(Circulation. 1999;99:744-750.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Early Contrast-Enhanced MRI Predicts Late Functional Recovery After Reperfused Myocardial Infarction
From the Division of Cardiology, Department of Medicine, Allegheny General Hospital, Pittsburgh, Pa.
Correspondence to Walter J. Rogers, Jr, MS, Division of Cardiology, Allegheny General Hospital, 320 E North Ave, Pittsburgh, PA 15212.
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Abstract |
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Background—We have observed 3 abnormal patterns on contrast-enhanced MRI early after reperfused myocardial infarction (MI): (1) absence of normal first-pass signal enhancement (HYPO), (2) normal first pass signal followed by hyperenhanced signal on delayed images (HYPER), or (3) both absence of normal first-pass enhancement and delayed hyperenhancement (COMB). This study examines the association between these patterns in the first week after MI and late recovery of myocardial contractile function by use of magnetic resonance myocardial tissue tagging.
Methods and Results—Seventeen patients (14 men) with a mean age of 53±12 years were studied after a reperfused first MI. Contrast-enhanced images were acquired immediately after bolus administration of gadolinium and 7±2 minutes later. Tagged images were acquired at weeks 1 and 7. Circumferential segment shortening (%S) was measured in regions displaying HYPER, COMB, or HYPO contrast patterns and in remote regions (REMOTE) at weeks 1 and 7. At week 1, %S was depressed in HYPER, COMB, and HYPO (9±8%, 7±6%, and 5±4%, respectively) and were less than REMOTE (18±6%, P<0.003). However, in HYPER, %S improved at week 7 from 9±8% to 18±5% (P<0.001 versus week 1). In contrast, HYPO did not improve significantly (5±4% to 6±3%, P=NS) and COMB tended to improve 7±6% to 11±6% (P=0.06).
Conclusions—HYPER has partially reversible dysfunction and represents predominantly viable myocardium. COMB shows borderline improvement and likely contains an admixture of viable and necrotic myocardium. HYPO shows little functional improvement at 7 weeks, presumably because of irreversible myocardial damage.
Key Words: magnetic resonance imaging • reperfusion • contrast media
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Prompt reperfusion salvages myocardium at risk after coronary artery occlusion.1 2 Significant improvement in mortality and morbidity may be achieved even when reperfusion occurs up to 6 to 12 hours after acute myocardial infarction (MI).3 However, protracted ischemia may produce an admixture of necrotic and viable myocardium. Although stunned viable myocardium differs structurally and metabolically from irreversibly injured myocardium, both may display similarly depressed mechanical function at rest early after MI.
Recently, a number of studies have investigated the potential value of T1-shortening contrast agents, combined with rapid MRI, in the characterization of regional myocardial perfusion, ischemia, and infarction with and without reperfusion.4 5 6 7 8 9 10 Normal myocardium displays signal enhancement immediately after passage of the contrast bolus through the left ventricle (LV) because of the T1 shortening effect of the contrast material. Previously ischemic, reperfused myocardium has been shown to display 2 different types of contrast "defects": first-pass regions of reduced signal enhancement and regions with relatively increased signal intensity on delayed images.6 7 The relationship between these 2 patterns and subsequent regional recovery of mechanical function has not been determined. In addition, most previous studies have used only delayed imaging, but it is now possible to image dynamically through the first-pass period. Thus, the goals of the present study were to combine first-pass and delayed image data to assess contrast abnormalities and to quantify the relationship between changes in regional mechanical function between 1 and 7 weeks after MI in regions with abnormal contrast patterns by use of myocardial tissue tagging.
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Methods |
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Subject Population
Twenty-seven subjects, 10 normal (from medical history and age) control subjects who underwent contrast imaging only (4 men; mean age, 37±6 years) and 17 patients (14 men) with a mean age of 53±12 years were included. Patients were studied after a reperfused first MI. Average time from initial cardiac symptoms to initiation of reperfusion therapy was 280±170 minutes. Table 1
summarizes the clinical
parameters associated with each patient. All patients had
TIMI grade 3 flow in the infarct-related artery after therapy and
before week 1 contrast MRI.
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Image Acquisition
The normal control group underwent first-pass and delayed
contrast-enhanced imaging to establish normal values for contrast
kinetics and regional signal variability. In patients, MRI was
performed 1 (5±2 days) and 7 (7±2 weeks) weeks after MI. We used a
Siemens 1.5-T clinical scanner with patients in the prone position
using an elliptical surface receiver coil. Scout images in the coronal
and parasagittal long axis were used to identify the LV short and long
axes. End systole was timed on the basis of minimum cavity area from a
rapid midlevel short-axis cine with a time of resistance of 40
ms and a matrix of 64x128.
Tagged short-axis cine-segmented k-space MRI allowed data to be gathered during breath-hold periods of 16 to 18 cardiac cycles. Contiguous 7-mm short-axis slices were acquired from the LV apex to base at weeks 1 and 7. Seven phase lines were acquired for every cardiac cycle. A 280x280-mm field of view was imaged, including 112 to 126 phase lines and 256 frequency lines. Two sets of perpendicularly oriented tags, with 7-mm interstripe spacing, were generated by use of binomial radiofrequency pulses immediately before image acquisition. Images were acquired at 5 points across the cardiac cycle, with interphase delay adjusted to ensure timing of an image at end systole.
To position the contrast image plane, tagged short-axis images at multiple levels were reviewed in cine format to locate the region of mechanical dysfunction in each patient. On the basis of this information, a tagged long-axis cine was acquired in the center of dysfunction in the short axis to verify dysfunction in the same plane that would be used for the contrast-enhanced images. Contrast-enhanced images were acquired at week 1 with 0.1 mmol/kg nonionic gadolinium (Gadoteridol, Bracco Diagnostics) as described by Atkinson et al.11 A venous line was positioned in the antecubital vein, and a contrast bolus was injected by hand over 4 to 6 seconds. T1-weighted, inversion-prepared Turboflash images were then sequentially acquired at a single location immediately after contrast injection (repetition time=rr interval, matrix=96x128, echo time=2 ms, flip angle=10°, slice thickness=10 mm, and field of view=30 cm) in the center of the dysfunctional region. A sufficient number of images were acquired before contrast arrival in the LV to allow magnetization to reach steady state. The delay from the 180° inversion pulse to image acquisition was adjusted to minimize steady-state myocardial signal. Thus, images were acquired in diastole. A complete image was acquired in 360 ms during each of 64 sequential cardiac cycles. A delayed set of 10 inversion recovery images was acquired in the same orientation 7±2 minutes after contrast administration.
Image Analysis
First-pass and delayed contrast images were reviewed in cine
format and used in combination to define 2 types of abnormal contrast
pattern qualitatively. On the first-pass images, regions were
classified by 2 experienced, blinded observers as either normal in
intensity or hypointense. On the delayed images, regions were
characterized as normal in intensity or hyperintense. Regions
displaying first-pass hypoenhancement without delayed hyperenhancement
were defined as HYPO. Regions displaying no first-pass HYPO but delayed
hyperenhancement were defined as HYPER. Regions displaying combined
first-pass hypoenhancement and delayed hyperenhancement were defined as
COMB. Normal-appearing regions remote from either functional or
contrast abnormalities were defined as REMOTE.
Contrast images were reviewed by 2 blinded reviewers for determination of location and transmurality of contrast patterns. Defects were defined as being limited to the endocardial half of the LV wall (ENDO), the epicardial half of the wall (EPI), or transmural (TRANS).
Matching between week 1 tagged short- and long-axis perfusion images
was accomplished with a custom computer program. The 3-dimensional
coordinates defining the tagged short-axis image plane locations were
graphically superimposed on the long-axis contrast image that best
represented HYPO and HYPER in the first-pass and delayed
postcontrast images, respectively (Figure 1). Intersections between contrast
defects and short-axis tagged image locations were used to select the
tagged short-axis image planes that would be used for analysis
of segment shortening (%S). In addition, the circumferential location
and transmural extent (EPI, ENDO, or TRANS) of the contrast
abnormality were matched to the tagged images to assign %S loci to
HYPO, HYPER, COMB, or REMOTE. The transmural and circumferential
locations used to compute %S at week 1 were used for analysis
of week 7 function. Slice level between weeks 1 and 7 tagged short-axis
images was matched by use of internal landmarks such as papillary
muscles, right ventricular insertion points, and absolute
distance from the apex.
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Contrast Quantification
In patients, time-intensity curves, including initial and
delayed time points, were calculated for regions of interest (ROIs)
positioned within HYPO, HYPER, COMB, and REMOTE myocardium.
Because of position-dependent changes in signal intensity resulting
from the use of a surface receiver coil, curves were normalized in both
patients and control subjects by dividing the absolute signal intensity
by the value obtained in the same ROI before contrast arrival in the LV
but after steady-state magnetization was reached. Normalized
time-intensity curves were used to determine the signal intensity in
HYPO (at peak first-pass REMOTE myocardial signal enhancement) and
HYPER (in delayed images) relative to that in REMOTE in patients during
the first-pass period and delayed contrast enhancement.
Signal intensity data in the control group were measured with 5 equally spaced circular ROIs (mean area, 0.4 cm2). Measurements before enhancement, at peak signal enhancement, and in delayed images were used to compute regional signal variability (expressed as the coefficient of variation) and the normal signal range (mean±2 SD). Visually selected HYPO and HYPER in patients were then quantitatively compared with the normal range.
Mechanical Function Analysis
Regional myocardial percent circumferential %S from end
diastole to mechanical end systole was calculated with the
VIDA software package (University of Iowa) as previously
described.12 %S was measured at 3 transmural locations
(epicardium, middle, and endocardium) at each circumferential location
and for all locations by a trained observer (T.M.T.) with no knowledge
of contrast imaging results. Results for %S at weeks 1 and 7 were
compared in HYPO, COMB, HYPER, and REMOTE.
Statistical Analysis
Results are expressed as mean±SD. Group differences in %S
between regions and time points were tested by the independent-samples
t test or the nonparametric Mann-Whitney
rank-sum test. Individual differences were tested by use of Fisher
(least-significant-difference) posttest analysis. ANOVA with
Fisher's posttest analysis was used to test differences
between REMOTE, HYPER, and HYPO signal intensities during first-pass
and delayed image acquisitions by analysis of time-intensity
curves. Reproducibility between observers was tested by use of the
statistic. The coefficient of variation was used to express the
variability of relative postcontrast signal intensity within the LV in
the normal control and patient groups.
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Results |
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Contrast Kinetics
Normal Control Subjects
Normal myocardium displayed rapid, uniform first-pass signal enhancement and a lack of delayed regional hyperenhancement. The coefficients of variation for the 5 ROIs evenly distributed within the long-axis contrast enhanced images were 12.7% at peak enhancement and 15.2% on delayed images. The mean signal intensity relative to a reference ROI was 1.02±0.1, resulting in a ±2-SD range of 0.82 to 1.22 at peak enhancement. On delayed images, the mean relative signal intensity was 0.98±0.15 of the reference ROI, resulting in a ±2-SD range of 0.68 to 1.28. These values were used to verify HYPO and HYPER in the patient group.
Patients
Contrast imaging in the 17 patients identified 5 HYPO, 13 HYPER,
10 COMB, and 17 REMOTE for a total of 28 regions. It was possible to
have >1 abnormal contrast region in each patient. HYPO and HYPER were
validated by comparison with quantitative data from the 10 normal
control subjects. In regions visually identified as HYPO or COMB, 15 of
15 (100%) had relative signal intensity >2 SD below mean normal
values on first-pass images. In regions identified as HYPER, 11 of 13
(85%) had relative signal intensity >2 SD above mean normal values on
delayed images; the remaining 2 (15%) had signal intensity >1 SD
above delayed mean normal. Of 10 regions defined as COMB, 6 (60%) had
relative signal intensity on delayed imaging >2 SD above normal
delayed values, 3 (30%) were >1 SD above normal, and 1 (10%) was <1
SD above the mean normal delayed value.
Figure 2 shows time-intensity curves for
ROIs positioned in the LV blood pool, REMOTE, and HYPO regions for a
sample patient during myocardial contrast transit. After a rapid
increase in blood pool signal intensity, there is an early and
persistent difference in myocardial signal intensity between HYPO and
REMOTE. HYPO is seen as a subendocardial region of hypointense signal
in the apical-septum in a first-pass, 4-chamber long-axis image of the
same patient (Figure 3). In contrast, in
HYPER (Figure 4), the early signal
increase is similar between HYPER and REMOTE. However, the signal
intensity in HYPER continues to increase, whereas REMOTE reaches a
plateau. This produces hyperintense myocardium on the
delayed postcontrast image shown in Figure 1
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),
REMOTE (
), and HYPO (
) regions. Curves derived from initial 63
successive images after contrast administration show persistent
reduction in signal intensity vs REMOTE.
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Quantitative Analysis of First-Pass Signal Intensity
in Patients
During the first pass of the contrast bolus, signal enhancement in
HYPO was 52±27% of that seen in REMOTE (P<0.0001),
whereas the signal intensity in HYPER was similar to REMOTE (91±31%).
In delayed contrast imaging, HYPER increased to 139±38% of REMOTE
(P<0.003). Signal enhancement in HYPO normalized in delayed
images (80±38% of REMOTE, P=NS). COMB showed first-pass
signal hypoenhancement (36±24%), which was different from both REMOTE
and HYPER (P<0.001) but not from HYPO. Delayed-imaging
hyperenhancement in COMB was 159±68% of remote (P<0.01).
This was similar to HYPER and greater than observed in delayed HYPO
(P<0.04). Table 2 displays
the results of interobserver reproducibility in qualitatively
identifying the type, location, and transmurality of myocardial
contrast patterns.
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Relationship Between Contrast Abnormalities and Mechanical Function
Over Time
Figure 5 compares 2 midlevel
end-systolic short-axis tagged images of a patient displaying
anteroseptal HYPER. Depressed myocardial deformation at week 1 is seen
as a region of undeformed tag grid (arrow) in the anteroseptal region.
The same portion of the LV displays noticeable improvement at week 7
(right) as indicated by a normal tag deformation pattern. Figure 6 displays %S data for HYPO, COMB, and
HYPER regions at weeks 1 and 7. At week 1, %S was similar in HYPO,
COMB, and HYPER at 5±6%, 7±6%, and 9±8%, respectively. %S in
these 3 groups was significantly less (P<0.003) than the
18±6% measured in REMOTE. By week 7, however, %S in HYPER had
improved substantially to 18±5% (P<0.001 versus week 1),
whereas the change in %S within HYPO to 7±6% was not significant.
There was borderline improvement in %S in COMB from 7±6% to 11±5%
(P=0.06). REMOTE %S increased to 21±4% (P=NS
versus week 1). At week 7, HYPO, COMB, and HYPER displayed reduced %S
compared with REMOTE (P<0.05). HYPER displayed greater week
7%S compared with COMB (18±5% versus 11±5%, P<0.005)
and HYPO (18±5% versus 6±3%, P<0.001). At week 7, there
was a trend toward greater %S in COMB versus HYPO (P=0.12).
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P<0.005). |
Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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By combining information from first-pass and delayed MRI contrast-enhanced images with tissue tagging, we have shown that reperfused myocardial regions displaying a HYPER MRI contrast pattern show significant recovery of mechanical function at 7 weeks after MI. In contrast, HYPO does not show significant mechanical improvement, and there is a borderline improvement in COMB.
Our data and those from previous studies that used delayed imaging to identify HYPO (as defined in the present study) suggest that HYPO represents predominantly necrotic myocardium. Reduced signal intensity on first-pass MRI contrast images has been shown to be associated with reduced blood flow,4 although this relationship may not be linear when higher doses of extravascular gadolinium-based MRI contrast agents are used.13 In infarct regions, however, microvascular myocardial blood flow may not return to normal even after epicardial revascularization,14 the so-called no-reflow phenomenon. In 2-day-old reperfused canine MI, Judd et al7 reported a blunted and delayed increase in signal intensity in regions of infarcted myocardium. Hypointense regions correlated closely with regions delineated by thioflavin-S, a no-reflow marker. Regions of hypoenhancement have also been reported in patients with the use of a similar technique in healed infarcts after edema and other transient postischemic sequelae have likely resolved. Saeed et al10 also demonstrated hypointense regions in a rat model after 3.5 hours of occlusion without reperfusion using gadodiamide and T1-weighted spin-echo images. Thus, the lack of normal, first-pass signal enhancement after a bolus injection of MRI contrast has been shown to identify myocardium with reduced blood flow and in the present study is associated with little late functional recovery.
A number of interrelated factors, including reduced regional blood flow,4 5 15 increased capillary permeability,16 and increased interstitial volume,17 may produce HYPER within viable but previously ischemic myocardium. In the present study, HYPER differed in both contrast enhancement pattern and late myocardial function compared with HYPO, COMB, or REMOTE. The presence of regions with delayed hyperenhancement by use of extravascular contrast agents has been previously described.7 8 Using an isolated rabbit heart preparation, Kim et al15 quantified MRI contrast uptake and washout after reperfused MI. They concluded that hyperintense and hypointense contrast patterns are due primarily to alterations in wash-in/washout time constants that in turn result from differences in capillary density. Three different regions were analyzed: infarct center, infarct rim, and remote. These regions differed in extent and severity of ischemic damage and are roughly comparable to regions defined as HYPO, HYPER, and REMOTE in the present study. In the Kim et al15 study, signal-to-intensity ratios compared with REMOTE during the early wash-in phase were 40.4±2.1% and 84.9±3.6% (mean±SEM) for infarct center and infarct rim, respectively. These were similar to our values of 52±27% and 91±31% for HYPO and HYPER, respectively. Kim et al15 also reported infarct core and infarct rim signal intensity ratios of 95.9±6.6% and 114.8±2.7%, respectively, on delayed images. These are not dissimilar to our HYPO and HYPER values of 80±38% and 139±38%, respectively. We have shown that exclusively HYPER displays significant week 7 improvement and therefore must represent at least partially viable myocardium.
In a study evaluating MRI contrast patterns in patients after reperfused MI, Lima et al8 found that there was a good correlation between fixed 201Tl defect size and delayed contrast-enhanced MRI when both hyperintense and hypointense regions were combined but did not assess recovery of mechanical function. Fixed 201Tl defects are often associated with nonviable myocardium. Thus, these data may seem to be at odds with the results of the present study. However, Lima et al6 did not perform first-pass imaging. Furthermore, in the present study, all vessels had TIMI grade 3 flow before imaging, whereas the population studied by Lima et al included TIMI 0 to 3 flow. Incomplete reperfusion may account for such apparent reduced viability in HYPER. Another possibility may be that regions identified on stress-redistribution 201Tl imaging as "fixed" may contain both viable and nonviable myocardium. Recently, Dilsizian et al18 showed that 201Tl reinjection identifies a significant volume of viable myocardium within "fixed" defects by stress-redistribution-reinjection 201Tl scintigraphy. Judd et al7 reported in a canine contrast MRI study that the hyperintense regions on delayed images were generally smaller than the risk region but larger (12%) than regions of necrosis as defined by triphenyltetrazolium chloride staining. This would indicate that at least part of the delayed hyperintense regions contain viable myocardium.
Yokota et al9 used T1-weighted nonsegmented spin-echo imaging 5 to 10 minutes after Gd-DTPA administration in patients with nonreperfused myocardial infarction. They qualitatively compared contrast MRI results to peak creatine phosphokinase levels, wall motion, and coronary angiography and concluded that subendocardial or transmural hyperenhancement may reflect the existence of viable myocardium, whereas subendocardial hypoenhancement was associated with necrotic myocardium.
In the present study, there was a significant number (10 of 28) of abnormal regions that displayed both first-pass hypoenhancement and delayed hyperenhancement. It is likely that this group contains an admixture of viable and nonviable myocardium. There was a trend for improvement from week 1 to 7 in COMB (P=0.12) and for a difference in %S between COMB and HYPO in week 7 (P=0.06).
Study Limitations
%S measurements were repeated over time. This required matching
of regions within the LV between weeks 1 and 7. Intrinsic cardiac
landmarks were used to maintain registration as previously reported by
Kramer et al19 However, changes in LV shape or volume
between imaging sessions could affect the precision of the match.
Technical constraints limited MRI contrast imaging to a single image
plane. Thus, care in positioning of the contrast plane in the center of
the MI was essential. Given the limited spatial resolution of perfusion
imaging, a conservative approach was assigning the transmural extent of
contrast patterns as limited to EPI, the ENDO, or TRANS. There was a
trend for greater week 7%S in COMB versus HYPO (P=0.12).
Power analysis (independent-samples t test)
indicated that analysis of an additional 12 subjects would
result in a significant difference. Thus, the present study may be
limited in detecting differences in %S between these 2 groups.
Conclusions
Myocardium displaying hypoenhanced signal
(HYPO) during first-pass transit, regardless of delayed contrast
pattern, shows limited recovery of mechanical function by week 7 and is
likely to be predominantly infarcted. In contrast, regions displaying
hyperenhancement of delayed images in the absence of initial
hypoenhancement show substantial functional late recovery and likely
represent predominantly viable myocardium.
Therefore, combining the information from first-pass and delayed
contrast-enhanced MRI may predict late functional recovery in
reperfused MI. Advances in MRI acquisition speed should permit imaging
of all the LV during contrast first-pass and the delayed period,
allowing clinically relevant application of the present study.
Received June 8, 1998; revision received October 16, 1998; accepted October 26, 1998.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Koren GT, Hasin Y, Appelbaum D, Luria MH, Gotsman MS. Prevention of myocardial damage in acute myocardial ischemia by early treatment with intravenous streptokinase. N Engl J Med. 1985;313:1384–1389.[Abstract]
2. Gruppo Italiano per lo Studio della Stretochinasi nell' Infarto Miocardico (GISSI). Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Lancet. 1986;1:397–401.[Medline] [Order article via Infotrieve]
3. Stone GW, Grines CL, Browne KF, Marco J, Rothbaum D, O'Keefe J, Hartzler GO, Overlie P, Donohue B, Chelliah N, Timmis GC, Vlietstra R, Strzelecki M, Puchrowicz-Ochocki S, O'Neill WW. Predictors of in-hospital and 6-month outcome after acute myocardial infarction in the reperfusion era: the Primary Angioplasty in Myocardial Infarction (PAMI) trial. J Am Coll Cardiol. 1995;25:370–377.[Abstract]
4. Wilke N, Simm C, Zhang J, Ellermann J, Ya X, Merkle H, Path G, Ludemann H, Bache RJ, Ugurbil K. Contrast-enhanced first-pass myocardial perfusion imaging: correlation between myocardial blood flow in dogs at rest and during hyperemia. Magn Reson Med. 1993;29:485–497.[Medline] [Order article via Infotrieve]
5. Diesbourg LD, Prato FS, Wisenberg G, Drost DJ, Marshall TP, Carroll SE, O'Neill B. Quantification of myocardial blood flow and extracellular volumes using a bolus injection of Gd-DTPA: kinetic modeling in canine ischemic disease. Magn Reson Med. 1992;23:239–253.[Medline] [Order article via Infotrieve]
6. Eichenberger AC, Schuiki E, Kochll VD, Amann FW, McKinnon GC, Schulthess GKV. Ischemic heart disease: assessment with gadolinium-enhanced ultrafast MR imaging and dipyridamole-stress. J Magn Reson Imaging. 1994;4:425–431.[Medline] [Order article via Infotrieve]
7.
Judd RM, Lugo-Olivieri CH, Arai M, Kondo T, Croisille
P, Lima JAC, Mohan V, Becker LC, Zerhouni EA.
Physiological basis of myocardial contrast
enhancement in fast magnetic resonance images of 2-day-old reperfused
canine infarcts. Circulation. 1995;92:1902–1910.
8.
Lima JAC, Judd RM, Bazille A, Schulman SP, Atalar E,
Zerhouni EA. Regional heterogeneity of human myocardial
infarcts demonstrated by contrast enhanced MRI: potential mechanisms.
Circulation. 1995;92:1117–1125.
9. Yakota C, Nonogi H, Miyazaki S, Goto Y, Maeno M, Daikoku S, Itoh A, Haze K, Yamada N. Gadolinium-enhanced magnetic resonance imaging in acute myocardial infarction. Am J Cardiol. 1995;75:577–581.[Medline] [Order article via Infotrieve]
10.
Saeed M, Wendland M, Takehara Y, Masui Takayuki Higgins
CB. Reperfusion and irreversible myocardial injury: identification with
a nonionic MR imaging contrast medium. Radiology. 1992;182:675–683.
11.
Atkinson DJ, Burstein D, Edelman RR. First-pass cardiac
perfusion: evaluation with ultrafast MR imaging. Radiology. 1990;174:757–762.
12.
Clark N, Reichek N, Bergey P, Hoffman EA, Brownson D,
Palmon L, Axel L. Normal segmental myocardial function: assessment by
magnetic resonance imaging using spatial modulation of magnetization.
Circulation. 1991;84:67–74.
13. Burstein D, Taratuta E, Manning WJ. Factors in myocardial "perfusion" imaging with ultrafast MRI and Gd-DTPA administration. Magn Reson Med. 1991;20:299–305.[Medline] [Order article via Infotrieve]
14. Kloner RA, Ganote CE, Jennings RB. The. "no-reflow" phenomenon after temporary coronary occlusion in the dog. J Clin Invest. 1974;54:1496–1508.
15.
Kim RJ, Chen R-L, Lima JAC, Judd RM. Myocardial Gd-DTPA
kinetics determine MRI contrast enhancement and reflect the extent and
severity of myocardial injury after acute reperfused infarction.
Circulation. 1996;94:3318–3326.
16.
Dauber IM, Van Benthuysen KM, McMurtry IF, Wheeler GS,
Lesnefsky EJ, Horwitz LD, Weil JV. Functional coronary
microvascular injury evident as increased permeability due to brief
ischemia and reperfusion. Circ Res. 1990;66:986–998.
17. Saeed M, Wendland MF, Masui T, Higgins CB. Reperfused myocardial infarctions on T1- and susceptibility-enhanced MRI: evidence for loss of compartmentalization of contrast media. Magn Reson Med. 1994;31:31–39.[Medline] [Order article via Infotrieve]
18. Dilsizian V, Rocco TP, Freedman NMT, Leon MB, Bonow RO. Enhanced detection of ischemic by viable myocardium by the reinjection of thallium after stress-redistribution imaging. N Engl J Med. 1990;323:141–146.[Abstract]
19. Kramer CM, Rogers WJ, Thedobald TM, Power TP, Geskin G, Reichek N. Dissociation between changes in intramyocardial function and left ventricular volumes in the 8 weeks after first anterior myocardial infarction. J Am Coll Cardiol. 1997;30:1625–1632.The association between postreperfusion MRI contrast patterns and recovery of myocardial function was studied in 17 patients. Circumferential shortening (%S) was measured in regions of first-pass hypoenhancement (HYPO), normal first pass with delayed hyperenhancement (HYPER), regions displaying both patterns (COMB) and remote myocardium at weeks 1 and 7. Week 1%S was similar in HYPO, COMB, and HYPER (5±4%, 7±6%, and 9±8%, respectively). Week 7%S improved in HYPER to 18±5% (P<0.001 versus week 1) but not in HYPO or COMB (6±3% and 11±6%, respectively; P=NS). Thus, MRI contrast patterns early after reperfused myocardial infarction may predict functional recovery.[Abstract]
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|
|
|
T. Dickfeld, R. Kato, M. Zviman, S. Lai, G. Meininger, A. C. Lardo, A. Roguin, D. Blumke, R. Berger, H. Calkins, et al. Characterization of Radiofrequency Ablation Lesions With Gadolinium-Enhanced Cardiovascular Magnetic Resonance Imaging J. Am. Coll. Cardiol., January 17, 2006; 47(2): 370 - 378. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Koyama, H. Matsuoka, T. Mochizuki, H. Higashino, H. Kawakami, S. Nakata, J. Aono, T. Ito, M. Naka, Y. Ohashi, et al. Assessment of Reperfused Acute Myocardial Infarction with Two-Phase Contrast-enhanced Helical CT: Prediction of Left Ventricular Function and Wall Thickness Radiology, June 1, 2005; 235(3): 804 - 811. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N G Bellenger, Z Yousef, K Rajappan, M S Marber, and D J Pennell Infarct zone viability influences ventricular remodelling after late recanalisation of an occluded infarct related artery Heart, April 1, 2005; 91(4): 478 - 483. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. M. Kramer The prognostic significance of microvascular obstruction after myocardial infarction as defined by cardiovascular magnetic resonance Eur. Heart J., March 2, 2005; 26(6): 532 - 533. [Full Text] [PDF]
|
|
|
|
|
|
T. Ibrahim, S. G. Nekolla, M. Hornke, H. P. Bulow, J. Dirschinger, A. Schomig, and M. Schwaiger Quantitative measurement of infarct size by contrast-enhanced magnetic resonance imaging early after acute myocardial infarction: Comparison with single-photon emission tomography using Tc99m-sestamibi J. Am. Coll. Cardiol., February 15, 2005; 45(4): 544 - 552. [Abstract] [Full Text] [PDF]
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|
|
|
|
|
L. C. Amado, B. L. Gerber, S. N. Gupta, D. W. Rettmann, G. Szarf, R. Schock, K. Nasir, D. L. Kraitchman, and J. A.C. Lima Accurate and objective infarct sizing by contrast-enhanced magnetic resonance imaging in a canine myocardial infarction model J. Am. Coll. Cardiol., December 21, 2004; 44(12): 2383 - 2389. [Abstract] [Full Text] [PDF]
|
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|
|
|
|
R. J. Gibbons, U. S. Valeti, P. A. Araoz, and A. S. Jaffe The quantification of infarct size J. Am. Coll. Cardiol., October 19, 2004; 44(8): 1533 - 1542. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Cochet, M. Zeller, Y. Cottin, C. Robert-Valla, A. Lalande, I. L'Huilllier, A. Comte, P. M. Walker, J. Desgres, J.-E. Wolf, et al. The extent of myocardial damage assessed by contrast-enhanced MRI is a major determinant of N-BNP concentration after myocardial infarction Eur J Heart Fail, August 1, 2004; 6(5): 555 - 560. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Bolli, L. Becker, G. Gross, R. Mentzer Jr, D. Balshaw, and D. A. Lathrop Myocardial Protection at a Crossroads: The Need for Translation Into Clinical Therapy Circ. Res., July 23, 2004; 95(2): 125 - 134. [Abstract] [Full Text] [PDF]
|
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|
|
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W. P. Ingkanisorn, K. L. Rhoads, A. H. Aletras, P. Kellman, and A. E. Arai Gadolinium delayed enhancement cardiovascular magnetic resonance correlates with clinical measures of myocardial infarction J. Am. Coll. Cardiol., June 16, 2004; 43(12): 2253 - 2259. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 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]
|
|
|
|
|
|
Z. Yang, S. S. Berr, W. D. Gilson, M.-C. Toufektsian, and B. A. French Simultaneous Evaluation of Infarct Size and Cardiac Function in Intact Mice by Contrast-Enhanced Cardiac Magnetic Resonance Imaging Reveals Contractile Dysfunction in Noninfarcted Regions Early After Myocardial Infarction Circulation, March 9, 2004; 109(9): 1161 - 1167. [Abstract] [Full Text] [PDF]
|
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|
|
|
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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]
|
|
|
|
|
|
M.B. Britten, N.D. Abolmaali, B. Assmus, R. Lehmann, J. Honold, J. Schmitt, T.J. Vogl, H. Martin, V. Schachinger, S. Dimmeler, et al. Infarct Remodeling After Intracoronary Progenitor Cell Treatment in Patients With Acute Myocardial Infarction (TOPCARE-AMI): Mechanistic Insights From Serial Contrast-Enhanced Magnetic Resonance Imaging Circulation, November 4, 2003; 108(18): 2212 - 2218. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
C. R. Weiss, A. H. Aletras, J. F. London, J. L. Taylor, F. H. Epstein, R. Wassmuth, R. S. Balaban, and A. E. Arai Stunned, Infarcted, and Normal Myocardium in Dogs: Simultaneous Differentiation by Using Gadolinium-enhanced Cine MR Imaging with Magnetization Transfer Contrast Radiology, March 1, 2003; 226(3): 723 - 730. [Abstract] [Full Text] [PDF]
|
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|
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|
M. Saeed, N. Watzinger, G. A. Krombach, G. K. Lund, M. F. Wendland, M. Chujo, and C. B. Higgins Left Ventricular Remodeling after Infarction: Sequential MR Imaging with Oral Nicorandil Therapy in Rat Model Radiology, September 1, 2002; 224(3): 830 - 837. [Abstract] [Full Text] [PDF]
|
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|
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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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P Andrassy, M Zielinska, R Busch, A Schomig, and C Firschke Myocardial blood volume and the amount of viable myocardium early after mechanical reperfusion of acute myocardial infarction: prospective study using venous contrast echocardiography Heart, April 1, 2002; 87(4): 350 - 355. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. G. Rehwald, D. S. Fieno, E.-L. Chen, R. J. Kim, and R. M. Judd Myocardial Magnetic Resonance Imaging Contrast Agent Concentrations After Reversible and Irreversible Ischemic Injury Circulation, January 15, 2002; 105(2): 224 - 229. [Abstract] [Full Text] [PDF]
|
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|
|
|
J. N. Oshinski, Z. Yang, J. R. Jones, J. F. Mata, and B. A. French Imaging Time After Gd-DTPA Injection Is Critical in Using Delayed Enhancement to Determine Infarct Size Accurately With Magnetic Resonance Imaging Circulation, December 4, 2001; 104(23): 2838 - 2842. [Abstract] [Full Text] [PDF]
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|
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S. KAUL Coronary angiography cannot be used to assess myocardial perfusion in patients undergoing reperfusion for acute myocardial infarction Heart, November 1, 2001; 86(5): 483 - 484. [Full Text] [PDF]
|
|
|
|
|
|
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]
|
|
|
|
 |
|
 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]
|
|
|
|
 |
|
 M. Saeed New Concepts in Characterization of Ischemically Injured Myocardium by MRI Exp Biol Med, May 1, 2001; 226(5): 367 - 376. [Abstract] [Full Text] [PDF]
|
|
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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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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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|
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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|
D. S. Fieno, R. J. Kim, E.-L. Chen, J. W. Lomasney, F. J. Klocke, and R. M. Judd Contrast-enhanced magnetic resonance imaging of myocardium at risk: Distinction between reversible and irreversible injury throughout infarct healing J. Am. Coll. Cardiol., November 15, 2000; 36(6): 1985 - 1991. [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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|
|
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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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C. B. Higgins Prediction of Myocardial Viability by MRI Circulation, February 16, 1999; 99(6): 727 - 729. [Full Text] [PDF]
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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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