组织多普勒应变成像评价犬急性心肌缺血左心室顿抑区的跨壁力学状态

Left ventricular transmural mechanics at stunned myocardium in dogs with acute myocardial ischemia using tissue Doppler strain imaging

背景:急性心肌缺血后跨壁峰值应变的改变不仅出现在梗死区域,而且出现在顿抑区域。但对顿抑区域的心内膜下层心肌、中层心肌及心外膜下层心肌的跨壁力学特征的研究还鲜有报道。目的:实验拟应用应变成像评价犬急性心肌缺血顿抑区不同层次心肌径向峰值应变及应变达峰时间,并观察其跨壁力学特征。设计、时间及地点:随机对照实验,于2007-10在四川省医学科学院·四川省人民医院超声医学中心完成。材料:雌性Beagle实验动物犬11只,平均体质量11.5kg,开胸结扎左冠状动脉前降支建立心肌缺血模型。方法:在组织速度成像条件下,基础状态采集标准心尖短轴切面的3个完整心动周期内的二维动态组织多普勒速度图像,同步记录心电图,存于TDI-Q工作站。在缺血基础状态下,采集左心室短轴切面心尖水平的3个完整心动周期内的动态图像,同步记录心电图,存于TDI-Q工作站。主要观察指标:基础状态、缺血后顿抑区的节段整体及心内膜下心肌、中层心肌(medium,mid)及心外膜下心肌的径向峰值应变及达峰时间。结果:Beagle犬2只死于室颤,9只成功制成缺血模型。①顿抑区心内膜下心肌峰值应变(Ssubendo)与基础状态值相比降低(P<0.05),中层心肌峰值应变(Smid)与基础状态值相比差异无显著性(P>0.05),心外膜下心肌峰值应变(Ssubepi)比基础状态值增高(P<0.05);节段整体达峰时间(Tsegment)以及各层次达峰时间(Tlayers)延长(P<0.05)。②基础状态Ssubendo及Smid分别与其节段整体的峰值应变(Ssegment)有较好的相关性(rSsubendo vs Ssegment=0.617,rSmid vs Ssegment=0.556,P均<0.01)。结论:急性心肌缺血后,顿抑区域呈Ssubendo降低、Ssubepi增高和Tlayers延长,该跨壁力学状态是缺血区域和非缺血区域不同层次心肌力学机制相互作用的结果。推测此力学状态是决定心室重构进程以及最终向缺血性心肌病演变的重要触发机制之一。

BACKGROUND： After acute myocardial ischemia, changes in transmural peak radial strain not only appear at infarcted region, but also appear at stunned region. There were rarely reports on transmural mechanics of different layers at stunned region including subendocardial layer, intercellular layer and subepicardial layer. OBJECTIVE： To assess peak radial strain and strain time-to-peak of stunned different layers myocardium using tissue Doppler strain imaging, and to observe its transmural mechanics characteristics during dog acute myocardial ischemia. DESIGN, TIME AND SETTING： The randomized controlled experiment was performed at the Sichuan Provincial Academy of Medical Science, Center of Ultrasonic Medicine, Sichuan People＇s Hospital during October 2007. MATERIALS： Eleven female Beagle dogs weighing 11.5 kg were used in this study. Dog models of myocardial ischemia were established by ligating left anterior descending coronary artery. METHODS： The two-dimensional apical short-axis views of the left ventricle in three complete cardiac cycles were acquired and stored in TDI-Q workstation at baseline （the control group of stunned myocardium） and during acute myocardial ischemia. MAIN OUTCOME MEASURES： Transmural peak radial strain and strain time-to-peak of segment, subendocardiac muscle, midmyocardium and subepicardiac muscle at stunned region and baseline. RESULTS： Two dogs died of ventricular fibrillation. Nine dog models of ischemia were successfully established. （1）Peak radial strain at stunned subendocardiac muscle （Ssubendo） decreased compared with the baseline （P 〈 0.05）. No significant difference between those at baseline and at stunned medium （Smid） （P 〉 0.05）. Peak radial strain at stunned subepicardium （Ssubepi） increased （P 〈 0.05）. Strain time-to-peak of the whole segment （Tsegment） and at different layers （Tlayers） of stunned myocardium was significantly postponed （P 〈 0.05）. （2） There was a good correlation of peak radial strain of Ssubendo and Smid to Ssegment at baseline （rSsubendo vs Ssement=0.617, rSmid vs Ssegment=0.556, P 〈 0.01）. CONCLUSION： Acute myocardial ischemia induces Ssubendo reduction, Ssubepi increase and Tlayers prolongation at stunned myocardium. The transmural mechanical remodeling is the myocardium. It is concluded that this mechanic state is processes and resulting in ischemic cardiomyopathy. results of mechanical interactions between ischemic and nonischemic an important trigger mechanism, which can determine remodeling