Marked Suppression of Pulmonary Vein Firing After Circumferential Pulmonary Vein Isolation in Patients With Paroxysmal Atrial Fibrillation

Is Pulmonary Vein Firing an Epiphenomenon?

Ru-Hong Jiang, M.S.; Chen-Yang Jiang, M.D.; Xia Sheng, M.D.; Zu-Wen Zhang, B.S.; Ya-Xun Sun, Ph.D.; Qiang Liu, M.S.; Guo-Sheng Fu, M.D.; Sunny S. Po, M.D., Ph.D.

Disclosures

J Cardiovasc Electrophysiol. 2014;25(2):111-118. 

In This Article

Abstract and Introduction

Abstract

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.

Introduction

Since the landmark report by Haissaguerre et al. that rapid firing (Rap-F) in pulmonary veins (PVs) was the major cause of paroxysmal atrial fibrillation (PAF),[1] atrial fibrillation (AF) ablation has evolved from eliminating the focal source of rapid PV firing (PV-F) to circumferential PV isolation (CPVI) to prevent Rap-F from entering the left atrium (LA) to initiate AF.[2] Recent studies reported that the long-term outcome of CPVI for PAF (single procedure, without antiarrhythmic drugs) was disappointing, underlying the necessity for better understanding of the mechanisms responsible for PAF and subsequently better selection of the ablation targets for PAF.[3,4] Recovery of PV-LA conduction has been shown as the major determinant for AF recurrence after CPVI,[3–5] while others found the isolation of PVs was not crucial for the outcome of AF ablation,[6,7] and similar proportion of PV reconnection was found in patients with and without AF recurrence after CPVI procedure.[8] If the trigger or substrate for PAF is located outside the CPVI line, a repeat CPVI to treat AF recurrence may not have enough impact on the outcome.

Recent experimental and clinical reports have indicated that the intrinsic cardiac autonomic nervous system (CANS) may play a critical role in the initiation and maintenance of AF[9–13] and additional autonomic denervation appeared to improve the success of CPVI.[14–16] It is well known that PV-LA junction is the site with the highest density of autonomic innervation.[17,18] We hypothesized that if the PVs and adjacent atrial tissue themselves are the true sources of PV-F, PV-F should continue after CPVI since all the tissues within the isolation lines remain intact. Based on prior experimental studies demonstrating that PV-F required simultaneous activation of both the sympathetic and parasympathetic components of the intrinsic CANS, we co-administered adenosine triphosphate (ATP) and isoproterenol (ISP) intravenously before and after CPVI. The former simulates the action of acetylcholine by shortening the action potential duration and the latter (a β-agonist) enhances the intracellular calcium transient, leading to early afterdepolarizations and subsequently rapid PV-F.[10,11]

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