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Published online before print May 27, 2004, 10.1148/radiol.2321031127
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(Radiology 2004;232:49-57.)
© RSNA, 2004


Cardiac Imaging

Acute Myocardial Infarction: Evaluation with First-Pass Enhancement and Delayed Enhancement MR Imaging Compared with 201Tl SPECT Imaging1

Gunnar K. Lund, MD, Alexander Stork, MD, Maythem Saeed, DVM, PhD, Martin P. Bansmann, MD, Jann H. Gerken, MD, Vika Müller, MD, Janos Mester, PhD, Charles B. Higgins, MD, Gerhard Adam, MD and Thomas Meinertz, MD

1 From the Departments of Cardiology (G.K.L., J.H.G., T.M.), Diagnostic and Interventional Radiology (A.S., M.P.B., J.H.G., G.A.), and Nuclear Medicine (V.M., J.M.), University Hospital Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany; and Department of Radiology, University of California, San Francisco (M.S., C.B.H.). From the 2002 RSNA scientific assembly. Received July 18, 2003; revision requested October 2; revision received October 29; accepted January 5, 2004. Supported in part by Schering, Berlin, Germany, and by the Pinguin Stiftung Düsseldorf, Germany. Address correspondence to G.K.L. (e-mail: glund@uke.uni-hamburg.de).


    ABSTRACT
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 APPENDIX
 REFERENCES
 
PURPOSE: To evaluate acute myocardial infarction by using first-pass enhancement (FPE) and delayed enhancement (DE) magnetic resonance (MR) imaging compared with thallium 201 (201Tl) single photon emission computed tomography (SPECT).

MATERIALS AND METHODS: Contrast material–enhanced FPE MR, inversion-recovery DE MR, and rest-redistribution 201Tl SPECT images were obtained in 60 consecutive patients (53 men, seven women; mean age [± SD], 56 years ± 13; range, 30–78 years) at 6 days ± 3 after reperfused first myocardial infarction. Presence of microvascular obstruction was determined on FPE MR images. Infarct size was defined on DE MR images as percentage of left ventricular (LV) area and compared with uptake defect on redistribution 201Tl SPECT images. Differences in continuous data were analyzed with Student t test. Linear regression and Bland-Altman analysis were used to compare measurements of infarct size.

RESULTS: Mean infarct size was not significantly different between DE MR imaging (20.7% ± 11.5% of LV area) and 201Tl SPECT (19.4% ± 14.3% of LV area; P = .26); good correlation (r = 0.73; P < .001) and agreement were found, with a mean difference of +1.3% ± 9.8% of LV area. 201Tl SPECT failed to depict infarct in six (20%) of 30 patients with inferior myocardial infarction (mean size, 6.4% ± 5.7% of LV area on DE MR images), whereas DE MR images showed the infarct in all patients (P < .01). FPE MR images depicted microvascular obstruction in 23 (38%) of 60 patients; these patients had larger infarctions at DE MR imaging than did patients without microvascular obstruction (30.4% ± 9.0% vs 15.1% ± 8.4% of LV area, P < .001). 201Tl SPECT showed larger infarcts in patients with microvascular obstruction (26.7% ± 16.2% vs 15.0% ± 11.2% of LV area, P < .01).

CONCLUSION: Good correlation and agreement with 201Tl SPECT indicate DE MR imaging may be used to estimate infarct size 6 days after reperfused acute myocardial infarction. DE MR imaging is more sensitive for detection of inferior infarction than is 201Tl SPECT. Patients with microvascular obstruction on FPE MR images have larger infarcts.

© RSNA, 2004

Index terms: Coronary vessels, stenosis or obstruction, 54.771 • Myocardium, infarction, 511.771 • Myocardium, MR, 511.121413, 511.12143 • Myocardium, SPECT, 511.12162 • Single photon emission computed tomography (SPECT), comparative studies, 511.121413, 511.12162


    INTRODUCTION
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 APPENDIX
 REFERENCES
 
Delayed enhancement (DE) magnetic resonance (MR) imaging has been used in the detection and measurement of acute and chronic myocardial infarction. Results of previous studies have documented the accuracy of inversion-recovery DE MR imaging in determining infarct size in patients with chronic infarction, validated with nuclear imaging techniques (1,2). However, few studies have been performed to analyze the accuracy of DE MR imaging for estimating infarct size in patients with acute myocardial infarction(3,4). Choi et al (4) showed close correlation between infarct size at DE MR imaging and peak release of creatine kinase (CK)-MB. In a study of 12 patients, Lima et al (3) revealed good correlation between DE MR imaging and thallium 201 (201Tl) single photon emission computed tomography (SPECT) for estimation of acute infarct size. However, authors of several animal studies have questioned the accuracy of DE MR imaging for quantifying acute infarct size because results of these studies revealed an overestimation of infarct size with DE MR imaging compared with histologic evaluation (59).

Contrast material–enhanced MR imaging also has the potential to allow identification of regional microvascular obstruction at first-pass enhancement (FPE) (6,10,11). The phenomenon of microvascular obstruction frequently occurs in the first few days after acute myocardial infarction, despite successful revascularization of the infarct-related artery (12). Results of experimental studies have shown that microvascular obstruction is related to endothelial swelling, to myocyte edema, and to obstruction of the capillaries by neutrophils, erythrocytes, and debris (12). Presence of microvascular obstruction is associated with greater myocardial damage, based on electrocardiographic and echocardiographic criteria (3,11). Furthermore, results of clinical studies have indicated that microvascular obstruction is associated with left ventricular (LV) remodeling and increased risk of mortality and morbidity (11,13).

Acute infarct size estimated at 201Tl SPECT has close correlation with true infarct size obtained from pathologic specimens (14). In humans, defect size at 201Tl SPECT correlates well with other physiologic measurements, including myocardial enzyme release (15,16) and LV ejection fraction (16), as well as with infarct size at technetium 99m sestamibi (17,18). Results of studies performed in patients with acute myocardial infarction have shown that the redistribution images allow one to accurately distinguish viable from scarred myocardium, whereas the early images may lead to underestimation of infarct size (19). SPECT is widely used to estimate infarct size after reperfusion therapy (19) and to predict outcome according to infarct size (20).

The purpose of our study was to evaluate patients with acute myocardial infarction by using FPE and DE MR imaging in comparison with 201Tl SPECT.


    MATERIALS AND METHODS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 APPENDIX
 REFERENCES
 
Study Protocol and Patient Characteristics
This study was approved by the institutional ethics committee (at University Hospital Eppendorf), and all patients gave written informed consent after the nature of the study and procedures had been fully explained. Sixty-three consecutive patients with first myocardial infarction were prospectively enrolled. Acute myocardial infarction was defined by prolonged chest pain, a peak CK-MB level more than twice the normal upper limit (5 U/L), and 1.0 mm or greater ST segment elevation in two or more leads at initial electrocardiography. Patients were included if they had undergone reperfusion therapy by means of angioplasty or thrombolysis and had no contraindication to MR imaging (pacemaker, intracranial metal, claustrophobia, or obesity [>150 kg body weight]) or 201Tl SPECT (obesity [>150 kg body weight] or severe renal failure).

Coronary angiography was performed in all patients to identify the infarct-related artery. Perfusion of the infarct-related artery was determined at consensus reading by two observers (G.K.L. and M.P.B., 10 and 2 years of experience reading coronary angiograms, respectively) by using the Thrombolysis in Myocardial Infarction (TIMI) trial criteria (see Appendix). Subsequently, the infarct-related artery underwent revascularization in all patients with reduced TIMI flow before the imaging examinations were performed. MR imaging and SPECT were performed within 24 hours and later than 3 days after myocardial infarction. Two patients discontinued MR imaging because of claustrophobia, and another patient withdrew informed consent to 201Tl SPECT. No patient was excluded for reasons of technical or image quality.

Thus, 60 patients completed the study. There were 53 men and seven women, with a mean age (± SD) of 56 years ± 13 (age range, 30–78 years). Age among men (mean age, 57 years ± 12; age range, 30–78 years) was not statistically different from that among women (mean age, 53 years ± 15; age range, 32–75 years; P = .42). Furthermore, no other patient characteristics were statistically different between the men and women. Q-wave infarction was present in 38 patients (63%). Peak CK level was 1,038 U/L ± 840, with a peak CK-MB isoenzyme level of 112 U/L ± 71. The infarct-related artery was the left anterior descending artery in 30 (50%), the right coronary artery in 17 (28%), and the circumflex artery in 13 patients (22%). In 47 patients (78%), myocardial infarction was successfully treated with direct angioplasty. In one patient scheduled to undergo direct angioplasty, revascularization was not performed because this patient had a spontaneous thrombolysis with TIMI flow grade 3 and no restenosis. The remaining 12 patients received thrombolytic agents, and revascularization was performed before the imaging procedures at 6 days ± 4 after infarction by means of angioplasty (n = 11) or bypass surgery (n = 1). Examinations with both imaging modalities were performed at 6 days ± 3 (range, 3–14 days) after infarction.

MR Imaging
MR imaging was performed with a 1.5-T system (Vision; Siemens Medical Systems, Erlangen, Germany) by using a phased-array chest coil and electrocardiographic triggering. All images were acquired during breath-hold sequences in double oblique planes along the short axis of the LV. FPE MR imaging was used to detect regional microvascular obstruction, whereas DE MR imaging was used to estimate infarct size. For FPE MR imaging, a bolus of 0.1 mmol of gadopentetate dimeglumine (Magnevist; Schering, Berlin, Germany) per kilogram of body weight was injected into an antecubital vein, followed by saline solution. Injection was performed at 3 mL/sec with a power injector (Spectris; Medrad, Indianola, Pa). Immediately after injection, one image per R-R interval was acquired for the next 60 heartbeats at a single midventricular section along the short axis by using a T1-weighted turbo fast low-angle shot sequence with a 90° saturation-recovery preparatory pulse. Imaging parameters were as follows: repetition time, 2.4 msec; echo time, 1.2 msec; effective inversion time, 118 msec; section thickness, 10 mm; field of view, 350 x 306 mm (7/8 rectangular field of view); image matrix, 128 x 90; and pixel size, 2.7 x 3.4 mm.

At 10 minutes after injection, DE MR imaging was performed in three short-axis LV sections at the apical, midventricular, and basal levels by using a T1-weighted turbo fast low-angle shot sequence with a segmented 180° inversion-recovery preparatory pulse (21). Imaging parameters were as follows: repetition time, 7.6 msec; echo time, 3.4 msec; inversion time, 220–300 msec to null the signal intensity of normal myocardium; delay after trigger, 400 msec; section thickness, 6 mm; field of view, 350 x 262 mm (6/8 rectangular field of view); image matrix, 256 x 132; and pixel size, 1.37 x 2.0 mm. Images were obtained every other heartbeat to allow time for more complete inversion recovery.

MR Data Analysis
MR images were transferred to a computer (Macintosh; Apple Computer, Cupertino, Calif), and data analysis was performed by using a public domain program (NIH Image, version 1.62; U.S. National Institutes of Health; available at rsb.info.nih.gov/nih-image). All MR measurements were performed independently by two of three observers (G.K.L., A.S., and M.P.B., with 5, 3, and 2 years of experience interpreting cardiac MR images, respectively) who were blinded to the results of 201Tl SPECT, as well as to all clinical data. MR data are given as mean values from the two readings. Microvascular obstruction was identified on single-section FPE MR images as an area of persistent subendocardial hypoenhancement with signal intensity more than 2 SDs lower than that of the surrounding hyperenhanced myocardium (22). The size of microvascular obstruction was measured on the image that showed peak enhancement in remote normal myocardium. Delayed hyperenhancement was considered present if the signal intensity was more than 2 SDs higher than that of remote normal myocardium on DE MR images (22). Images were thresholded to these levels, and the size of microvascular obstruction and infarct was measured and expressed as a percentage of the LV area. On DE MR images, the size of a zone of persistent subendocardial hypoenhancement within a hyperenhanced area was also measured, and this area was included in measurements of infarct size (23).

201Tl SPECT
Patients underwent 201Tl SPECT at rest after injection of 1 MBq (0.03 mCi) of 201Tl (Bristol-Myers Squibb Pharma, Brussels, Belgium) per kilogram of body weight. Rest-redistribution images were acquired 4 hours after injection; images were acquired with a dual-head gamma camera equipped with a low-energy high-spatial-resolution collimator (ECAM; Siemens Medical Systems). Thirty-two projections were acquired over a 90° arc, with an acquisition time of 40 seconds each. Transverse images were reconstructed in a 64 x 64-pixel matrix by using a filtered back projection with a Butterworth filter with an order of 5 and a cutoff frequency of 0.5 cycles per pixel. SPECT images were independently evaluated by one observer (V.M., 5 years of experience interpreting cardiac SPECT images) who was blinded to all other data by using a polar projection–based image analysis program (4D-MSPECT; University of Michigan, Ann Arbor). A volumetric sampling algorithm was used to delineate a maximum count surface, which was transformed into a polar map. Each polar map was normalized to maximum uptake of the tracer. Infarct size was calculated as a percentage of the LV area by using an uptake threshold more than –2.5 SDs (24,25) below the normal threshold established at the University of Michigan.

Statistical Analysis
Continuous data are expressed as mean ± SD. Differences in continuous data between or within groups were analyzed by using the Student t test for unpaired or paired data, respectively. Categorical variables were analyzed by using the {chi}2 test. Linear regression and Bland-Altman analysis were used for analysis of correlation and agreement in measurements of infarct size. Concordance between microvascular obstruction on FPE MR images and persistent hypoenhancement on DE MR images was analyzed by using {kappa} statistics for paired data. Diagnostic accuracy of DE MR imaging in the detection of microvascular obstruction was calculated, including the corresponding 95% CIs. P < .05 was required to show statistical significance.


    RESULTS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 APPENDIX
 REFERENCES
 
Comparison between DE MR Imaging and 201Tl SPECT
Figure 1 shows representative multisection DE MR and 201Tl SPECT images in patients with anterior (Fig 1a) and inferior (Fig 1b) infarction. Mean size of myocardial infarct was not significantly different between DE MR imaging (20.7% ± 11.5% of the LV area) and 201Tl SPECT (19.4% ± 14.3% of the LV area; P = .26). Regression analysis revealed good correlation between the two measurements (r = 0.73; P < .001; Fig 2). Bland-Altman analysis showed close agreement between the modalities, with a mean difference of +1.3% ± 9.8% of the LV area (Fig 3). Moderate correlations were found between peak CK-MB and infarct size determined with 201Tl SPECT (r = 0.46; P < .001; Fig 4a) and DE MR imaging (r = 0.59; P < .001; Fig 4b). 201Tl SPECT failed to depict small infarcts in six (20%) of 30 patients with inferior infarction, whereas DE MR imaging depicted the infarction in all cases (P < .01). The mean size of small infarctions that were missed at 201Tl SPECT was 6.4% ± 5.7% of the LV area at DE MR imaging. All six of these patients had an elevated CK-MB level (49 U/L ± 44; range, 15–135 U/L); at coronary angiography, the infarct-related artery was identified as the right coronary artery in five patients and the circumflex artery in one patient. DE MR imaging was more sensitive for detecting inferior infarction compared with 201Tl SPECT (100% vs 80%, P < .01). A better agreement between modalities was found for anterior infarction (mean difference, –3.1% ± 8.3% of the LV area) compared with inferior infarction (mean difference, +5.6% ± 9.4% of the LV area). The mean difference between observers was 0.1% ± 3.1% of the LV area at DE MR imaging and 0.6% ± 2.4% of the LV area at FPE MR imaging.



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Figure 1a. T1-weighted multiple-section short-axis DE MR images obtained with inversion-recovery turbo fast low-angle shot sequence and corresponding short-axis 201Tl SPECT images in two patients with acute myocardial infarction. (a) In a patient with anterior infarction, size and location of contrast-enhanced area (arrowheads) on DE MR images correspond with uptake defect on 201Tl SPECT images. (b) In a patient with inferior infarction, a small but distinct area of enhancement in the inferior wall (arrowheads) is seen on DE MR images but not on 201Tl SPECT images.

 


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Figure 1b. T1-weighted multiple-section short-axis DE MR images obtained with inversion-recovery turbo fast low-angle shot sequence and corresponding short-axis 201Tl SPECT images in two patients with acute myocardial infarction. (a) In a patient with anterior infarction, size and location of contrast-enhanced area (arrowheads) on DE MR images correspond with uptake defect on 201Tl SPECT images. (b) In a patient with inferior infarction, a small but distinct area of enhancement in the inferior wall (arrowheads) is seen on DE MR images but not on 201Tl SPECT images.

 


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Figure 2. Graph shows strong correlation between infarct size at 201Tl SPECT and DE MR imaging in 60 patients with acute myocardial infarction (Y = 9.7 + 0.58X; r = 0.73; P < .001; standard error of the estimate, 7.88).

 


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Figure 3. Graph shows good agreement between 201Tl SPECT and DE MR imaging in the estimation of infarct size in 60 patients with acute myocardial infarction (mean difference, +1.3% ± 9.8% of the LV area).

 


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Figure 4a. Graphs show correlation of estimation of infarct size (a) between peak CK-MB level and 201Tl SPECT (Y = 9.1 ± 0.09X; r = 0.46; P < .001; standard error of the estimate, 12.82) and (b) between peak CK-MB level and DE MR imaging (Y = 10.5 ± 0.09X; r = 0.59; P < .001; standard error of the estimate, 9.30). 201Tl SPECT failed to depict myocardial infarct in six patients with significant elevation of CK-MB level, whereas DE MR imaging depicted infarct in all patients.

 


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Figure 4b. Graphs show correlation of estimation of infarct size (a) between peak CK-MB level and 201Tl SPECT (Y = 9.1 ± 0.09X; r = 0.46; P < .001; standard error of the estimate, 12.82) and (b) between peak CK-MB level and DE MR imaging (Y = 10.5 ± 0.09X; r = 0.59; P < .001; standard error of the estimate, 9.30). 201Tl SPECT failed to depict myocardial infarct in six patients with significant elevation of CK-MB level, whereas DE MR imaging depicted infarct in all patients.

 
Microvascular Obstruction: Imaging Characteristics
In 23 patients (38%), microvascular obstruction was observed on FPE MR images as a subendocardial hypoenhanced area surrounded by hyperenhanced myocardium (Fig 5); in the remaining 37 patients, there was no evidence of microvascular obstruction. In 17 of 23 patients in whom microvascular obstruction was depicted on FPE MR images, DE MR images also depicted a subendocardial zone of persistent hypoenhancement surrounded by a larger hyperenhanced area (Fig 5; Table 1). Conversely, in 35 of 37 patients in whom microvascular obstruction was not depicted on FPE MR images, DE MR images showed no persistent hypoenhancement. A high concordance was found between microvascular obstruction on FPE MR images and persistent hypoenhancement on DE MR images at 10 minutes after contrast material injection ({kappa} value, 0.71). Discordant findings were present in eight patients; in six of these patients, microvascular obstruction was depicted on FPE MR images, but no persistent hypoenhancement was seen on DE MR images. In the remaining two patients, no microvascular obstruction was observed on FPE MR images, but DE MR images revealed persistent hypoenhancement. One of these two patients had an anterior infarction, and DE MR images showed persistent hypoenhancement only in the apical section, whereas the other patient with inferior infarction had persistent hypoenhancement solely in the basal section on DE MR images.



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Figure 5. Corresponding midventricular short-axis images in a patient with microvascular obstruction (top row) and a patient without microvascular obstruction (bottom row). An inversion-recovery T1-weighted turbo fast low-angle shot sequence was used for FPE and DE MR imaging. In the patient with microvascular obstruction, the perfusion defect is depicted as a subendocardial hypoenhanced region on the FPE MR image (arrowheads). DE MR image shows a persistent hypoenhanced zone (open arrowheads), surrounded by a larger hyperenhanced area (solid arrowheads). In the patient without microvascular obstruction on the FPE MR image, homogeneous enhancement of the area affected by infarction (arrowheads) is seen on the DE MR image. In both patients, the uptake defect on the 201Tl SPECT image corresponds to the enhanced zone on the DE MR image.

 

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TABLE 1. Concordance between Microvascular Obstruction on FPE MR Images and Persistent Hypoenhancement on DE MR Images

 
With FPE MR imaging used as the reference standard, DE MR imaging was shown to have a sensitivity, specificity, and accuracy for detection of microvascular obstruction of 74% (95% CI: 52%, 90%), 95% (95% CI: 82%, 99%), and 87% (95% CI: 75% 94%), respectively. Quantitative measurement revealed that the size of microvascular obstruction on FPE MR images was larger than that of persistent hypoenhancement on corresponding midventricular DE MR images (13.5% ± 5.7% vs 4.4% ± 5.1% of the LV area; P < .001), which suggested slow diffusion of the contrast medium into the region of microvascular obstruction.

Size of Myocardial Infarct
Patients with microvascular obstruction had larger infarcts at DE MR imaging in comparison with patients without obstruction (30.4% ± 9.0% vs 15.1% ± 8.4% of the LV area; P < .001; Fig 6). Use of 201Tl SPECT confirmed larger infarcts in patients with microvascular obstructions (26.7% ± 16.2% vs 15.0% ± 11.2% of the LV area; P < .01). Presence of microvascular obstruction was indicative of a large infarct (ie, infarct size larger than 20% of the LV area). Twenty (87%) of 23 patients with microvascular obstruction had large infarcts compared with those in 11 (30%) of 37 patients without microvascular obstruction (P < .001).



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Figure 6. Bar graph shows that infarct size was larger in patients with microvascular obstruction (MO) than in patients without obstruction. P < .001 at DE MR imaging (*), P < .01 at 201Tl SPECT ({dagger}), and P < .001 for size of microvascular obstruction versus infarct size on DE MR images in patients with microvascular obstruction ({ddagger}).

 
Clinical Findings
Reduced TIMI flow of the infarct-related artery before revascularization was found more often in patients with microvascular obstruction than in those without microvascular obstruction (Table 2). Furthermore, peak releases of CK and CK-MB were significantly higher in patients with microvascular obstruction (P < .001). No statistically significant differences were found with respect to age, gender, presence of Q-wave infarction, involvement of the infarct-related artery, or treatment of myocardial infarction by means of direct angioplasty or thrombolysis.


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TABLE 2. Characteristics in Patients with and without Microvascular Obstruction

 

    DISCUSSION
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 APPENDIX
 REFERENCES
 
The major findings among 60 patients with acute myocardial infarction were as follows: (a) A good correlation and agreement were found between DE MR imaging and 201Tl SPECT in the measurement of infarcts of various sizes 6 days after reperfused myocardial infarction; (b) DE MR imaging was more sensitive for detecting small inferior infarcts, in comparison with 201Tl SPECT; and (c) cases in patients with microvascular obstruction identified at FPE MR imaging were characterized by large infarcts determined at DE MR imaging, 201Tl SPECT, or maximal release of CK and CK-MB.

Correlation between DE MR Imaging and 201Tl SPECT
A number of animal studies have been performed to analyze the accuracy of DE MR imaging with gadopentetate dimeglumine to quantify the size of acute myocardial infarction (5,79,23,26). These studies revealed confounding results; results of some studies demonstrated excellent correlation between DE MR imaging and histopathologic validation (23,26), whereas results of other studies indicated that DE MR images may cause overestimation of infarct size by 12%–40% of the LV area (59). Results of two animal studies showed that the time point of MR imaging after injection of gadopentetate dimeglumine is crucial for the accuracy of DE MR imaging after acute infarction (7,8). In one of these studies, in which spin-echo MR imaging and a constant inversion time were used, the gadolinium-enhanced region caused the true infarct size to be greatly overestimated when imaging was performed immediately after injection of the contrast medium (8). The enhanced region gradually receded, and estimation closely matched true infarct size after an elapsed time of 21 minutes ± 4. Similar data were determined in a study by Ni et al (7). By using an inversion-recovery turbo fast low-angle shot sequence, Ni et al revealed that the agreement between DE MR imaging and true infarct size was closest at 30 minutes after administration of the contrast medium. Possible explanations for overestimation early after the occurrence of acute myocardial infarction include (a) an altered washout characteristic of the contrast medium in ischemically injured but viable myocardium compared with necrotic myocardium or (b) an increased distribution volume for gadopentetate dimeglumine in the edematous but viable periinfarction zone (5).

Our study, performed in humans, revealed good agreement between 201Tl SPECT and DE MR imaging with a delay of 10 minutes between injection of contrast medium and start of MR imaging. This good agreement may be related to the use of a variable inversion time for nulling the signal intensity of normal myocardium after contrast medium injection. Authors of one recent study emphasized the importance of adjusting the inversion time after administration of contrast medium because the concentration of gadopentetate dimeglumine decreases continuously after injection (21). Another possible explanation is that, in our study, MR imaging was performed at a later time after infarction compared with that in the animal studies in which infarct overestimation was demonstrated. In those studies, MR imaging was performed early, within the first 48 hours after infarction (59). Prolonged reperfusion may eliminate the edematous periinfarction zone and may improve the accuracy of infarct size measurement. Results of a previous study support the notion that the rate of infarct size overestimation with DE MR imaging decreases within days after infarction (9). In that study, a significant reduction in overestimation of infarct size was found, from 12.4% to 8.3% of the LV area measured within the first 24 hours of reperfusion.

Although a large number of animal studies have been performed, to our knowledge, there has been only one prior human study in which the accuracy of DE MR imaging was compared with that of a nuclear imaging technique to estimate acute infarct size (3). In that study, 12 patients were examined at DE MR imaging and at stress-redistribution 201Tl SPECT. Size of myocardial infarct was estimated at a single midventricular level with use of each method. Results of that study also showed good correlation between DE MR imaging and stress-redistribution 201Tl SPECT (r = 0.92; P < .001). The large number of patients evaluated in our study permits greater confidence in the results of DE MR imaging, as well as testing of the method in a wide range of infarct sizes. Unlike measurements in previous studies (3,27), quantitative measurements were performed in our study in multiple sections by two observers using a threshold method to distinguish between infarction and normal myocardium. With this approach, a low mean difference was found between observers, which underlines the reproducibility of the MR measurements. The close agreement between the results of 201Tl SPECT and DE MR imaging demonstrates the clinical usefulness of MR imaging for estimating the size of acute myocardial infarcts. However, at this stage it is not clear whether the regions measured with the two modalities represented only nonviable myocardium or also included a periinfarction zone of viable myocardium. Future MR studies that include administration of a necrosis-specific contrast medium may be useful for addressing this issue.

DE MR imaging was more sensitive in demonstrating small inferior infarcts than was 201Tl SPECT. Our finding has been recently confirmed by Wagner et al (28) in a study of patients with chronic myocardial infarction. Detection of small infarcts is important because patients with previous infarction are at a high risk for recurrent infarction and death (29). The higher sensitivity of DE MR imaging is a result of several factors. First, 201Tl SPECT has limited ability to measure tracer uptake in the inferior myocardium because of diaphragmatic photon attenuation. Second, mean 201Tl uptake is lower and has a larger SD in the inferior wall compared with that in the anterior wall (30). The larger SD of tracer uptake results in an increased threshold, which most likely causes the reduced sensitivity of 201Tl SPECT in depicting small inferior infarcts. Third, 201Tl SPECT has limited spatial resolution, with a pixel size approximately 60 times larger than that at DE MR imaging, which also may have prevented detection of small infarcts (29).

Effect of Microvascular Obstruction on Infarct Size
Previous studies have shown that patients with microvascular obstruction have larger areas of myocardial damage according to electrocardiographic and echocardiographic criteria (3) and measurement of infarct size (11). The data from our study confirm previous findings and extend the knowledge about the association between microvascular obstruction and infarct size. Patients with microvascular obstruction had larger infarcts, quantified with three independent methods, compared with patients without microvascular obstruction. Quantitative measurement showed that almost all patients with microvascular obstruction had large infarcts (>20% of the LV area). This infarct size is an important threshold because results of animal studies have indicated that LV remodeling occurs if more than 20% of the myocardium is affected by infarction (31). Therefore, detection of microvascular obstruction and accurate sizing of myocardial infarction are good indicators for identifying patients who are at risk for LV remodeling. Further studies are needed to analyze the relative abilities of microvascular obstruction and infarct size to predict LV remodeling and eventual outcome.

Microvascular Obstruction and Persistent Hypoenhancement
Presence of persistent hypoenhancement on DE MR images has been noted before (3,23), and it has been suggested that this finding may be related to a closed infarct-related artery (23). The data from our study show that persistent hypoenhancement occurs in the presence of an open epicardial vessel, because all patients underwent revascularization before imaging examinations were performed.

The high concordance between microvascular obstruction on FPE MR images and persistent hypoenhancement on DE MR images may suggest that DE MR images can be used for identification of microvascular obstruction. However, the sensitivity of DE MR images was only 74% for the detection of microvascular obstruction with FPE MR images used as the reference standard. In six (26%) of 23 patients with microvascular obstruction, no persistent hypoenhancement was present on DE MR images. This result is most likely related to the observed reduction in size of the areas of microvascular obstruction on FPE MR images compared with the size of areas of persistent hypoenhancement on DE MR images. The reduction in size of the hypoenhanced zone indicates that the edges of the perfusion defect are filled in over time by contrast material, through collateral flow or slow diffusion. Thus, FPE MR imaging preferably should be used for visualization of microvascular obstruction.

Limitations
In two patients, FPE MR imaging revealed no microvascular obstruction, but a persistent hypoenhancement was detected at DE MR imaging. This discordant finding was probably related to the fact that FPE MR imaging was performed in a single midventricular section, whereas DE MR imaging was performed in three sections. This limitation can be avoided with the acquisition of FPE MR images in multiple sections by using faster sequences and more rapid data acquisition strategies.

It has been shown that attenuation correction improves the homogeneity of tracer distribution on 201Tl SPECT images (30). However, this methodology is still being developed and evaluated, and no clinical evaluation study has produced results showing a significant improvement in sensitivity of SPECT with attenuation correction (32). Thus, attenuation correction was not performed in our study.

The software we used for 201Tl SPECT images (4D-MSPECT) compared our data to pooled data of healthy subjects. This analysis may have added a layer of manipulation to the SPECT data. A simple threshold analysis might have overcome some limitations of the analysis we performed. However, in a previous study of patients with acute myocardial infarction, results of a comparison of the use of the threshold method with that of the polar map method for measuring infarct size on 201Tl SPECT images revealed no differences (18). Furthermore, a recent study showed that a threshold analysis of SPECT images also missed a number of subendocardial infarcts similar to that in our study (29). Therefore, it is unlikely that a threshold analysis would have improved the diagnostic accuracy of SPECT imaging in our study.

For assessment of infarct size, fluorodeoxyglucose positron emission tomography (PET) may be a more suitable technique to compare with DE MR imaging in future studies, because PET images have fewer attenuation artifacts and scatter effects. Another possibility would be the use of necrosis-specific MR contrast media (7,9); however, these agents are not approved for human use. In patients with acute myocardial infarction, the lack of an accurate reference standard makes it difficult to verify the ability of imaging modalities to depict solely necrotic myocardium.

Clinical Implications
The good correlation and agreement between 201Tl SPECT and DE MR imaging indicate that DE MR imaging may be used to estimate various infarct sizes 6 days after reperfused acute myocardial infarction. Combined FPE and DE MR imaging may be useful for stratifying patients after acute myocardial infarction into a low-risk group, with no microvascular obstruction and small infarcts, and a high-risk group, with microvascular obstruction and large infarcts. However, besides infarct size and presence of microvascular obstruction, there are other parameters, such as LV ejection fraction, presence of inducible ischemia with exercise, or identification of reversible LV dysfunction, that have been used for risk stratification after acute myocardial infarction (33). Further studies have to be performed to demonstrate the importance and utility of the proposed MR imaging measurements to predict eventual outcome in a low-risk group of patients receiving reperfusion therapy, particularly in comparison with existing parameters.


    APPENDIX
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 APPENDIX
 REFERENCES
 
The TIMI trial criteria define the perfusion of the infarct-related artery on the basis of flow of contrast medium at coronary angiography, beyond the point of occlusion (34), as follows: grade 0 (no perfusion), there is no antegrade flow beyond the point of occlusion; grade 1 (penetration without perfusion), the contrast medium passes beyond the area of obstruction but fails to opacify the entire coronary bed; grade 2 (partial perfusion), the contrast medium passes the obstruction and slowly opacifies the entire coronary bed; and grade 3 (complete perfusion), there is prompt antegrade flow into the bed distal to the obstruction. A TIMI flow of grade 2 or 3 represents a successful reperfusion.


    FOOTNOTES
 
Abbreviations: CK = creatine kinase, DE = delayed enhancement, FPE = first-pass enhancement, LV = left ventricular, TIMI = Thrombolysis in Myocardial Infarction

Author contributions: Guarantors of integrity of entire study, G.K.L., M.S., G.A., T.M.; study concepts, G.K.L., M.S., C.B.H.; study design, G.K.L., A.S., M.S., J.M.; literature research, G.K.L., A.S.; clinical studies, G.K.L., A.S., M.P.B., J.H.G., V.M., J.M.; data acquisition and analysis/interpretation, G.K.L., A.S., M.P.B., J.H.G., V.M., J.M.; statistical analysis, G.K.L., A.S.; manuscript preparation and definition of intellectual content, G.K.L., A.S., M.S.; manuscript editing, G.K.L., M.S.; manuscript revision/review and final version approval, all authors


    REFERENCES
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 APPENDIX
 REFERENCES
 

  1. Klein C, Nekolla SG, Bengel FM, et al. Assessment of myocardial viability with contrast-enhanced magnetic resonance imaging: comparison with positron emission tomography. Circulation 2002; 105:162-167.[Abstract/Free Full Text]
  2. Mahrholdt H, Wagner A, Holly TA, et al. Reproducibility of chronic infarct size measurement by contrast-enhanced magnetic resonance imaging. Circulation 2002; 106:2322-2327.[Abstract/Free Full Text]
  3. Lima JA, 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.[Abstract/Free Full Text]
  4. Choi KM, Kim RJ, Gubernikoff G, Vargas JD, Parker M, Judd RM. Transmural extent of acute myocardial infarction predicts long-term improvement in contractile function. Circulation 2001; 104:1101-1107.[Abstract/Free Full Text]
  5. Judd RM, Lugo-Olivieri CH, Arai M, et al. Physiological basis of myocardial contrast enhancement in fast magnetic resonance images of 2-day-old reperfused canine infarcts. Circulation 1995; 92:1902-1910.[Abstract/Free Full Text]
  6. Rochitte CE, Lima JA, Bluemke DA, et al. Magnitude and time course of microvascular obstruction and tissue injury after acute myocardial infarction. Circulation 1998; 98:1006-1014.[Abstract/Free Full Text]
  7. Ni Y, Pislaru C, Bosmans H, et al. Intracoronary delivery of Gd-DTPA and Gadophrin-2 for determination of myocardial viability with MR imaging. Eur Radiol 2001; 11:876-883.[CrossRef][Medline]
  8. Oshinski JN, Yang Z, Jones JR, Mata JF, French BA. Imaging time after Gd-DTPA injection is critical in using delayed enhancement to determine infarct size accurately with magnetic resonance imaging. Circulation 2001; 104:2838-2842.[Abstract/Free Full Text]
  9. Saeed M, Lund G, Wendland MF, Bremerich J, Weinmann H, Higgins CB. Magnetic resonance characterization of the peri-infarction zone of reperfused myocardial infarction with necrosis-specific and extracellular nonspecific contrast media. Circulation 2001; 103:871-876.[Abstract/Free Full Text]
  10. Wu KC, Kim RJ, Bluemke DA, et al. 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 1998; 32:1756-1764.[Abstract/Free Full Text]
  11. Wu KC, Zerhouni EA, Judd RM, et al. Prognostic significance of microvascular obstruction by magnetic resonance imaging in patients with acute myocardial infarction. Circulation 1998; 97:765-772.[Abstract/Free Full Text]
  12. Kloner RA, Ganote CE, Jennings RB. The "no-reflow" phenomenon after temporary coronary occlusion in the dog. J Clin Invest 1974; 54:1496-1508.
  13. Ito H, Maruyama A, Iwakura K, et al. Clinical implications of the ‘no reflow’ phenomenon: a predictor of complications and left ventricular remodeling in reperfused anterior wall myocardial infarction. Circulation 1996; 93:223-228.[Abstract/Free Full Text]
  14. Prigent F, Maddahi J, Garcia EV, Satoh Y, Van Train K, Berman DS. Quantification of myocardial infarct size by thallium-201 single-photon emission computed tomography: experimental validation in the dog. Circulation 1986; 74:852-861.[Abstract/Free Full Text]
  15. Tamaki S, Nakajima H, Murakami T, et al. Estimation of infarct size by myocardial emission computed tomography with thallium-201 and its relation to creatine kinase-MB release after myocardial infarction in man. Circulation 1982; 66:994-1001.[Abstract/Free Full Text]
  16. Mahmarian JJ, Pratt CM, Borges-Neto S, Cashion WR, Roberts R, Verani MS. Quantification of infarct size by 201Tl single-photon emission computed tomography during acute myocardial infarction in humans: comparison with enzymatic estimates. Circulation 1988; 78:831-839.[Abstract/Free Full Text]
  17. Wackers FJ, Gibbons RJ, Verani MS, et al. Serial quantitative planar technetium-99m isonitrile imaging in acute myocardial infarction: efficacy for noninvasive assessment of thrombolytic therapy. J Am Coll Cardiol 1989; 14:861-873.[Abstract]
  18. Christian TF, O’Connor MK, Hopfenspirger MR, Gibbons RJ. Comparison of reinjection thallium 201 and resting technetium 99m sestamibi tomographic images for the quantification of infarct size after acute myocardial infarction. J Nucl Cardiol 1994; 1:17-28.[Medline]
  19. Dilsizian V, Bonow RO. Current diagnostic techniques of assessing myocardial viability in patients with hibernating and stunned myocardium. Circulation 1993; 87:1-20.[Free Full Text]
  20. Miller TD, Christian TF, Hopfenspirger MR, Hodge DO, Gersh BJ, Gibbons RJ. Infarct size after acute myocardial infarction measured by quantitative tomographic 99mTc sestamibi imaging predicts subsequent mortality. Circulation 1995; 92:334-341.[Abstract/Free Full Text]
  21. Simonetti OP, Kim RJ, Fieno DS, et al. An improved MR imaging technique for the visualization of myocardial infarction. Radiology 2001; 218:215-223.[Abstract/Free Full Text]
  22. Gerber BL, Garot J, Bluemke DA, Wu KC, Lima JA. Accuracy of contrast-enhanced magnetic resonance imaging in predicting improvement of regional myocardial function in patients after acute myocardial infarction. Circulation 2002; 106:1083-1089.[Abstract/Free Full Text]
  23. Fieno DS, Kim RJ, Chen EL, Lomasney JW, Klocke FJ, Judd RM. Contrast-enhanced magnetic resonance imaging of myocardium at risk: distinction between reversible and irreversible injury throughout infarct healing. J Am Coll Cardiol 2000; 36:1985-1991.[Abstract/Free Full Text]
  24. Klocke FJ, Baird MG, Bateman TM, et al. ACC/AHA/ASNC guidelines for the clinical use of cardiac radionuclide imaging: a report from the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASNC Committee to Revise the 1995 Guidelines for the Clinical Use of Radionuclide Imaging). American College of Cardiology Web Site. Available at: www.acc.org/clinical/guidelines/radio/index.pdf. Accessed October 24, 2003.
  25. Hendel RC, Henry TD, Rocha-Singh K, et al. Effect of intracoronary recombinant human vascular endothelial growth factor on myocardial perfusion: evidence for a dose-dependent effect. Circulation 2000; 101:118-121.[Abstract/Free Full Text]
  26. Kim RJ, Fieno DS, Parrish TB, et al. Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation 1999; 100:1992-2002.[Abstract/Free Full Text]
  27. Holman ER, van Jonbergen HP, van Dijkman PR, van der Laarse A, de Roos A, van der Wall EE. Comparison of magnetic resonance imaging studies with enzymatic indexes of myocardial necrosis for quantification of myocardial infarct size. Am J Cardiol 1993; 71:1036-1040.[CrossRef][Medline]
  28. Wagner A, Mahrholdt H, Holly TA, et al. Contrast-enhanced MRI and routine single photon emission computed tomography (SPECT) perfusion imaging for detection of subendocardial myocardial infarcts: an imaging study. Lancet 2003; 361:374-379.[CrossRef][Medline]
  29. Donges K, Schiele R, Gitt A, et al. Incidence, determinants, and clinical course of reinfarction in-hospital after index acute myocardial infarction (results from the pooled data of the maximal individual therapy in acute myocardial infarction [MITRA], and the myocardial infarction registry [MIR]). Am J Cardiol 2001; 87:1039-1044.[CrossRef][Medline]
  30. Ficaro EP, Fessler JA, Ackermann RJ, Rogers WL, Corbett JR, Schwaiger M. Simultaneous transmission-emission thallium-201 cardiac SPECT: effect of attenuation correction on myocardial tracer distribution. J Nucl Med 1995; 36:921-931.[Abstract/Free Full Text]
  31. Pfeffer MA. Left ventricular remodeling after acute myocardial infarction. Annu Rev Med 1995; 46:455-466.[CrossRef][Medline]
  32. Hendel RC, Corbett JR, Cullom SJ, DePuey EG, Garcia EV, Bateman TM. The value and practice of attenuation correction for myocardial perfusion SPECT imaging: a joint position statement from the American Society of Nuclear Cardiology and the Society of Nuclear Medicine. J Nucl Cardiol 2002; 9:135-143.[CrossRef][Medline]
  33. Ryan TJ, Anderson JL, Antman EM, et al. ACC/AHA guidelines for the management of patients with acute myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction). J Am Coll Cardiol 1996; 28:1328-1428.[CrossRef][Medline]
  34. TIMI Study Group. The Thrombolysis in Myocardial Infarction (TIMI) trial: phase I findings. N Engl J Med 1985; 312:932-936.[Medline]



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