title: Critical mass hypothesis revisited: role of dynamical wave stability in spontaneous termination of cardiac fibrillation.
abstract: The tendency of atrial or ventricular fibrillation to terminate spontaneously in finite-sized tissue is known as the critical mass hypothesis. Previous studies have shown that dynamical instabilities play an important role in creating new wave breaks that maintain cardiac fibrillation, but its role in self-termination, in relation to tissue size and geometry, is not well understood. This study used computer simulations of two- and three-dimensional tissue models to investigate qualitatively how, in relation to tissue size and geometry, dynamical instability affects the spontaneous termination of cardiac fibrillation. The major findings are as follows: 1) Dynamical instability promotes wave breaks, maintaining fibrillation, but it also causes the waves to extinguish, facilitating spontaneous termination of fibrillation. The latter effect predominates as dynamical instability increases, so that fibrillation is more likely to self-terminate in a finite-sized tissue. 2) In two-dimensional tissue, the average duration of fibrillation increases exponentially as tissue area increases. In three-dimensional tissue, the average duration of fibrillation decreases initially as tissue thickness increases as a result of thickness-induced instability but then increases after a critical thickness is reached. Therefore, in addition to tissue mass and geometry, dynamical instability is an important factor influencing the maintenance of cardiac fibrillation.
authors.affiliation: Department of Medicine (Cardiology), David Geffen School of Medicine at UCLA, 47-123 CHS, 10833 Le Conte Ave., Los Angeles, CA 90095, USA. zqu@mednet.ucla.edu
authors.forename: Zhilin
authors.initials: Z
authors.lastname: Qu
mesh_terms: D001281:Atrial Fibrillation / Q000503:physiopathology; D003198:Computer Simulation; D006321:Heart / Q000033:anatomy & histology*; D008955:Models, Cardiovascular; D014693:Ventricular Fibrillation / Q000503:physiopathology