VORTEX DYNAMICS IN 3-DIMENSIONAL CONTINUOUS MYOCARDIUM WITH FIBER ROTATION - FILAMENT INSTABILITY AND FIBRILLATION

Wave propagation in ventricular muscle is rendered highly anisotropic by the intramural rotation of the fiber. This rotational anisotropy is especially important because it can produce a twist of; electrical vo rtices, which measures the rate of rotation (in degree/mm) of activati on wavefronts in successive planes perpendicular to a line of phase si ngularity, or filament. This twist can then significantly alter the dy namics of the filament. This paper explores this dynamics via numerica l simulation. After a review of the literature, we present modeling to ols that include: (i) a simplified ionic model with three membrane cur rents that approximates well the restitution properties and spiral wav e behavior of more complex ionic models of cardiac action potential (B eeler-Reuter and others), and (ii) a semi-implicit algorithm for the f ast solution of monodomain cable equations with rotational anisotropy. We then discuss selected results of a simulation study of vortex dyna mics in a parallelepipedal slab of ventricular muscle of varying wall thickness (S) and fiber rotation rate (theta(z)). The main finding is that rotational anisotropy generates a sufficiently large twist to des tabilize a single transmural filament and cause a transition to a wave turbulent state characterized by a high density of chaotically moving filaments. This instability is manifested by the propagation of local ized disturbances along the filament and has no previously known analo g in isotropic excitable media. These disturbances correspond to highl y twisted and distorted regions of filament, or ''twistons,'' that cre ate vortex rings when colliding with the natural boundaries of the ven tricle. Moreover, when sufficiently twisted, these rings expand and cr eate additional filaments by further colliding with boundaries. This i nstability mechanism is distinct from the commonly invoked patchy fail ure or wave breakup that is not observed here during the initial insta bility. For modified Beeler-Reuter-like kinetics with stable reentry i n two dimensions, decay into turbulence occurs in the left ventricle i n about one second above a critical wall thickness in the range of 4-6 mm that matches experiment. However this decay is suppressed by unifo rmly decreasing excitability. Specific experiments to test these resul ts, and a method to characterize the filament density during fibrillat ion are discussed. Results are contrasted with other mechanisms of fib rillation and future prospects are summarized. (C) 1998 American Insti tute of Physics.