VENTRICULAR-FIBRILLATION AND ATRIAL-FIBRILLATION ARE 2 DIFFERENT BEASTS

Although the mechanisms of fibrillation are no doubt multi-faceted, th e geometry of the heart may play a major role in the dynamics of wave propagation during fibrillation [A. T. Winfree, Science 266, 1003-1006 (1994)]. The ventricles are thick chambers made up of sheets of paral lel muscle fibers with the direction of fibers rotating across the ven tricular walls (rotational anisotropy). The thick walls of the ventric les allow reentry to develop transmurally, provided the wavelength is sufficiently small. Depending on the kinetics of heart cells, the dyna mics of rotating waves in three dimensions may be fundamentally differ ent than in two dimensions, leading to destabilization of reentry and Ventricular fibrillation (VF) in thick ventricles. The atria have an i ntricate geometry comprised of a thin sheet of cardiac tissue attached to a very complex network of pectinate muscles. The branching geometr y of the pectinate muscles may lead to destabilization of two-dimensio nal reentry via ''long-distance'' electrical connections giving rise t o atrial fibrillation (AF). Therefore, although fibrillation occurs vi a complex three-dimensional wave propagation in the ventricles and the atria, the underlying mechanisms and factors that sustain VF and AF a re probably different. (C) 1998 American Institute of Physics.