Alterations in electrophysiology and tissue structure of the left atrial posterior wall in a canine model of atrial fibrillation caused by chronic atrial dilatation.
BACKGROUND
Chronic left atrial dilatation (CDLA) is associated with an increased incidence of atrial fibrillation (AF). The electrophysiological functions of the left atrial posterior wall (LAPW) are not well understood.


RESULTS
Eight control dogs and 8 with CDLA (developed 6 months after partial mitral valve avulsion) were studied. An electrophysiological study was performed using the noncontact mapping system. The conduction velocity was significantly decreased in the LAPW in the CDLA group. During atrial extrastimulation, a sharp curvature in the activation wavefront became apparent in the LAPW of 6 CDLA dogs, with unidirectional block in 1 dog. The effective refractory periods increased homogeneously throughout the atrium in the CDLA group. AF was much more easily inducible in the CDLA dogs than in the controls. After the onset of AF, the LAPW exhibited the earliest disorganized activity as compared with other sites in the left atrial. In the CDLA dogs, the most extensive interstitial fibrosis was observed in the LAPW.


CONCLUSIONS
Alterations in the electrophysiologic properties and tissue structure of the LAPW were observed in the CDLA dogs. This study supports the idea that the LAPW may play a role in the mechanism of AF induced by CDLA.
Tang
Min
M
Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, Beijing, China.
Zhang
Shu
S
Sun
Qi
Q
Huang
Congxin
C
D000818:Animals; D001281:Atrial Fibrillation / Q000473:pathology* / Q000503:physiopathology*; D004108:Dilatation, Pathologic / Q000473:pathology; D004195:Disease Models, Animal; D004285:Dogs; D004562:Electrocardiography; D022062:Electrophysiologic Techniques, Cardiac / Q000379:methods*; D006325:Heart Atria / Q000473:pathology* / Q000503:physiopathology*; D006329:Heart Conduction System / Q000473:pathology / Q000503:physiopathology; D008944:Mitral Valve Insufficiency / Q000473:pathology / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000502:physiology