EDITORIAL COMMENT
Emerging Applications of T2-Weighted Cardiac Magnetic Resonance Imaging in Acute Ischemic Syndromes*
Francis J. Klocke, MD*
Feinberg Cardiovascular Research Institute and Department of Medicine (Division of Cardiology), Feinberg School of Medicine, Northwestern University, Chicago, Illinois
* Reprint requests and correspondence: Dr. Francis J. Klocke, Apartment 5102, 950 North Michigan Avenue, Chicago, Illinois 60611-7532 (Email: f-klocke{at}northwestern.edu).
Key Words: T2-weighted CMR • acute myocardial ischemia • reversible myocardial injury • myocardial area-at-risk • myocardial salvage
Recent studies (1–3) indicate that T2-weighted cardiovascular magnetic resonance imaging (CMR) can retrospectively identify the area at risk in acute myocardial infarction. In this issue of the Journal, Abdel-Aty et al. (4) explore the possibility that T2 imaging can identify areas of ischemic myocardium before irreversible injury has occurred.
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Background
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The use of magnetic resonance to identify areas of recent myocardial injury was originally investigated in the 1980s, using myocardium examined ex vivo in small-bore or relatively low-strength magnets. Several early findings remain pertinent to current applications:- 1 T2 (transverse magnetization) relaxation times are increased systematically in acutely infarcted myocardium (5).
- 2 Increases in T2 relaxation time following coronary ligation tend to be augmented by reperfusion, sometimes markedly so, and can persist for days to weeks (6–8).
- 3 Areas of increased T2 signal are usually larger than the zone of infarction but comparable to the total at-risk zone defined autoradiographically (9) or using fluorescein staining (8).
- 4 T2 signal intensity is importantly (though not exclusively) related to myocardial water content. In early studies, increases in water content following acute infarction averaged 3% to 5% in nonreperfused infarcts (5,7) and as much as 28% in reperfused infarcts (7).
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Evolving technology
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Although the feasibility of in vivo T2-weighted imaging of injured areas was also demonstrated in the 1980s (10), systematic studies awaited the development of improved scanners and imaging sequences. As cogently reviewed by Abdel-Aty et al. (11), T2 imaging technology has improved greatly during the past 10 to 15 years. Multiechocardiographic techniques can now provide high-resolution, black-blood images of the heart with improved blood and fat signal suppression in a single breath-hold. Improved signal intensity correction algorithms have facilitated the use of phased array surface coils. "Hyperintense" areas on T2-weighted images are often identified using a pre-selected threshold difference in signal intensity between affected and remote myocardial regions rather than visual analysis.
Despite these advances, relatively small differences in signal-to-noise ratio between injured and normal myocardium remain challenging. Although increases in T2 are thought primarily to reflect local edema, increases in myocardial water content can be quite small, for example, 1.8 ± 0.9% in the current study of Abdel-Aty et al. (4). Inflammatory responses and the location of edema (intracellular vs. interstitial) may also influence signal intensity. The most troublesome pitfall in image interpretation continues to be incomplete suppression of blood signal in areas of slow flow. As illustrated in Figure 4 of the Abdel-Aty et al. study (4), this often mimics subendocardial signal enhancement. Areas of low T2 signal within an infarction (perhaps related to "no reflow") and inadequate windowing of low contrast-to-noise images during visual analysis can also be problematic.
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Area at risk in acute infarction
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Experimentally, Aletras et al. (1) and Tilak et al. (2) at the National Heart, Lung, and Blood Institute have demonstrated that hyperintense zones on in vivo images obtained 2 days following mid-left anterior descending coronary occlusion accurately define the ischemic area at risk retrospectively in both reperfused (1) and nonreperfused infarctions (2). In both situations, the area at risk systematically exceeded infarct size measured by triphenyltetrazolium chloride staining. Contrast-to-noise ratios, defined as the differences in signal-to-noise ratio between areas at risk and remote myocardium, averaged 2.9 and  2.1 in reperfused and nonreperfused infarcts on day 2, but did not differ in reperfused infarcts reimaged at 2 months.
Clinically, Friedrich et al. (3) have reported that the proportion of an area at risk that has been irreversibly injured in acutely reperfused infarction can also be assessed retrospectively by comparing T2-weighted and late-gadolinium-enhancement CMR images. In successfully reperfused patients studied within a few days after the acute event, areas at risk identified with T2 imaging were consistently transmural and exceeded areas of irreversible injury defined by late-gadolinium-enhancement CMR by 16 ± 11%. Abdel-Aty et al. (12) have also reported that the presence or absence of increased T2 signal can differentiate acute and chronic myocardial infarction.
Thus, state-of-the-art T2-weighted imaging is a valuable emerging tool for identifying areas at risk in acute infarction. It appears to have particular value in studies of myocardial salvage and may also prove helpful in patients presenting late after the onset of infarction in whom immediate revascularization is not an obvious choice (13).
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Ischemia without apparent infarction
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In their present study, Abdel-Aty et al. (4) report that visually detectible changes in T2 signal intensity developed 28 ± 4 min following mid-left anterior descending coronary occlusion in open-chest dogs. Reperfusion was instituted as soon as increased T2 signals were identified but continued only until blood troponin sampling and repeat CMR imaging could be performed. Contrast-to-noise ratios were higher than in other studies but were calculated slightly differently and derived from regions of interest drawn within areas of maximal T2 signal intensity in the ischemic zone. In the absence of both late gadolinium enhancement and troponin elevation during reperfusion, Abdel-Aty et al. (4) conclude that T2-weighted imaging can detect acute myocyte injury before the onset of irreversible injury. The conclusion does presume that troponin elevations and/or late-gadolinium-enhancement CMR can identify myocardium committed to irreversible injury during the earliest stages of reperfusion.
As Abdel-Aty et al. (4) carefully point out, their findings remain subject to practical as well as technical limitations and are not easily extrapolated to situations other than sudden coronary occlusion. The profound degree of ischemia following sudden occlusion caused immediate contractile dysfunction, while the concomitant T2 abnormality became apparent only 20 to 40 min later. The utility of T2-weighted imaging in cases of less severe ischemia, and shorter durations or repetitive episodes of ischemia, remains to be established. In a study of infarctions induced by septal artery embolization in patients with hypertrophic cardiomyopathy (14), increases in T2 signal could not be detected 1 h following embolization but were present consistently at 3 to 28 days. In a recent emergency department study of CMR in chest pain patients presenting with normal biomarkers and electrocardiograms (15), the addition of T2-weighted imaging was sometimes helpful in identifying ongoing ischemia and in distinguishing between recent and remote infarction.
As efforts to improve T2-weighted imaging continue (16), even modest additional advances may substantially increase the value of this modality in ischemic syndromes.
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Footnotes
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* Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. 
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References
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1. 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 Circulation 2006;113:1865-1870.[Abstract/Free Full Text]2. Tilak GS, Hsu L-Y, Hoyt Jr. RF, Arai AE, Aletras AH. In vivo T2-weighted magnetic resonance imaging can accurately determine the ischemic area at risk for 2-day-old nonreperfused myocardial infarction Invest Radiol 2008;43:7-15.[CrossRef][Web of Science][Medline] 3. Friedrich MG, Abdel-Aty H, Taylor A, Schulz-Menger J, Messroghli D, Dietz R. The salvaged area at risk in reperfused acute myocardial infarction as visualized by cardiovascular magnetic resonance J Am Coll Cardiol 2008;51:1581-1587.[Abstract/Free Full Text] 4. Abdel-Aty H, Cocker M, Meek C, Tyberg JV, Friedrich MG. Edema as a very early marker for acute myocardial ischemia: a cardiovascular magnetic resonance study J Am Coll Cardiol 2009;53:1194-1201.[Abstract/Free Full Text] 5. Higgins CB, Herfkens R, Lipton MJ, et al. Nuclear magnetic resonance imaging of acute myocardial infarction in dogs: alterations in magnetic relaxation times Am J Cardiol 1983;52:184-188.[CrossRef][Web of Science][Medline] 6. Johnston DL, Brady TJ, Ratner AV, et al. Assessment of myocardial ischemia with proton magnetic resonance: effects of a three hour coronary occlusion with and without reperfusion Circulation 1985;71:595-601.[Abstract/Free Full Text] 7. 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.[Abstract/Free Full Text] 8. Johnston DL, Homma S, Liu P, et al. Serial changes in nuclear magnetic resonance relaxation times after myocardial infarction in the rabbit: relationship to water content, severity of ischemia, and histopathology over a six-month period Magn Reson Med 1988;8:363-379.[Web of Science][Medline] 9. Buda AJ, Aisen AM, Juni JE, Gallagher KP, Zotz RJ. Detection and sizing of myocardial ischemia and infarction by nuclear magnetic resonance imaging in the canine heart Am Heart J 1985;110:1284-1290.[CrossRef][Web of Science][Medline] 10. Wesbey G, Higgins CB, Lanzer P, Botvinick E, Lipton MJ. Imaging and characterization of acute myocardial infarction in vivo by gated nuclear magnetic resonance Circulation 1984;69:125-130.[Abstract/Free Full Text] 11. Abdel-Aty H, Simonetti O, Friedrich MG. T2-weighted cardiovascular magnetic resonance imaging J Magn Reson Imaging 2007;26:452-459.[CrossRef][Web of Science][Medline] 12. 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] 13. Pennell D. Myocardial salvage Circulation 2006;113:1821-1823.[Free Full Text] 14. Schulz-Menger J, Gross M, Messroghli D, Uhlich F, Dietz R, Friedrich MG. Cardiovascular magnetic resonance of acute myocardial infarction at a very early stage J Am Coll Cardiol 2003;42:513-518.[Abstract/Free Full Text] 15. Cury RC, Shash K, Nagurney JT, et al. Cardiac magnetic resonance with T2-weighted imaging improves detection of patients with acute coronary syndrome in the emergency department Circulation 2008;118:837-844.[Abstract/Free Full Text] 16. Arai AE. Using magnetic resonance imaging to characterize recent myocardial injury Circulation 2008;118:795-796.[Free Full Text]
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Background
Evolving technology