A computer heart model incorporating anisotropic propagation: IV. Simulation of regional myocardial ischemia

Abstract

The main goal of this study was to simulate clinical body surface potential maps, recorded during percutaneous transluminal coronary angioplasty protocols, using a realistic geometry computer heart model. Other objectives were to address the question of reciprocal ST-segment changes observed in the 12-lead electrocardiogram during ischemia and to verify the hypothesis that the shortening of the QRS duration observed in left anterior descending (LAD) coronary artery occlusion may be explained by conduction delay in the septal His-Purkinje system. Simulation was achieved by first introducing into the heart model three transmural zones of mild, moderate, and severe ischemia for assumed occlusions in the LAD, left circumflex, and right coronary arteries. The heart model was then excited, in turn, with these three zones present for assumed occlusions in the LAD, left circumflex, and right coronary arteries. Myocardial conduction velocities in the regions of moderate and severe ischemia were assumed to be reduced to 75 and 50% of normal, respectively. Model action potentials in the mild, moderate, and severely ischemic zones were also altered to reflect known ischemic changes in these action potentials. Body surface potential maps and electrocardiograms were computed by placing the heart model inside a numerical torso model. Simulated map patterns during both ST-segment and QRS were qualitatively similar to clinical maps. Reciprocal ST-segment depression was observed for all three occlusions in remote leads that did not overlie the ischemic zones. QRS shortening due to septal His-Purkinje conduction delay was verified. The simulation results attest to the model's ability to reproduce body surface potential distributions recorded following percutaneous transluminal coronary angioplasty protocols. The simulations also showed that reciprocal ST-segment changes occur as a natural consequence of the primary ischemic region and that there is no need to invoke a second region of ischemia. Finally, the model demonstrated that QRS shortening can occur in LAD occlusion despite a slowing of conduction down the septal His-Purkinje system.