This computational study explores how conduction inhomogeneities influence spiral breakup and reentry dynamics in a model of ventricular fibrillation.
Cautions against clinical extrapolation from this model; leaves open the role of inhomogeneity in human reentry mechanisms.
Ventricular fibrillation (VF), the major reason behind sudden cardiac death, is turbulent cardiac electrical activity in which rapid, irregular disturbances in spatiotemporal electrical activation of heart make it incapable of any concerted pumping action. We give a brief overview of the simple Panfilov model for ventricular fibrillation, with emphasis on studies that have elucidated the nature of spiral turbulence which is the analog of VF here. The control of such turbulence is briefly touched upon. Preliminary results are presented for the effects of conduction inhomogeneity on spiral breakup, and the transition from functional to anatomical reentry as a function of the size and position of the inhomogeneity.
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Shajahan et al. (2003) studied this question.
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