Kilpatrick David, Johnston Peter R, Li D S
Medicine, University of Tasmania, Hobart, Australia.
J Electrocardiol. 2003;36 Suppl:7-12. doi: 10.1016/j.jelectrocard.2003.09.002.
The origin of ST depression in ischemia remains poorly understood. The accepted source is of intracellular current flowing between the ischemic and non ischaemic muscle both in systole and diastole such that the AC recorded electrocardiogram shows ST elevation over the ischemic area. The difficulty comes with partial thickness ischemia where the body surface changes do not allow localisation of the ischemic region. In an animal model we have shown that the reason one cannot see the region on the body surface is that the epicardial distribution of ST segment is almost identical for partial thickness ischaemia in the left anterior descending coronary artery, (LAD) and circumflex coronary artery (Cx) territories. Dissection of the reasons for this finding has lead to 3 contributing factors. The first is the role of the right ventricular blood mass, the second the boundary between ischemia and normal and the third the presence of anisotropy and its contribution. In a block of myocardium with anisotropy included we have shown marked differences between the distributions depending on the anisotropy. We have also shown that the published values of conductivity for use in the bidomain model produce unacceptably disparate results.
缺血时ST段压低的起源仍未得到很好的理解。公认的来源是在收缩期和舒张期缺血和非缺血心肌之间流动的细胞内电流，使得体表记录的心电图显示缺血区域上方的ST段抬高。困难在于心肌部分厚度缺血，此时体表变化无法确定缺血区域的位置。在一个动物模型中，我们已经表明，在体表看不到该区域的原因是，左前降支冠状动脉（LAD）和左旋支冠状动脉（Cx）区域的部分厚度缺血时，心外膜ST段分布几乎相同。对这一发现原因的剖析导致了三个促成因素。第一个是右心室血容量的作用，第二个是缺血与正常组织之间的边界，第三个是各向异性的存在及其影响。在包含各向异性的心肌块中，我们已经表明，根据各向异性的不同，分布存在显著差异。我们还表明，双域模型中使用的已发表电导率值会产生令人无法接受的不同结果。
