Experimental and clinical AF mechanisms: bridging the divide.
There is general agreement that AF is most likely a reentrant rhythm disturbance. However, the precise pathophysiological bases for its initiation and maintenance have not been fully resolved. In the original description of the multiple wavelet hypothesis of atrial fibrillation, as put forward by Moe et al. and later substantiated by Allessie et al., the wavelets were thought to move randomly throughout the atria. However, more recent studies that have applied high resolution mapping of wave propagation and rigorous analyses in the time and frequency domains to long episodes of AF, have provided evidence that atrial fibrillation is not random, but is accompanied by a high degree of spatiotemporal periodicity. This has led to the hypothesis that maintenance of AF may depend on the uninterrupted periodic activity of a small number of discrete reentrant sites, established by the interaction of propagating waves with anatomical heterogeneities in the atria. It has been proposed also that the rapidly successive wave fronts emanating from these sources propagate through both atria and interact with anatomical and/or functional obstacles, leading to fragmentation and wavelet formation. In support of this idea, observations made during radiofrequency ablation of AF in humans suggest that, in some patients, a single, repetitive focal source of activity propagate impulses from an individual pulmonary vein to the remainder of the atrium as fibrillatory waves. These studies underscore the need for identification of continuing AF sources at localized sites, and of transient AF "triggers", which may involve normal or abnormal pacemaker mechanisms or even reentrant activity, and of the manner in which electrical activity initiated by such triggers interacts with the normally propagating electrical waves to initiate fibrillatory activity in the atria.
Jalife
José
J
SUNY Upstate Medical University, 766 Irving Avenue, Syracuse, NY 13210, USA. jalifej@upstate.edu
D000818:Animals; D001281:Atrial Fibrillation / Q000209:etiology* / Q000503:physiopathology; D016275:Atrial Function / Q000502:physiology; D006325:Heart Atria / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology; D006801:Humans; D015995:Prevalence; D014481:United States / Q000453:epidemiology