Computational mapping identifies localized mechanisms for ablation of atrial fibrillation.

Atrial fibrillation (AF) is the most common heart rhythm disorder in the Western world and a common cause of hospitalization and death. Pharmacologic and non-pharmacologic therapies have met with limited success, in part due to an incomplete understanding of the underlying mechanisms for AF. AF is traditionally characterized by spatiotemporally disorganized electrical activation and, although initiating triggers for AF are described, it is unclear whether AF is sustained by spatially meandering continuous excitation (re-entrant waves), localized electrical sources within the atria, or some other mechanism.

Dynamically-Induced Spatial Dispersion of Repolarization and the Development of VF in an Animal Model of Sudden Death.

Spatial dispersion of refractoriness and discordant action potential duration (APD) alternans, resulting in local conduction block, have been shown to cause wavebreak that can lead to ventricular fibrillation (VF). Previously, we developed a theory, based on action potential restitution functions, that predicts when the requisite conduction block can be created through a series of premature beats. The theory was applied successfully to normal beagle dogs; however, restitution functions in these animals were similar, both between right and left ventricles in a given animal and across animals.

Dynamic mechanism for initiation of ventricular fibrillation in vivo.

Background: Dynamically induced heterogeneities of repolarization may lead to wave-front destabilizations and initiation of ventricular fibrillation (VF). In a computer modeling study, we demonstrated that specific sequences of premature stimuli maximized dynamically induced spatial dispersion of refractoriness and predisposed the heart to the development of conduction block. The purpose of this study was to determine whether the computer model results pertained to the initiation of VF in dogs in vivo.