Mechanisms of ST change in partial thickness ischemia

Abstract 

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.

Keywords:  ST depression, partial ischemia, anisotrophy, bidomain modeling thickness