Key result
Despite isolation of the triggering pulmonary vein, paroxysmal atrial fibrillation continued in 53% of patients, suggesting nontriggering veins also contribute to arrhythmia maintenance.
Why the study?
Does isolation of the triggering pulmonary vein alone terminate sustained paroxysmal atrial fibrillation in patients with isoproterenol-induced PAF?
Observational (n=26)
Does isolation of the triggering pulmonary vein alone terminate sustained paroxysmal atrial fibrillation in patients with isoproterenol-induced PAF?
While triggering structures harbor the fastest electrical activity during sustained paroxysmal AF, non-triggering pulmonary veins also contribute to arrhythmia maintenance, indicating that isolating only the triggering vein is often insufficient.
Single triggering vein isolation should not yet alter ablation strategy in PAF; hypothesis-generating for multi-vein approaches requiring randomized confirmation.
BACKGROUND: Triggers from thoracic veins have been implicated not only in the initiation, but also in the perpetuation of paroxysmal atrial fibrillation (PAF). To investigate their role we studied the distribution and stability of dominant frequencies (DFs) during PAF and the response to isolation of the triggering pulmonary vein (PV). METHODS AND RESULTS: Triggering structures inducing PAF were identified during isoproterenol challenge in 26 patients (15 males, 55 ± 8.5 years). During sustained PAF, sequential recordings were made with a decapolar circular mapping catheter from each PV and the left atrial posterior wall (LAPW), together with coronary sinus (CS) and right atrium (RA) recordings. DF was determined using fast Fourier transformation. Recordings were repeated after ≥15 minutes of PAF. Radiofrequency ablation was directed first at the triggering PVs. PAF initiated from the PVs in 24 patients and from RA in two. There was a significant frequency gradient from the triggering structure to the PVs, CS, LAPW, and RA (P < 0.0001). During the second recording, DF decreased at all sites (P < 0.02), but the frequency gradient remained unchanged. Despite isolation of the triggering PV, PAF continued in 53% of patients, although DF measured in the CS was lower. AF termination occurred with contralateral PV isolation in half of the remaining patients and further AF slowing was noted in the rest. CONCLUSIONS: Triggering structures harbor the fastest activity during sustained PAF pointing to their leading role in arrhythmia perpetuation. However, nontriggering PVs also seem to contribute to PAF maintenance.
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Traykov et al. (2013) conducted an observational in Paroxysmal atrial fibrillation (n=26). Radiofrequency ablation of triggering pulmonary veins was evaluated on Continuation of paroxysmal atrial fibrillation after isolation of the triggering pulmonary vein. Despite isolation of the triggering pulmonary vein, paroxysmal atrial fibrillation continued in 53% of patients, suggesting nontriggering veins also contribute to arrhythmia maintenance.
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