Publications by authors named "Valentin I Krinsky"

Controlling the complex spatio-temporal dynamics underlying life-threatening cardiac arrhythmias such as fibrillation is extremely difficult, because of the nonlinear interaction of excitation waves in a heterogeneous anatomical substrate. In the absence of a better strategy, strong, globally resetting electrical shocks remain the only reliable treatment for cardiac fibrillation. Here we establish the relationship between the response of the tissue to an electric field and the spatial distribution of heterogeneities in the scale-free coronary vascular structure.

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High-energy defibrillation shock is the only therapy for ventricular tachyarrhythmias. However, because of adverse side effects, lowering defibrillation energy is desirable. We investigated mechanisms of unpinning, destabilization, and termination of ventricular tachycardia (VT) by low-energy shocks in isolated rabbit right ventricular preparations (n = 22).

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We show that for a class of bistable reaction-diffusion systems, zero-velocity fronts can be robust in the singular limit where one of the diffusion coefficients vanishes. In this case, stationary fronts can persist along variations of the system parameters. This property contrasts with the standard result that the front velocity v(&mgr;), expressed as a function of a control parameter &mgr;, is zero only at some isolated values &mgr;(0), and thus not giving robustness to zero-velocity fronts when &mgr; is varied.

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Steady, nonpropagating, fronts in reaction diffusion systems usually exist only for special sets of control parameters. When varying one control parameter, the front velocity may become zero only at isolated values (where the Maxwell condition is satisfied, for potential systems). The experimental observation of fronts with a zero velocity over a finite interval of parameters, e.

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Classical theory of potential distribution in cardiac muscle (cable theory) postulates that all effects of electric field (internally or externally applied) should decay exponentially with a space constant of the order of the tissue space constant ( approximately 1 mm). Classical theory does not take into account the cellular structure of the heart. Here, we formulate a mathematical model of excitation propagation taking into account cellular gap junctions.

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