Role of fibrillation cycle length in spontaneous and drug-induced termination of human atrial fibrillation.
The aim of this study was to investigate the mechanism of spontaneous termination of atrial fibrillation (AF) by comparing it with drug-induced termination on the basis of changes in fibrillation cycle length (FCL). Fast Fourier transform analysis was carried out on the electrocardiogram (ECG) records of 27 patients with paroxysmal AF without organic heart disease. In 8 patients with drug-induced termination of AF, spectral analysis of the data from surface ECG lead V1 was performed before and after class I antiarrhythmic drug infusion for 10 min. In 19 patients with spontaneous termination of AF, the analysis used the Holter ECG recordings at 10 min before the spontaneous termination and at the termination. FCL was calculated from the peak frequency of each epoch and the mean FCL and the coefficient of variation (CV) of FCL were determined from the data of 20 epochs. In the 8 episodes of drug-induced AF termination, the mean FCL increased significantly with class I drugs (from 151+/-17 to 203+/-21 ms, p<0.001), whereas in the 19 episodes of spontaneous termination, the mean FCL and CV of FCL at termination did not differ from those at 10 min before the termination. Of the 19 episodes, 10 episodes terminating in the morning showed a significant increase in the FCL of the last epoch of the termination period (from 158 +/-22 to 172+/-17 ms, p<0.05). In the 9 episodes terminating in either the afternoon or the evening, the FCL of the last epoch did not change significantly. Although drug-induced termination of paroxysmal AF may depend on a gradual increase in FCL, the pattern of spontaneous termination may depend on the time of day. Spontaneous termination in the morning may be caused by an abrupt increase in FCL related to vagolytic autonomic balance.
The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan. fujiki@ms.toyama-mpu.ac.jp
Akira
A
Fujiki
Masao
M
Sakabe
Kunihiro
K
Nishida
Koichi
K
Mizumaki
Hiroshi
H
Inoue
D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000188:drug therapy* / Q000503:physiopathology*; D004562:Electrocardiography / Q000187:drug effects* / Q000379:methods; D006801:Humans; D007093:Imidazoles / Q000627:therapeutic use; D008875:Middle Aged; D011342:Procainamide / Q000627:therapeutic use; D012075:Remission, Spontaneous
D000889:Anti-Arrhythmia Agents; D007093:Imidazoles; D011342:Procainamide; C032151:cifenline