Abstract-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 (rϭ0.77Ϯ0.14, PϽ0.0001), 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.(Circ Res. 1998;82;957-970.)Key Words: ST depression Ⅲ potential mapping Ⅲ bidomain model Ⅲ subendocardial ischemia Ⅲ regional myocardial blood flow E lectrocardiographic ST-segment depression has long been recognized as a sign of ischemia, 1,2 but the explanations of the responsible mechanisms have been controversial. [3][4][5][6] Much of the current opinion regarding the genesis of ST-segment depression is derived from interpretations based on certain theoretical considerations 7,8 and indirect evidence from animal experiments. 1,2 Ischemic muscle generates intracellular currents, which effectively cause TQ depression and ST elevation over the ischemic area 9,10 and which conventional electrocardiography with AC-coupled amplifiers reflects as ST elevation. ST-segment depression recorded at the epicardium has been considered to be secondary to an injury current in the underlying subendocardium. [11][12][13][14] In conventional stress testing, as myocardial demand exceeds the ability of the narrowed coronary arterial bed to increase blood flow, the ischemic threshold is exceeded, and reversible ST-segment depression is produced. However, the location of this ST depression does not enable us to localize...
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...
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