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Early-after depolarizations (EADs) are changes in the action potential plateau that can lead to cardiac arrhythmia. At the cellular level, these oscillations are irregular and change from beat to beat due to the sensitivity of voltage repolarization to subcellular stochastic processes. However, the behavior of EADs in tissue, where cells are strongly coupled by gap junctions, is less understood. In this study, we develop a computational model of EADs caused by a reduction in the rate of calcium-induced inactivation of the L-type calcium channel. We find that, as inactivation decreases EADs occur with durations varying randomly from beat to beat. In cardiac tissue, however, gap junction coupling between cells dampens these fluctuations, and it is unclear what dictates the formation of EADs. In this study we show that EADs in cardiac tissue can be modeled by the deterministic limit of a stochastic single-cell model. Analysis of this deterministic model reveals that EADs emerge in tissue after an abrupt transition to alternans, where large populations of cells suddenly synchronize, causing EADs on every other beat. We analyze this transition and show that it is due to a discontinuous bifurcation that leads to a large change in the action potential duration in response to very small changes in pacing rate. We further demonstrate that this transition is highly arrhythmogenic, as the sudden onset of EADs on alternate beats in cardiac tissue promotes conduction block and reentry. Our results highlight the importance of EAD alternans in arrhythmogenesis and suggests that ectopic beats may not be required. 

Cardiac arrythmias are a form of heart disease that contributes toward making heart disease a significant cause of death globally. Irregular rhythms associated with cardiac arrythmias are thought to arise due to singularities in the heart tissue that generate reentrant waves in the underlying excitable medium. A normal approach to removing such singularities is to apply a high voltage electric shock, which effectively resets the phase of the cardiac cells. A concern with the use of this defibrillation technique is that the high-energy shock can cause lasting damage to the heart tissue. Various theoretical works have investigated lower-energy alternatives to defibrillation. In this work, we demonstrate the effectiveness of a low-energy defibrillation method in an experimental 2D Belousov–Zhabotinsky (BZ) system. When implemented as a 2D spatial reaction, the BZ reaction serves as an effective analog of general excitable media and supports regular and reentrant wave activity. The defibrillation technique employed involves targeted low-energy perturbations that can be used to “teleport” and/or annihilate singularities present in the excitable BZ medium.