A computer simulation of ST segment shift in myocardial ischaemia

This thesis presents a computer simulation of electrocardiographic ST segment shift in myocardial ischaemia to elucidate the source of ST changes in both subendocardial and transmural ischaemia. A realistic torso model was constructed, in which the myocardium was represented by the bidomain model. In a normal heart, there is no current source during the ST segment and there is a minimal ST potential field. With myocardial ischaemia, the transmembrane potential of ischaemic cells changes, allowing current to flow between the ischaemic and nonischaemic regions, which generates ST segment shift. The ischaemic regions included in the model were those measured using fluorescent microspheres in a sheep model, and the transmembrane potentials were generated from values extracted from the literature. Subendocardial ischaemia in the territory supplied by either the left anterior descending coronary artery (LAD) or left circumflex coronary artery (LOX) was simulated, showing that the current source is produced at the ischaemic boundary, with the positive source at the ischaemic and the negative source at the normal side of the boundary. At the intramural boundary, the current flow is highly localised around the boundary, while at the lateral boundary normal to the endocardium, current flows both by crossing the boundary and through the intracavity blood. Epicardial ST depression is seen over the lateral boundary while endocardial ST elevation appears over the ischaemic region. The source in the septum is not seen on the epicardium because it is surrounded by highly conductive blood. LAD and LCX ischaemia share the lateral boundary and produce a similar pattern of epicardial ST depression on the left free wall. Transmural ischaemia of varying size was studied. Transmural ischaemia of a small region produces localised ST elevation over the ischaemic region with little ST depression elsewhere on the epicardium and a similar pattern on the endocardium with a much lower amplitude. Ischaemia in either the LAD or LCX territory produces a strong dipole on the epicardium over the left lateral region, with ST elevation on the ischaemic region and ST depression on the nonischaemic region. ST depression in transmural ischaemia is generated with ST elevation and is an integral part of the source, thus it is inevitable that ST depression on the body surface will be generated during ischaemia of a large region of myocardium. The effect of the myocardial anisotropy on ST potentials was also studied. The inclusion of myocardial anisotropy produces results somewhat closer to measured results in animal models. In conclusion, the bidomain model is successful in modelling the ST potential and the simulation in this study successfully explains the observations of ST segment shift during myocardial ischaemia. It provides useful guidance for the clinical interpretation of ST segment shift.