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he coherent steady-state free precession (SSFP) pulse sequence is increasingly being used in cine imaging for evaluating the cardiac function. Compared to the spoiled gradient echo MRI, which has usually been performed for cardiac cine imaging, the SSFP imaging sequence provides a higher signal-to-noise ratio (SNR) by recycling the residual transverse magnetization, and there is less of an inflow effect by using a very short repetition time. A few studies have recently reported that contrast-enhanced (CE) cineSSFP imaging could be used for estimating the viability of infarcted myocardium with or without the simultaneous evaluation of the ventricular function (1). Since the contrast of the SSFP sequence imaging is based on the ratio of T2 to T1, T1-shortening contrast-enhancement is shown as hyperenhancement, which is similar to that in the delayed-enhanced T1-imaging. In this issue of the Korean Journal of Radiology, Kim et al. (2) have reported that the CE-cine-SSFP sequence could be used for differentiating the acutely infarcted myocardium from chronic myocardial scar with a sensitivity of 95.8%. This was a new approach for evaluating the age of myocardial infarction (MI) by using MRI. The most important pathologic changes of infarcted myocardium that influence the signal intensities (SI) on the T1and T2-weighted imaging (WI) are the edema in acute MI and the fibrosis in chronic MI. The T1 and T2 relaxation times are directly correlated with the water content and they are inversely correlated with the collagen content (3) (Table 1). The abnormal signal intensity of infarcted myocardium on the T2-WI is usually conspicuous compared to that on the T1-WI. Therefore, to evaluate the age of an infarct, the T2-WI could be added to the infarct MRI (4). T2-WI reveals a high signal intensity of edema, which inevitably accompanies acutely infarcted myocardium and it is intensified by reperfusion therapy. The abnormal signal intensity of infarcted myocardium on the cine-SSFP images should reflect the T2 SI more than the T1 SI. However, the low SI of the infarcted myocardium that was seen in the chronic MI of this study is in disagreement with those findings of Abdel-Aty et al., in which the T2 SI of the infarcted myocardium in chronic MI showed as isosignal intensity compared to the noninfarcted myocardium (4). This discrepancy may be due to the usage of contrast-enhancement in Kim et al’s study. Hyperenhancement of infarcted myocardium on the delayed contrast-enhanced (DCE) MRI has been well established for evaluating an infarct’s location and size. However, there is the same degree of hyperenhancement of the infarcted myocardium on the DCE MRI regardless of the infarct’s age. The low SI of infarcted myocardium in chronic MI could be accounted for by the slow enhancement of fibrosis in the relatively early phase compared to the DCE, which occurred two minutes after contrast administration in Kim’s study, as contrasted with the enhancement of the surrounding normal myocardium. Although the concept of early enhancement, which is different from the first-pass perfusion, has not been well established in cardiac imaging, dynamic enhancement has already been used as a diagnostic imaging technique for the radiological examination for various pathologies; this was recently recognized to be different from the delayed T Byoung Wook Choi, MD Department of Radiology, Yonsei University, College of Medicine, Severance Hospital, Seoul 120-752, Korea

Differentiation of Acute Myocardial Infarction from Chronic Myocardial Scar with MRI