应变成像评价犬左心室急性心肌缺血边缘区跨壁力学状态

Study of left ventricular transmural mechanics at peri - infarct myocardium in vivo using tissue Doppler strain imaging

目的应用应变成像观察犬左室急性心肌缺血边缘区不同层次心肌径向峰值应变及应变达峰时间，评价其跨壁力学特征。方法9只Beagle犬开胸结扎左冠状动脉前降支建立心肌缺血模型，分别于基础状态、缺血状态采集连续3个心动周期的左室心尖二维短轴观图像存于TDI—Q工作站，在脱机状态下应用软件衍生M型组织多普勒速度图，采样分析基础状态、缺血后边缘区的节段整体、心内膜下心肌、中层心肌及心外膜下心肌（subepicardium，subepi）的径向峰值应变（S）及达峰时间（T）。统计数据分析采用两独立样本t检验和配对t检验以及直线相关分析。结果边缘区心内膜下心肌峰值应变较基础状态值降低（P〈0．05），中层心肌峰值应变与基础状态值相比无明显差异（P〉0．05），心外膜下心肌峰值应变较基础状态值增高（P〈0．05）；节段整体达峰时间以及各层次达峰时间延长（P〈0．05）；同时观察到基础状态心内膜下层心肌及中层心肌分别与其节段整体的峰值应变有较好的相关性（r=（0.617，r=0．556，P均〈0．01），而梗死边缘区这种相关性消失（r=0．287，r=0．243，P均〉0．05）。结论急性心肌缺血后，边缘区呈心内膜下层心肌峰值应变降低、心外膜下层心肌峰值应变增高和各层次达峰时间延长，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。

Objective To observe left ventrieular transmural peak radial strain and strain time-to-peak of peri infarct different layers myocardium using tissue Doppler strain imaging, to assess its mechanical pattern during acute myocardial ischemia. Methods Left anterior descending coronary artery（LAD） were ligated in experimental open-chest Beagle dog models （n = 9）, the two-dimensional apical short-axis views of left ventricle in three complete cardiac cycles were acquired and stored in TDI-Q workstation at baseline（the control group of periinfarc myocardium） and during acute myocardial ischemia respectively. Sampling volume was uesd to measure the peak radial strain and the strain time-to-peak consesquently on the derived M mode tissue Doppler velocity images at peri-infarct myocardium before and after ischemic segments and different layers （subendocardium, medium, subepicardium）. Statistical analies was performed using student＇s t - test or Pearson＇s correlations. Results Peak radial strain decreased at peri-infarct subendocardium （ P 〈 0. 05） with no significant difference between those at baseline and at peri infarct medium （P〉0.05）, the peak radial strain increasd at peri-infarct subepicardium （P 〈0. 05） ,and the strain time-to-peak at different layers of peri-infarct myocardium was significantly postponed （ P〈0.05）. There was a good correlationship of peak radial strain between subendocardium and segment as well as between the medium and segment （ r = 0. 617, P 〈0.01 ; r = 0. 556, P 〈0.01 ）. This correlationship disappeared at peri infarct myocardial segment （ r = 0. 287, P 〉 0.05, r = 0.243, P 〉 0.05）. Conclusions The left ventricular transmural mechanical remodeling at peri infarct myocardium is the integrant of result of mechanical interactions between ischemic and nonischemic myocardium,which might be one of the trigger the structural and fundational remodeling processes involving in the pathophysiological foundation of ischemic cardiomyopathy.