Organization of Ventricular Fibrillation in the Human Heart

Abstract

Abstract-Sudden cardiac death is a major cause of death in the industrialized world, claiming approximately 300 000 victims annually in the United States alone. In most cases, sudden cardiac death is caused by ventricular fibrillation (VF). Experimental studies in large animal hearts have shown that the uncoordinated contractions during VF are caused by large numbers of chaotically wandering reentrant waves of electrical activity. However, recent clinical data on VF in the human heart seem to suggest that human VF may have a markedly different organization. Here, we use a detailed model of the human ventricles, including a detailed description of cell electrophysiology, ventricular anatomy, and fiber direction anisotropy, to study the organization of human VF. We show that characteristics of our simulated VF are qualitatively similar to the clinical data. Furthermore, we find that human VF is driven by only approximately 10 reentrant sources and thus is much more organized than VF in animal hearts of comparable size, where VF is driven by approximately 50 sources. We investigate the influence of anisotropy ratio, tissue excitability, and restitution properties on the number of reentrant sources driving VF. We find that the number of rotors depends strongest on minimum action potential duration, a property that differs significantly between human and large animal hearts. Based on these findings, we suggest that the simpler spatial organization of human VF relative to VF in large animal hearts may be caused by differences in minimum action potential duration. Both the simpler spatial organization of human VF and its suggested cause may have important implications for treating and preventing this dangerous arrhythmia in humans. (Circ Res. 2007;100:e87-e101.)Key Words: ventricular fibrillation Ⅲ computer simulation Ⅲ spatial organization V entricular fibrillation (VF) is the single most common cause of sudden cardiac death, the largest cause of death in the Western world. During VF, the contraction of the ventricles becomes rapid, uncoordinated, and highly ineffective, causing this condition to be lethal within minutes, unless halted by defibrillation. The highly disorganized contractions during VF are caused by a severely disturbed, turbulent conduction of the electrical excitation wave.Experimental studies in animal hearts and tissue 1-6 have shown that the turbulent electrical activity typical of VF is caused by the presence of multiple reentrant waves of electrical excitation. Because of their reentrant behavior and high frequency, these rotors act as self-perpetuating, independent sources of excitation that take over control from the slower sinus node. The number of rotors present during VF is a good quantifier of the complexity and amount of disorganization of the excitation pattern. Results in animal hearts suggest that the number of reentrant sources present during VF increases as a function of heart size. For example, in rabbit hearts, VF can be driven by just 1 or 2 sources, 2,7 whereas in sheep hearts, VF...

Small size ionic heterogeneities in the human heart can attract rotors

“…For a more detailed description, we refer to Ref. 36. This model takes anisotropy into account by reconstructing the fiber direction field described in Ref.…”

Control of electrical turbulence by periodic excitation of cardiac tissue

“…First direct experimental observations of such states were reported almost 20 years ago 6,7 . Recent experimental and simulations studies 8,9 show a complex picture with states dominated by one or a few mother rotors as well as multiple wave dynamics characterized by a mean number of 10 vortices on the surface of, e. g., a human heart. The fluctuations in vortex number resemble a Poissonian statistics.…”

Modeling Defibrillation

“…FEM and FVM are both very well suited for spatial discretizations of complex geometries with smooth representations of the boundaries, which is a key feature when polarization patterns induced via extracellularly applied currents are to be studied. Both FVM and FEM have been used to model electrical activity in anatomical realistic models of the atria (Harrild & Henriquez, 2000;Seemann et al, 2006;Vigmond et al, 2004;Virag et al, 2002) as well as the ventricles (Ashihara et al, 2008;Plank et al, 2009;Potse et al, 2006;Ten Tusscher et al, 2007). Mesh generation requirements are similar for both techniques, that is, the domain of interest has to be tessellated into a set of non-overlapping and conformal geometric primitives (Fig.…”