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Controlled Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't
Marked suppression of pulmonary vein firing after circumferential pulmonary vein isolation in patients with paroxysmal atrial fibrillation: is pulmonary vein firing an epiphenomenon?
Journal of Cardiovascular Electrophysiology 2014 Februrary
INTRODUCTION: Rapid firing in pulmonary veins (PVs) is a leading cause of paroxysmal atrial fibrillation. We hypothesized that PV firing (PV-F) should continue after circumferential PV isolation (CPVI) because the PV tissue responsible for PV-F remains intact.
METHODS AND RESULTS: In Group-1 (n = 92), isoproterenol (ISP) and adenosine triphosphate (ATP) were co-administered to provoke PV-F before and after CPVI. The site of rapid focal discharge that initiated atrial fibrillation (AF) defined PV-F versus non-PV-F. Additional 17 patients with PV-F induced by ISP+ATP before CPVI were enrolled into Group-2 and various pacing maneuvers were used in conjunction to ISP+ATP to provoke PV-F after CPVI. In Group-1, AF was induced in 47/81 (58.0%) and 16/88 (18.2%) patients before and after CPVI, respectively (P < 0.01). Before CPVI, 43/47 (91.5%) of the rapid firing originated from PV. After successful CPVI, 88/92 patients were in sinus rhythm and non-PV-F was induced in 14/88 patients. PV-F was induced in 2/88 patients, which was eliminated by ganglionated plexus ablation outside the CPVI line. In Group-2, various pacing maneuvers with ISP+ATP only induced PV-F in 1/17 patients after CPVI.
CONCLUSION: Marked suppression of PV-F after CPVI strongly suggests that the real source of PV-F is located in the atrium. PV-F may be an epiphenomenon.
METHODS AND RESULTS: In Group-1 (n = 92), isoproterenol (ISP) and adenosine triphosphate (ATP) were co-administered to provoke PV-F before and after CPVI. The site of rapid focal discharge that initiated atrial fibrillation (AF) defined PV-F versus non-PV-F. Additional 17 patients with PV-F induced by ISP+ATP before CPVI were enrolled into Group-2 and various pacing maneuvers were used in conjunction to ISP+ATP to provoke PV-F after CPVI. In Group-1, AF was induced in 47/81 (58.0%) and 16/88 (18.2%) patients before and after CPVI, respectively (P < 0.01). Before CPVI, 43/47 (91.5%) of the rapid firing originated from PV. After successful CPVI, 88/92 patients were in sinus rhythm and non-PV-F was induced in 14/88 patients. PV-F was induced in 2/88 patients, which was eliminated by ganglionated plexus ablation outside the CPVI line. In Group-2, various pacing maneuvers with ISP+ATP only induced PV-F in 1/17 patients after CPVI.
CONCLUSION: Marked suppression of PV-F after CPVI strongly suggests that the real source of PV-F is located in the atrium. PV-F may be an epiphenomenon.
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