SELF-ORGANIZATION AND THE DYNAMICAL NATURE OF VENTRICULAR-FIBRILLATION

This article reviews recent data supporting the conjecture that, in th e structurally and electrophysiologically normal heart, cardiac fibril lation is not a totally random phenomenon. Experimental and numerical studies based on the theory of excitable media suggest that fibrillati on in the mammalian ventricles is the result of self-organized three-d imensional (3-D) electrical rotors giving rise to scroll waves that mo ve continuously (i.e., drift) throughout the heart at varying speeds. A brief review of studies on the dynamics of rotors in two-dimensional (2-D) and 3-D excitable media is presented with emphasis on the exper imental demonstration of such dynamics in cardiac muscle of various sp ecies. The discussion is centered on rotor dynamics in the presence an d the absence of structural heterogeneities, and in the phenomena of d rifting and anchoring, which in the electrocardiogram (EGG) may manife st as life-threatening cardiac rhythm disturbances. For instance, in t he rabbit heart, a single electrical rotor that drifts rapidly through out the ventricles gives rise to complex patterns of excitation. In th e ECG such patterns an indistinguishable from ventricular fibrillation . On the other hand, a rotor that anchors to a discontinuity or defect in the muscle (e.g., a scar, a large artery or a bundle of connective tissue) may result in stationary rotating activity, which in the ECG is manifested as a form of so-called ''monomorphic'' ventricular tachy cardia. More recent data show that ventricular fibrillation occurs in mammals irrespective of size or species. While in small hearts, such a s those of mice and rabbits, a single drifting or meandering rotor can result in fibrillation, in larger hearts, such as the sheep and possi bly the human, fibrillation occurs in the form of a relatively small n umber of coexisting but short-lived rotors. Overall, the work discusse d here has paved the way for a better understanding of the mechanisms of fibrillation in the normal, as well as diseased human heart. (C) 19 98 American Institute of Physics.