Circulation. 2003;107:2615-2622
Published online before print May 5, 2003, doi: 10.1161/01.CIR.0000066915.15187.51
Published online before print May 5, 2003, doi: 10.1161/01.CIR.0000066915.15187.51
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(Circulation. 2003;107:2615.)
© 2003 American Heart Association, Inc.
Basic Science Reports |
Alterations in Atrial Electrophysiology and Tissue Structure in a Canine Model of Chronic Atrial Dilatation Due to Mitral Regurgitation
From Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Ind.
Correspondence to Jeffrey Olgin, MD, Chief, Cardiac Electrophysiology, University of California San Francisco, 500 Parnassus Ave, MU East 4/Box 1354, San Francisco, CA 94143-1354. E-mail olgin{at}medicine.ucsf.edu
Background— Clinically, chronic atrial dilatation is associated with an increased incidence of atrial fibrillation (AF), but the underlying mechanism is not clear. We have investigated atrial electrophysiology and tissue structure in a canine model of chronic atrial dilatation due to mitral regurgitation (MR).
Methods and Results— Thirteen control and 19 MR dogs (1 month after partial mitral valve avulsion) were studied. Dogs in the MR group were monitored using echocardiography and Holter recording. In open-chest follow-up experiments, electrode arrays were placed on the atria to investigate conduction patterns, effective refractory periods, and inducibility of AF. Alterations in tissue structure and ultrastructure were assessed in atrial tissue samples. At follow-up, left atrial length in MR dogs was 4.09±0.45 cm, compared with 3.25±0.28 at baseline (P<0.01), corresponding to a volume of 205±61% of baseline. At follow-up, no differences in atrial conduction pattern and conduction velocities were noted between control and MR dogs. Effective refractory periods were increased homogeneously throughout the left and right atrium. Sustained AF (>1 hour) was inducible in 10 of 19 MR dogs and none of 13 control dogs (P<0.01). In the dilated MR left atrium, areas of increased interstitial fibrosis and chronic inflammation were accompanied by increased glycogen ultrastructurally.
Conclusions— Chronic atrial dilatation in the absence of overt heart failure leads to an increased vulnerability to AF that is not based on a decrease in wavelength.
Key Words: fibrillation • electrophysiology • tissue
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