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Myocardial Edema Imaging of the Area at Risk in Acute Myocardial Infarction

Seeing Through Water^_*

Franz-Volhard-Klinik, Charité Universitätsmedizin Berlin, Berlin, Germany, and Cardio Imaging Center Berlin, Berlin-Wilmersdorf, Germany

Key Words: myocardial infarction • area at risk • myocardial edema • cardiac magnetic resonance • T2-weighted myocardial salvage

"Water is the driving force of all nature"

Leonardo da Vinci (1)

Sudden occlusion of a coronary artery marks the rapid onset of an array of functional, metabolic, and structural injuries within a certain time window in the myocardial area supplied by this coronary artery (2). If not timely reperfused, this area is at definite risk of ischemic death. Currently, quantification of this area at risk (AAR) per se is more interesting from a research rather than a clinical perspective. It is, however, the relation between the AAR and the dynamically evolving wavefront of necrosis within its territory that gives the AAR its clinical importance. In the setting of revascularization, this relation enables quantifying the volume of myocardium that reperfusion successfully salvaged from ischemic death. For quantitative assessment of the AAR, radionuclide imaging with its known limitations has been traditionally used. Several surrogate injuries like defective perfusion or loss of function are characteristics of the AAR and might be detectable noninvasively with echocardiography, radionuclide imaging, or cardiac magnetic resonance (CMR). The clinical value of these surrogates, however, is limited: although these approaches are sensitive in detecting an overwhelming ischemic event like that after coronary occlusion, they have a low specificity to identify the acuity of such an event, simply because a loss of perfusion and function are also features of chronic coronary artery disease or remote infarctions.

Water accumulation within tissues subjected to acute injury such as ischemia and reperfusion occurs in almost every organ in the body. In the brain, acute tissue edema can be detected through diffusion imaging, allowing for the quantification of the "penumbra," the term used for the cerebral AAR. Unlike the brain, the heart does not have a barrier between blood and tissue and also differs in other structural aspects. Because of these differences, there is an early relative and absolute increase of free water protons and accordingly T2 imaging—a far less technically challenging approach than diffusion imaging—can be used to detect the myocardial AAR. Edematous myocardium "shines" through its free water within the dark myocardium with its bound water.

Edema imaging is an interesting candidate to image the AAR for several reasons. First, it is a low-threshold ischemic injury occurring in reversibly injured myocardium (3,4) like that of the AAR. Second, it is both sensitive (5) and specific (6) to the acuity of an event. Third, edema is a tissue footprint of the AAR lasting for up to 2 weeks after the event, enabling an extended window to assess myocardial salvage (e.g., before patients' discharge).

A landmark study by Aletras et al. (3) established the concept that the area of high T2 signal (edematous myocardium) in CMR reflects the AAR in reperfused acute myocardial infarction (AMI). This confirmed findings from preliminary basic science (7) as well as clinical reports (8) and paved the way for the large patients' study by Friedrich et al. (5), which systematically assessed the AAR in 92 AMI patients with T2 edema imaging. In combination with late gadolinium enhancement, CMR, which accurately quantifies irreversible injury (9), myocardial salvage can thus be visualized and quantified with a simple CMR protocol.

In this issue of iJACC, Wright et al. (10) present data from 108 patients with reperfused AMI in whom the AAR was quantified with 3 different approaches: T2 edema imaging, endocardial surface length (ESL) of late gadolinium enhancement, and finally coronary angiography (BARI [Bypass Angioplasty Revascularization Investigation] score). The authors note a good correlation between T2 and ESL and a moderate correlation between T2 and BARI. The volume of T2 abnormality was consistently larger than that of late enhancement, confirming multiple previous reports (5,8,11). The T2 edema imaging of AMI has recently gained considerable interest, but concerns have been raised regarding its robustness, reproducibility, and vendor- or sequence-dependent differences of its performance. To this end, the current study is a welcome contribution, solidifying knowledge from previous reports in a large number of patients. The correlations presented are definitely interesting from a pathophysiological point of view, but unfortunately their clinical impact is reduced by the study design. Instead of comparing a novel approach (T2 in this case) with a clinically established approach with known limitations (invasiveness, cost, availability, and so forth) with the ultimate goal of replacing the "old" method (e.g., radionuclide imaging in this setting) with a novel one, the reported comparisons do not meet such criteria. The correlation of AAR with the angiographically determined BARI score is not a strong clinical argument, because BARI is rarely—if at all—clinically used to assess salvage in clinical settings and T2 will not replace angiography, which is an integral part of percutaneous coronary interventions. The other correlation deviates even further from such a "replacement" approach by comparing one CMR sequence (T2) with another (late enhancement). These design limitations might have been mandated by the retrospective nature of the analysis (ESL has been only recently proposed [12], whereas patients' recruitment for this study began several years earlier [10]). Despite that, the study should be viewed as a welcome contribution to our knowledge in a widening context of edema imaging in AMI with emerging data confirming its clinical feasibility and utility.

Future research should be directed toward addressing the technical challenges involved and standardizing image acquisition and analysis tools. Furthermore, there is a need to show that myocardial salvage as defined by a CMR-derived index correlates with other well-established methods of salvage assessment, such as radionuclide imaging, and that it does indeed offer a clear advantage over mere necrosis assessment (late enhancement) for assessing novel reperfusion strategies.

There is much to see through water.

	Footnotes

 
^_* Editorials published in JACC: Cardiovascular Imaging reflect the views of the authors and do not necessarily represent the views of JACC: Cardiovascular Imaging or the American College of Cardiology.

^_* Reprint requests and correspondence: Dr. Hassan Abdel-Aty, Cardio Imaging Center Berlin, Paretzer Str. 12, 10713 Berlin-Wilmersdorf, Germany (Email: abdel-aty{at}cardiomrt.de).

	REFERENCES

Top REFERENCES

 

1. da Vinci L. http://thinkexist.comAccessed March 18, 2009.
2. Reimer KA, Jennings RB. The "wavefront phenomenon" of myocardial ischemic cell death. II. Transmural progression of necrosis within the framework of ischemic bed size (myocardium at risk) and collateral flow. Lab Invest 1979;40:633-644.[Web of Science][Medline]
3. 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]
4. Abdel-Aty H, Cocker M, Meek C, Tyberg J, Friedrich MG. Edema as a very early marker for acute myocardial ischemia: a cardiovascular magnetic resonance study J Am Coll Cardiol 2009;53:1194-1212.[Abstract/Free Full Text]
5. 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]
6. 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]
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. Stork A, Lund GK, Bansmann M, et al. Comparison of an edema-sensitive HASTE-TIRM sequence with delayed contrast enhancement in acute myocardial infarcts Rofo 2003;175:194-198.[Web of Science][Medline]
9. 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]
10. Wright J, Adriaenssens T, Dymarkowski S, Desmet W, Bogaert J. Quantification of myocardial area at risk with T2-weighted CMR: comparison with contrast-enhanced CMR and coronary angiography J Am Coll Cardiol Img 2009;2:825-831.[Abstract/Free Full Text]
11. Stork A, Lund GK, Muellerleile K, et al. Characterization of the peri-infarction zone using T2-weighted MRI and delayed-enhancement MRI in patients with acute myocardial infarction Eur Radiol 2006;16:2350-2357.[CrossRef][Web of Science][Medline]
12. Ortiz-Perez JT, Meyers SN, Lee DC, et al. Angiographic estimates of myocardium at risk during acute myo cardial infarction: validation study using cardiac magnetic resonance imaging Eur Heart J 2007;28:1750-1758.[Abstract/Free Full Text]

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