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. 1999 Sep;82(3):319-24.
doi: 10.1136/hrt.82.3.319.

Incidence and modes of onset of early reinitiation of atrial fibrillation after successful internal cardioversion, and its prevention by intravenous sotalol

Affiliations

Incidence and modes of onset of early reinitiation of atrial fibrillation after successful internal cardioversion, and its prevention by intravenous sotalol

H F Tse et al. Heart. 1999 Sep.

Abstract

Objectives: To study the incidence and mode of onset of early reinitiation of atrial fibrillation (ERAF) following successful internal cardioversion of chronic atrial fibrillation, and to determine the effects of sotalol in the prevention of ERAF.

Design: The incidence and modes of onset of ERAF and the acute effects of intravenous sotalol in the prevention of ERAF were studied retrospectively.

Setting: Electrophysiology laboratory at a university teaching hospital.

Patients: 64 patients, mean (SD) age 62 (10) years, who underwent internal cardioversion of chronic atrial fibrillation (mean duration of atrial fibrillation 31 (39) months).

Main outcome measures: ECGs and intracardiac electrograms recorded during the internal cardioversion of atrial fibrillation using 3/3 ms biphasic, R wave synchronised shocks.

Results: 52 patients (81%) had successful electrical cardioversion, and 20 (31%) of these had ERAF during the procedure. There was no clinical predictor for the occurrence of ERAF. Fifty eight episodes of ERAF were observed. Five ERAF episodes (9%) had preceding bradycardia and 53 (91%) of these were triggered by atrial premature beats with normal preceding heart rate. Atrial premature beats that reinitiated atrial fibrillation had a shorter coupling interval (333 (43) ms v 396 (100), p < 0.001) and a lower prematurity index (0.44 (0.11) v 0. 55 (0.14), p < 0.001) than those that did not reinitiate atrial fibrillation. Repeated shock delivery and increasing the defibrillation energy did not prevent ERAF. Intravenous sotalol infusion decreased the numbers of atrial premature beats and prolonged their coupling interval, and prevented ERAF after repeated defibrillation in 83% of patients with ERAF.

Conclusions: ERAF is a significant clinical problem after successful internal cardioversion of chronic atrial fibrillation, and was observed in up to 31% of patients. In most episodes, ERAF was triggered by short coupling atrial premature beats with preceding normal heart rate. Intravenous sotalol was effective in preventing ERAF in most cases.

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Figures

Figure 1
Figure 1
Flow chart showing the outcome of patients after low energy internal cardioversion of atrial fibrillation (AF) and the results of treatment for spontaneous reinitiation of atrial fibrillation by repeated defibrillation, intravenous sotalol and atropine, and atrial pacing. SR, sinus rhythm.
Figure 2
Figure 2
Different modes of onset of early reinitiation of atrial fibrillation (AF). (A) AF reinitiation preceding by bradycardia (mean atrial cycle length = 1240 ms). (B) AF was reinitiated an atrial premature beat (APB) after a short period of organised electrical activity. Note the normal heart rate preceding the onset of APB. (C) AF was reinitiated by APB with preceding long/short cycles. HRA, high right atrium.

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