构建急性心肌梗死模型犬梗死区的跨壁力学变化

Transmural mechanics at the infarcted myocardium of a dog model of acute myocardial infarction

背景:急性心肌梗死起病急,病情凶险,但目前对超急性期的辅助诊断主要靠心电图,实验主要利用组织多普勒应变成像的优点,对急性心肌梗死的早期诊断提供帮助。目的:应用组织多普勒应变成像技术观测犬急性心肌梗死前、后心内膜下层心肌、中层心肌、心外膜下层心肌径向峰值应变及应变达峰时间,分析其力学变化特征。方法:16只Beagle犬,开胸结扎左冠状动脉前降支的第一对角支建立急性心肌缺血模型。同步记录心电图,在组织速度成像模式下,分别在急性心肌梗死前、后采集标准心尖短轴切面的连续5个完整心动周期内的二维动态组织多普勒速度图像,存于TDI-Q工作站。分别观测梗死区缺血前、后局部及心内膜下层心肌、中层心肌、心外膜下层心肌径向峰值应变及应变达峰时间。结果与结论:急性心肌梗死后,梗死区局部以及心内膜下层心肌、中层心肌、心外膜下层心肌的峰值应变较梗死前明显降低(P<0.05);梗死区心肌各层次间峰值应变梯度消失;梗死区局部以及各层次心肌达峰时间均较缺血前延长(P<0.05)。同时观察到梗死区基础状态心内膜下心肌及中层心肌分别与其局部心肌的峰值应变呈正相关(r=0.617,P<0.01;r=0.556,P<0.01),而与梗死区则无相关性(r=0.338,P>0.05;r=0.218,P>0.05)。提示急性心肌梗死后,梗死区不同层次心肌间峰值应变梯度消失,局部及不同层次心肌峰值应变明显减低,而达峰时间明显延长,是梗死区心肌结构异常、功能障碍的反映,从而导致心脏整体运动不协调,引起心脏整体的非同步化运动,是触发心力衰竭的重要力学机制之一。

BACKGROUND：Acute myocardial infarction with acute onset is dangerous, but the aided diagnosis for hyperacute disease mainly depends on electrocardiogram. The advantages of tissue Doppler strain imaging were utilized to help early diagnosis of acute myocardial infarction. 〈br〉 OBJECTIVE：To observe left ventricular transmural peak radial strain and strain time-to-peak of subendocardiac muscle, midmyocardium and subepicardiac muscle using tissue Doppler strain imaging in dogs before and after acute myocardial infarction, and to assess its mechanical characteristics. 〈br〉 METHODS：A total of 16 Beagle dog models of acute myocardial ischemia were established by ligating left anterior descending coronary artery. The two-dimensional apical short-axis views of the left ventricle in five complete cardiac cycles were acquired and stored in TDI-Q workstation before and after acute myocardial ischemia. Transmural peak radial strain and strain time-to-peak of segment, subendocardiac muscle,＆amp;nbsp;midmyocardium and subepicardiac muscle at infarct region and baseline were observed. 〈br〉 RESULTS AND CONCLUSION：Peak radial strains at infarct and subendocardiac muscle, midmyocardium and subepicardiac muscle were decreased compared with the baseline （P〈0.05）. Peak strain gradient disappeared in each layer of infarct myocardium. Strain time-to-peak of the whole segment and infarct myocardium at different layers was significantly postponed （P〈0.05）. There was a positive correlation of peak radial strain between subendocardium and segment as wel as between medium and segment at baseline （r=0.617, P〈0.01;r=0.556, P〈0.01）. This relationship disappeared at infarct region （r=0.338, P〉0.05;r=0.218, P〉0.05）. Results indicated that after acute myocardial infarction, peak strain gradient disappeared at different layers at infarct region. Acute myocardial ischemia induces peak radial strain decrease at subendocardium, medium, subepicardium and strain time-to-peak at infarct region was significantly postponed, which reflected abnormal cardiac structure and dysfunction, resulted in uncoordinated cardiac motion and asynchronous heart movement. This may be an important mechanical mechanism triggering heart failure.