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(Circulation. 1995;92:1117-1125.)
© 1995 American Heart Association, Inc.
Articles |
Regional Heterogeneity of Human Myocardial Infarcts Demonstrated by Contrast-Enhanced MRI
Potential Mechanisms
From the Cardiology Division, Department of Medicine, and the Division of Thoracic and Magnetic Resonance Imaging, Department of Radiology, of the Johns Hopkins Hospital, Baltimore, Md.
Correspondence to Joao A.C. Lima, MD, Assistant Professor of Medicine, Carnegie 568, Cardiology Division, Johns Hopkins Hospital, 600 N Wolfe St, Baltimore, MD 21287.
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Abstract |
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 Top Abstract IntroductionMethods Results Discussion References |
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Background Myocardial reperfusion is pivotal to the prognosis of patients with acute myocardial infarction. In these patients, coronary flow is generally assessed by angiography and tissue perfusion by tracer scintigraphy. This study was designed to examine whether magnetic resonance imaging (MRI) provides information on myocardial perfusion and damage beyond that supplied by angiography and thallium scintigraphy after acute myocardial infarction.
Methods and Results Twenty-two patients with recent myocardial infarction had ECG, echocardiography, coronary angiography, and fast contrast-enhanced MRI. Twelve patients also had exercise thallium scintigraphy. Time-intensity curves obtained from infarcted and noninfarcted regions were correlated with coronary anatomy and left ventricular function. Two perfusion patterns were observed in infarcted regions by comparison with the normal myocardial pattern. All patients but 1 had persistent myocardial hyperenhancement within the infarcted region up to 10 minutes after contrast. In 10 patients, this hyperenhanced region surrounded a subendocardial area of decreased signal at the center of the infarcted region associated with coronary occlusion at angiography, Q waves on ECG, and greater regional dysfunction by echocardiography. Moreover, the extent and location of the MRI abnormalities correlated well with the extent and location of the fixed single-photon emission computed tomography thallium defects.
Conclusions Large human infarcts, associated with prolonged obstruction of the infarct-related artery, are characterized by central dark zones surrounded by hyperenhanced regions on MRI. Conversely, reperfused infarcts with less regional dysfunction have uniform signal hyperenhancement. The MRI hyperenhanced segment correlates well with the fixed scintigraphic defect in patients with acute myocardial infarction.
Key Words: reperfusion • edema • magnetic resonance imaging • myocardial infarction
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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The timing and adequacy of myocardial reperfusion largely determine the prognosis of patients with acute myocardial infarction.1 2 When myocardial perfusion is quickly restored after coronary occlusion and maintained to the entire territory at risk, myocardial infarction may be aborted.3 In most cases, however, only partial restoration of coronary blood flow is achieved after significant injury to the threatened segment of the left ventricular wall has already occurred.1 2 4 Therefore, methods to evaluate the extent and adequacy of spontaneous or therapeutically induced reperfusion are necessary to assess the prognosis and management of patients with myocardial infarction.
Coronary angiography is currently the method of choice to evaluate the efficacy of reperfusion after myocardial infarction.5 Although it reflects flow only in the large epicardial vessels and thus provides limited information on the extent of myocardial tissue reperfusion, its impact on the treatment of patients after infarction is well established.5 6 Radionuclide scintigraphy, generally used to assess myocardial reperfusion,7 8 is limited in terms of spatial resolution and its dependence on both myocardial blood flow and tracer cellular uptake. The limitations of the present methods are particularly relevant in view of recent reports of incomplete myocardial reperfusion after successful thrombolysis8 or angioplasty9 in patients with acute myocardial infarction.
The advent of fast magnetic resonance imaging (MRI)10 permits the acquisition of MR tomograms during a breath-hold. This creates the possibility of studying the influence of paramagnetic contrast agents on myocardial signal intensity with much greater temporal resolution11 12 than achieved before by spin-echo MRI. Previous experimental work using spin-echo MRI identified different contrast enhancement patterns in animals with occlusive versus reperfused infarcts.13 14 15 16 Our study was designed to examine whether, in patients with acute myocardial infarction, contrast-enhanced fast MRI provides information on myocardial perfusion and myocardial tissue damage additional to that supplied by coronary angiography and thallium scintigraphy.
In patients with acute myocardial infarction, we identified different contrast enhancement patterns that are correlated with epicardial vessel patency defined by coronary angiography and perfusion defects assessed by thallium scintigraphy. The interpretation of these enhancement patterns is based on the knowledge of the fundamental mechanisms of MR contrast enhancement defined in isolated myocardial tissue and experimental models.13 14 15 16 17 In addition, we demonstrate that these patterns relate to the severity of acute myocardial damage modulated by attempts to restore coronary blood flow to the infarcted region.
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Methods |
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TopAbstractIntroductionMethods Results Discussion References |
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Study Patients
The study group consisted of 22 patients (16 men) with a mean age of 58 years (range, 40 to 76 years) (Table 1
). The
entry criteria included typical symptoms of acute myocardial
infarction, accompanied by a creatine phosphokinase rise above two
times the upper limits of normal, with an at least 5% MB band. All
patients gave written informed consent according to the standards
established by the Joint Committee for Clinical Investigation of the
Johns Hopkins Hospital.
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Two-dimensional echocardiography was performed by standard techniques (Hewlett Packard Sonos 1000) in all patients within the first week after infarction. Twelve patients performed a predischarge treadmill exercise test (Naughton protocol), and at peak exercise, a dose of 3 mCi (111 MBq) of [201Tl]thallium chloride was administered intravenously. Single-photon emission computed tomography (SPECT) thallium scintigraphy was performed according to our standard clinical protocol.18 Thirty 1-minute projection images over 180° (from 45° right anterior oblique to 225° left posterior oblique) were obtained in a 64x64 matrix by use of a low-energy, all-purpose collimator and a 35x35-cm field of view. SPECT images were reconstructed by uniformity correction with a 150 million count flood, center-of-rotation correction and low-pass filtering, no attenuation correction, and reconstruction into 1-pixel-thick (5.3-mm) transaxial sections. Oblique angle reorientation and summation produced 3-pixel-thick short-axis left ventricular images. Correction algorithms were applied to the projection images to compensate for motion artifacts.
MRI Protocol
Images were acquired during multiple
breath-holds on a 1.5-T
whole-body magnet (Signa, General Electric). The pulse sequence used in
this study19 is similar to an inversion-recovery
turboFLASH sequence11 in that pixel intensity is heavily
T1-weighted. It was specifically designed to minimize contamination of
pixel intensity by both T2 effects, by spoiling magnetization in the
xy plane19 achieved by use of standard
radiofrequency phasing algorithms,20 and T2* effects, by
use of a very short TE (2.3 ms). Briefly, within each RR interval, 60
nonselective dummy radiofrequency pulses are transmitted before imaging
to drive magnetization to steady state. These are followed immediately
by 32 image phase-encoding steps acquired with TR=6.5 ms, TE=2.3
ms,
and flip angle=45°. A total of 96 phase-encoding steps per image
were
acquired, such that each image was completed in three cardiac cycles.
K-space lines 1, 4, 7. . . etc; 2, 5, 8. . . etc; and 3, 6,
9. . . etc were acquired during the first, second, and third beats,
respectively. Matrix size was 256x96, field of view was 36 cm, and
voxel size was 0.9x3.7x10.0 mm.
After scout images were completed, four base-to-apex short-axis cross sections were acquired with prospective ECG gating during each 12-heartbeat breath-hold every 30 seconds for 5 minutes and then at each minute to complete a 10-minute interval begun immediately before contrast administration. The nonionic contrast agent gadoteridol (Squibb, 0.1 mmol/kg) was administered as a bolus by hand injection in a peripheral vein. The entire examination lasted 45 minutes on average, and there were no untoward reactions to gadoteridol.
MRI Data Analysis
Signal-intensity curves over time were
generated with the aid of
a commercially available software package (GPIX, General
Electric). In brief, regions of interest were defined inside the
infarcted region represented as a region of hyperenhanced
or hypoenhanced signal in the territory perfused by the infarct-related
artery determined by coronary angiography. Regions of interest
were also defined inside the noninfarcted territory and left
ventricular cavity. In patients with hypoenhanced
subendocardial zones at the center of the infarcted region, the central
region of interest was defined within the central dark zone, while the
other regions of interest were placed within regions of increased
signal intensity surrounding the central dark zone. The pulse sequence
used in these studies produces dark and homogeneous
precontrast cardiac images (Fig 1). Signal intensity
from each image was quantified, and the time-intensity curves generated
for each patient (Fig 2) were expressed as the percent
increase in signal intensity (SI) over baseline precontrast signal
intensity as shown below:
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) and noninfarcted regions (
) is
sharp, with slow decay after contrast. Signal intensity in the
periphery of the infarcted region (
) also rises rapidly after
contrast but persists at an elevated level, while blood signal
intensity is falling. The center of the infarcted region exhibits
reduced signal intensity in the first minutes after contrast
administration (
), followed by a progressive rise secondary to
delayed contrast penetration into the infarct core.
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Normalized time-intensity curves were sampled at three time points (50, 160, and 600 seconds) to describe the time course of myocardial enhancement beyond contrast first pass. The time courses of myocardium-to-blood normalized signal-intensity ratios were analyzed at the same time points. The assessment of the extracellular volume index (ECVi, see "Appendix" for details) was performed in 10 patients, with large areas of signal hyperenhancement uncontaminated by central dark zones. The ECVi was calculated according to the following equation:
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Study Outcomes
The circumferential extent of the sum of
hyperenhanced plus
hypoenhanced regions was compared with the circumferential extent of
the fixed SPECT thallium defect assessed visually from MRI images and
thallium scans by two independent investigators. Only the short-axis
images obtained at the redistribution phase of the thallium studies,
which therefore delineated the fixed thallium defects, were used in
this analysis. Both MRI and thallium SPECT abnormalities were
quantified at the mid left ventricular wall level and
matched by location along the left ventricular long axis.
The match was performed by calculating the relative distance of
short-axis images from the left ventricular base
represented by the mitral valve level. Because only four
MRI cross sections were available for seven or eight thallium SPECT
cross sections, the thallium short-axis scan that best approximated the
MRI short-axis location along the left ventricular long
axis was selected for comparison. The average time interval between
thallium scintigraphy and MRI was 1 day (range, 0 to 7
days). Thallium scans were interpreted for the presence of fixed or
redistribution defects by independent observers who were unaware of the
MRI results.
Coronary angiograms were classified by two independent observers in relation to the extent of radiographic contrast penetration downstream from a coronary lesion according to the criteria proposed by the Thrombolysis in Myocardial Infarction (TIMI) study group9 : grade 0 (no flow), grade 1 (minimal penetration of contrast), grade 2 (delayed flow of contrast), or grade 3 (brisk flow of contrast). Vessels with TIMI grade 0 or 1 were considered occluded and those with grade 2 or 3 were considered patent for statistical analysis purposes. Since 16 of our 22 patients had coronary angioplasty, TIMI flow in the infarct-related artery was assessed both before and after coronary angioplasty. The average time interval between coronary angiography and MRI was 4 days (range, 0 to 10 days).
Echocardiograms were quantified by an independent observer blinded in relation to the MRI and thallium scintigraphic results according to methodology previously described.21 Global parameters included left ventricular volumes and ejection fraction. The left ventricular wall, defined by endocardial and epicardial contours, was divided into 16 segments by equiangular radial lines placed around the left ventricular cross section.21 Wall thickness was calculated as the ratio of the segment area to the average of the endocardial and epicardial arc lengths in the short-axis images. Systolic wall thickening was calculated as [(end-systolic minus end-diastolic wall thickness) divided by the end-diastolic wall thickness]x100. Regional dysfunction was characterized as the percent circumferential extent of the sum of segments with systolic wall thickening <5%. ECGs were analyzed by two observers for the presence of Q waves and for infarct location, defined by ECG leads demonstrating Q waves and/or ST-segment changes.
Statistical Analysis
The changes over time of signal
intensity obtained from
infarcted regions in the MRI scans were compared with the patterns
obtained from noninfarcted regions by repeated-measures
ANOVA.22 Differences between specific regions at specific
time points were isolated by Bonferroni t
tests.22 Moreover, differences in the
myocardium-to-blood signal-intensity ratio between patients
with open and closed infarct-related arteries were analyzed by
profile analysis with repeated-measures ANOVA.22
Fisher's exact probability tests, Student's t tests, and
linear regression analyses were also used, as indicated in the
text. The data are presented as mean±SEM.
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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Myocardial Infarction and Reperfusion
Therapeutic myocardial reperfusion was attempted in 18 of the 22 patients (see Table 1
). Thrombolytics were used in 17
patients, combined with rescue angioplasty in 4 patients. Direct
angioplasty was performed in 1 patient. Four patients had
contraindications to therapeutic reperfusion and were treated
conservatively. Except for the 5 patients who had either rescue or
direct angioplasty, all patients had catheterization at
least 48 hours after the onset of myocardial infarction. Eleven of
these 17 patients had percutaneous coronary
angioplasty at that time. The average time interval between
coronary angiography and myocardial infarction was 4 days
(range, 0 to 11 days).
Myocardial MRI Enhancement Patterns
Three patterns of
myocardial signal enhancement on MRI were
observed in patients with acute myocardial infarction (see Figs 1 through
3). In noninfarcted regions, a
rapid increase in
signal intensity reflecting adequate tissue contrast delivery is
followed by a slower decay (110±17%, 85±12%, and 57±9% at
50,
160, and 600 seconds after contrast, respectively, Fig 3)
caused by the
combination of a slowly decaying blood contrast concentration and the
extravasation of contrast material into the interstitial
space.17 23 24
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The second
enhancement pattern is characterized by a similarly sharp
rise in myocardial signal intensity, followed, however, by a continued
rise in signal intensity over the first 2 minutes and a slower decay
than that observed in normal noninfarcted regions (128±21%,
151±26%, and 116±20% at 50, 160, and 600 seconds, ANOVA
P<.001 versus noninfarcted, Fig 3). This
enhancement
pattern is seen as a "bright area" occupying the infarcted region
and was found in 21 of the 22 patients. One patient had a normal and
uniform enhancement pattern despite a clinical diagnosis of myocardial
infarction.
The third pattern, characterized by a slower rate of
signal-intensity
increase after contrast administration, was present in 10 patients
(37±9%, 41±10%, and 39±9% at 50, 160, and 600 seconds,
ANOVA
P<.02 versus noninfarcted, Fig 3). It was seen as a
"dark zone" involving the subendocardial half of the left
ventricular wall at the center of the infarcted region
surrounded by regions of hyperenhanced signal intensity. Eventually,
protracted contrast penetration into the infarct core produced signal
enhancement in the central dark zones, observed in images obtained 5 to
10 minutes after contrast injection (Figs 1 and
2).
Precontrast absolute signal-intensity levels were not different in noninfarcted versus infarcted regions (59.3±8.3 versus 53.2±7.5 for all patients, P=NS). In patients with central dark zones, precontrast signal intensity was similar in noninfarcted (56.4±12.6) and infarcted regions, which later appeared hyperenhanced (52.9±12.6) and hypoenhanced (57.8±15.3, P=NS, ANOVA).
Infarct-Related Artery Patency and Myocardial Enhancement
Patterns
Infarct-related artery obstruction at the time of cardiac
catheterization was related to the presence of
subendocardial dark zones by MRI. When the first angiogram obtained
after myocardial infarction was analyzed, coronary
arteries with TIMI flow 0 or 1 were associated with a high prevalence
(75%) of central dark zones by MRI. The prevalence was lower (20%) in
patients with patent coronary arteries but with slow antegrade
flow (TIMI 2) and was nil in patients with brisk antegrade flow (TIMI
3, P<.003, Table 2).
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The analysis was
repeated taking into consideration the last
angiogram obtained before the MRI study, because 16 patients had
coronary angioplasty before MRI (Table 2). Four patients who
initially had occluded infarct-related arteries (TIMI 1 or 0) and 3
patients previously in the TIMI 2 group crossed over to the group of
patients with patent arteries and brisk antegrade flow (TIMI 3) after
angioplasty. The prevalence of patients with central dark zones
increased in both groups (83% and 36% in patients with TIMI flow 0 or
1 and TIMI flow 3, respectively), thereby reducing the statistical
strength of the association between infarct-related artery obstruction
and the presence of hypoenhanced regions by MRI (P<.056,
Table 2).
Conversely, the presence of hyperenhanced regions on MRI was not related to patency of the culprit artery by angiography. All patients had either normal or hyperenhanced infarcted regions, indicating that at least the peripheral areas of most human infarcts are perfused by antegrade or collateral blood flow a few days after infarction.
Creatine Phosphokinase, ECG, and Left Ventricular
Function
Peak creatine phosphokinase rise was not associated with
myocardial perfusion patterns by MRI (1411+309 IU/L for patients with
hypoenhanced regions versus 1109+366 IU/L for those without
hypoenhanced regions, P=NS). However, the pattern of
myocardial perfusion by contrast-enhanced MRI was related to the
presence of Q waves on serial ECGs obtained at the time of infarction.
Patients with Q-wave infarcts were more likely (60%) to have
hypoenhanced zones than those with non–Q-wave infarcts (14%,
P<.07, Fisher's exact probability). Ten infarcts were
anterior, 10 inferior, and 2 lateral by ECG criteria.
Patients with and
without hypoenhanced subendocardial zones within the
infarcted regions had similar left ventricular
end-diastolic volume (145.3±23.4 versus 130.4±21.6 mL),
end-systolic volume (96.1±19.9 versus 68.7±12.2 mL), and
ejection
fraction (39.7±14.9% versus 46.1±14.9%, respectively,
P=NS), despite a trend for greater volumes and lower
ejection fractions in those with MRI hypoenhanced zones. However,
regional dysfunction characterized as a reduction in percent systolic
wall thickening <5% was greater in patients with hypoenhanced zones
(45.9±8.1%) than those without (22.3±5.6%, P<.03,
Fig 4). The relation was still present, although
statistically weaker, when the threshold for dysfunction was set at 0%
systolic wall thickening (36.8±10.6% with versus 16.0±2.3%
without
hypoenhanced zones, P<.07, Fig 4).
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) and without (
) central
hypoenhanced zones for 16 segments distributed around the left
ventricular short-axis echocardiograms. Wall-thickening
maps from individual patients were averaged by superimposing the center
of the segments containing the most severe wall thickening
abnormalities. Comparisons between patients with and without central
hypoenhanced zones were performed by arbitrary selection of the 5% and
0% thresholds (see "Methods").
Thallium Scintigraphy
Thallium scintigraphy was obtained in
12 patients
during exercise and after tracer redistribution 4 hours later. Ten
patients had fixed defects corresponding to the acute infarction, but 2
patients had no scintigraphic evidence of infarction despite a rise in
creatine phosphokinase. Eight of the 10 patients with fixed thallium
defects also had adjacent redistribution defects, suggesting the
presence of myocardial ischemia.
The topographic location of fixed
thallium defects correlated well with
the location of hyperenhanced regions defined by contrast-enhanced MR
images (Fig 5). In addition, the circumferential extent
of the fixed thallium defect in the redistribution scan correlated well
with the total extent of the MRI abnormality (the sum of the
hypoenhanced plus hyperenhanced regions) in patients with acute
myocardial infarction (Fig 6).
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Potential Mechanisms of Myocardial Hyperenhancement After Acute
Myocardial Infarction
The mechanisms of signal hyperenhancement that
characterize
infarcted myocardium were explored by study of the time
course of signal intensity in myocardium relative to blood
after contrast administration. The ratio was not a function of time in
noninfarcted regions (Fig 7). However, in the infarcted
regions of patients with occluded infarct-related arteries (TIMI 0 or
1), the ratio increased progressively during the first 10 minutes that
followed contrast administration, reflecting the contribution of
impaired contrast wash-in/washout kinetics as a mechanism of local
myocardial hyperenhancement (Fig 7A). Conversely, in patients
with open
arteries (TIMI 3), the immediate delivery of contrast material to
infarcted territory was followed by a further increase in the ratio
during the following 2 minutes, reaching a plateau beyond that time
point (Fig 7B).
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). However, in infarcted territory (
), the ratio
increased initially (P<.003, ANOVA), reaching a plateau
after 160 seconds (time-group interaction P<.02 by ANOVA
versus patients with closed arteries). This relation suggests a
combination of impaired contrast kinetics with an increased contrast
volume of distribution in reperfused regions.
The upward horizontal displacement of
the
myocardium-to-blood signal-intensity ratio relative to
normal regions suggests the presence of an increased contrast volume of
distribution as a mechanism of myocardial hyperenhancement in infarcted
territory. This possibility was further explored by plotting myocardial
against blood signal intensity for individual images acquired after 2
minutes following contrast administration in 10 patients. Fig 8
shows that all data points obtained from noninfarcted
regions lie essentially on the same straight line (myocardial
SI=-0.8+0.32 blood SI, r=.96). The slope of
this relation,
which characterizes the volume of distribution for the contrast agent
in normal myocardium, principally reflects the
extracellular compartment volume.23 24 The index of
extracellular volume, derived from similar relations for each
individual patient (see "Appendix"), was greater in infarcted
than in noninfarcted myocardium (45.1±2.9% versus
28.4±1.9%, respectively, P<.001). These results suggest
that the contrast volume of distribution is increased in infarcted
regions and may contribute to local myocardial hyperenhancement in
infarcted but perfused myocardium.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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Contrast-enhanced MRI allows the identification of two perfusion patterns within human infarcts by comparison with the perfusion pattern of normal, noninfarcted regions. Virtually all patients with clinical myocardial infarction had an area of increased signal intensity within the infarcted region in images obtained 2 to 10 minutes after contrast bolus administration. The only patient who did not have hyperenhancement of the infarcted region had a normal perfusion pattern. In addition, the extent of this area of hyperenhanced signal intensity correlated well with the size of the fixed thallium defect, and its presence was not related to the patency of the infarct-related artery. Therefore, our study, by contrast-enhanced MRI, demonstrates the presence of myocardial blood perfusion within all human infarcts a few days after coronary occlusion. This observation is in agreement with prior studies that used pyrophosphate scintigraphy to demonstrate tracer uptake within infarcted territory after permanent coronary occlusion.25 26
The second pattern consisted of a dark hypoenhanced area located in the subendocardium of the infarcted region within 2 minutes of intravenous contrast bolus administration. These regions were surrounded by areas of increased signal intensity and slowly diminished in size over the course of 5 to 8 minutes after contrast injection. They were associated with closed or nearly closed infarct-related arteries at the time of cardiac catheterization, the presence of Q waves on the ECG, and greater segmental dysfunction by echocardiography. They probably result from protracted contrast penetration with or without hemorrhage, probably caused by severe capillary damage and obstruction at the center of the infarcted region.
The presence of flow inhomogeneity inside infarcted territory is well
known from experimental studies using radioactive microspheres
after coronary occlusion, which have shown a greater reduction
in myocardial blood flow in the subendocardial half of the infarct
core.27 28 In addition, previous clinical studies
have
shown flow inhomogeneity inside the infarcted region by contrast
echocardiography immediately after direct
angioplasty.9 Our study extends the findings of previous
work to demonstrate the persistence of flow inhomogeneity several days
after coronary occlusion in association with failure to achieve
adequate patency of the infarct-related artery after myocardial
infarction and with larger regions of myocardial damage by ECG and
echocardiographic criteria. Hypoenhanced zones within
the infarcted region were also documented in 2 patients with widely
patent infarct-related arteries who failed thrombolysis and
underwent successful rescue angioplasty (Fig 5). These central
dark
regions correlate well with "no-reflow" regions, characterized in
previous experimental27 28 and
clinical8 9
studies by the failure to achieve complete myocardial reperfusion after
reestablishment of blood supply to the infarcted territory.
Prior experimental studies using spin-echo MRI have demonstrated dark
zones surrounded by regions of hyperenhanced signal in occlusive
infarcts and basically hyperenhanced signal in infarcted but reperfused
myocardium.13 14 15 16 Our
findings correlate well
with the results of those animal studies in which patency of the
infarct-related artery could be accurately controlled. Spin-echo
contrast-enhanced MRI techniques have also shown
heterogeneous enhancement patterns within infarcted
territory in patients with acute infarction.29 However,
those patterns were difficult to interpret because of the limited
temporal resolution of the spin-echo imaging sequence used in those
studies. Given the time course of regional enhancement patterns after
contrast bolus administration (Figs 2 and 3),
the temporal and
topographic features of hypoenhanced zones within the injured territory
are best characterized by fast imaging techniques. However, it is
theoretically possible to assess the different MRI perfusion patterns
documented in our study by conventional or fast spin-echo MRI.
Several previous studies using spin-echo imaging have documented a good correlation between infarct sizes estimated by MRI and by other techniques.15 30 31 32 Our results are in agreement with those studies that also used the planimetered area encompassed by the MRI signal-intensity abnormality to estimate the extent of ischemic and/or infarcted myocardium. However, because of the trade-off between temporal resolution and number of image planes obtained during a given breath-hold, infarct size was not measured in our study. In addition, in our study, images represent the average of three cardiac cycles with loss of beat-to-beat variations of signal intensity during the contrast bolus first pass through the heart. However, since we did not attempt to extract information on myocardial perfusion from the ascending limb of the time-intensity curves,11 33 it is unlikely that the latter factor influenced our results.
Finally, we explored the mechanisms of signal hyperenhancement in
infarcted myocardial tissue to gain insight into the pathophysiology of
myocardial damage within infarcted regions. Potential mechanisms to
explain differences in the time course of the
myocardium-to-blood signal-intensity ratio (Fig 7) include
(1) impaired myocardial contrast wash-in/washout kinetics, (2)
increased contrast volume of distribution, and (3) binding of contrast
material to proteins released within injured myocardial tissue.
Our study documents a progressive increase in the infarcted myocardium-to-blood signal-intensity ratio in patients with a totally occluded or nearly occluded infarct-related artery. This finding suggests impairment of contrast wash-in/washout kinetics as a mechanism of myocardial hyperenhancement observed in those patients. Moreover, we estimated the magnitude of extracellular volume expansion in the injured territory of patients with acute myocardial infarction. The almost doubled extracellular space that characterizes human infarcted tissue could represent extracellular edema formation and/or membrane rupture, with consequent diffusion of gadoteridol into the intracellular space. However, although gadoteridol protein binding in normal myocardium is minimal,34 the possibility of contrast protein binding within infarcted territory cannot be excluded and could potentially contribute to myocardial hyperenhancement in damaged areas after coronary occlusion. Future studies should be directed toward gaining further insight into these mechanisms, which could provide the means to assess myocardial viability after coronary occlusion by MRI.
In conclusion, human myocardial infarcts containing central regions of impaired myocardial blood flow are associated with persistent occlusion of the infarct-related artery and greater regional left ventricular dysfunction. Conversely, infarcts showing uniform contrast hyperenhancement on fast MRI are associated with patent infarct-related arteries and less damage by ECG and echocardiography. Myocardial hyperenhancement by fast MRI results at least in part from impaired contrast kinetics and extracellular space expansion, which may reflect edema formation and/or ruptured cell membranes. Therefore, contrast-enhanced MRI provides unique information on regional myocardial blood perfusion and tissue damage within acute human infarcts.
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Acknowledgments |
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Supported by Grant-in-Aid 92-10-26-01 of the American Heart Association, Dallas, Tex, and NHLBI grant HL-45090, NIH, Bethesda, Md.
Increased Contrast Volume of Distribution as a Potential
Mechanism
of Signal Hyperenhancement in Infarcted
Myocardium
The interpretation of the first-pass events that follow
bolus
administration of contrast are complex.17 The results of
this study, however, in which at best only a single breath-hold
occurred under first-pass conditions, are somewhat easier to interpret.
By 1 minute after contrast administration, which comprises the vast
majority of our data, the contrast agent would be expected to be mixed
within the body blood pool. In addition, within myocardial tissue,
contrast concentrations between the blood and interstitium would be
equilibrated on the basis of known extravasation of this
agent17 and molecules of similar size.35
Furthermore, the rate of contrast clearance from the blood pool by
renal elimination and interstitial space diffusion is slow
relative to the time required for equilibration between the myocardial
blood pool and the interstitial space.36 These
approximations for noninfarcted regions are supported by our results
showing myocardial enhancement as a fixed percentage of blood
enhancement (Figs 7 and 8). Thus, our data were
acquired at a time when
myocardial interstitial contrast concentration equals that
of the blood.
Fig 9 shows the hypothetical myocardial
distribution of
the contrast agent under these conditions. Given the above assumptions,
the change in pixel intensity in the tissue (
SItissue)
due to the contrast agent can be obtained
by
 |
where IVV is intravascular volume, ISV is interstitial volume, k is the slope of pixel intensity versus 1/T1 for the specific pulse sequence used in this study,19 R is the relaxivity of the contrast agent as further discussed below, [plasma] is plasma contrast concentration, and Hcttissue is tissue hematocrit. Similarly, for blood:
 |
If we take the ratio of tissue to blood pixel intensity changes, the constants k, R, and [plasma] cancel:
 |
From this equation, an ECVi can be defined that differs from true extracellular volume in that the volume of red cells within the myocardium is included as cell volume:
 |
This equation implicitly assumes that (1) myocardial water exchange rates are fast and (2) the imaging pulse sequence results in pixel intensities that are linearly related to 1/T1. These points are individually addressed below.
First, under these nontransient conditions, it is valid to assume that myocardial water exchange rates are fast17 23 24 and that the change in myocardial 1/T1 is linearly related to tissue contrast concentration. Thus, the ratio of the change in 1/T1 of tissue to that of blood is proportional to extracellular volume.
Second, pixel intensities for the pulse sequence used in this study are linearly related to 1/T1 over the range of 0 to 10 s-1.19 After the first pass of a 0.1 mmol/kg gadoteridol IV bolus, blood and myocardial voxel contrast concentrations would be approximately 0.3 and 0.1 mmol/L, respectively, assuming a myocardial extracellular volume of 30%.36 For a gadoteridol relaxivity of 4.3 (mmol/L)-1 · s-117 and assuming fast myocardial water exchange,23 24 36 the change in 1/T1 of blood and tissue would be about 1.3 and 0.43 s-1, respectively. These values are well within the range in which image pixel intensity is linearly related to contrast concentration for our pulse sequence,19 such that the ratio of the change in tissue to blood pixel intensity is proportional to extracellular volume.
Thus, as shown in Fig 8, all
patients have a similar extracellular
volume index for normal myocardium and, within the bounds
of the above assumptions, the slope of this line reflects the average
extracellular space. In infarcted regions, the above arguments equally
apply, and the increased index documented in these hyperenhanced
regions (see "Results") reflects, at least in part, a local
augmentation in the contrast volume of distribution secondary to an
increased extracellular space.
Received December 13, 1994; revision received March 6, 1995; accepted March 10, 1995.
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S.R. Underwood, J. J Bax, J. v. Dahl, M. Y Henein, A. C van Rossum, E. R Schwarz, J.-L. Vanoverschelde, E. E.v. d. Wall, and W. Wijns Imaging techniques for the assessment of myocardial hibernation: Report of a Study Group of the European Society of Cardiology Eur. Heart J., May 2, 2004; 25(10): 815 - 836. [Abstract] [Full Text] [PDF]
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L. C. Amado, D. L. Kraitchman, B. L. Gerber, E. Castillo, R. C. Boston, J. Grayzel, and J. A. C. Lima Reduction of "no-reflow" phenomenon by intra-aortic balloon counterpulsation in a randomized magnetic resonance imaging experimental study J. Am. Coll. Cardiol., April 7, 2004; 43(7): 1291 - 1298. [Abstract] [Full Text] [PDF]
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K. Shan, G. Constantine, M. Sivananthan, and S. D. Flamm Role of Cardiac Magnetic Resonance Imaging in the Assessment of Myocardial Viability Circulation, March 23, 2004; 109(11): 1328 - 1334. [Full Text] [PDF]
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T. K. F. Foo, D. W. Stanley, E. Castillo, C. E. Rochitte, Y. Wang, J. A. C. Lima, D. A. Bluemke, and K. C. Wu Myocardial Viability: Breath-hold 3D MR Imaging of Delayed Hyperenhancement with Variable Sampling in Time Radiology, March 1, 2004; 230(3): 845 - 851. [Abstract] [Full Text] [PDF]
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 K. C. Wu and J. A.C. Lima Noninvasive Imaging of Myocardial Viability: Current Techniques and Future Developments Circ. Res., December 12, 2003; 93(12): 1146 - 1158. [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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J. A. C. Lima Myocardial viability assessment by contrast-enhanced magnetic resonance imaging J. Am. Coll. Cardiol., September 3, 2003; 42(5): 902 - 904. [Full Text] [PDF]
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R. J. Kim and R. M. Judd Gadolinium-Enhancedmagnetic resonance imagingin hypertrophic cardiomyopathy: In vivo imaging of the pathologic substrate for premature cardiac death? J. Am. Coll. Cardiol., May 7, 2003; 41(9): 1568 - 1572. [Full Text] [PDF]
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S. Flacke, J. S. Allen, J. M. Chia, J. H. Wible, M. P. Periasamy, M. D. Adams, I. K. Adzamli, and C. H. Lorenz Characterization of Viable and Nonviable Myocardium at MR Imaging: Comparison of Gadolinium-based Extracellular and Blood Pool Contrast Materials versus Manganese-based Contrast Materials in a Rat Myocardial Infarction Model Radiology, March 1, 2003; 226(3): 731 - 738. [Abstract] [Full Text] [PDF]
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S. S. Lee, H. W. Goo, S. B. Park, C. H. Lim, G. Gong, J. B. Seo, and T.-H. Lim MR Imaging of Reperfused Myocardial Infarction: Comparison of Necrosis-Specific and Intravascular Contrast Agents in a Cat Model Radiology, March 1, 2003; 226(3): 739 - 747. [Abstract] [Full Text] [PDF]
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 J.-P. Laissy, B. Messin, O. Varenne, B. Iung, D. Karila-Cohen, E. Schouman-Claeys, and P. G. Steg MRI of Acute Myocarditis: A Comprehensive Approach Based on Various Imaging Sequences Chest, November 1, 2002; 122(5): 1638 - 1648. [Abstract] [Full Text] [PDF]
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B. L. Gerber, J. Garot, D. A. Bluemke, K. C. Wu, and J. A.C. Lima Accuracy of Contrast-Enhanced Magnetic Resonance Imaging in Predicting Improvement of Regional Myocardial Function in Patients After Acute Myocardial Infarction Circulation, August 27, 2002; 106(9): 1083 - 1089. [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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B. Kumbasar, K. C. Wu, I. R. Kamel, J. A. C. Lima, and D. A. Bluemke Left Ventricular True Aneurysm: Diagnosis of Myocardial Viability Shown on MR Imaging Am. J. Roentgenol., August 1, 2002; 179(2): 472 - 474. [Full Text] [PDF]
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H. Mahrholdt, A. Wagner, R.M. Judd, and U. Sechtem Assessment of myocardial viability by cardiovascular magnetic resonance imaging Eur. Heart J., April 2, 2002; 23(8): 602 - 619. [Full Text] [PDF]
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J. J. W. Sandstede, T. Pabst, M. Beer, C. Lipke, K. Baurle, F. Butter, K. Harre, W. Kenn, W. Voelker, S. Neubauer, et al. Assessment of Myocardial Infarction in Humans with 23Na MR Imaging: Comparison with Cine MR Imaging and Delayed Contrast Enhancement Radiology, October 1, 2001; 221(1): 222 - 228. [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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S. B. Yeon, N. Reichek, B. A. Tallant, J. A. C. Lima, L. P. Calhoun, N. R. Clark, E. A. Hoffman, K. K. L. Ho, and L. Axel Validation of in vivo myocardial strain measurement by magnetic resonance tagging with sonomicrometry J. Am. Coll. Cardiol., August 1, 2001; 38(2): 555 - 561. [Abstract] [Full Text] [PDF]
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S. B. Reeder, Y. P. Du, J. A. C. Lima, and D. A. Bluemke Advanced Cardiac MR Imaging of Ischemic Heart Disease RadioGraphics, July 1, 2001; 21(4): 1047 - 1074. [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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 U. Sechtem Imaging myocardial area at risk and final infarct size Eur. Heart J. Suppl., June 1, 2001; 3(suppl_C): C36 - C46. [PDF]
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 M. Saeed New Concepts in Characterization of Ischemically Injured Myocardium by MRI Experimental Biology and Medicine, May 1, 2001; 226(5): 367 - 376. [Abstract] [Full Text]
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S. J. Flacke, S. E. Fischer, and C. H. Lorenz Measurement of the Gadopentetate Dimeglumine Partition Coefficient in Human Myocardium in Vivo: Normal Distribution and Elevation in Acute and Chronic Infarction Radiology, March 1, 2001; 218(3): 703 - 710. [Abstract] [Full Text]
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M. Saeed, G. Lund, M. F. Wendland, J. Bremerich, H.-J. Weinmann, and C. B. Higgins Magnetic Resonance Characterization of the Peri-Infarction Zone of Reperfused Myocardial Infarction With Necrosis-Specific and Extracellular Nonspecific Contrast Media Circulation, February 13, 2001; 103(6): 871 - 876. [Abstract] [Full Text] [PDF]
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 T. Wolf, L. Gepstein, G. Hayam, A. Zaretzky, R. Shofty, D. Kirshenbaum, G. Uretzky, U. Oron, and S. A. Ben-Haim Three-dimensional endocardial impedance mapping: a new approach for myocardial infarction assessment Am J Physiol Heart Circ Physiol, January 1, 2001; 280(1): H179 - H188. [Abstract] [Full Text] [PDF]
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O. P. Simonetti, R. J. Kim, D. S. Fieno, H. B. Hillenbrand, E. Wu, J. M. Bundy, J. P. Finn, and R. M. Judd An Improved MR Imaging Technique for the Visualization of Myocardial Infarction Radiology, January 1, 2001; 218(1): 215 - 223. [Abstract] [Full Text]
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K. Lauerma, P. Niemi, H. Hänninen, T. Janatuinen, L.-M. Voipio-Pulkki, J. Knuuti, L. Toivonen, T. Mäkelä, M. A. Mäkijärvi, and H. J. Aronen Multimodality MR Imaging Assessment of Myocardial Viability: Combination of First-Pass and Late Contrast Enhancement to Wall Motion Dynamics and Comparison with FDG PET-Initial Experience Radiology, December 1, 2000; 217(3): 729 - 736. [Abstract] [Full Text]
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 R. J. Kim, E. Wu, A. Rafael, E.-L. Chen, M. A. Parker, O. Simonetti, F. J. Klocke, R. O. Bonow, and R. M. Judd The Use of Contrast-Enhanced Magnetic Resonance Imaging to Identify Reversible Myocardial Dysfunction N. Engl. J. Med., November 16, 2000; 343(20): 1445 - 1453. [Abstract] [Full Text] [PDF]
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C. M. Kramer, W. J. Rogers Jr., S. Mankad, T. M. Theobald, D. L. Pakstis, and Y.-L. Hu Contractile reserve and contrast uptake pattern by magnetic resonance imaging and functional recovery after reperfused myocardial infarction J. Am. Coll. Cardiol., November 15, 2000; 36(6): 1835 - 1840. [Abstract] [Full Text] [PDF]
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C. E. Rochitte, R. J. Kim, H. B. Hillenbrand, E.-l. Chen, and J. A. C. Lima Microvascular Integrity and the Time Course of Myocardial Sodium Accumulation After Acute Infarction Circ. Res., October 13, 2000; 87(8): 648 - 655. [Abstract] [Full Text] [PDF]
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K. Rajappan, N. G. Bellenger, L. Anderson, and D. J. Pennell The role of cardiovascular magnetic resonance in heart failure Eur J Heart Fail, September 1, 2000; 2(3): 241 - 252. [Abstract] [Full Text] [PDF]
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B. L. Gerber, C. E. Rochitte, J. A. Melin, E. R. McVeigh, D. A. Bluemke, K. C. Wu, L. C. Becker, and J. A. C. Lima Microvascular Obstruction and Left Ventricular Remodeling Early After Acute Myocardial Infarction Circulation, June 13, 2000; 101(23): 2734 - 2741. [Abstract] [Full Text] [PDF]
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J. J. W. Sandstede, C. Lipke, M. Beer, K. Harre, T. Pabst, W. Kenn, S. Neubauer, and D. Hahn Analysis of First-Pass and Delayed Contrast-Enhancement Patterns of Dysfunctional Myocardium on MR Imaging: Use in the Prediction of Myocardial Viability Am. J. Roentgenol., June 1, 2000; 174(6): 1737 - 1740. [Abstract] [Full Text]
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A. J. Duerinckx Myocardial Viability Using MR Imaging: Is It Ready for Clinical Use? Am. J. Roentgenol., June 1, 2000; 174(6): 1741 - 1743. [Full Text]
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H. Arheden, M. Saeed, C. B. Higgins, D.-W. Gao, P. C. Ursell, J. Bremerich, R. Wyttenbach, M. W. Dae, and M. F. Wendland Reperfused Rat Myocardium Subjected to Various Durations of Ischemia: Estimation of the Distribution Volume of Contrast Material with Echo-planar MR Imaging Radiology, May 1, 2000; 215(2): 520 - 528. [Abstract] [Full Text]
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P. R. Sensky, A. Jivan, N. M. Hudson, R. P. Keal, B. Morgan, J. L. Tranter, D. de Bono, N. J. Samani, and G. R. Cherryman Coronary Artery Disease: Combined Stress MR Imaging Protocol-One-Stop Evaluation of Myocardial Perfusion and Function Radiology, May 1, 2000; 215(2): 608 - 614. [Abstract] [Full Text]
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R. J. Kim, D. S. Fieno, T. B. Parrish, K. Harris, E.-L. Chen, O. Simonetti, J. Bundy, J. P. Finn, F. J. Klocke, and R. M. Judd Relationship of MRI Delayed Contrast Enhancement to Irreversible Injury, Infarct Age, and Contractile Function Circulation, November 9, 1999; 100(19): 1992 - 2002. [Abstract] [Full Text] [PDF]
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H. Arheden, M. Saeed, C. B. Higgins, D.-W. Gao, J. Bremerich, R. Wyttenbach, M. W. Dae, and M. F. Wendland Measurement of the Distribution Volume of Gadopentetate Dimeglumine at Echo-planar MR Imaging to Quantify Myocardial Infarction: Comparison with 99mTc-DTPA Autoradiography in Rats Radiology, June 1, 1999; 211(3): 698 - 708. [Abstract] [Full Text]
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W. J. Rogers Jr, C. M. Kramer, G. Geskin, Y.-L. Hu, T. M. Theobald, D. A. Vido, S. Petruolo, and N. Reichek Early Contrast-Enhanced MRI Predicts Late Functional Recovery After Reperfused Myocardial Infarction Circulation, February 16, 1999; 99(6): 744 - 750. [Abstract] [Full Text] [PDF]
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K. Ramani, R. M. Judd, T. A. Holly, T. B. Parrish, V. H. Rigolin, M. A. Parker, C. Callahan, S. W. Fitzgerald, R. O. Bonow, and F. J. Klocke Contrast Magnetic Resonance Imaging in the Assessment of Myocardial Viability in Patients With Stable Coronary Artery Disease and Left Ventricular Dysfunction Circulation, December 15, 1998; 98(24): 2687 - 2694. [Abstract] [Full Text] [PDF]
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K. C. Wu, R. J. Kim, D. A. Bluemke, C. E. Rochitte, E. A. Zerhouni, L. C. Becker, and J. A. C. Lima Quantification and time course of microvascular obstruction by contrast-enhanced echocardiography and magnetic resonance imaging following acute myocardial infarction and reperfusion J. Am. Coll. Cardiol., November 15, 1998; 32(6): 1756 - 1764. [Abstract] [Full Text] [PDF]
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 J. D. Kasprzak, W. B. Vletter, J. R.T.C. Roelandt, J. R. van Meegen, R. Johnson, and F. J. Ten Cate Visualization and quantification of myocardial mass at risk using three-dimensional contrast echocardiography Cardiovasc Res, November 1, 1998; 40(2): 314 - 321. [Abstract] [Full Text] [PDF]
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C. E. Rochitte, J. A. C. Lima, D. A. Bluemke, S. B. Reeder, E. R. McVeigh, T. Furuta, L. C. Becker, and J. A. Melin Magnitude and Time Course of Microvascular Obstruction and Tissue Injury After Acute Myocardial Infarction Circulation, September 8, 1998; 98(10): 1006 - 1014. [Abstract] [Full Text] [PDF]
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G. Geskin, C. M. Kramer, W. J. Rogers, T. M. Theobald, D. Pakstis, Y.-L. Hu, and N. Reichek Quantitative Assessment of Myocardial Viability After Infarction by Dobutamine Magnetic Resonance Tagging Circulation, July 21, 1998; 98(3): 217 - 223. [Abstract] [Full Text] [PDF]
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