Author + information
- Received October 31, 1994
- Revision received February 7, 1995
- Accepted February 27, 1995
- Published online July 1, 1995.
- ↵*Address for correspondence: Dr. Stanley Nattel, Research Center, Montreal Heart Institute, 5000 Belanger Street, Montreal, Quebec H1T 1C8, Canada.
Objectives. This study sought to determine the mechanisms of idiopathic atrial fibrillation and the atrial antifibrillatory action of flecainide in dogs.
Background. In a small subset of dogs, sustained atrial fibrillation can be readily induced in the absence of vagal tone. The electrophysiologic mechanisms underlying this ability to sustain atrial fibrillation, and of flecainide action on the arrhythmia, are unknown.
Methods. Six dogs with inducible sustained atrial fibrillation were studied before and after flecainide administration and compared with a control group of 10 dogs.
Results. Dogs with atrial fibrillation differed in displaying more shortening of the atrial refractory period with increased rate, resulting in a significantly shorter refractory period and wavelength for reentry at rapid rates, and in increased regional dispersion in refractoriness. Activation maps during sustained fibrillation showed a mean (± SE) of 6.3 ± 0.4 coexistent zones of reentry, compatible with short wavelengths, whereas in control dogs activation during self-limited atrial fibrillation was better organized, and the number of reentrant circuits was smaller. Quantitative analysis demonstrated significantly greater inhomogeneity of activation during atrial fibrillation in dogs with atrial fibrillation than in control animals. Flecainide terminated atrial fibrillation by increasing the duration and homogeneity of atrial refractoriness at rapid rates, thereby reducing the number of reentry circuits and the heterogeneity of activation.
Conclusions. The ability of atrial fibrillation to sustain itself resulted from enhanced rate-dependent shortening of atrial refractoriness and increased regional heterogeneity. Flecainide reversed these changes and restored sinus rhythm. These results suggest potential mechanisms of idiopathic atrial fibrillation and are pertinent to understanding the clinical actions of flecainide.
This study was supported by the Medical Research Council of Canada, Ottawa; the Quebec Heart Foundation, Montreal; and the Fonds de Recherche de l'Institut de Cardiologie de Montréal, Montreal. Dr. Wang is the recipient of a studentship award from the Canadian Heart Foundation, Ottawa. Riker-3M Pharmaceuticals provided the flecainide used in this study.
- Received October 31, 1994.
- Revision received February 7, 1995.
- Accepted February 27, 1995.
- The American College of Cardiology