Epicardial ST Depression in Acute Myocardial Infarction

Abstract

Abstract-The presence of electrocardiographic ST depression in acute infarction remains controversial and poorly explained. A combined animal and modeling study was performed to evaluate the source of ST changes in acute infarction. In anaesthetized sheep, small infarcts showed uniform ST elevation over the infarction whereas larger infarcts showed marked ST depression over the normal myocardium in addition to the ST elevation. These findings were replicated by bidomain models of the heart. A hollow sphere was used to model a gradually increasing infarct, and this showed that there was a decrease in the ratio of ST elevation to ST depression as the infarct was increased. The current flowing out of the heart must be identical to the current flowing back into the heart. This means that any infarction will produce ST depression as well as ST elevation, the ratio between the two being related to the size of the infarction. Small infarction is associated with a small region of ST elevation and minor ST depression of the remaining myocardium, and as the infarct region increases, the amplitude of the epicardial ST elevation falls and the amplitude of the ST depression increases. Infarction size is proportional to both the height of the ST depression on the epicardium and the strength of the epicardial ST segment dipole. (Circ Res. 1999;85:959-964.)Key Words: electrocardiography Ⅲ epicardial potential Ⅲ acute infarction Ⅲ bidomain model Ⅲ ST depression T he origins and significance of ST depression associated with acute myocardial infarction are poorly understood and controversial. [1][2][3][4][5][6][7][8] As part of a study looking at partial-thickness ischemia in an experimental animal model, 9 we observed that ST depression accompanied some episodes of full-thickness ischemia and not others. The literature reflecting experimental infarction has shown that full-thickness ischemia was associated with a region of epicardial ST elevation over the ischemia with minimal changes elsewhere. 10 -16 This discrepancy between clinical observation and experimental results has been more fully evaluated by detailed epicardial, endocardial, and body surface ECG mapping of acute infarction in different territories and of different sizes in an experimental sheep model. The electrical changes were correlated with regional blood flow measured by fluorescent microspheres. To explain the results of the experimental infarction, we have developed several levels of a bidomain model based on that described by Tung, 17 including a hollow thick-walled sphere, and a finite element model of the heart that replicated the experimental observations. Materials and Methods Experimental AnimalsA total of 33 sheep were randomized into three groups. Transmural ischemia was achieved by completely ligating the obtuse marginal branch (OM) in group 1, the proximal left circumflex coronary artery (LCX) in group 2, and the proximal left anterior descending coronary artery (LAD) in group 3 for a minimum of 20 minutes. The epicardial ST potential fields were re...

The importance of anisotropy in modeling ST segment shift in subendocardial ischaemia

“…The model also predicts ST depression just outside the ischaemic boundary and this depression increases in magnitude as the size of the ischaemic region increases. This fact was also observed by Li et al [23]. Model predictions also fit with the simple model of Holland and Brooks [11].…”

“…2-4). In each case, the highest amplitude of ST elevation was obtained at the boundary of the ischaemic region, as was observed by Li et al [23] with ligation of the LAD and LCX arteries. However, this behavior was not observed with the occlusion of the obtuse marginal artery, nor was it observed in the experimental studies of Smith et al [12] where a more convex distribution was observed.…”

Mathematical Cardiac Electrophysiology

“…One way to locate ischemia in clinical electrocardiography is the so-called ST segment elevation in the electrocardiogram (ECG), but both the choice of this criterion and the mechanism underlying ST shifts are still controversial. Several experimental works have studied these phenomena: Samson et al [453], Prinzmetal et al [403], Kjekshus et al [286], and Kleber et al [279], suggested that subendocardial ischemia produces ST elevation at the epicardial level, while Wolferth et al [565] and Li et al [298] found ST depression. MacLeod et al [314] observed depression only under conditions of combined coronary occlusion and elevated heart rate.…”

The role of extracellular potassium transport in computer models of the ischemic zone

“…Many important results can be obtained with ''static'' simulations of ischemia, in which only the effect of the offset in resting V m is simulated [19,23,24,29,31,34]. For such simulations, the profile of resting V m across the ischemic border is of interest.…”