Abstract
The current study evaluated the capability of magnetic resonance imaging (MRI) to detect acutely injured myocardium in the first 5 hr after a 1-hr period of occlusion followed by reperfusion of the coronary artery and to determine if magnetic relaxation times could be used to differentiate injured from normal myocardium. Fourteen dogs underwent left anterior descending coronary arterial occlusion for 1 hr, followed by reperfusion. Electrocardiographic gated MRI was performed before and during coronary artery occlusion and immediately after reperfusion, and serially up to 5 hr postreperfusion. In all dogs with postmortem evidence of myocardial infarction (n = 7), regional increase of signal intensity was observed in the anterior wall of the left ventricle as early as 30 min after reestablishing blood flow to the jeopardized myocardium. The area of increased signal intensity in the myocardium conformed to the site of myocardial infarction found at autopsy. The signal intensities of the jeopardized myocardium were significantly (p less than 0.01) greater than those of normal myocardium at 30 to 300 min postreperfusion. The T2 (spin-spin) relaxation time was significantly (p less than 0.05-p less than 0.01) prolonged in the region of the reperfused myocardial infarct at 30 min (59.6 +/- 13.1 msec) and remained prolonged up to 300 min (62.6 +/- 12 msec) postreperfusion compared with the T2 of normal myocardium (40.6 +/- 5.2 msec). Of the remaining seven dogs, four developed fatal arrhythmias during the reperfusion procedure and three dogs had no evidence of myocardial infarction at pathologic examination. Signal intensities and T2 relaxation times in these three dogs did not change during the experiment. Thus, acutely infarcted and reperfused myocardium can be detected by in vivo gated MRI, using the spin-echo technique, as early as 30 min after reperfusion. The jeopardized myocardium is characterized by a prolonged T2 relaxation time and, therefore, best visualized on T2-weighted images.
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