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(Circulation. 1999;100:1992-2002.)
© 1999 American Heart Association, Inc.
Basic Science Reports |
Relationship of MRI Delayed Contrast Enhancement to Irreversible Injury, Infarct Age, and Contractile Function
From Northwestern University Medical School Feinberg Cardiovascular Research Institute (R.J.K., D.S.F., T.B.P., K.H., E.-L.C., J.P.F., F.J.K., R.M.J.), Departments of Medicine (R.J.K., F.J.K.), Radiology (T.B.P., J.P.F.), and Biomedical Engineering (D.S.F., F.J.K., R.M.J.), and Siemens Medical Systems (O.S., J.B.), Chicago, Ill.
Correspondence to Robert M. Judd, PhD, Feinberg Cardiovascular Research Institute, Northwestern University Medical School, 303 E 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—Contrast MRI enhancement patterns in several pathophysiologies resulting from ischemic myocardial injury are controversial or have not been investigated. We compared contrast enhancement in acute infarction (AI), after severe but reversible ischemic injury (RII), and in chronic infarction.
Methods and Results—In dogs, a large coronary artery was occluded to study AI and/or chronic infarction (n=18), and a second coronary artery was chronically instrumented with a reversible hydraulic occluder and Doppler flowmeter to study RII (n=8). At 3 days after surgery, cine MRI revealed reduced wall thickening in AI (5±6% versus 33±6% in normal, P<0.001). In RII, wall thickening before, during, and after inflation of the occluder for 15 minutes was 35±5%, 1±8%, and 21±10% and Doppler flow was 19.8±5.3, 0.2±0.5, and 56.3±17.7 (peak hyperemia) cm/s, respectively, confirming occlusion, transient ischemia, and reperfusion. Gd-DTPA–enhanced MR images acquired 30 minutes after contrast revealed hyperenhancement of AI (294±96% of normal, P<0.001) but not of RII (98±6% of normal, P=NS). Eight weeks later, the chronically infarcted region again hyperenhanced (253±54% of normal, n=8, P<0.001). High-resolution (0.5x0.5x0.5 mm) ex vivo MRI demonstrated that the spatial extent of hyperenhancement was the same as the spatial extent of myocyte necrosis with and without reperfusion at 1 day (R=0.99, P<0.001) and 3 days (R=0.99, P<0.001) and collagenous scar at 8 weeks (R=0.97, P<0.001).
Conclusions—In the pathophysiologies investigated, contrast MRI distinguishes between reversible and irreversible ischemic injury independent of wall motion and infarct age.
Key Words: magnetic resonance imaging • myocardial infarction • ischemia
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Introduction |
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The extent and degree of myocardial injury after an acute ischemic event are strong predictors of patient outcome, and interventions that reduce injury significantly improve prognosis.1 MRI contrast enhancement observed early (tens of seconds) after contrast is affected by large-artery patency2 3 and microvascular obstruction4 5 and is thought to relate to perfusion. Delayed enhancement patterns, defined as those appearing more than a few minutes after contrast (eg, >5 minutes), may reflect different physiological information. After acute infarction, hyperenhancement is observed both with4 5 6 7 8 9 10 11 12 and without11 12 13 14 15 reperfusion and predicts prognosis over the next 2 years.16
The role of contrast-enhanced MRI in evaluating pathophysiologies other than acute infarction is not well established. For example, it is unknown whether delayed hyperenhancement occurs in dysfunctional but viable myocardium or whether hyperenhancement occurs in reversibly injured regions surrounding acute infarcts. Furthermore, there are conflicting reports concerning the utility of contrast MRI after infarct healing. In this study, we examined delayed contrast enhancement and wall motion after severe but reversible ischemic injury, acute infarction with and without reperfusion, and chronic infarction in chronically instrumented dogs.
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Methods |
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Experimental Preparation
The care and treatment of the eighteen 25- to 30-kg mongrel dogs was in accordance with the "Position of the American Heart Association on Research Animal Use." Animals were premedicated with 1 mL Innovar-Vet IM (0.4 mg/mL fentanyl and 20 mg/mL droperidol) followed by 11 mg/kg brevital IV. The animals were then intubated and ventilated with gas anesthesia (halothane). In 8 dogs, the left circumflex (LCx) coronary artery was instrumented with a hydraulic occluder and a 20-MHz Doppler flowmeter for the study of transient ischemia, and the LAD and/or diagonal(s) were permanently ligated to produce infarction (see Figure 1
). In all other dogs, a single
coronary artery (LAD or LCx) either was permanently ligated to
study nonreperfused infarction (n=6) or was transiently occluded for 90
minutes to study reperfused infarction (n=4).
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MRI and Experimental Protocol
Animals were imaged by MRI at 1 day (n=3), 3 days (n=13), and 8
(7.9±0.6) weeks after surgery (n=9). Seven dogs were imaged at both 3
days and 8 weeks.
All animals were anesthetized with sodium pentobarbital 25 mg/kg IV, intubated, and studied on a clinical 1.5-T scanner (Siemens Symphony) in the right lateral decubitus position. A 14x28-cm flexible surface coil was used for imaging. ECG-gated cine MR images encompassing the entire left ventricle were acquired during repeated breath-holds (10 to 15 seconds) to examine wall motion.
In the 8 animals with the reversible occluder, at 3 days after surgery,
severe but reversible ischemic injury was produced in the
magnet by a 15-minute total occlusion.17 18 On the basis
of the cine images and knowledge of the intervention, 2 short-axis and
1 long-axis views were chosen as being likely to include the territory
distal to the occluder (see Figure 1
). Cine MR images of these
views were acquired before, during, and after occlusion.
Contrast enhancement was studied after Gd-DTPA 0.3 mmol/kg IV. The
agent was injected 30 minutes after release of the occluder, and images
were acquired 20 to 30 minutes after Gd-DTPA. T1 weighting was achieved
with an inversion-recovery fast low-angle shot (IR-FLASH) pulse
sequence. Typical parameters were TE=2 ms, TR=6 ms, voxel
size=1x1x6 mm, 300-ms inversion delay, k-space data segmented
over 4 cardiac cycles (32 lines per cycle), with data acquired every
other cardiac cycle. Images were acquired during breath-hold (
8
seconds) and were ECG-gated to end diastole.
Ex Vivo MRI and Histology
Hearts from 3 dogs euthanized at 1 day (2 reperfused, 1
nonreperfused), 4 dogs at 3 days (2 reperfused, 2 nonreperfused), and 2
dogs at 8 weeks were subjected to detailed comparison of ex vivo MRI
and necrosis defined by
triphenyltetrazolium chloride (TTC) over
the entire left ventricle. In these animals, the hearts were removed 45
to 60 minutes after Gd-DTPA and quickly rinsed in cold (4°C) saline.
To facilitate registration of the ex vivo images, 3 markers were glued
to the epicardium near the base. T1-weighted 3D gradient-echo images
were acquired with an isometric resolution of 500 µm (TR=20,
TE=3.2 ms, flip angle 70°). The hearts were then stiffened by
immersion in 95% ethanol precooled to -80°C and sectioned from base
to apex into 2-mm-thick short-axis slices with a commercial rotating
meat slicer. The cutting plane was defined by use of the 3 markers. All
slices were then stained with 2% TTC and photographed. Selected tissue
samples were processed for light microscopy (hematoxylin and eosin
and/or Masson’s trichrome).
Data Analysis
Wall Motion
Wall thickening was determined with commercial software (ARGUS,
Siemens) in 36 segments by the modified centerline
method.19
Contrast Enhancement
Image intensities after Gd-DTPA were measured in 3 regions:
normal myocardium, myocardium undergoing
transient coronary occlusion, and myocardium
subtended by permanent coronary occlusion (see Figure 1). These regions were defined on the basis of wall motion.
First, the myocardial segment with the worst contractile function was
identified in the preocclusion cine MR images. A preliminary normal
region was then defined as all segments in the half of the heart
opposite the severe contractile abnormality, and the mean±SD of wall
thickening was calculated for this territory. On the basis of these
values, the 3 regions were defined as follows: normal region 
any group of segments in which wall thickening was within 1 SD of the
mean before and during occlusion; transient occlusion region
any group of segments in which wall thickening was within 1 SD of the
mean before occlusion but fell below 2 SD of the mean during occlusion;
and permanent occlusion region any group of segments in which
wall thickening was <2 SD of the mean before coronary
occlusion.
The locations of these regions were then transferred to the
post–Gd-DTPA images, and image intensity was measured in the normal
region. An observer was then instructed to determine whether
hyperenhanced zones, defined as image intensities >2 SD above the mean
of the normal region, were present or absent within the transient
and permanent occlusion territories. If hyperenhancement was not
present, the entire region was outlined. If hyperenhancement was
present, the observer thresholded image intensities at a level
equal to 2 SD above the mean of the normal region and outlined only the
hyperenhancement region to account for nontransmural involvement (see
Figures 3 and 4).
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Ex Vivo MRI and Histology
For each of the slices stained with TTC, ex vivo images were
extracted from the 3D MRI data set. Selection of images was facilitated
by the 3 epicardial markers and the uniform slice thickness afforded by
the commercial slicer. An independent observer blinded to the MR
results analyzed the tissue slices, and a second independent
observer blinded to the tissue results analyzed the MR images
using the same procedure as described for the in vivo images.
Statistical Analysis
All results were expressed as mean±SD. Wall thickening and
image intensity values were compared by 2-factor and single-factor
repeated-measures ANOVA, respectively. Bonferroni correction was used
for multiple comparisons. All tests were 2-tailed, and a value of
P<0.05 was considered significant.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Results at 1 and 3 Days
In vivo enhancement patterns in infarcted regions were similar at 1 and 3 days. Figure 2
compares
enhancement patterns in the infarcted region with that of the region
subjected to reversible ischemic injury in 1 animal at 3 days
after surgery. Before occlusion, cine MRI revealed normal thickening in
the LCx territory but reduced thickening in the permanent
occlusion territory (3- to 5-o’clock position; LAD diagonal in this
animal). During occlusion, verified by the flowmeter (Figure 2, top), cine MRI revealed a dramatic reduction in thickening in the
distal LCx territory (6- to 9-o’clock position), confirming that this
area became ischemic. After reperfusion, wall thickening
remained moderately reduced in the transient occlusion territory.
Before administration of Gd-DTPA, image intensities in all regions were
similar (Figure 2, bottom). After Gd-DTPA, the infarct territory
became hyperenhanced, whereas the transient occlusion territory did not
become hyperenhanced compared with normal myocardium (10-
to 2-o’clock position).
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Figure 3A shows similar results in 3
additional animals. In each case, infarcted myocardium
became hyperenhanced, whereas myocardial regions after severe transient
ischemia with concomitant regional dysfunction did not
hyperenhance. Figure 3B summarizes the wall-thickening data at 3
days. In normal regions, thickening remained high before, during, and
after transient occlusion (32.8±6.2%, 37.4±5.1%, and 36.9±4.9%,
respectively; P=NS). In the permanent occlusion territory,
thickening was significantly lower than normal regions before, during,
and after occlusion (4.5±5.9%, 3.7±5.5%, and 3.5±4.9%,
respectively, P<0.001 compared with normal for all times).
In the transient occlusion territory, thickening was not different from
that of the normal region before occlusion (35.1±5.4%,
P=NS) but became significantly lower during occlusion
(1.1±8.3%, P<0.001) and remained moderately reduced after
reperfusion (20.9±10.1%, P<0.001). Doppler flow
before, during, and after occlusion was 19.8±5.3, 0.2±0.5, and
56.3±17.7 (peak hyperemia) cm/s, respectively, confirming
successful occlusion and reperfusion for all animals. Eight weeks
later, wall thickening in the transient occlusion territory returned to
baseline levels (38.7±5.4%, P=NS).
Figure 3C summarizes post–Gd-DTPA image intensities at 3 days
in the 8 animals subjected to transient occlusion and the 10 animals
subjected to permanent occlusion. Image intensities in the transient
occlusion territory were the same as those of the normal region
(98.1±5.7% of normal, P=NS). In all animals, no evidence
of irreversible injury was found in the region distal to the hydraulic
occluder at 8 weeks, confirming that the ischemic injury at 3
days was reversible. Conversely, contrast-enhanced image intensity in
the infarcted territory was much higher than in the normal region at 1
day (506±51.5% of normal, P<0.001) and 3 days
(294.4±96.1% of normal, P<0.001). In all cases,
hyperenhancement was easily detected in regions later found to reveal
histological evidence of infarction. In 2 animals, the
region distal to the permanent occlusion site did not hyperenhance
(101.0±9.0%), and histochemical staining revealed no evidence of
infarction.
Results at 8 Weeks
Figure 4, top, shows results in the
same animal at 3 days and at 8 weeks. Contrast hyperenhancement is
clearly seen after Gd-DTPA administration in both acute and chronic
infarction. The photograph of the sectioned heart shows the chronic
infarction, which correlated closely in location with the hyperenhanced
zone in the MR images. Trichrome staining revealed that the infarct was
nontransmural (see inset), and the transmural extent of the scar
observed histologically (blue region) appeared to
correspond to the transmural extent of the hyperenhanced region in the
8-week MR image. At higher magnification, the trichrome stain revealed
that the chronic infarction was a dense collagen matrix.
Figure 4, bottom, summarizes the change in myocardial volume
(cm3) from 3 days to 8 weeks for both the
hyperenhanced and nonhyperenhanced regions based on images encompassing
the entire left ventricle. Of the 7 dogs imaged at both 3 days and 8
weeks, 2 had no infarction. The absolute volume of the hyperenhanced
regions in the remaining 5 dogs decreased by a factor of 3.4±1.4 at 8
weeks compared with 3 days. In all 7 dogs, the absolute volume of the
nonhyperenhanced regions increased (1.2±0.2-fold increase).
Ex Vivo MRI and Histology
Figure 5 compares ex vivo MR images
with slices stained with TTC in an animal with a nonreperfused infarct
euthanized at 3 days. The location, spatial extent, and 3D shape of the
regions of elevated MR image intensity were essentially identical to
those of the irreversibly injured regions defined by TTC. Similar
results were found in 3-day-old reperfused infarcts. Figure 6 shows similar results at 1 day for both
nonreperfused and reperfused infarcts. Figure 7 shows the corresponding results in an
animal euthanized at 8 weeks. Despite replacement of the infarct
territory with a collagenous scar (verified by light microscopy, see
also Figure 4), the regions of elevated MR image intensity were
again essentially identical to the irreversibly injured regions defined
by TTC. Figure 8 summarizes the results.
The regressions were y=1.02x+0.28
(R=0.99, SEE=1.97, P<0.001) at 1 day,
y=1.01x+0.59 (R=0.99, SEE=2.4,
P<0.001) at 3 days, and y=1.03x-0.14
(R=0.97, SEE=0.76, P<0.001) at 8 weeks.
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Figure 9 demonstrates the partial-volume
effect. Sixteen consecutive images 500 µm thick were extracted
from the 3D MR data set at the location shown in panel A. Hyperenhanced
regions had sharp, distinct borders that migrated significantly from
slice to slice. Summation of all 16 images resulted in the image in
panel B, which has an effective thickness of 8 mm. Intermediate
image intensities are introduced along the periphery of the
hyperenhancement zone (arrows) due to partial-volume effects and the
complex 3D shape of the infarct.
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Discussion |
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We found that both acute and chronic myocardial infarcts hyperenhance. Myocardial injury without necrosis due to severe, transient ischemia did not lead to hyperenhancement despite the presence of myocardial stunning. The spatial extent of hyperenhancement matched the spatial extent of myocyte necrosis at 1 and 3 days with and without reperfusion and collagenous scar at 8 weeks.
Acute Infarction
Our data are in agreement with previous studies demonstrating that
hyperenhancement occurs in both reperfused4 5 6 7 9 10 11 12 and
nonreperfused11 12 13 14 15 acute infarcts. However, some reports
suggest that hyperenhancement occurs not only in regions of cellular
necrosis but also in a border zone of injured but viable myocytes
surrounding the acute infarct,7 14 20 21 particularly in
the first 24 hours. Partial-volume effects may also play a role in the
overestimation of infarct size.22 23
The mechanism responsible for hyperenhancement of acutely necrotic
myocardium is not clear. Gd-DTPA, with a molecular weight
of 800 Da, is thought to be biologically inert and to passively
diffuse throughout the extracellular space.24 Other
markers of similar molecular weight increase their volume of
distribution significantly after myocyte death due to loss of sarcomere
membrane integrity.25 26 In a previous study of MRI
contrast enhancement mechanisms,23 we reported that
regions of hyperenhancement systematically revealed sarcomere membrane
rupture examined by electron microscopy. The data also revealed marked
changes in Gd-DTPA wash-in and washout kinetics within the infarct zone
compared with normal myocardium. Sarcolemmal rupture, in
itself, could affect myocardial Gd-DTPA kinetics, because additional
time may be required for contrast molecules to diffuse in and out of
isolated breaks in the cellular membrane. Accordingly, it is possible
that a physiological event specific for myocyte
death, such as myocyte membrane rupture, may relate to the strong
correlation between hyperenhancement and acute cellular necrosis.
Chronic Infarction
Contrast enhancement patterns after infarct healing have received
less attention than acute infarction. For images acquired more than a
few minutes after contrast, some reports suggest that chronic infarcts
appear hyperenhanced,27 28 but others do
not.29 30 31 Our data establish that delayed
hyperenhancement occurs in nonreperfused myocardial scar. The mechanism
responsible for hyperenhancement of healed infarcts is unknown.
Reversible Ischemic Injury
Whether or not hyperenhancement occurs in injured but viable
myocardial regions is controversial. One way to address this question
is to examine myocardium subjected to severe but reversible
ischemic injury by occluding a canine coronary artery
for 15 minutes.17 18 McNamara et al6
evaluated myocardial contrast enhancement in dogs that underwent 15
minutes of LAD occlusion followed by 24 hours of reperfusion. In
agreement with our findings, ex vivo MRI did not show hyperenhancement
of the LAD territory.
A related question is whether hyperenhancement occurs in reversibly injured myocardium surrounding regions of myocyte necrosis, particularly in the first week after infarction.14 21 Schaefer et al7 reported that in the first few hours after infarction, regions of hyperenhancement overestimated infarct size when the contrast agent was injected 5 minutes after reperfusion. Previous studies by our group and others suggest that the spatial extent of hyperenhancement may be similar to that of acute myocyte necrosis.5 22 23 Few other studies have directly addressed this issue.
This issue, however, is critical to the interpretation of many MRI
observations. In the present study, for example, we found that the
absolute volume of hyperenhanced myocardium decreased by a
factor of 3.4 between 3 days and 8 weeks (Figure 4). One
interpretation of this is that hyperenhancement includes both acutely
necrotic regions and surrounding reversibly injured regions at 3 days
but that by 8 weeks, the reversibly injured regions have recovered and
no longer hyperenhance. Our finding that the spatial extent of
hyperenhancement was identical to the spatial extent of myocyte
necrosis at 3 days (Figures 5 and 8), however,
contradicts this interpretation. Another interpretation of the data of
Figure 4 is that the spatial extent of collagenous scar at 8
weeks was 3.4 times smaller than the spatial extent of acute myocyte
necrosis at 3 days. Reimer and Jennings report that infarcts shrink
4-fold between 4 days and 6 weeks.32 33 Accordingly,
the data of the lower left panel of Figure 4 could be explained
by infarct shrinkage during the transition from myocyte necrosis to
collagenous scar. Extending this concept, the data of the lower right
panel of Figure 4 might be explained by compensatory
hypertrophy.
Our results also suggest that partial-volume effects should be
considered in the interpretation of contrast-enhanced MRI (Figure 9). Whether or not partial-volume effects influenced the results
of previous studies is unknown.
On the basis of our findings that hyperenhancement does not occur in
purely reversibly injured regions (Figure 3), that the spatial
extent of hyperenhancement is identical to that of acute myocyte
necrosis and scar (Figure 8), and that the temporal changes in
the spatial extent of hyperenhancement (Figure 4) can be
explained by infarct shrinkage,32 33 we conclude that
hyperenhancement does not occur in reversibly injured regions in the
pathophysiologies investigated. Our data do not exclude the possibility
of enhancement of a peripheral region surrounding the
infarction that resolves by 24 hours.
Clinical Implications
Identification of the spatial extent of viable
myocardium is of established clinical importance. Several
investigators have reported MRI approaches to identifying viable
myocardium, such as wall thickness and
dobutamine challenge. Our data suggest a different
approach. In the pathophysiologies investigated, the size and shape of
regions exhibiting delayed hyperenhancement are identical to regions of
irreversible injury. Accordingly, regions that fail to hyperenhance are
viable. This finding implies that it is not necessary to consider wall
motion in the MRI definition of viability. In fact, the data in Figures 2 and 3 underscore that wall thickening by cine MRI and
viability by contrast MRI are dissociated. This dissociation, combined
with the ability of contrast MRI to clearly distinguish the transmural
extent of acute myocyte necrosis and collagenous scar, suggests that
MRI may play an important clinical role in the evaluation of
ischemic heart disease. Specifically, our results suggest that
contrast MRI in combination with cine MRI might be used in the acute
setting to distinguish between acute myocardial infarction
(hyperenhanced and with contractile dysfunction), injured but viable
myocardium (not hyperenhanced but with contractile
dysfunction), and normal myocardium (not hyperenhanced and
with normal function). In the setting of chronic coronary
artery disease, the combination of contrast and cine MRI may be used
similarly to distinguish between myocardial scar, hibernating
myocardium, and normal myocardium.
The ability to measure the 3D spatial extent of nonviable and viable
myocardium serially over time suggests additional clinical
roles. Figure 10 shows
contrast-enhanced MR images in a patient 12 days and 10 weeks after a
large myocardial infarction in the LAD territory. Similar to the
results in Figure 4, this patient showed a reduction in volume
of hyperenhanced myocardium (16 mL) along with an increase
in the volume of nonhyperenhanced myocardium (34 mL). These
results indicate infarct resorption and viable tissue
hypertrophy over the 8 weeks between the 2 MRI studies and
suggest that contrast MRI may allow noninvasive regional evaluation of
ventricular remodeling after ischemic injury with
high spatial resolution and full ventricular coverage.
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Acknowledgments |
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This work was supported in part by a Biomedical Engineering Research Grant from the Whitaker Foundation and NIH-NHLBI grant R29-HL-53411 (both to Dr Judd).
Received March 9, 1999; revision received June 15, 1999; accepted June 22, 1999.
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