Assmann P E, Slager C J, Dreysse S T, van der Borden S G, Oomen J A, Roelandt J R
Department of Clinical Echocardiography, Thoraxcenter, University Hospital Rotterdam-Dijkzigt, The Netherlands.
J Am Soc Echocardiogr. 1988 Nov-Dec;1(6):393-405. doi: 10.1016/s0894-7317(88)80021-x.
To establish an appropriate echocardiographic model for wall motion analysis we first determined the precise dynamic geometry of the left ventricle during systole, as visualized by two-dimensional echocardiography. With the epicardial apex and the aortic-ventricular and mitral-ventricular junctions as anatomic landmarks, we quantitatively analyzed apical long-axis views in 61 normal subjects, 41 patients with anterior myocardial infarction, and nine patients with posterior myocardial infarction. Thoracic impedance registration allowed exclusion of extracardiac motion from the measurements. In normal subjects the epicardial apex moved outwardly only 0.6 +/- 0.3 mm (mean +/- standard error). Examination of 15 hearts fixed in formalin revealed apical myocardial thickness of 1.5 +/- 0.2 mm. These data suggest that the observed inward motion of the endocardial apex (4.1 +/- 0.7 mm) resulted from obliteration of the apical cavity as a result of inward motion of the adjacent walls. Translation of the base was considerable in normal subjects (14.1 +/- 0.4 mm) and decreased in myocardial infarction (9.1 +/- 0.5 mm, p less than 0.0001). Unequal shortening of the adjacent walls in anterior and posterior myocardial infarction caused basal rotation in the opposite direction (-9.1 +/- 0.8 degrees and 9.7 +/- 1.4 degrees, respectively, p less than 0.0001 versus that of normal subjects, -3.4 +/- 0.7 degrees). Long-axis rotation was not clinically significant (less than 1 degree). We conclude that during ventricular contraction the apex serves as a stable point, whereas the base translates toward the apex because of shortening of the adjacent walls. We then propose a model for analyzing regional wall motion from two-dimensional echocardiograms on the basis of these observations.
为建立一个适用于室壁运动分析的超声心动图模型，我们首先通过二维超声心动图观察，确定了收缩期左心室精确的动态几何形态。以心外膜顶点以及主动脉 - 心室和二尖瓣 - 心室连接点作为解剖标志，我们对61名正常受试者、41名前壁心肌梗死患者和9名后壁心肌梗死患者的心尖长轴视图进行了定量分析。胸廓阻抗记录可排除测量中的心脏外运动。在正常受试者中，心外膜顶点仅向外移动0.6±0.3毫米（平均值±标准误）。对15颗用福尔马林固定的心脏进行检查发现，心尖心肌厚度为1.5±0.2毫米。这些数据表明，观察到的心内膜顶点向内运动（4.1±0.7毫米）是由于相邻壁向内运动导致心尖腔闭塞所致。在正常受试者中，心底的平移相当显著（14.1±0.4毫米），而在心肌梗死患者中则减少（9.1±0.5毫米，p<0.0001）。前壁和后壁心肌梗死时相邻壁缩短不均，导致心底向相反方向旋转（分别为-9.1±0.8度和9.7±1.4度，与正常受试者的-3.4±0.7度相比，p<0.0001）。长轴旋转在临床上不显著（小于1度）。我们得出结论，在心室收缩期间，心尖作为一个稳定点，而心底由于相邻壁的缩短而向心尖平移。然后，基于这些观察结果，我们提出了一个从二维超声心动图分析局部室壁运动的模型。
