Supported by the unrestricted Alumni Funds from Cornell University College of Veterinary Medicine, and in part by Grants PfH-HL39707 and R01-HL60843 from the National Heart, Lung, and Blood Institute of the National Institutes of Health.
Temporal Organization of Atrial Activity and Irregular Ventricular Rhythm During Spontaneous Atrial Fibrillation:
An In Vivo Study in the Horse
Article first published online: 20 APR 2007
Journal of Cardiovascular Electrophysiology
Volume 11, Issue 7, pages 773–784, July 2000
How to Cite
GELZER, A. R.M., MOISE, N. S., VAIDYA, D., WAGNER, K. A. and JALIFE, J. (2000), Temporal Organization of Atrial Activity and Irregular Ventricular Rhythm During Spontaneous Atrial Fibrillation:. Journal of Cardiovascular Electrophysiology, 11: 773–784. doi: 10.1111/j.1540-8167.2000.tb00049.x
- Issue published online: 20 APR 2007
- Article first published online: 20 APR 2007
- Manuscript received 13 December 1999; Accepted for publication 27 March 2000.
- atrial fibrillation;
- spectral analysis;
- ventricular response;
Temporal Organization of Atrial Activity. Introduction: Atrial fibrillation (AF) is common in healthy horses. We studied the temporal organization of AF to test the hypothesis that the arrhythmia is governed by a high degree of periodicity and therefore is not random in the horse. Further, we surmised that concealed conduction of AF impulses in the AV node results in an inverse relationship between AF frequency and ventricular frequency.
Methods and Results: Fast Fourier transform (FFT) analysis of atrial activity was done on signal-averaged ECGs (n = 11) and atrial electrograms (n = 3) of horses with AF at control (C), after quinidine sulfate (22 mg/kg by mouth every 2 hours) at 50% time to conversion (T50), and immediately before conversion (T90) to sinus rhythm. FFT always revealed a single dominant frequency peak. The mean dominant frequency decreased until conversion (C = 6.84 ± 0.85 Hz, T50 = 4.87 ± 1.5 Hz, T90 = 3.41 ± 1.18 Hz; P < 0.001). Mean AA intervals (n = 5WM gradually increased after quinidine. Mean RR intervals (n = 500), standard deviation of the mean ISDM), Poincaré plots, and serial autocorrelograms (SACs) of 500 RR intervals were measured at C and T90 to determine the ventricular response to AF and quinidine-induced changes in the variability of the ventricular response. Mean RR interval and SDM were reduced after quinidine (C = 1431 ± 266 msec and 695 ± 23 msec; T90 = 974 ± 116 msec and 273 ± 158 msec, respectively: P < 0.01). Poincaré plots and SAC at C and at T90 revealed a significant correlation of consecutive RR intervals typical of a system with a deterministic behavior. At T90, the variability of RR intervals was reduced and the overall periodicity of RR intervals was increased after quinidine administration.
Conclusion: In the horse, AF is a complex arrhythmia characterized by a high degree of underlying periodicity. The inverse AA-to-RR interval relationship and reduced variability of RR intervals after quinidine suggest that the ventricular response during AF results from rate-dependent concealment of AF wavelets bombarding the AV node, which nevertheless results in a significant degree of short-term predictability of beat-to-beat changes in RR intervals.