Response of atrial fibrillatory activity to carotid sinus massage in patients with atrial fibrillation.

In some cases carotid sinus massage (CSM) may induce AF, whereas it may terminate AF in others. The purpose of this study was to investigate the influence of CSM on atrial fibrillatory frequency using spectral analysis of the surface ECG. Continuous ECG recordings were made in 19 patients (12 men, 7 women, mean age 61 +/- 11 years) with AF. Unilateral CSM was performed in the standard fashion to one randomized bifurcation of the carotid artery at a time. Ventricular rate and fibrillatory frequency were assessed in 30-second ECG segments at baseline and during CSM. The frequency content of the fibrillatory baseline was quantified using digital signal processing (filtering, subtraction of averaged QRST complexes, and Fourier transformation). CSM resulted in a relative change in fibrillatory frequency of 4.5 +/- 3.9% (range 0%-13%). In 8 (42%) patients an increase in fibrillatory frequency was found (6.4 +/- 0.5 vs 6.8 +/- 0.5 Hz, P = 0.012). In 9 (47%) patients a decrease in fibrillatory frequency occurred (6.5 +/- 0.8 vs 6.1 +/- 0.8 Hz, P = 0.008) without AF termination. The remaining two patients showed no change in fibrillatory frequency. CSM on the contralateral side after 2 minutes produced fibrillatory frequency changes in the same direction in all patients with a good reproducibility in its magnitude (r = 0.59, P = 0.05). Calcium channel blockers were more frequently used (78% vs 25%, P = 0.044) in patients with a decrease in fibrillatory frequency compared to patients with a frequency increase. There were no significant changes in ventricular rate during CSM. In conclusion, two different responses of atrial fibrillatory frequency to CSM were found. This might explain why CSM may facilitate AF induction in some cases and AF termination in others. Calcium channel blocker treatment may prevent an increase in fibrillatory frequency provoked by CSM suggesting a blunted electrical remodeling process.

Circadian variations in atrial fibrillatory frequency in persistent human atrial fibrillation.

Atrial fibrillatory frequency reflects the atrial refractory period during AF. This study was conducted to investigate noninvasively the diurnal fluctuations of fibrillatory frequency in persistent human atrial fibrillation and to determine the relationship between changes in ventricular rate and fibrillatory frequency. Ambulatory ECGs were recorded in 30 patients (18 men, 12 women, mean age 60 +/- 11 years) with persistent AF (> 24 hours). AF frequency was measured in 1-minute ECG segments by subtracting averaged QRST complexes and applying Fourier analysis to the resulting signals at 4 PM, 10 PM, 4 AM, and 10 AM. Peak frequency was determined in the 3-12 Hz frequency band. Mean fibrillatory frequency measured 6.6 +/- 0.6 Hz (range 5.0-7.8 Hz). Two different frequency patterns were distinguished comparing maximal diurnal versus nocturnal fibrillatory frequency. In six (20%) patients an increase (P = 0.045) in nocturnal fibrillatory frequency (type I) was found. In the remaining 24 (80%) patients a decrease (P < 0.001) in fibrillatory frequency occurred (type II). Type I AF showed a strong inverse correlation between relative changes (percent) in ventricular rate and fibrillatory frequency obtained from two consecutive measurement points (r = -0.88 to -.97, P < 0.01), whereas in type II AF a moderate positive correlation (r = 0.36 to 0.41, P < 0.05) was detected. These data indicate a circadian pattern in AF frequency that concurs with ventricular rate changes suggesting a modulating influence of the autonomic nervous system on atrial electrophysiology in persistent human AF.

Non-invasive assessment of fibrillatory activity in patients with paroxysmal and persistent atrial fibrillation using the Holter ECG.

OBJECTIVE: Automatic analysis of the frequency content of the fibrillatory baseline on the surface ECG accurately reflects the average rate of atrial fibrillation (AF). This frequency measurement correlates with the behavior of AF and predicts the response to administration of ibutilide, a new antiarrhythmic drug. Neither the temporal pattern of fibrillatory frequency in spontaneous paroxysmal or persistent AF, nor its response to chronic antiarrhythmic medication has been studied so far. METHODS AND RESULTS: Holter ECG recordings were made in 20 patients during AF. One minute ECG segments were selected for analysis. The frequency content of the fibrillatory baseline was then quantified using digital signal processing. After high-pass filtering, the QRST complexes were subtracted using a template matching algorithm. The resulting fibrillatory baseline signal was subjected to Fourier transformation, displayed as a frequency power spectrum and the peak frequency (f) was determined. In 11 patients (7 male, 4 female, age 62 +/- 10 years) 31 paroxysmal AF episodes were analyzed. Duration ranged from 1 min to 665 min (115 +/- 175 min). Initial mean peak f measured 5.1 +/- 0.7 Hz (range 3.9 to 6.9 Hz). There was a positive correlation between f and AF duration (R = 0.53, p = 0.002). AF of less than 15 min duration (n = 13) showed a lower f (4.8 +/- 0.6 Hz) when compared with longer lasting episodes (n = 18, 5.3 +/- 0.7 Hz, p = 0.03). In short AF episodes f was constant, whereas in longer-lasting episodes f increased to 5.8 +/- 0.5 Hz (p < 0.001) within 5 min. In 9 patients (9 male, age 58 +/- 8 years) with persistent AF oral antiarrhythmic drugs (amiodarone n = 5, sotalol n = 3, flecainide n = 1) were given prior to electrical cardioversion for prophylaxis of AF recurrence. Frequency measurements were obtained at baseline and 3 to 5 days after initiation of drug administration. At baseline mean f measured 6.9 +/- 0.4 Hz. Frequency was reduced by antiarrhythmic drugs to 5.8 +/- 0.4 Hz (p < 0.001). CONCLUSIONS: (1) The duration of paroxysmal AF episodes can be predicted using spectral analysis of ECG recordings of AF episodes. (2) An increase in fibrillatory frequency is associated with AF persistence. (3) This technique can be used to monitor the response to antiarrhythmic medication.