Evolution of spiral and scroll waves of excitation in a mathematical model of ischaemic border zone

TL;DR

This paper presents a theoretical analysis of spiral and scroll wave dynamics at ischemic cardiac tissue boundaries, explaining their formation, drift, pinning, and potential to cause fibrillation-like states.

Contribution

It introduces an asymptotic theory of spiral and scroll wave drift based on response functions, extending 2D insights into 3D and exploring conditions for wave expansion or collapse.

Findings

Spiral waves can drift, pin, and penetrate tissue boundaries.

Scroll waves may expand and multiply under certain conditions.

Collapse of scroll waves is not guaranteed; they can lead to fibrillation-like activity.

Abstract

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.