A COMPUTER HEART MODEL INCORPORATING ANISOTROPIC PROPAGATION .4. SIMULATION OF REGIONAL MYOCARDIAL-ISCHEMIA

The main goal of this study was to simulate clinical body surface pote ntial maps, recorded during percutaneous transluminal coronary angiopl asty protocols, using a realistic geometry computer heart model. Other objectives were to address the question of reciprocal ST-segment chan ges observed in the 12-lead electrocardiogram during ischemia and to v erify the hypothesis that the shortening of the QRS duration observed in left anterior descending (LAD) coronary artery occlusion may be exp lained by conduction delay in the septal His-Purkinje system. Simulati on was achieved by first introducing into the heart model three transm ural zones of mild, moderate, and severe ischemia for assumed occlusio ns in the LAD, left circumflex, and right coronary arteries. The heart model was then excited, in turn, with these three zones present for a ssumed occlusions in the LAD, left circumflex, and right coronary arte ries. Myocardial conduction velocities in the regions of moderate and severe ischemia were assumed to be reduced to 75 and 50% of normal, re spectively. Model action potentials in the mild, moderate, and severel y ischemic zones were also altered to reflect known ischemic changes i n these action potentials. Body surface potential maps and electrocard iograms were computed by placing the heart model inside a numerical to rso model. Simulated map patterns during both ST-segment and QRS were qualitatively similar to clinical maps. Reciprocal ST-segment depressi on 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 mo del's ability to reproduce body surface potential distributions record ed 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.