Incomplete reentry and epicardial breakthrough patterns during atrial fibrillation in the sheep heart.
BACKGROUND
The mechanisms underlying atrial fibrillation and its initiation are not fully understood. Our hypothesis is that atrial fibrillation results from complex activation involving the subendocardial muscle network.


RESULTS
We have used video imaging to study the sequence of activation on the surface of the right atrium of the Langendorff-perfused sheep heart during pacing, atrial fibrillation, and its initiation. We recorded transmembrane potentials simultaneously from over 20,000 sites. We observed two types of patterns of wave propagation during the initiation of atrial fibrillation. The first type resulted from heterogeneties of refractoriness and transmural propagation near the stimulating electrode. The second type involved heterogeneity in conduction away from the pacing site. During atrial fibrillation, the average period of activation was 138 +/- 25 ms (n = 6), and complete reentrant pathways were never observed. Propagation patterns were characterized by a combination of incomplete reentry, breakthrough patterns, and wave collisions. Incomplete reentry occurred when waves propagated around thin lines of block and then terminated. Breakthrough patterns were frequent and occurred every 215 ms on average. The location of these breakthrough sites and the lines of block during incomplete reentry were not randomly distributed but appeared to be related to preferential propagation in the underlying subendocardial muscle structures. A computer model of atrial free wall connected to a pectinate muscle suggested that subendocardial muscles lead to epicardial breakthrough patterns that act to destabilize reentry.


CONCLUSIONS
These results suggest that the complex three-dimensional structure of the atria plays a major role in the activation sequences during atrial fibrillation and its initiation.
Gray
R A
RA
Department of Pharmacology, State University of New York Health Science Center at Syracuse 13210, USA. gray@suntan.pharm.hscsyr.edu
Pertsov
A M
AM
Jalife
J
J
D000200:Action Potentials; D000818:Animals; D016880:Anisotropy; D001281:Atrial Fibrillation / Q000503:physiopathology*; D016280:Atrial Function, Right; D002304:Cardiac Pacing, Artificial; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology; D006339:Heart Rate; D008297:Male; D008955:Models, Cardiovascular; D009431:Neural Conduction; D055095:Optics and Photonics; D010496:Pericardium / Q000503:physiopathology*; D011930:Reaction Time; D012032:Refractory Period, Electrophysiological; D012756:Sheep; D013997:Time Factors