title: Rotors and focal sources for human atrial fibrillation: mechanistic paradigm with direct clinical relevance.
abstract: Outcomes for patients with atrial fibrillation (AF) have changed little despite many advances in technology. In large part, this reflects fundamental uncertainty about the mechanisms for AF in humans, which must reconcile diverse observations. Despite the complexity of AF, many electrophysiologists have witnessed modulation of 'chaotic' AF after the first few ablation lesions, or before lines are complete or trigger sites are isolated, and numerous analyses demonstrate temporospatial stability in AF. These common observations challenge the concept that AF is driven by spatially disorganized, widespread mechanisms. Using mathematical techniques applied to other complex systems, evidence is rapidly accumulating that human AF is largely sustained by localized rotors and focal sources. Elimination of sources by Focal Impulse and Rotor Modulation (FIRM)-guided ablation has been shown by independent laboratories to substantially improve success compared with pulmonary vein isolation alone. These data advance our mechanistic understanding of AF. Randomized trials are underway to verify the relative efficacy of ablation at AF sources (substrate) vs. conventional trigger ablation. The renewed focus on AF substrates is a paradigm shift, but also a re-alignment of concepts for AF towards those for other cardiac arrhythmias that are generally defined by sustaining mechanisms (substrates).
authors.affiliation: University of California Medical Center, Veterans Affairs San Diego.
authors.forename: Gautam G
authors.initials: GG
authors.lastname: Lalani
authors.forename: Rishi
authors.initials: R
authors.lastname: Trikha
authors.forename: David E
authors.initials: DE
authors.lastname: Krummen
authors.forename: Sanjiv M
authors.initials: SM
authors.lastname: Narayan
mesh_terms: D001281:Atrial Fibrillation / Q000503:physiopathology* / Q000628:therapy*; D055724:Electrophysiological Phenomena; D006801:Humans; D008955:Models, Cardiovascular