  Abnormal electrical activity from the boundaries of ischemic cardiac tissue
is recognized as one of the major causes in generation of ischemia-reperfusion
arrhythmias. Here we present theoretical analysis of the waves of electrical
activity that can rise on the boundary of cardiac cell network upon its
recovery from ischaemia-like conditions. The main factors included in our
analysis are macroscopic gradients of the cell-to-cell coupling and cell
excitability and microscopic heterogeneity of individual cells. The interplay
between these factors allows one to explain how spirals form, drift together
with the moving boundary, get transiently pinned to local inhomogeneities, and
finally penetrate into the bulk of the well-coupled tissue where they reach
macroscopic scale. The asymptotic theory of the drift of spiral and scroll
waves based on response functions provides explanation of the drifts involved
in this mechanism, with the exception of effects due to the discreteness of
cardiac tissue. In particular, this asymptotic theory allows an extrapolation
of 2D events into 3D, which has shown that cells within the border zone can
give rise to 3D analogues of spirals, the scroll waves. When and if such scroll
waves escape into a better coupled tissue, they are likely to collapse due to
the positive filament tension. However, our simulations have shown that such
collapse of newly generated scrolls is not inevitable and that under certain
conditions filament tension becomes negative, leading to scroll filaments to
expand and multiply leading to a fibrillation-like state within small areas of
cardiac tissue.
