Frequency analysis of human atrial fibrillation using the surface electrocardiogram and its response to ibutilide.

This study assesses a technique for quantifying the frequency spectrum of atrial fibrillation (AF) using the surface electrocardiogram. Electrocardiograhic recordings were obtained in 61 patients during AF. After bandpass filtering, the QRST complexes were subtracted using a template-matching algorithm. The resulting fibrillatory baseline signal was subjected to Fourier transformation and displayed as a frequency power spectrum. These frequency spectra were compared to direct measurements from the right atrium and coronary sinus in 35 patients undergoing electrophysiologic study. The clinical use of this technique was explored by correlating fibrillatory frequency with the behavior of the arrhythmia in 26 patients referred for cardioversion. The electrocardiographic frequency spectrum during AF was characterized by a single peak that varied widely between patients (range 228 to 480 beats/min). There was a strong correlation between electrocardiographic peak frequency and that measured in the right atrium and coronary sinus (r = 0.79 to 0.98, p <0.0001). Episodes of AF that terminated in < 5 minutes had a lower frequency than those that persisted > 5 minutes (324 +/- 36 vs 402 +/- 78 beats/min, p = 0.001). Chronic AF (< 3 months in duration) had a lower frequency than chronic AF (present > 3 months) (336 +/- 48 vs 408 +/- 60 beats/ min, p = 0.012). Fibrillation frequency was an accurate predictor of conversion with ibutilide. Success rate was 100% in patients with peak frequency < 360 beats/min versus 29% in patients with frequencies > or = 360 beats/min (p = 0.003). Automatic analysis of the frequency content of the fibrillatory baseline on the surface electrocardiogram accurately reflects the average rate of AF. This measurement correlates with the clinical pattern of the arrhythmia and predicts the response to administration of ibutilide.

Effects of high energy shocks on pacing impedance during transvenous ICD implantation.

The purpose of the current study was to characterize the effects of transvenous ICD shocks on myocardial impedance. Rather than recording impedance during shocks, it was measured during continuous pacing in order to minimize confounding effects such as electrode polarization. Pacing impedance (reflecting the combined impedances of the electrode-tissue interface, myocardium, and blood pool) was measured every 5 seconds before and after 58 single shocks in 22 patients undergoing ICD implantation with a Transvene (n = 14) or Endotak (n = 8) lead. There was a progressive and long-lasting decrease in impedance after shocks. The magnitude of this change was similar for 0.6-J test shocks and shocks > or = 5 J (28 +/- 32 omega vs 23 +/- 16 omega; P = 0.8). However, the drop in impedance was more abrupt after high energy shocks. Because impedance continued to decline throughout the 5-minute interval between shocks, successive shocks had a cumulative effect, with a decrease of 46 +/- 42 omega after four discharges. In conclusion, a progressive decline in pacing impedance is a characteristic response to transvenous ICD discharges.