Funding: Dr. Traykov is supported by a grant from the Szívritmus foundation.
Role of Triggering Pulmonary Veins in the Maintenance of Sustained Paroxysmal Atrial Fibrillation
Article first published online: 19 MAR 2013
©2013, The Authors. Journal compilation ©2013 Wiley Periodicals, Inc.
Pacing and Clinical Electrophysiology
Volume 36, Issue 7, pages 845–854, July 2013
How to Cite
TRAYKOV, V. B., PAP, R., GINGL, Z., CHADAIDE, S., HAQQANI, H. M., KLAUSZ, G., GALLARDO, R., FORSTER, T., CALLANS, D. J. and SÁGHY, L. (2013), Role of Triggering Pulmonary Veins in the Maintenance of Sustained Paroxysmal Atrial Fibrillation. Pacing and Clinical Electrophysiology, 36: 845–854. doi: 10.1111/pace.12121
This work was partially supported by the Hungarian National Research Fund (OTKA K69018).
Conflict of interests: None related to this study.
- Issue published online: 1 JUL 2013
- Article first published online: 19 MAR 2013
- Manuscript Accepted: 13 JAN 2013
- Manuscript Revised: 4 JAN 2013
- Manuscript Received: 6 AUG 2012
- Szívritmus foundation
- Hungarian National Research Fund. Grant Number: OTKA K69018
- paroxysmal atrial fibrillation;
- dominant frequency;
- frequency gradient;
- fast Fourier transformation
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.
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.