Self-organization and the dynamical nature of ventricular fibrillation.

This article reviews recent data supporting the conjecture that, in the structurally and electrophysiologically normal heart, cardiac fibrillation is not a totally random phenomenon. Experimental and numerical studies based on the theory of excitable media suggest that fibrillation in the mammalian ventricles is the result of self-organized three-dimensional (3-D) electrical rotors giving rise to scroll waves that move 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 experimental demonstration of such dynamics in cardiac muscle of various species. The discussion is centered on rotor dynamics in the presence and the absence of structural heterogeneities, and in the phenomena of drifting and anchoring, which in the electrocardiogram (ECG) may manifest as life-threatening cardiac rhythm disturbances. For instance, in the rabbit heart, a single electrical rotor that drifts rapidly throughout the ventricles gives rise to complex patterns of excitation. In the ECG such patterns are 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 tachycardia. More recent data show that ventricular fibrillation occurs in mammals irrespective of size or species. While in small hearts, such as those of mice and rabbits, a single drifting or meandering rotor can result in fibrillation, in larger hearts, such as the sheep and possibly the human, fibrillation occurs in the form of a relatively small number of coexisting but short-lived rotors. Overall, the work discussed here has paved the way for a better understanding of the mechanisms of fibrillation in the normal, as well as diseased human heart. (c) 1998 American Institute of Physics.