Electrical, contractile and structural remodeling during atrial fibrillation.
The natural history of atrial fibrillation (AF) is characterized by a gradual worsening with time. The recent finding that AF itself produces changes in atrial function and structure has provided a possible explanation for the progressive nature of this arrhythmia. Electrical remodeling (shortening of atrial refractoriness) develops within the first days of AF and contributes to an increase in stability of AF. However, 'domestication of AF' must also depend on a 'second factor' since the persistence of AF continues to increase after electrical remodeling has been completed. Atrial contractile remodeling (loss of contractility) leads to a reduced atrial transport function after cardioversion of AF. An important clinical consequence is that during several days after restoration of sinus rhythm, the risk of atrial thrombus formation is still high. In addition, the reduction of atrial contractility during AF may enhance atrial dilatation which may add to the persistence of AF. Tachycardia-induced structural remodeling takes place in a different time domain (weeks to months). Myolysis probably contributes to the loss of atrial contractile force. Although it might explain the loss of efficacy of pharmacological cardioversion and the development of permanent AF, the role of structural remodeling in the progression of AF is still unclear. Atrial structural remodeling also occurs as a result of heart failure and other underlying cardiovascular diseases. The associated atrial fibrosis might explain intra-atrial conduction disturbances and the susceptibility for AF. Thus, both AF itself and the underlying heart disease are responsible for the development of the arrhythmogenic substrate. New strategies for prevention and termination of AF should be build on our knowledge of the mechanisms and time course of AF-induced atrial remodeling.
Allessie
Maurits
M
Department of Physiology, Cardiovascular Research Institute Maastricht, University of Maastricht, P.O. Box 616, 6200 MD Maastricht, The Netherlands. m.allessie@fys.unimaas.nl
Ausma
Jannie
J
Schotten
Ulrich
U
D000818:Animals; D001281:Atrial Fibrillation / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D016275:Atrial Function; D002304:Cardiac Pacing, Artificial; D004554:Electric Countershock; D004594:Electrophysiology; D006041:Goats; D006325:Heart Atria / Q000503:physiopathology / Q000648:ultrastructure; D006801:Humans; D023421:Models, Animal; D009206:Myocardium / Q000648:ultrastructure; D013997:Time Factors