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On complex dynamics in a Purkinje and a ventricular cardiac cell model
Cardiac muscle cells can exhibit complex patterns including irregular behaviour such as chaos or (chaotic) early afterdepolarisations (EADs), which can lead to sudden cardiac death. Suitable mathematical models and their analysis help to predict the occurrence of such phenomena and to decode their mechanisms. The focus of this paper is the investigation of dynamics of cardiac muscle cells described by systems of ordinary differential equations. This is generically performed by studying a Purkinje cell model and a modified ventricular cell model. We find chaotic dynamics with respect to the leak current in the Purkinje cell model, and EADs and chaos with respect to a reduced fast potassium current and an enhanced calcium current in the ventricular cell model — features that have been experimentally observed and are known to exist in some models, but are new to the models under present consideration. We also investigate the related monodomain models of both systems to study synchronisation and the behaviour of the cells on macro-scale in connection with the discovered features. The models show qualitatively the same behaviour to what has been experimentally observed. However, for certain parameter settings the dynamics occur within a non-physiological range.
Analysis and simulation of a modified cardiac cell model gives accurate predictions of the dynamics of the original one
The 19-dimensional TP06 cardiac muscle cell model is reduced to a 17-dimensional version, which satisfies the required conditions for performing an analysis of its dynamics by means of bifurcation theory. The reformulated model is shown to be a good approximation of the original one. As a consequence, one can extract fairly precise predictions of the behaviour of the original model from the bifurcation analysis of the modified model. Thus, the findings of bifurcations linked to complex dynamics in the modified model - like early afterdepolarisations (EADs), which can be precursors to cardiac death - predicts the occurrence of the same dynamics in the original model. It is shown that bifurcations linked to EADs in the modified model accurately predicts EADs in the original model at the single cell level. Finally, these bifurcations are linked to wave break-up leading to cardiac death at the tissue level.