title: Revisiting heart activation-conduction physiology, part I: atria.
abstract: This discussion paper re-examines the conduction-activation of the atria, based on observations, with respect to the complexity of the heart as an organ with a brain, and its evolution from a peristaltic tube. The atria do not require a specialized conduction system because they use the subendocardial layer to produce centripetal transmural activation fronts, regardless of the anatomical and histological organization of the transmural atrial wall. This has been described as "two-layer" physiology which provides robust transmission of activation from the sinus to the AV node via a centripetal transmural activation front. New productive insights can come from re-examining the physiology, not only during sinus rhythm but also during atrial tachycardias, in particular atrial flutter and atrial fibrillation (AF). During common flutter, the areas of slow conduction, in the isthmus and following trabeculations, particularly the subendocardial layer confines conduction through the trabeculations which supports re-entry. During experimental or postoperative flutter, the circular 2D activation around the obstacle follows the physiological transmural activation. Understanding this physiology offers insights into AF. During acute or protracted AF, the presence of stationary or drifting rotors is characteristic and consistent with normal physiological 2D atrial activation, suggesting that suppressing physiological transmural activation of AF will permanently restore normal sinus node atrial activation. In contrast, during permanent AF, normal 2D activation is abolished; the presence of transmural, serpentine, and chaotic atrial activation suggests that the normal physiological activation pattern has been replaced by a new, irreversible variety of atrial conduction that is a new physiology, which is consistent with evolution of complex systems.
authors.affiliation: Canadian Surgical Technologies and Advance Robotics, Lawson Health Research Institute, London Health Science Center, London, Ontario, Canada, gguiraud@uwo.ca.
authors.forename: Gerard M
authors.initials: GM
authors.lastname: Guiraudon
authors.forename: Douglas L
authors.initials: DL
authors.lastname: Jones
mesh_terms: D001281:Atrial Fibrillation / Q000503:physiopathology*; D016275:Atrial Function / Q000502:physiology*; D016279:Atrial Function, Left / Q000502:physiology; D016280:Atrial Function, Right / Q000502:physiology; D022062:Electrophysiologic Techniques, Cardiac; D004699:Endocardium / Q000502:physiology; D006321:Heart / Q000196:embryology; D006329:Heart Conduction System / Q000502:physiology*; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology; D011690:Purkinje Fibers / Q000502:physiology