DOI: 10.1148/radiol.2451061590
(Radiology 2007;245:245-250.)
© RSNA, 2007
Recent Myocardial Infarction: Assessment with Unenhanced T1-weighted MR Imaging1
James W. Goldfarb, PhD,
Sheeba Arnold, MS, and
Jing Han, PhD
1 From the Department of Research and Education, DeMatteis MRI, St Francis Hospital, 100 Port Washington Blvd, Roslyn, NY 11576 (J.W.G., S.A., J.H.); and Program in Biomedical Engineering, SUNY Stony Brook, Stony Brook, NY (J.W.G.). Received September 13, 2006; revision requested November 9; revision received December 5; accepted January 15, 2007; final version accepted March 7. Supported by a grant from the American Heart Association (0635029N).
Address correspondence to J.W.G. (e-mail: James.Goldfarb{at}chsli.org).
 |
ABSTRACT
|
|---|
The purpose of the study was to prospectively evaluate a T1-weighted technique for detection of myocardial edema resulting from recent myocardial infarction (MI) or intervention. This study was HIPAA compliant and institutional review board approved. Fifteen men and one woman (mean age, 57.8 years ± 11.5 [standard deviation]) were examined with T1-weighted magnetic resonance (MR) imaging and inversion-recovery cine pulse sequence in two groups, recent MI and chronic MI, and gave informed consent. T1 relaxation times of MI and adjacent myocardium were compared (Student t test and correlation analysis). In patients with recent MI, areas of myocardial edema were well depicted with T1-weighted MR imaging. T1 relaxation times of recent infarcts were longer than those of older MIs (925 msec ± 169 vs 551 msec ± 107, P < .001). From local edema, T1 relaxation time of infarcted myocardium is increased, may remain elevated for 2 months, and enables imaging with T1-weighted techniques.
© RSNA, 2007
 |
INTRODUCTION
|
|---|
Detection of myocardial infarction (MI) with cardiac magnetic resonance (MR) imaging has become a clinically viable protocol. Sometimes (1,2), there are no substantial differences between recent and chronic myocardial injuries on cine functional (3) or delayed hyperenhanced (DHE) (4) images. The detection of and differentiation between acute and chronic MI with MR imaging has been proposed with unenhanced T2-weighted MR imaging (1,5–11) and contrast agent kinetic techniques (12,13). Recently, it has been reported that T2-weighted MR imaging can help accurately define the myocardial "area at risk" (14), but image quality with T2-weighted MR imaging has the disadvantages of long breath-hold times, image artifacts, and poor contrast between myocardium and the left ventricular blood pool (15,16). Gadolinium-based contrast agent kinetic techniques are in development but require extended imaging times.
When a patient presents with chest pain, the knowledge of a recent MI plays an important role in the risk stratification process. Often, a chronic MI can be defined by wall thinning, but this is not the case for many subendocardial infarcts (17). To date, a definitive robust test to differentiate between recent and chronic myocardial injury on a segmental basis does not exist.
A recent MI is known to have local edema, which normally resolves over time (18–20). This edema can be increased or created through reperfusion (21). Myocardial edema and, more generally, body fluid (eg, pericardial effusion or cerebrospinal fluid) have both long T1 and long T2 MR relaxation times. Early attempts to detect an MI with T1-weighted MR imaging before administration of contrast material have yielded highly variable results (6). Contrast material–enhanced imaging of the myocardium with T1-weighted inversion-recovery (IR) techniques has been refined for DHE imaging (22,23). IR MR pulse sequences are heavily T1 sensitive and capable of providing excellent contrast between tissues with only small differences in T1 relaxation times. The purpose of our study was to prospectively evaluate a T1-weighted imaging technique for the detection of myocardial edema resulting from a recent MI or intervention.
 |
MATERIALS AND METHODS
|
|---|
Patients
This study complied with the Health Insurance Portability and Accountability Act. We evaluated 16 patients (15 men and one woman; mean age, 57.8 years ± 11.5 [standard deviation]; range, 43.4–84.8 years) from April 2003 to March 2005. The study was approved by the Saint Francis Hospital institutional review board. After the nature of the procedure had been fully explained, written informed consent was obtained from all patients. Patients were included in the study if they had had a prior MI that was documented with serum cardiac markers or positive nuclear stress testing results. Patients with contraindications to MR imaging, such as claustrophobia or metallic implants, were not considered for study inclusion. Eight patients had experienced an MI within 2 months of MR imaging (mean MI age, 0.05 years ± 0.03; range, 0.03–0.13 years) and eight had older MIs (mean MI age, 1.7 years ± 1.2; range, 0.4–3.5 years).
MR Imaging
Imaging was performed with a 1.5-T unit (Magnetom Sonata; Siemens, Erlangen, Germany) with gradients that had a capability of 40 mT/m and 200 (mT·m–1)/msec. The standard four-channel body phased-array coil was used for signal reception. After localizer imaging, cine true fast imaging with steady-state precession imaging (TrueFISP; Siemens Medical Systems, Erlangen, Germany) (3) was performed in several long-axis planes (two-, three-, and four-chamber views) of the heart, and parallel short-axis sections from the apex to the base of the left ventricle were acquired for volumetric analysis. Patients underwent unenhanced T1-weighted MR imaging by using a true fast imaging with steady-state precession IR cine technique (12,24,25). Sequence parameters were as follows: (repetition time msec/echo time msec, 2.5/1.25; flip angle, 50°; bandwidth, 965 Hz/pixel; voxel size, 2.5 x 1.8 x 8.0 mm3; 15 k-space lines per cardiac cycle; and 19 segments per cardiac cycle, yielding 19 images with inversion times increasing by 40 msec). A single section was positioned (J.W.G.) on the basis of cine MR wall motion imaging to include regions with both dysfunctional and functional myocardium. After injection of 0.2 mmol per kilogram body weight of a gadolinium-based contrast agent (Omniscan; GE Healthcare, Buckinghamshire, England) with an automated injector (Spectris; Medrad, Pittsburgh, Pa), the same true fast imaging with steady-state precession IR cine sequence was used repeatedly to assess delayed hyperenhancement. After a delay of 20–30 minutes (26), DHE imaging was performed by using an IR fast low-angle shot protocol (22) (11.0/4.3; flip angle, 30°; bandwidth, 140 Hz/pixel; voxel size, 1.7 x 1.3 x 8.0 mm3) or an IR true fast imaging with steady-state precession sequence (23,27) (2.6/1.3; flip angle, 45°; bandwidth, 1180 Hz/pixel; voxel size, 1.8 x 1.3 x 8.0 mm3).
Image Analysis
Volumetric analysis of the short-axis cine true fast imaging with steady-state precession images was performed by an author (S.A.) by using dedicated software (QMASS MR; Medis, Leiden, the Netherlands). The epicardial and endocardial contours of the heart were hand drawn from the apex to the base of the left ventricle. End-systolic and diastolic left ventricular volumes and myocardial mass were measured from the drawn contours, and the left ventricular ejection fraction was calculated (28).
An image analyst with 2 years of cardiac MR experience (S.A.), who was blinded to the patient information, was presented with each unenhanced T1-weighted MR image set. Four unenhanced images with equally spaced inversion times that showed the infarct were selected, and the mean signal intensity of the infarct region was measured. Cine IR steady-state free precession images show the same heart segments over the cardiac cycle with different image contrasts throughout the IR of up to one heartbeat. When possible, the four selected images depicted the infarct region as both hypointense and hyperintense compared with adjacent viable myocardium. A region of interest of approximately 10 pixels was placed adjacent to the infarct segment and the mean signal intensity of the adjacent myocardium was measured. T1 relaxation times for the infarct and adjacent myocardium were calculated by using a four-point least-squares fit to the analytic signal intensity formula (12,25).
Statistical Analysis
All statistical analyses were performed by an author (J.H.) with software (SAS, version 9.1; SAS Institute, Cary, NC). Means, standard deviations, and ranges of T1 relaxation times in the MI and adjacent myocardium were calculated. Data were tested for normality by using the Kolmogorov-Smirnov test. The relationship between T1 relaxation times of the infarct and infarct age was evaluated by using the Pearson correlation. An unpaired two-tailed Student t test was used to determine whether there was a significant difference between the T1 relaxation times of infarcts with an age less than 2 months and of infarcts with an age greater than 2 months. A paired two-tailed Student t test was used to compare the T1 relaxation times in the infarct and adjacent myocardium. Data are presented as means ± standard deviations. A poststudy power analysis was performed to determine whether the sample sizes used in this study were appropriate. A difference with a P value of .05 or less was considered significant.
 |
RESULTS
|
|---|
All patients successfully completed the study. Although the ages of the MIs differed between groups, the patients' ages, left ventricular ejection fractions, and left ventricular masses were similar (Table 1).
Detection of Recent MI with Unenhanced T1-weighted MR Imaging
In patients who developed an MI within the last 2 months, areas of myocardial edema in areas of MI shown with DHE imaging were well depicted with unenhanced T1-weighted MR imaging (Fig 1). At early inversion times, unenhanced T1-weighted MR imaging depicted infarcted regions as hyperintense when compared with adjacent myocardium (Fig 2). Because of the T1 weighting of the MR pulse sequence, both the signal intensity values of the MI and the viable myocardium changed as a function of the inversion time. The image contrast was dependent on the inversion time for both the unenhanced and enhanced acquisitions, demonstrating the difference in T1 relaxation time before and after contrast agent administration (Fig 2). The unenhanced T1 relaxation times were significantly different (P < .001) between the infarcted region and the adjacent myocardium for recent MIs (Fig 3) but were only slightly significantly different (P = .049) for older MIs (Table 2).

View larger version (93K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 1: Top: Precontrast T1-weighted (2.5/1.3, 50° flip angle) MR images. Bottom: Postcontrast DHE (2.6/1.3, 45° flip angle) images. Optimal contrast between infarcted regions (arrow) and adjacent myocardium is observed. Infarcts are 10, 15, and 48 days old, from left to right.
|
|

View larger version (80K):
[in this window]
[in a new window]
[Download PPT slide]
|
Figure 2: Short-axis T1-weighted MR images obtained in a 48-year-old patient with a recent (10-day-old) MI (arrowheads) by using true fast imaging with steady-state precession IR cine technique (2.5/1.3, 50° flip angle). Top: Precontrast images show a midcavity inferolateral region (T1 = 1265 msec) that is hyperintense at inversion time (TI) of less than 435 msec. Bottom: Postcontrast images in the same region show the area to be hypointense for inversion time of less than 223 msec. The postcontrast image at inversion time of 308 msec would be considered optimal for DHE imaging. Images are windowed individually for optimal contrast.
|
|
Comparison of Recent and Chronic MIs with Unenhanced T1-weighted MR Imaging
The T1 relaxation times for the recent infarcts were significantly longer (P < .001) than those for the older MIs (925 msec ± 169 vs 551 msec ± 107) (Fig 4). The measured adjacent myocardial T1 relaxation times were not significantly different between the two groups. Results of Pearson correlation analysis indicated that there was no statistically significant correlation (P > .05) between infarct age and T1 relaxation times of either infarct or adjacent normal myocardium.
Poststudy Power Analysis
With use of a sample size of eight, T1-weighted imaging will have 99% power for detection of a difference in mean T1 relaxation times of 291 msec relative to adjacent myocardium, with assumption of a standard deviation of differences of 134 msec. For discrimination between recent and older MIs by using T1 measurements, a sample size of eight in each of two groups will have 99% power for detection of a difference in mean T1 relaxation times of 373 msec, with the assumption that the common standard deviation is 141 msec.
 |
DISCUSSION
|
|---|
In our study, we have shown the capability of unenhanced T1-weighted MR imaging to depict an MI and provide information that permits infarct characterization. Dating of infarcts may be performed by using unenhanced T1-weighted MR imaging or T1 relaxation time measurements. Our data not only demonstrate a significant difference between T1 relaxation times of a recent infarct and those of adjacent myocardium but also show a difference between the T1 relaxation times of recent and chronic MIs. The clinical implications of determining the MI ages have been discussed in the literature (1,29). The addition of T1-weighted MR imaging to clinical imaging protocols may provide improved risk stratification and help direct further therapy.
After MI or intervention, local edema increases not only the T2 relaxation time but also the T1 relaxation time of infarcted myocardium. Imaging of myocardial edema can be performed by using T1-weighted MR techniques, which can provide an image quality that may be difficult to achieve with T2-weighted MR imaging. T2-weighted MR imaging typically has longer breath-hold times than does T1-weighted MR imaging, depends on the flow of blood out of the imaging plane, often results in ghosting, and may fail in patients with extreme cardiac dysfunction (1,15,16). T1-weighted MR imaging has many variants. We used an IR cine true fast imaging with steady-state precession technique, but T1-weighted MR imaging can also be performed in a single heartbeat (23,27), in a three-dimensional acquisition (30), or during free breathing (31).
T2-weighted MR imaging was recently shown to accurately depict the myocardial area at risk, a zone of reversible and irreversibly injured myocardium associated with reperfused subendocardial infarctions (14). After acute infarction, knowledge of the area at risk may allow interventions and, thus, help save potentially functional heart muscle (32). Unenhanced T1-weighted MR imaging can be performed by using the same MR pulse sequences as those used for DHE imaging, with only a change in the inversion time. This would allow almost perfect registration and direct comparison of edema-sensitive and contrast agent–sensitive (DHE) images, with identical resolution and field-of-view restrictions.
As with DHE imaging, the quality of unenhanced T1-weighted MR images is dependent on the inversion time. This is due to the patient-specific T1 relaxation time of the edematous region, which can vary with the amount of edema. In this study, there was a wide range of measured unenhanced T1 relaxation times. It is necessary to iteratively adjust the inversion time so that signal from adjacent myocardium is minimized (33). Alternatively, the optimal inversion time can be measured (24) or a phase-sensitive reconstruction (34) can be used.
In our study, we did not address the issue of quantitative infarct size measurements. A single section was used in all T1-weighted MR calculations. The acquisition of multiple sections would allow measurement of edema and DHE infarct volume. Although the sample size in our study was small, there were significant differences between the T1 relaxation times of recent infarcts and those of adjacent myocardium. A larger sample size may show that to be true also for chronic MIs as a result of their increased fat content (35–37). Because of the variety of infarct size, locations, and other variables, larger sample sizes are needed to determine the associations of the T1 relaxation times of recent infarcts with the age of infarcts and other clinical variables. Potential selection bias is a limitation of the study. Individual participation was limited by the desire and ability due to the overall health of the patients. Myocardial edema in this study may not only be due to MI but also to reperfusion. Reperfusion introduces myocardial edema, the magnitude of which depends mainly on the duration and severity of ischemia (21). Replacement of intravascular fluid creates an osmotic gradient, resulting in myocardial edema. T1-weighted MR imaging before and after interventions would be capable of helping determine the amount of edema that can be attributed to interventions. T2-weighted MR images were not obtained in most cases, and a study in which T1- and T2-weighted MR imaging are compared with respect to the detection of myocardial edema is warranted. Only MIs resulting from coronary artery disease were included in this study. Further study of unenhanced T1-weighted MR imaging is necessary to determine its usefulness in a wide array of myocardial injuries, such as myocarditis and necrosis in cardiomyopathy.
As a result of local edema, the T1 relaxation time of infarcted myocardium is increased and may remain elevated up to 2 months after MI. The detection and characterization of a recent MI on a segmental basis can be performed with unenhanced T1-weighted MR imaging.
 |
ADVANCES IN KNOWLEDGE
|
|---|
- Recent myocardial infarction (MI) can be detected by using unenhanced T1-weighted MR imaging techniques.
- The T1 relaxation times of recent MI and adjacent myocardium are significantly different (P < .001).
- The T1 relaxation times of recent MI and chronic MI are significantly different (P < .001).
 |
IMPLICATIONS FOR PATIENT CARE
|
|---|
- Recent MI can be detected by using T1-weighted MR imaging techniques, which provide image quality that may be difficult to achieve with T2-weighted MR imaging.
- T1 relaxation times can be used to determine the age of MI.
 |
ACKNOWLEDGMENTS
|
|---|
We thank Marguerite Roth, RN, and Jeanette McLaughlin, RN, for their help with patient recruitment.
 |
FOOTNOTES
|
|---|
Abbreviations: DHE = delayed hyperenhanced IR = inversion recovery MI = myocardial infarction
Author contributions:Guarantor of integrity of entire study, J.W.G.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript revision for important intellectual content, all authors; approval of final version of submitted manuscript, all authors; literature research, J.W.G.; clinical studies, J.W.G., S.A.; statistical analysis, J.W.G., J.H.; and manuscript editing, all authors
Authors stated no financial relationship to disclose.
 |
References
|
|---|
- Abdel-Aty H, Zagrosek A, Schulz-Menger J, et al. Delayed enhancement and T2-weighted cardiovascular magnetic resonance imaging differentiate acute from chronic myocardial infarction. Circulation 2004;109:2411–2416. [Abstract/Free Full Text]
- 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]
- Carr JC, Simonetti O, Bundy J, Li D, Pereles S, Finn JP. Cine MR angiography of the heart with segmented true fast imaging with steady-state precession. Radiology 2001;219:828–834. [Abstract/Free Full Text]
- Kim RJ, Wu E, Rafael A, et al. The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med 2000;343:1445–1453. [Abstract/Free Full Text]
- Simonetti OP, Finn JP, White RD, Laub G, Henry DA. "Black blood" T2-weighted inversion-recovery MR imaging of the heart. Radiology 1996;199:49–57. [Abstract/Free Full Text]
- Pflugfelder PW, Wisenberg G, Prato FS, Turner KL, Carroll SE. Serial imaging of canine myocardial infarction by in vivo nuclear magnetic resonance. J Am Coll Cardiol 1986;7:843–849. [Abstract]
- Miller S, Helber U, Brechtel K, et al. MR imaging at rest early after myocardial infarction: detection of preserved function in regions with evidence for ischemic injury and non-transmural myocardial infarction. Eur Radiol 2003;13:498–506. [Medline]
- Miller S, Helber U, Kramer U, et al. Subacute myocardial infarction: assessment by STIR T2-weighted MR imaging in comparison to regional function. MAGMA 2001;13:8–14. [CrossRef][Medline]
- Johnston DL, Wendt RE III, Mulvagh SL, Rubin H. Characterization of acute myocardial infarction by magnetic resonance imaging. Am J Cardiol 1992;69:1291–1295. [CrossRef][Medline]
- Thompson RC, Liu P, Brady TJ, Okada RD, Johnston DL. Serial magnetic resonance imaging in patients following acute myocardial infarction. Magn Reson Imaging 1991;9:155–158. [CrossRef][Medline]
- Garcia-Dorado D, Oliveras J, Gili J, et al. Analysis of myocardial oedema by magnetic resonance imaging early after coronary artery occlusion with or without reperfusion. Cardiovasc Res 1993;27:1462–1469. [Medline]
- Goldfarb JW, Mathew ST, Reichek N. Quantitative breath-hold monitoring of myocardial gadolinium enhancement using inversion recovery TrueFISP. Magn Reson Med 2005;53:367–371. [CrossRef][Medline]
- Kim RJ, Chen EL, Lima JA, 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. [Abstract/Free Full Text]
- Aletras AH, Tilak GS, Natanzon A, et al. 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 2006;113:1865–1870. [Abstract/Free Full Text]
- Keegan J, Gatehouse PD, Prasad SK, Firmin DN. Improved turbo spin-echo imaging of the heart with motion-tracking. J Magn Reson Imaging 2006;24:563–570. [CrossRef][Medline]
- Vignaux OB, Augui J, Coste J, et al. Comparison of single-shot fast spin-echo and conventional spin-echo sequences for MR imaging of the heart: initial experience. Radiology 2001;219:545–550. [Abstract/Free Full Text]
- Willerson JT, Buja LM. Q-wave versus non-Q-wave myocardial infarction. Cardiovasc Clin 1989;20:183–195. [Medline]
- Buja LM, Willerson JT. Abnormalities of volume regulation and membrane integrity in myocardial tissue slices after early ischemic injury in the dog: effects of mannitol, polyethylene glycol, and propranolol. Am J Pathol 1981;103:79–95. [Abstract]
- Willerson JT, Scales F, Mukherjee A, et al. Abnormal myocardial fluid retention as an early manifestation of ischemic injury. Am J Pathol 1977;87:159–188. [Abstract]
- Reimer KA, Jennings RB. The changing anatomic reference base of evolving myocardial infarction: underestimation of myocardial collateral blood flow and overestimation of experimental anatomic infarct size due to tissue edema, hemorrhage and acute inflammation. Circulation 1979;60:866–876. [Free Full Text]
- Garcia-Dorado D, Oliveras J. Myocardial oedema: a preventable cause of reperfusion injury? Cardiovasc Res 1993;27:1555–1563.
- 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]
- Li W, Li BS, Polzin JA, Mai VM, Prasad PV, Edelman RR. Myocardial delayed enhancement imaging using inversion recovery single-shot steady-state free precession: initial experience. J Magn Reson Imaging 2004;20:327–330. [CrossRef][Medline]
- Gupta A, Lee VS, Chung YC, Babb JS, Simonetti OP. Myocardial infarction: optimization of inversion times at delayed contrast-enhanced MR imaging. Radiology 2004;233:921–926. [Abstract/Free Full Text]
- Scheffler K, Hennig J. T(1) quantification with inversion recovery TrueFISP. Magn Reson Med 2001;45:720–723. [CrossRef][Medline]
- Wagner A, Mahrholdt H, Thomson L, 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 2006;47:2027–2033. [Abstract/Free Full Text]
- Huber A, Bauner K, Wintersperger BJ, et al. Phase-sensitive inversion recovery (PSIR) single-shot TrueFISP for assessment of myocardial infarction at 3 tesla. Invest Radiol 2006;41:148–153. [CrossRef][Medline]
- Maceira AM, Prasad SK, Khan M, Pennell DJ. Normalized left ventricular systolic and diastolic function by steady state free precession cardiovascular magnetic resonance. J Cardiovasc Magn Reson 2006;8:417–426. [CrossRef][Medline]
- Nieman K, Cury RC, Ferencik M, et al. Differentiation of recent and chronic myocardial infarction by cardiac computed tomography. Am J Cardiol 2006;98:303–308. [CrossRef][Medline]
- Dewey M, Laule M, Taupitz M, Kaufels N, Hamm B, Kivelitz D. Myocardial viability: assessment with three-dimensional MR imaging in pigs and patients. Radiology 2006;239:703–709. [Abstract/Free Full Text]
- Goldfarb JW, Shinnar M. Free-breathing delayed hyperenhanced imaging of the myocardium: a clinical application of real-time navigator echo imaging. J Magn Reson Imaging 2006;24:66–71. [CrossRef][Medline]
- Pennell D. Myocardial salvage: retrospection, resolution, and radio waves. Circulation 2006;113:1821–1823. [Free Full Text]
- Kim RJ, Shah DJ, Judd RM. How we perform delayed enhancement imaging. J Cardiovasc Magn Reson 2003;5:505–514. [CrossRef][Medline]
- Kellman P, Arai AE, McVeigh ER, Aletras AH. Phase-sensitive inversion recovery for detecting myocardial infarction using gadolinium-delayed hyperenhancement. Magn Reson Med 2002;47:372–383. [CrossRef][Medline]
- Goldfarb JW, Arnold S, Roth M, Han J. T1-weighted magnetic resonance imaging shows fatty deposition after myocardial infarction. Magn Reson Med 2007;57:828–834. [CrossRef][Medline]
- Baroldi G, Silver MD, De Maria R, Parodi O, Pellegrini A. Lipomatous metaplasia in left ventricular scar. Can J Cardiol 1997;13:65–71. [Medline]
- Su L, Siegel JE, Fishbein MC. Adipose tissue in myocardial infarction. Cardiovasc Pathol 2004;13:98–102. [Medline]
This article has been cited by other articles:

|
 |

|
 |
 
M. G. Friedrich
A closer look on the battlefield the salvaged area at risk as an outcome marker for myocardial reperfusion.
J. Am. Coll. Cardiol. Img.,
May 1, 2009;
2(5):
577 - 579.
[Full Text]
[PDF]
|
 |
|