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EXPERIMENTAL STUDY

Contrast-enhanced magnetic resonance imaging of myocardium at risk

Distinction between reversible and irreversible injury throughout infarct healing

David S. Fieno, PhD^* , Raymond J. Kim, MD, FACC^* , Enn-Ling Chen, PhD^*, Jon W. Lomasney, MD^* , Francis J. Klocke, MD, MACC^* and Robert M. Judd, PhD^*

^* Northwestern University Medical School Feinberg Cardiovascular Research Institute, Chicago, Illinois, USA
Department of Medicine, Chicago, Illinois, USA
Department of Pathology, Chicago, Illinois, USA
Department of Biomedical Engineering, Chicago, Illinois, USA

Manuscript received April 14, 2000; revised manuscript received May 23, 2000, accepted July 12, 2000.

Reprint requests and correspondence: Dr. Robert M. Judd, Feinberg Cardiovascular Research Institute, Northwestern University Medical School, 303 E Chicago Avenue, Tarry 12-723, Chicago, Illinois 60611-3008
rjudd{at}nwu.edu

	Abstract

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OBJECTIVES

We sought to determine the relationship of delayed hyperenhancement by contrast magnetic resonance imaging (MRI) to viable and nonviable myocardium within the region at risk throughout infarct healing.

BACKGROUND

The relationship of delayed MRI contrast enhancement patterns to injured but viable myocardium within the ischemic bed at risk has not been established.

METHODS

We compared in vivo and ex vivo MRI contrast enhancement to histopathologic tissue sections encompassing the entire left ventricle in dogs (n = 24) subjected to infarction with (n = 12) and without (n = 12) reperfusion at 4 h, 1 day, 3 days, 10 days, 4 weeks and 8 weeks. In vivo MR imaging was performed 30 min after contrast injection.

RESULTS

The sizes and shapes of in vivo myocardial regions of elevated image intensity (828 ± 132% of remote) were the same as those observed ex vivo (241 slices, r = 0.99, bias = 0.05 ± 1.6% of left ventricle [LV]). Comparison of ex vivo MRI to triphenyltetrazolim chloride–stained sections demonstrated that the spatial extent of hyperenhancement was the same as the spatial extent of infarction at every stage of healing (510 slices, lowest r = 0.95, largest bias = 1.7 ± 2.9% of LV). Conversely, hyperenhanced regions were smaller than the ischemic bed at risk defined by fluorescent microparticles at every stage of healing (239 slices, 35 ± 24% of risk region, p < 0.001). Image intensities of viable myocardium within the risk region were the same as those of remote, normal myocardium (102 ± 9% of remote, p = NS).

CONCLUSIONS

Delayed contrast enhancement by MRI distinguishes between viable and nonviable regions within the myocardium at risk throughout infarct healing.

Abbreviations and Acronyms   ceMRI = contrast-enhanced magnetic resonance imaging   LOA = limits of agreement   LV = left ventricle   MRI = magnetic resonance imaging   ROI = region of interest   TTC = triphenyltetrazolium chloride

In a recent study by our group (4), we found a strong association between irreversible myocardial injury and delayed (>5 min) hyperenhancement in magnetic resonance images (MRI) following administration of Gd-DTPA. Hyperenhancement occurred in infarcted regions but was not observed in regions subjected to purely reversible ischemic injury (15 min coronary occlusion) despite the presence of myocardial stunning at the time of the MRI. Other recent reports, however, suggest a different perspective. Rogers et al. (5) studied Gd-DTPA enhancement in 17 patients and found that hyperenhanced regions observed one week after reperfused infarction partially recovered contractile function by seven weeks. The authors interpreted this finding as evidence that hyperenhancement can occur in viable myocardial regions. Pislaru et al. (6) studied an investigational "necrosis avid" MRI contrast agent, Gadophrin-2, in a canine model of acute infarction based in part on the assumption that FDA-approved contrast agents such as Gd-DTPA do not distinguish between reversible and irreversible ischemic injury.

While the physiologic interpretation of contrast-enhanced MRI (ceMRI) remains to be fully elucidated, the quality of the images continues to improve. Segmented inversion-recovery MRI pulse sequences now typically result in hyperenhanced image intensities that are 300% to 500% greater than nonhyperenhanced regions (4), greatly reducing observer subjectivity regarding the shape and transmural extent of hyperenhanced regions. In patients with ischemic heart disease, cine MRI is easily combined with contrast MRI to examine regional wall motion and contrast enhancement with perfect registration in multiple short and long axis views. Considering the wide availability of MRI scanners and the routine use of Gd-DTPA and similar agents for noncardiac clinical indications (5,7,8), these recent improvements in image quality underscore the importance of establishing the relationship of delayed myocardial hyperenhancement to the underlying pathophysiology.

In the present study, we evaluated ceMRI of postischemic myocardium following administration of Gd-DTPA at different times throughout infarct healing. Dogs were subjected to either transient 90-min or permanent coronary artery occlusion, imaged in vivo by MRI, and sacrificed at either 4 h, 1 day, 3 days, 10 days, 4 weeks or 8 weeks. All hearts were imaged ex vivo at 500 x 500 x 500-µm spatial resolution and then sectioned into registered contiguous 2-mm-thick tissue slices encompassing the entire left ventricle (LV). Regions of MRI hyperenhancement were compared to regions at risk of infarction defined by fluorescent microparticles, to infarcted regions defined by triphenyltetrazolium chloride (TTC) staining and to histology by light microscopy.

	Methods

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Experimental preparation.   Twenty-eight 25- to 30-kg mongrel dogs were studied. The care and treatment of all animals was in accordance with the Position of the American Heart Association on Research Animal Use, adopted November 15, 1984. Under sterile technique, a lateral thoracotomy was performed, the pericardium was opened, and the proximal left anterior descending or left circumflex artery was carefully dissected and occluded to produce an infarction. In one group of animals (n = 12), the artery was permanently occluded with a snare ligature; in another group (n = 16), the artery was occluded for 90 min with a removable soft occluder, and then reperfusion was restored. In animals to be studied at one day and beyond, the chest was then sutured closed, and the animals were allowed to recover.

MRI and experimental protocol.   Animals were studied at 4 h, 1 day, 3 days, 10 days, 4 weeks and 8 weeks.

In vivo imaging.   In vivo images were acquired for all time points except 4 h (due to scanner scheduling limitations). Animals were anesthetized, intubated, transported to the MRI facility and imaged in the right lateral decubitus position (1.5T Siemens Symphony; Erlangen, Germany). Approximately 30 min after 0.3 mmol/kg Gd-DTPA i.v., contiguous 5-mm-thick short-axis T₁-weighted images were acquired from base to apex (ca. 15 per heart) using a segmented inversion-recovery pulse sequence described in detail elsewhere (9). Animals were then sacrificed and the hearts removed for further study. In the animals with reperfused infarcts, the coronary artery was reoccluded before sacrifice and 120 ml of 1.3% fluorescent microparticles (1 to 10 µm in diameter; Duke Scientific Corporation; Palo Alto, California) was injected into the left atrium to identify the myocardium at risk of infarction (10–12).

To test whether or not the observed enhancement patterns were specific to the use of Gd-DTPA, eight animals were imaged on consecutive days using Gd-HP-DO3A on the first day and Gd-DTPA on the next day. Gd-HP-DO3A (ProHance; Bracco Diagnostics, Inc.; Milan, Italy) is another clinically approved contrast agent that has a molecular weight (ca. 800 daltons), T₁ relaxivity (ca. 4 mmol^–1 s^–1), and biologic distribution (extracellular) similar to Gd-DTPA. Two animals were studied at each of four time points (3 days, 10 days, 4 weeks and 8 weeks).

Ex vivo imaging.   After excision, hearts were quickly immersed in cold (4°C) saline solution, rinsed, and ventricular cavities were blotted dry. Balloons containing 99.9% deuterated water (D₂O) were placed in the ventricular cavities and three fiduciary markers defining the short axis of the heart were glued to the epicardium near the base. The hearts were then suspended vertically in a standard knee coil and three-dimensional gradient-echo images (TR = 20 ms, TE = 3.2 ms) were acquired with a spatial resolution of 500 x 500 x 500 µm. T₁-weighting was achieved by the use of a large flip angle (70°).

Histochemical staining.   Following ex vivo imaging, hearts were cooled and made partially stiff by short, repeated immersions in 95% ethanol precooled to –80°C and then sectioned into 2-mm-thick short axis slices from base to apex (ca. 25 per heart) using a commercial rotating meat slicer along the plane defined by the three epicardial markers. All slices were stained with 2% TTC and photographed under room light to determine infarct size and under ultraviolet light to determine the myocardium at risk.

Light microscopy.   In 24 animals, one transmural block of tissue was obtained from the infarct territory and a second transmural block was obtained from a normal region opposite the infarct territory. Each tissue block was photographed under room light (for TTC) and ultraviolet light (for fluorescent microparticles) and then stained with hematoxylin and eosin (H&E) and Masson’s trichrome.

Data analysis.   In vivo hyperenhancement
Image intensities were measured in hyperenhanced and remote, nonhyperenhanced regions of myocardium using a software package (NIH Image, National Institute of Health, Bethesda, Maryland). Hyperenhancement was defined as an image intensity >3 SDs above the mean of remote myocardium. The spatial extent of hyperenhancement was expressed as a percentage of the LV on a slice-by-slice basis. Consistent with previous analyses (4,13), the measurement of the spatial extent of hyperenhancement included subendocardial regions of hypoenhancement within the core of the hyperenhanced region if these regions were present.

In vivo versus ex vivo hyperenhancement
For each animal, the ex vivo images were registered to the in vivo images for blinded comparison of hyperenhancement patterns. First, the short-axis slice locations acquired in vivo were displayed on an in vivo long-axis image (Fig. 2). Next, each high resolution ex vivo data set was loaded into a multiplanar reconstruction tool (MPR; Siemens Medical Systems; Erlangen, Germany) and contiguous 5-mm-thick short-axis ex vivo images were extracted from the three dimensional data set according to the slice positions displayed in the in vivo long-axis image. A separate observer measured hyperenhanced regions in the same manner used for the in vivo images.

View larger version (95K): [in this window] [in a new window]   Figure 2 Hyperenhancement observed in vivo was similar to that observed ex vivo.

Light microscopy
Pairs of H&E- and trichrome-stained tissue sections were presented to a pathologist (J.W.L.) blinded to the results of the MRI, TTC and fluorescent microparticle examinations. The pathologist examined each section for the presence or absence of irreversible injury and, if present, outlined regions without viable myocytes by hand on the glass slides. Irreversible injury was defined using standard histologic criteria such as coagulation and contraction band necrosis acutely and collagen replacement chronically. Based on these outlines, the percent surface area of each irreversibly injured region was calculated for later comparison to TTC-negative regions and to regions without fluorescent microparticles based on photographs of the same tissue blocks taken before H&E and trichrome staining (see "Experimental Protocol").

Statistical analysis.   All results were expressed as mean ± SD. The method of Bland and Altman (14) was used to compare in vivo versus ex vivo hyperenhancement, hyperenhancement with infarct size and hyperenhancement with the region at risk. Image intensities amongst regions were compared using repeated measures analysis of variance with Bonferronni correction. All tests were two tailed and p < 0.05 was considered significant.

	Results

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In vivo and ex vivo contrast enhancement.   Hyperenhancement was observed in vivo at 1 day, 3 days, 10 days, 4 weeks and 8 weeks in both nonreperfused and reperfused infarcts (Fig. 1). Image intensities in hyperenhanced regions were 828 ± 132% of remote, normal myocardium. Subendocardial hypoenhanced regions within the central core of the hyperenhanced region were observed in 12 of the 24 animals 30 min postcontrast. These hypoenhanced regions were most prominent for nonreperfused infarcts; however, they were also present in large reperfused infarcts.

View larger version (94K): [in this window] [in a new window]   Figure 1 Hyperenhancement was observed at 1 day, 3 days, 10 days, 4 weeks and 8 weeks after nonreperfused (top row) and reperfused (bottom row) myocardial infarction.

Hyperenhancement versus infarct size.   Figure 3 compares ex vivo ceMRI to corresponding TTC-stained sections. The location and spatial extent of ceMRI hyperenhancement appeared to be the same as the infarct zone delineated by TTC. Linear regression analysis revealed a high correlation coefficient (510 slices, lowest r = 0.95). Bland-Altman analysis showed a high degree of agreement between MRI and TTC at every stage of infarct healing regardless of reperfusion status (largest bias = 1.7% of LV area; maximum LOA = bias ± 5.7% of LV area). Similarly, when total infarct size by TTC (mean, 8.0 ± 1.6% of LV; range, 0.5 to 29.2) was compared to the spatial extent of in vivo hyperenhancement (8.2 ± 1.5%; range, 1.0 to 30.5), a correlation coefficient of 0.96 was found and Bland-Altman analysis showed a high degree of agreement (bias: 0.24% of LV; limits of agreement of +8.0 and –7.6% of LV).

View larger version (75K): [in this window] [in a new window]   Figure 3 The size and shape of hyperenhanced regions by MRI closely matched those of irreversible injury defined by TTC throughout infarct healing.

View larger version (47K): [in this window] [in a new window]   Figure 4 The size and shape of regions with reduced perfusion ("at risk") were larger than the hyperenhanced areas by ceMRI.

View larger version (125K): [in this window] [in a new window]   Figure 5 Comparison of MRI hyperenhancement (left upper panel), TTC staining (left middle panel) and the myocardium at risk (region without fluorescent microparticles, left lower panel) in an animal with a 1-day-old reperfused infarction. Light microscopy views of region 1 (not at risk, not infarcted), region 2 (at risk but not infarcted) and region 3 (infarcted) are shown on the right panels. Arrows point to contraction bands. See text for details.

View larger version (19K): [in this window] [in a new window]   Figure 6 Hyperenhancement was not observed in "at risk but not infarcted" regions.

Gd-HP-DO3A versus Gd-DTPA.   For the eight animals in which in vivo ceMRI was performed using both contrast agents, no differences were detected in the spatial extent of hyperenhancement (92 slices, bias = 0.4 ± 3.2% of LV area, p = NS).

	Discussion

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The main findings of this study were as follows: 1) the spatial extent of in vivo and ex vivo hyperenhancement was identical when the same slice thickness was used (5 mm); 2) the spatial extent of ex vivo hyperenhancement at high resolution (0.5 x 0.5 x 0.5 mm) was the same as infarct size defined by TTC; and 3) within the risk region, viable myocardium was distinguished from nonviable myocardium as nonhyperenhanced and hyperenhanced regions, respectively. These findings held throughout infarct healing and irrespective of reperfusion status.

Comparison to previous studies.   Several previous studies by our group (13,15) and others (16–22) have compared contrast enhancement to infarct size using "thick" histologic sections cut by hand and typically not precisely oriented in the same plane as the images. In a recent report by our group (4), we developed a method by which high resolution ex vivo images could be accurately registered with "thin" (2 mm) histologic sections. The purpose of the current study was to apply this method to address three key issues raised but not addressed by our recent report (4) or by previous studies (16–22). First, we systematically compared in vivo to ex vivo enhancement to determine if the data comparing ex vivo images to histology can be used as a basis for the interpretation of in vivo images. Second, we used fluorescent microparticles to determine whether hyperenhancement occurs in viable regions at risk of infarction that surround infarcted regions. Third, we studied hyperenhancement throughout infarct healing because it remained unclear whether or not hyperenhancement would be observed at all stages of infarct healing and how hyperenhancement, if present, would relate to the profound cellular-level changes that occur during the transition from acutely necrotic myocytes to collagenous scar. Study of these issues with a level of detail significantly beyond that of previous studies was motivated by observations of clearly defined, nontransmural regions of hyperenhancement in patients with coronary artery disease (4,9).

Timing of in vivo imaging.   All images were acquired approximately 30 min postcontrast for two reasons. First, in earlier studies (8,13,15), we found that "delayed" hyperenhancement is established by approximately 5 min postcontrast. Second, we have empirically observed that the endocardial border is often more easily detected at later times because the image intensity of the blood pool decreases at a faster rate than that of hyperenhanced myocardial regions. The data of the current study do not address the time course of first-pass contrast enhancement or the time course of contrast penetration in regions of microvascular damage (13,15).

Contrast enhancement of the risk region.   We found that the myocardial region at risk is characterized by two different enhancement patterns: hyperenhanced and nonhyperenhanced. Hyperenhancement appeared in a subregion within the risk region and was exclusively associated with nonviable myocardium. Regions without hyperenhancement but within the risk region were found to contain viable myocytes both by TTC staining and light microscopy. The association of hyperenhancement to nonviable myocardium was observed throughout infarct healing and was unaffected by reperfusion status.

To our knowledge, our data are the first in which contrast enhancement within the risk region has been studied beyond 24 h postinfarct. One of the few studies to address this issue within the first 24 h is that of Schaefer et al. (16) who, unlike our current findings, reported that hyperenhancement overestimated infarct size. It should be noted, however, that the animals in the study by Schaefer et al. (16) received the MRI contrast agent during reactive hyperemia, suggesting that hyperenhancement may have occurred in hyperemic regions without infarction as well as in infarcted regions. In a smaller group of animals reported in the same article, Schaefer et al. (16) found that when the contrast agent was administered 90 min after reperfusion, the hyperemic response was no longer present and the spatial extent of hyperenhancement was much smaller (8.6 vs. 25.9% of LV) despite similar regions at risk and infarct sizes.

Contrast enhancement of the infarct zone.   In agreement with previous findings, our data show hyperenhancement of acute infarcts 4 h to 3 days old both with (15–18,21,22) and without (19,20,23,24) reperfusion. For older infarcts, the data of some previous studies indicate that hyperenhancement is observed (8,22,25) whereas others do not (26,27). In the present study, we found that hyperenhancement persists at 10 days, 4 weeks and 8 weeks. Discrepant findings regarding whether or not older infarcts hyperenhance may relate to both the process of infarct healing and the MRI technique employed. Myocardial infarcts may shrink by as much as 400% during infarct healing (28) making older infarcts inherently more difficult to detect. In addition, pulse sequences with a more limited ability to distinguish differences in postcontrast longitudinal relaxation times (T₁) may reduce an observer’s ability to detect infarcted regions (9).

In a previous study of two-day-old reperfused infarcts (13), we found that the spatial extent of in vivo hyperenhancement was 12% larger than infarcted regions. The method of our current study was developed specifically to improve our ability to examine this issue. In vivo spatial resolution was approximately eightfold higher (1.2 x 3.3 x 10 mm/1 x 1 x 5 mm 8) and the number of histologic slices per animal was 25 compared to 5 in our previous study (13). Perhaps more importantly, the intermediate stage of ex vivo imaging greatly improved our ability to register individual slices. When examined at this level of detail, the data indicate that the spatial extent of hyperenhancement is identical to infarct size. It is important to note that the spatial extent of hyperenhancement may appear slightly larger than infarct size when spatial resolution is not adequate to portray the three-dimensional shape of the infarct (4) (partial volume effect).

Subendocardial regions of hypoenhancement within larger regions of hyperenhancement were detected in 12 of the 24 animals. Impeded contrast penetration may relate to microvascular occlusion (13,18,29) in reperfused and nonreperfused infarcts and/or a closed infarct-related artery in the nonreperfused group.

In summary, when spatial resolution is adequate, regions "at risk but not infarcted" do not hyperenhance and hyperenhancement is identical to infarct size throughout infarct healing. We conclude that delayed contrast enhancement by MRI distinguishes between viable and nonviable regions within the myocardium at risk.

	Acknowledgments

 
The authors wish to thank Orlando P. Simonetti, PhD, for the imaging pulse sequence, Friedrich Cavagna, PhD, for the Gd-HP-DO3A, and Kathleen R. Harris, S.R.S., for the surgical preparation.

	Footnotes

 
This work was supported in part by grants NIH-NHLBI R29-HL53411 and R01-HL63268 (R.M.J.), and a Graduate Fellowship from the Whitaker Foundation (D.S.F.).

	References

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				J. D. Dodd, G. Holmvang, U. Hoffmann, M. Ferencik, S. Abbara, T. J. Brady, and R. C. Cury Quantification of Left Ventricular Noncompaction and Trabecular Delayed Hyperenhancement with Cardiac MRI: Correlation with Clinical Severity Am. J. Roentgenol., October 1, 2007; 189(4): 974 - 980. [Abstract] [Full Text] [PDF]

				B. Ibanez, S. Prat-Gonzalez, W. S. Speidl, G. Vilahur, A. Pinero, G. Cimmino, M. J. Garcia, V. Fuster, J. Sanz, and J. J. Badimon Early Metoprolol Administration Before Coronary Reperfusion Results in Increased Myocardial Salvage: Analysis of Ischemic Myocardium at Risk Using Cardiac Magnetic Resonance Circulation, June 12, 2007; 115(23): 2909 - 2916. [Abstract] [Full Text] [PDF]

				M. Habis, A. Capderou, S. Ghostine, B. Daoud, C. Caussin, J.-Y. Riou, P. Brenot, C. Y. Angel, B. Lancelin, and J.-F. Paul Acute Myocardial Infarction Early Viability Assessment by 64-Slice Computed Tomography Immediately After Coronary Angiography: Comparison With Low-Dose Dobutamine Echocardiography J. Am. Coll. Cardiol., March 20, 2007; 49(11): 1178 - 1185. [Abstract] [Full Text] [PDF]

				J. Chan, L. Hanekom, C. Wong, R. Leano, G.-Y. Cho, and T. H. Marwick Differentiation of Subendocardial and Transmural Infarction Using Two-Dimensional Strain Rate Imaging to Assess Short-Axis and Long-Axis Myocardial Function J. Am. Coll. Cardiol., November 21, 2006; 48(10): 2026 - 2033. [Abstract] [Full Text] [PDF]

				M. Becker, R. Hoffmann, H. P. Kuhl, H. Grawe, M. Katoh, R. Kramann, A. Bucker, P. Hanrath, and N. Heussen Analysis of myocardial deformation based on ultrasonic pixel tracking to determine transmurality in chronic myocardial infarction Eur. Heart J., November 1, 2006; 27(21): 2560 - 2566. [Abstract] [Full Text] [PDF]

				C. Jackowski, A. Christe, M. Sonnenschein, E. Aghayev, and M. J. Thali Postmortem unenhanced magnetic resonance imaging of myocardial infarction in correlation to histological infarction age characterization Eur. Heart J., October 2, 2006; 27(20): 2459 - 2467. [Abstract] [Full Text] [PDF]

				M.-T. Wu, W.-Y. I. Tseng, M.-Y. M. Su, C.-P. Liu, K.-R. Chiou, V. J. Wedeen, T. G. Reese, and C.-F. Yang Diffusion Tensor Magnetic Resonance Imaging Mapping the Fiber Architecture Remodeling in Human Myocardium After Infarction: Correlation With Viability and Wall Motion Circulation, September 5, 2006; 114(10): 1036 - 1045. [Abstract] [Full Text] [PDF]

				C. M. Bove, J. M. DiMaria, S. Voros, M. R. Conaway, and C. M. Kramer Dobutamine Response and Myocardial Infarct Transmurality: Functional Improvement after Coronary Artery Bypass Grafting--Initial Experience Radiology, September 1, 2006; 240(3): 835 - 841. [Abstract] [Full Text] [PDF]

				C. Ebeling Barbier, T. Bjerner, L. Johansson, L. Lind, and H. Ahlstrom Myocardial Scars More Frequent Than Expected: Magnetic Resonance Imaging Detects Potential Risk Group J. Am. Coll. Cardiol., August 15, 2006; 48(4): 765 - 771. [Abstract] [Full Text] [PDF]

				G. L. Raff, W. W. O'Neill, R. E. Gentry, A. Dulli, K. G. Bis, A. N. Shetty, and J. A. Goldstein Microvascular Obstruction and Myocardial Function after Acute Myocardial Infarction: Assessment by Using Contrast-enhanced Cine MR Imaging. Radiology, August 1, 2006; 240(2): 529 - 536. [Abstract] [Full Text] [PDF]

				R. M. Setser, J. K. Kim, Y. C. Chung, K. Chen, A. E. Stillman, R. Loeffler, O. P. Simonetti, J. A. Weaver, M. L. Lieber, and R. D. White Cine Delayed-Enhancement MR Imaging of the Heart: Initial Experience Radiology, June 1, 2006; 239(3): 856 - 862. [Abstract] [Full Text] [PDF]

				M. Dewey, M. Laule, M. Taupitz, N. Kaufels, B. Hamm, and D. Kivelitz Myocardial Viability: Assessment with Three-dimensional MR Imaging in Pigs and Patients Radiology, June 1, 2006; 239(3): 703 - 709. [Abstract] [Full Text] [PDF]

				A. Wagner, H. Mahrholdt, L. Thomson, S. Hager, G. Meinhardt, W. Rehwald, M. Parker, D. Shah, U. Sechtem, R. J. Kim, et al. Effects of Time, Dose, and Inversion Time for Acute Myocardial Infarct Size Measurements Based on Magnetic Resonance Imaging-Delayed Contrast Enhancement J. Am. Coll. Cardiol., May 16, 2006; 47(10): 2027 - 2033. [Abstract] [Full Text] [PDF]

				J. Vogel-Claussen, C. E. Rochitte, K. C. Wu, I. R. Kamel, T. K. Foo, J. A. C. Lima, and D. A. Bluemke Delayed enhancement MR imaging: utility in myocardial assessment. RadioGraphics, May 1, 2006; 26(3): 795 - 810. [Abstract] [Full Text] [PDF]

				A. H. Aletras, G. S. Tilak, A. Natanzon, L.-Y. Hsu, F. M. Gonzalez, R. F. Hoyt Jr, and A. E. Arai Retrospective Determination of the Area at Risk for Reperfused Acute Myocardial Infarction With T2-Weighted Cardiac Magnetic Resonance Imaging: Histopathological and Displacement Encoding With Stimulated Echoes (DENSE) Functional Validations Circulation, April 18, 2006; 113(15): 1865 - 1870. [Abstract] [Full Text] [PDF]

				R. M. Setser, T. P. O'Donnell, N. G. Smedira, J. F. Sabik, S. S. Halliburton, A. E. Stillman, and R. D. White Coregistered MR Imaging Myocardial Viability Maps and Multi-Detector Row CT Coronary Angiography Displays for Surgical Revascularization Planning: Initial Experience Radiology, November 1, 2005; 237(2): 465 - 473. [Abstract] [Full Text] [PDF]

				J.-P. Laissy, F. Hyafil, L. J. Feldman, J.-M. Juliard, E. Schouman-Claeys, P. G. Steg, and M. Faraggi Differentiating Acute Myocardial Infarction from Myocarditis: Diagnostic Value of Early- and Delayed-Perfusion Cardiac MR Imaging Radiology, October 1, 2005; 237(1): 75 - 82. [Abstract] [Full Text] [PDF]

				A. Giorgetti, A. Pingitore, B. Favilli, A. Kusch, M. Lombardi, and P. Marzullo Baseline/Postnitrate Tetrofosmin SPECT for Myocardial Viability Assessment in Patients with Postischemic Severe Left Ventricular Dysfunction: New Evidence from MRI J. Nucl. Med., August 1, 2005; 46(8): 1285 - 1293. [Abstract] [Full Text] [PDF]

				V. Fuster and R. J. Kim Frontiers in Cardiovascular Magnetic Resonance Circulation, July 5, 2005; 112(1): 135 - 144. [Full Text] [PDF]