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犬再灌注心肌梗死的磁共振成像

MRI of reperfused myocardial infarct in dogs.

作者信息

Tscholakoff D, Higgins C B, Sechtem U, Caputo G, Derugin N

出版信息

AJR Am J Roentgenol. 1986 May;146(5):925-30. doi: 10.2214/ajr.146.5.925.

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.

摘要

本研究评估了磁共振成像(MRI)在冠状动脉闭塞1小时后再灌注的最初5小时内检测急性损伤心肌的能力,并确定磁弛豫时间是否可用于区分损伤心肌与正常心肌。14只犬接受左前降支冠状动脉闭塞1小时,随后再灌注。在冠状动脉闭塞前、闭塞期间以及再灌注后立即进行心电图门控MRI检查,并在再灌注后连续检查至5小时。在所有有心肌梗死尸检证据的犬(n = 7)中,早在恢复对濒危心肌的血流后30分钟,就观察到左心室前壁信号强度区域增加。心肌中信号强度增加的区域与尸检时发现的心肌梗死部位相符。在再灌注后30至300分钟,濒危心肌的信号强度显著高于正常心肌(p < 0.01)。与正常心肌的T2(自旋-自旋)弛豫时间(40.6±5.2毫秒)相比,再灌注心肌梗死区域的T2弛豫时间在30分钟时显著延长(p < 0.05 - p < 0.01)(59.6±13.1毫秒),并一直延长至再灌注后300分钟(62.6±12毫秒)。在其余7只犬中,4只在再灌注过程中发生致命性心律失常,3只犬在病理检查中无心肌梗死证据。这3只犬在实验过程中信号强度和T2弛豫时间未发生变化。因此,使用自旋回波技术,通过体内门控MRI最早可在再灌注后30分钟检测到急性梗死和再灌注的心肌。濒危心肌的特征是T2弛豫时间延长,因此在T2加权图像上显示最佳。

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