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J Am Coll Cardiol, 1999; 33:1217-1226 © 1999 by the American College of Cardiology Foundation |
* Division of Cardiology, Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, China
InControl, Redmond, Washington, USA
Manuscript received May 26, 1998; revised manuscript received November 6, 1998, accepted December 23, 1998.
Reprint requests and correspondence: Prof. C. P. Lau, Chief, Division of Cardiology, Department of Medicine, University of Hong Kong, Hong Kong, China
cplau{at}hkucc.hku.hk
OBJECTIVES
Our aim was to evaluate a potential focal source of atrial fibrillation (AF) by unmasking spontaneous early reinitiation of AF after transvenous atrial defibrillation (TADF), and to describe a method of using repeated TADF to map and ablate the focus.
BACKGROUND
Atrial fibrillation may develop secondary to a rapidly discharging atrial focus that the atria cannot follow synchronously, with suppression of the focus once AF establishes. Focus mapping and radiofrequency (RF) ablation may be curative but is limited if the patient is in AF or if the focus is quiescent. Early reinitiation of AF has been observed following defibrillation, which might have a focal mechanism.
METHODS
We performed TADF in patients with drug-refractory lone AF using electrodes in the right atrium (RA) and the coronary sinus. When reproducible early reinitiation of AF within 2 min after TADF was observed that exhibited a potential focal mechanism, both mapping and RF ablation were performed to suppress AF reinitiation. Clinical and ambulatory ECG monitoring was used to assess AF recurrence.
RESULTS
A total of 44 lone AF patients (40 men, 4 women; 32 persistent, 12 paroxysmal AF) with a mean age of 58 ± 13 years underwent TADF. Sixteen patients had early reinitiation of AF after TADF, nine (20%; 5 paroxysmal) exhibited a pattern of focal reinitiation. Earliest atrial activation was mapped to the right superior (n = 4) and the left superior (n = 3) pulmonary vein, just inside the orifice, in the seven patients who underwent further study. At the onset of AF reinitiation, the site of earliest activation was 86 ± 38 ms ahead of the RA reference electrogram. The atrial activities from this site were fragmented and exhibited progressive cycle-length shortening with decremental conduction to the rest of the atrium until AF reinitiated. Radiofrequency ablation at the earliest activation site resulted in suppression of AF reinitiation despite pace-inducibility. Improved clinical outcome was observed over 8 ± 4 months’ follow-up.
CONCLUSIONS
Transvenous atrial defibrillation can help to unmask, map, and ablate a potential atrial focus in patients with paroxysmal and persistent AF. A consistent atrial focus is the cause of early reinitiation of AF in 20% of patients with lone AF, and these patients may benefit from this technique.
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