The mechanisms by which arrhythmias are generated in the heart remains a field of intensive research. Recent advances in computational biology and electrophysiology have enabled researchers to use an alternative tool in the study of arrhythmia mechanisms, the multi-scale modeling and simulation of cardiac arrhythmogenesis at the organ level. This article reviews the recent advances and achievements using this approach.
KeywordsArrhythmias; modeling; bidomain model Understanding how electric current delivered to the heart to terminate lethal arrhythmias traverses myocardial structures and interacts with wavefronts of fibrillation has been challenging researchers for many years. Of particular importance is insight into the mechanisms by which the shock fails -re-initiation of fibrillation is related not only to the effect of the shock on the electrical state of the myocardium, but also to the intrinsic properties of the tissue that lead to destabilization of post-shock activations and their degradation into electric turbulence. The complexity of the relationships and dependencies to be teased out and dissected in this quest has been staggering. Historically, overwhelming electrical artifacts had prevented researchers from recording during as well as shortly after the shock. A breakthrough in mapping cardiac activity associated with defibrillation occurred during the last decade of the 20th century with the introduction of potentiometric dyes, which allowed continuous recording of activity before, during, and after the shock.At the same time, the theoretical electrophysiology community adopted a novel modeling methodology, termed the bidomain model. The bidomain model [1] is a continuum representation of the myocardium that takes into consideration current distribution resulting from a particular characteristic of cardiac tissue: the fact that the two spaces comprising the myocardium, the intra-and extracellular, are both anisotropic but to a different degree; the myocardium is thus characterized with 'unequal anisotropy ratios'. Since the bidomain model accounts for the current flow in the interstitium, it became instantly a powerful modeling tool in the study of stimulation of cardiac tissue (with an eye on defibrillation), where current delivered in the extracellular space finds its way across the membranes of cardiac cells. The first significant achievement of this new approach was the study of the passive (i.e. the ionic currents are not accounted for) shock-induced change in The next big contribution of passive bidomain modeling was the detailed analysis of VEP etiology and its dependence on cardiac tissue structure and the configuration of the applied field; both were shown to be major determinants of the shape, location, polarity, and intensity of the shock-induced polarization [4]. In particular, theoretical considerations led to the recognition of two types of VEP: (1) 'surface VEP', which penetrates the ventricular wall over a few cell layers, due to current re-distribution near the boundaries se...