Li D, Li C Y, Yong A C, Kilpatrick D
The Discipline of Medicine, University of Tasmania, Hobart, Australia.
Circ Res. 1998 May 18;82(9):957-70. doi: 10.1161/01.res.82.9.957.
To clarify the source of electrocardiographic ST depression associated with ischemia, a sheep model of subendocardial ischemia was developed in which simultaneous epicardial and endocardial ST potentials were mapped, and a computer model using the bidomain technique was developed to explain the results. To produce ischemia in different territories of the myocardium in the same animal, the left anterior descending coronary artery and left circumflex coronary artery were partially constricted in sequence. Results from 36 sheep and the computer simulation are reported. The distributions of epicardial potentials from either ischemic source were very similar (r=0.77+/-0.14, P<0.0001), with both showing ST depression on the free wall of the left ventricle and no association between the ST depression and the ischemic region. However, endocardial potentials showed that ST elevation was directly associated with the region of reduced blood flow. Insulating the heart from the surrounding tissue with plastic increased the magnitude of epicardial ST potentials, which was consistent with an intramyocardial source. Increasing the percent stenosis of a coronary artery increased epicardial ST depression at the lateral boundary and resulted in ST elevation starting from the ischemic center as ischemia became transmural. Computer simulation using the bidomain model reproduced the epicardial ST patterns and suggested that the ST depression was generated at the lateral boundary between ischemic and normal territories. ST depression on the epicardium reflected the position of this lateral boundary. The boundaries of ischemic territories are shared, and only those appearing on the free wall contribute to external ST potential fields. These effects explain why body surface ST depression does not localize cardiac ischemia in humans.
为了阐明与缺血相关的心电图ST段压低的来源，建立了一个心内膜下缺血的绵羊模型，在该模型中同步绘制心外膜和心内膜的ST电位，并开发了一个使用双域技术的计算机模型来解释结果。为了在同一动物的心肌不同区域产生缺血，依次对左前降支冠状动脉和左旋支冠状动脉进行部分结扎。报告了36只绵羊的结果和计算机模拟结果。来自任一缺血源的心外膜电位分布非常相似（r = 0.77±0.14，P < 0.0001），两者均显示左心室游离壁ST段压低，且ST段压低与缺血区域无关联。然而，心内膜电位显示ST段抬高与血流减少区域直接相关。用塑料将心脏与周围组织隔离可增加心外膜ST电位的幅度，这与心肌内源性来源一致。增加冠状动脉狭窄百分比会增加外侧边界的心外膜ST段压低，并在缺血变为透壁性时导致从缺血中心开始的ST段抬高。使用双域模型的计算机模拟重现了心外膜ST模式，并表明ST段压低是在缺血区与正常区的外侧边界产生的。心外膜上的ST段压低反映了该外侧边界的位置。缺血区域的边界是共享的，只有那些出现在游离壁上的边界才会对外部ST电位场有贡献。这些效应解释了为什么体表ST段压低不能在人体中定位心脏缺血。
