abstract] [Full Text] [PDF]
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K. Kitagawa, H. Sakuma, T. Hirano, S. Okamoto, K. Makino, and K. Takeda Acute Myocardial Infarction: Myocardial Viability Assessment in Patients Early Thereafter--Comparison of Contrast-enhanced MR Imaging with Resting 201Tl SPECT Radiology, January 1, 2003; 226(1): 138 - 144. [Abstract] [Full Text] [PDF]
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E. C. Perin, G. V. Silva, R. Sarmento-Leite, A. L.S. Sousa, M. Howell, R. Muthupillai, B. Lambert, W. K. Vaughn, and S. D. Flamm Assessing Myocardial Viability and Infarct Transmurality With Left Ventricular Electromechanical Mapping in Patients With Stable Coronary Artery Disease: Validation by Delayed-Enhancement Magnetic Resonance Imaging Circulation, August 20, 2002; 106(8): 957 - 961. [Abstract] [Full Text] [PDF]
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J.o. Barkhausen, W. Ebert, J.o. F. Debatin, and H.-J. Weinmann Imaging of myocardial infarction: comparison of magnevist and gadophrin-3 in rabbits J. Am. Coll. Cardiol., April 17, 2002; 39(8): 1392 - 1398. [Abstract] [Full Text] [PDF]
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B. L. Gerber, C. E. Rochitte, D. A. Bluemke, J. A. Melin, P. Crosille, L. C. Becker, and J. A.C. Lima Relation Between Gd-DTPA Contrast Enhancement and Regional Inotropic Response in the Periphery and Center of Myocardial Infarction Circulation, August 28, 2001; 104(9): 998 - 1004. [Abstract] [Full Text] [PDF]
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J C Nilsson, G Nielsen, B A Groenning, T Fritz-Hansen, L Sondergaard, G B Jensen, and H B W Larsson Sustained postinfarction myocardial oedema in humans visualised by magnetic resonance imaging Heart, June 1, 2001; 85(6): 639 - 642. [Abstract] [Full Text]
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 G. A. Beller Noninvasive Assessment of Myocardial Viability N. Engl. J. Med., November 16, 2000; 343(20): 1487 - 1490. [Full Text]
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K. M. Choi, R. J. Kim, G. Gubernikoff, J. D. Vargas, M. Parker, and R. M. Judd Transmural Extent of Acute Myocardial Infarction Predicts Long-Term Improvement in Contractile Function Circulation, September 4, 2001; 104(10): 1101 - 1107. [Abstract] [Full Text] [PDF]
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