CONTRACTILE STATE OF MYOCARDIUM IN MYOCARDIAL INFARCTION

心肌梗死（MI）后，由于顿抑心肌的恢复，左心室功能可能会自发改善。 然而，是否在邻近心肌区域的收缩状态的变化可能有助于这一过程是未知的。 因此，本研究的目的是探讨心肌损伤的程度和室壁运动异常之间的关系在MI的早期阶段的变化。 通过永久性结扎冠状动脉前循环或后循环的动脉分支，在21只成年绵羊中制造MI。 实时三维超声心动图（RT 3D回波）图像获得立即（组I; n=10）或24小时（组II; n=11）后冠状动脉闭塞。 在I组动物中，在图像采集后将伊文思蓝染料注射到闭塞的冠状动脉中，用于随后的解剖识别和异常灌注心肌的面积测量。 在组II动物中，从病理标本中获得解剖梗死的直接面积测量。 使用基于Silicon Graphics工作站的交互式追踪技术，从RT 3D回波图像离线测量室壁运动异常的程度，并表示为具有异常室壁运动的内膜表面。 室壁运动异常的内膜表面与灌注缺损（I组）或心肌坏死（II组）的解剖范围之间的差异被认为是邻近心肌。结果如下：24小时时心肌坏死的解剖学范围（组II）明显大于灌注缺损的解剖学范围（组I）（15.8+/-2.8 vs. 11.6 +/-2.7 cm 2; P=0.002）。 相反，与结扎后即刻相比，24小时时室壁运动异常程度有降低的趋势（21.9+/-4.4 vs. 25.9+/-5.9 cm 2; P=0.09）。 值得注意的是，与冠状动脉闭塞后即刻相比，24小时时相邻心肌室壁运动异常的程度显著降低（6.1+/-2.1 vs. 14.2+/-2.7 cm 2; P<0.0001）。 结论：在永久性冠状动脉闭塞的动物模型中，梗塞区域周围的功能障碍心肌的程度早期减少。 这种现象可以部分解释急性心肌梗死后左心室功能的自发恢复。

Spontaneous improvement in left ventricular function may occur after myocardial infarction (MI) due to recovery of stunned myocardium. However, whether changes in the contractile state of neighboring myocardial regions may contribute to this process is unknown. Therefore, the present study was designed to investigate changes in the relation between the extent of myocardial injury and wall motion abnormalities in the early phase of MI. MI was created in 21 adult sheep by permanently ligating arterial branches on the anterior or posterior coronary circulation. Real-time 3-dimensional echocardiographic (RT3D echo) images were obtained either immediately (group I; n=10) or 24 hours (group II; n=11) after coronary occlusion. In group I animals, Evans blue dye was injected into the occluded coronary artery after image acquisition for subsequent anatomic identification and planimetry of abnormally perfused myocardium. In group II animals, direct planimetry measurements of the anatomic infarct were obtained from the pathologic specimens. Extent of wall motion abnormalities was measured off-line from RT3D echo images using an interactive tracing technique based on a Silicon Graphics workstation and expressed as endocardial surface with abnormal wall motion. The difference between endocardial surface with wall motion abnormalities and the anatomic extent of perfusion deficit (group I) or myocardial necrosis (group II) was considered neighboring myocardium. Results: The anatomic extent of myocardial necrosis at 24 hours (group II) was significantly greater than the anatomic extent of perfusion deficit (group I) (15.8+/-2.8 vs.11.6+/-2.7 cm2; P=0.002). In contrast, there was a trend toward decreased extent of wall motion abnormality at 24 hours compared to immediately following ligation (21.9+/-4.4 vs. 25.9+/-5.9 cm2; P=0.09). Of note, the extent of neighboring myocardium with wall motion abnormalities was significantly reduced at 24 hours compared to immediately after coronary occlusion (6.1+/-2.1 vs. 14.2+/-2.7 cm2; P<0.0001). Conclusion: In an animal model of permanent coronary occlusion, there is an early reduction in the extent of dysfunctional myocardium surrounding the infarcted area. This phenomenon may partly explain the spontaneous recovery in left ventricular function which may be observed following an acute MI.