Re-entry in computational models of ischaemic myocardium

The purpose of this study was to investigate how both the vulnerability to re-entry and the behaviour of re-entry are altered by regional abnormalities in a computational model of action potential propagation in the mammalian heart. We simulated the effect of regional ischaemia by separately increasing the voltage dependent background K+ current, reducing the voltage dependent Na+ current, and increasing the extracellular K+ concentration in part of a one-dimensional fibre. The vulnerability to re-entry was estimated from the timings of premature stimuli in the middle portion of the heterogeneous fibres that resulted in a unidirectionally propagating action potential. In general the vulnerability to re-entry increased as the heterogeneity of the fibre increased, although under some conditions the vulnerability decreased below the level for uniform tissue. In two-dimensional simulations with a central ischaemic region, re-entry once initiated was destabilised by the heterogeneity. This study shows how regional ischaemia in the whole heart might increase the vulnerability to arrhythmias, and how arrhythmias might degenerate to ventricular fibrillation (VF) once initiated.