Journal
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Volume 53, Issue 14, Pages 1194-1201Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jacc.2008.10.065
Keywords
cardiovascular magnetic resonance; acute myocardial ischemia; myocardial edema; myocardial infarction; myocardial viability
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Objectives This study was designed to determine whether imaging myocardial edema would identify acute myocardial ischemia before irreversible injury takes place. Background Early identification of acute myocardial ischemia is a diagnostic challenge. Methods We studied 15 dogs with serial T-2-weighted and cine imaging at baseline, during transient coronary occlusion of up to 35 min, and after reperfusion in a 1.5-T magnetic resonance imaging system. Late gadolinium enhancement and troponin measurements were used to assess for the presence of irreversible injury. Myocardial water content was measured to assess myocardial edema. Results We consistently observed a transmural area of high T-2 signal intensity matching areas with new onset regional akinesia 28 +/- 4 min after experimental coronary artery occlusion. At this time, the contrast-to-noise ratio between the ischemic and remote myocardium had significantly increased from 1.0 +/- 2.0 to 12.8 +/- 9.6 (p < 0.003), which further increased after reperfusion to 15.8 +/- 10.3 (p < 0.004 compared with baseline). Neither myocardial late gadolinium enhancement nor troponin elevation were noted at this time window. Myocardial water content of the ischemic segments was consistently higher (68.9 +/- 2% vs. 67.0 +/- 2%; p < 0.004) than in remote segments and the difference correlated significantly to the contrast-to-noise ratio in T-2 images (p < 0.04). Conclusions We provide the first evidence that T-2-weighted cardiovascular magnetic resonance imaging of edema detects acute ischemic myocyte injury before the onset of irreversible injury. T-2-weighted cardiovascular magnetic resonance imaging may serve as a very useful diagnostic marker in clinical settings such as unstable angina or evolving infarction. (J Am Coll Cardiol 2009; 53: 1194-201) (C) 2009 by the American College of Cardiology Foundation
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