QUARTERLY FOCUS ISSUE: HEART RHYTHM DISORDERS
The Role of Ganglionated Plexi in Apnea-Related Atrial Fibrillation
Muhammad Ghias, MD,
Benjamin J. Scherlag, PhD*,
Zhibing Lu, MD,
Guodong Niu, MD,
Annerie Moers, MD,
Warren M. Jackman, MD,
Ralph Lazzara, MD and
Sunny S. Po, MD, PhD
Heart Rhythm Institute, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
Manuscript received June 13, 2009;
revised manuscript received September 9, 2009,
accepted September 21, 2009.
* Reprint requests and correspondence: Dr. Benjamin J. Scherlag, Heart Rhythm Institute, 1200 Everett Drive (6E103), Oklahoma City, Oklahoma 73104 (Email: benjamin-scherlag{at}ouhsc.edu).
Objectives: This study was conducted to simulate sleep apnea-induced atrial fibrillation (AF) in an experimental model and to determine whether neural ablation will prevent AF.
Background: An increasing number of clinical reports have associated sleep apnea and AF, and many possible mechanisms responsible for this relationship have been proposed.
Methods: Thirty dogs anesthetized with Na-pentobarbital were ventilated by a positive pressure respirator. Protocol 1 (n = 14): After a right thoracotomy, atrial and pulmonary vein programmed pacing at 2x and 4x threshold determined the shortest atrial refractory period. Obstructive apnea was induced by turning off the respirator during end expiration for 2 min. During apnea, programmed pacing was performed with S1-S2 = 5 to 10 ms earlier than the atrial refractory period. Neural activity was monitored from the ganglionated plexi (GP) adjacent to the right pulmonary veins. Protocol 2 (n = 16): Electrical stimulation identified the GP at the right pulmonary artery (RPA). Programmed pacing was again instituted, below atrial refractory period, during 2 min of apnea. After radiofrequency ablation of the RPA GP, continuous programmed pacing was again repeated during 2 min of apnea. In 5 dogs, blood gases were determined at baseline and at 2 min of apnea.
Results: Protocol 1: During apnea, S1-S2 induced AF within 85 ± 38 s (9 of 10). In 1 case, AF occurred spontaneously at 1 min 36 s of apnea. Recorded GP neural activity progressively increased before AF onset. Systolic but not diastolic blood pressure rose significantly before AF (149 ± 26 mm Hg to 193 ± 38 mm Hg, p < 0.05). In 4 dogs, autonomic blockade prevented apnea-induced AF. Protocol 2: AF induced by pacing occurred in 8 of 11 dogs within the 2-min period of apnea, before neural ablation. After ablation, 0 of 6 showed AF during 2 min of apnea (p = 0.009).
Conclusions: This experimental model of apnea shows a reproducible incidence of AF. After neural ablation of the RPA GP or autonomic blockade, AF inducibility was significantly inhibited.
Key Words: atrial fibrillation • autonomic nervous system • sleep apnea
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Abbreviations and Acronyms
| | AF = atrial fibrillation | | ARGP = anterior right ganglionated plexi | | ARP = atrial refractory period | | AV = atrioventricular | | BP = blood pressure | | GP = ganglionated plexi | | PV = pulmonary vein | | RA = right atrial | | RPA = right pulmonary artery | | RSPV = right superior pulmonary vein | | SVC = superior vena cava |
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