Failure of impulse propagation in a mathematically simulated ischemic border zone: influence of direction of propagation and cell-to-cell electrical coupling.

INTRODUCTION It is suggested that heterogeneous extracellular potassium concentration, cell-to-cell coupling, and geometric nonuniformities of the ischemic border zone contribute to the incidence of unidirectional block and subsequent development of lethal ventricular arrhythmias. METHOD AND RESULTS A discrete electrical network was used to model a single cardiac fiber with a [K+]e gradient characteristic of an ischemic border zone. Directional differences in propagation were evaluated by creating discrete regions with increased gap junctional resistance within the [K+]e gradient. Furthermore, the effect of homogeneity/heterogeneity of call length on impulse propagation through the [K+]e gradient in the presence of increased gap junctional resistance was evaluated. The results indicate that failure of impulse propagation occurs at the junction between partially uncoupled and normally coupled cells. Furthermore, propagation failure was more likely to occur as the impulse propagated from a region of high [K+]e to low [K+]e. Heterogeneity in cell length contributes to the variability in the occurrence of unidirectional and bidirectional block. CONCLUSIONS The onset of cellular uncoupling in an ischemic border zone may interact with the inherent [K+]e gradient leading to unidirectional conduction block. This mechanism may be important for the generation of reentrant arrhythmias at the ischemic border zone.