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探讨急性心肌梗塞及再灌注的MRI征象及其病理学基础以及再灌注对心肌梗塞后左室重构的影响。材料和方法：13只小型猪开胸结扎冠状动脉左前降支制备心肌梗塞动物模型（6只）和心肌缺血再灌注动物模型（7只），于术前，术后7小时、5～7天、13～17大和1个月进行MRI检查，心脏标本进行病理检查。结果：梗塞组和再灌注组均见左心室前壁及空间隔前部T2WI上高信号，部分出现心脏内流动信号升高（其中梗塞组5例，再灌注组4例）。增强扫描两组均见心前壁明显强化，与T2WI上高信号部位、范围相同，病理检查证实其为梗塞心肌。随梗塞时间的进展，梗塞组（3只）左心室前壁变薄、膨展逐渐明显，左心室腔扩大，其中2例有室壁瘤形成；再灌注组（3只）仅1例左心室前壁变薄较明显，但无左室前壁明显膨展和左室腔扩大。结论：MRI能全面评价急性心肌梗塞的大小、范围和心脏的形态和功能等变化，对左室重构改变的评价有价值。再灌注对心肌梗塞后左室重构有限制作用。
To investigate the MRI features of acute myocardial infarction and reperfusion and its pathological basis and the effect of reperfusion on left ventricular remodeling after myocardial infarction. MATERIALS AND METHODS: Thirteen miniature pigs were subjected to thoracotomy and ligation of the left anterior descending coronary artery. Six animal models of myocardial infarction (MI) and 7 myocardial ischemia-reperfusion (I / R) Day, 13 ~ 17 and 1 month MRI examination, pathological examination of cardiac specimens. Results: In the infarction group and the reperfusion group, both the anterior wall of the left ventricle and the anterior segment of the anterior space had a high signal on T2WI, and some intracardiac flow signals were elevated (5 in the infarction group and 4 in the reperfusion group). Enhanced scanning of the two groups were significantly enhanced anterior heart wall, and T2WI high signal site, the same range, confirmed by pathological examination of myocardial infarction. With the progress of infarction time, the anterior wall of the left ventricle in the infarction group became thinner, the anterior wall of the left ventricle became thinner and the left ventricular cavity became larger gradually, including 2 cases of aneurysm. In the reperfusion group (3) The anterior wall thinning more obvious, but no significant left anterior wall expansion and left ventricular cavity expansion. Conclusion: MRI can evaluate the changes of acute myocardial infarction size, range and shape and function of heart completely, which is valuable for the evaluation of left ventricular remodeling changes. Reperfusion has a limited effect on left ventricular remodeling after myocardial infarction.