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J Am Coll Cardiol, 1990; 15:1355-1364
© 1990 by the American College of Cardiology Foundation
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Distinguishing viable from infarcted myocardium after experimental ischemia and reperfusion by using nuclear magnetic resonance imaging

T Ryan, RD Tarver, JL Duerk, SG Sawada, and NC Hollenkamp

Krannert Institute of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis 46202.

Early reperfusion has the potential for salvaging ischemic myocardium at risk for infarction. To test the ability of nuclear magnetic resonance (NMR) imaging to differentiate between stunned and infarcted myocardium early after reperfusion, 16 mongrel dogs underwent transient occlusion of the left anterior descending artery or a diagonal branch for 30, 60 or 180 min followed by reperfusion. To identify the area at risk for infarction and to assess the extent of hypoperfusion and reperfusion, two-dimensional and contrast echocardiography were performed at baseline study, during coronary occlusion and at three separate times during reperfusion (before NMR imaging, immediately after NMR imaging and 12 to 14 h later). Wall thickening in the control and ischemic zones and the circumferential extent of abnormal wall motion were analyzed at each time point using short-axis echocardiograms. Nuclear magnetic resonance imaging at 1.5 tesla was performed 2 to 3.5 h (mean 2.7 +/- 0.5) after reperfusion. Short-axis, multislice spin-echo images (TE 26 and TE 60) were obtained. Signal intensity was measured in the control and ischemic areas and expressed as a percent difference compared with normal myocardium. All dogs demonstrated a significant decrease in wall thickening and abnormal wall motion before and after NMR imaging. Seven of the eight dogs with infarction had an area of increased signal intensity on TE 60 images. The mean percent difference in signal intensity compared with adjacent normal myocardium was 127 +/- 68% (p = 0.002). None of the eight dogs without infarction had a visually apparent change in signal intensity on TE 60 images (mean percent difference versus control area 13 +/- 11%), despite regional systolic dysfunction documented by echocardiography at the time of imaging. The area of increased signal intensity correlated with infarct size (r = 0.69), although overestimation by NMR imaging occurred. The area of increased signal intensity did not correlate with the extent of echocardiographic contrast defect during coronary occlusion (risk area). This study demonstrates that NMR imaging can be applied early after coronary reperfusion to assess the potential for recovery of dysfunctional myocardium. In addition, by using a TE 60 multislice spin-echo imaging sequence at 1.5 tesla, quantification of the extent of infarction also may be possible.


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