Atrial Fibrillation Induction Rate Research Articles

Catheter-Based Renal Sympathetic Denervation Significantly Inhibits Atrial Fibrillation Induced by Electrical Stimulation of the Left Stellate Ganglion and Rapid Atrial Pacing

BackgroundSympathetic activity involves the pathogenesis of atrial fibrillation (AF). Renal sympathetic denervation (RSD) decreases sympathetic renal afferent nerve activity, leading to decreased central sympathetic drive. The aim of this study was to identify the effects of RSD on AF inducibility induced by hyper-sympathetic activity in a canine model.MethodsTo establish a hyper-sympathetic tone canine model of AF, sixteen dogs were subjected to stimulation of left stellate ganglion (LSG) and rapid atrial pacing (RAP) for 3 hours. Then animals in the RSD group (n = 8) underwent radiofrequency ablation of the renal sympathetic nerve. The control group (n = 8) underwent the same procedure except for ablation. AF inducibility, effective refractory period (ERP), ERP dispersion, heart rate variability and plasma norepinephrine levels were measured at baseline, after stimulation and after ablation.ResultsLSG stimulation combined RAP significantly induced higher AF induction rate, shorter ERP, larger ERP dispersion at all sites examined and higher plasma norepinephrine levels (P<0.05 in all values), compared to baseline. The increased AF induction rate, shortened ERP, increased ERP dispersion and elevated plasma norepinephrine levels can be almost reversed by RSD, compared to the control group (P<0.05). LSG stimulation combined RAP markedly shortened RR-interval and standard deviation of all RR-intervals (SDNN), Low-frequency (LF), high-frequency (HF) and LF/HF ratio (P<0.05). These changes can be reversed by RSD, compared to the control group (P<0.05).ConclusionsRSD significantly reduced AF inducibility and reversed the atrial electrophysiological changes induced by hyper-sympathetic activity.

GW24-e1132 β3-Adrenoceptor mediates metabolic remodelling in the rabbit model of tachypacing-induced atrial fibrillation

ObjectivesBeta 3-adrenoceptor (β3-AR) is closely associated with the energy metabolism. This study aimed to explore the role of β3-AR in energy remodelling in rabbit model of pacing-induced atrial fibrillation (AF).MethodsRabbits...

β3-Adrenoceptor Mediates Metabolic Protein Remodeling in a Rabbit Model of Tachypacing-Induced Atrial Fibrillation

Background: The beta 3-adrenoceptor (β3-AR) is closely associated with energy metabolism. This study aimed to explore the role of β3-AR in energy remodeling in a rabbit model of pacing-induced atrial fibrillation (AF). Methods: Rabbits with a sham-operation or pacing-induced AF were used for this study, and the latter group was further divided into three subgroups: 1) the pacing group, 2) the β3-AR agonist (BRL37344)-treated group, and 3) the β3-AR antagonist (SR59230A)-treated group. Atrial electrogram morphology and surface ECG were used to monitor the induction of AF and atrial effective refractory period (AERP). RT-PCR and western blot (WB) were used to show alterations in β3-AR and metabolic-related protein. Results: RT-PCR and WB results showed that β3-AR was significantly upregulated in the pacing group, and that it corresponded with high AF inducibility and significantly decreased AERP₂₀₀ and ATP production in this group. Inhibition of β3-AR decreased the AF induction rate, reversed AERP₂₀₀ reduction, and restored ATP levels in the AF rabbits. Further activation of β3-AR using agonist BRL37344 exacerbated AF-induced metabolic disruption. Periodic acid Schiff (PAS) and Oil Red O staining showed β3-AR-dependent glycogen and lipid droplet accumulation in cardiac myocytes with AF. Glucose transporter-4 (GLUT-4) and CD36, key transporters of glucose and fatty acids, were downregulated in the pacing group. Expression of carnitine-palmitoyltransferase I (CPT-1), a key regulator in fatty acid metabolism, was also significantly downregulated in the pacing group. Reduced glucose transportation and fatty acid oxidation could be restored by inhibition of β3-AR. Furthermore, key regulators of metabolism, peroxisome proliferator-activated receptor-α (PPARα) and PPAR co-activator (PGC-1α) can be regulated by pharmacological intervention of the β3-AR. Conclusions: β3-AR is involved in metabolic protein remodeling in AF. PPARα/PGC-1α signaling pathway might be the relevant down-stream molecular machinery in response to AF-induced activation of β3-AR. β3-AR might be a novel target in AF treatment.

STELLATE GANGLION ELECTRICAL STIMULATION FOR ESTABLISHING A CANINE MODEL OF ACUTE ATRIAL FIBRILLATION MEDIATED BY SYMPATHETIC NERVE

ObjectivesTo build the methodology of acute animal model of atrial fibrillation (AF) induced by increased sympathetic nerve activity.MethodsSixteen adult mongrel dogs weighing 18 to 25 kg were randomly divided into...

THE TIME COURSE OF ELECTRICAL REMODELLING, STRUCTURAL REMODELLING, NEURAL REMODELLING AND ENDOTHELIN-1 LEVEL IN ATRIAL FIBRILLATION

ObjectivesThe consistency between electrical remodelling, structural remodelling, neural remodelling and endothelin-1 level in atrial fibrillation (AF) has not been reported. The present study aimed to investigate the time course of...

The relationship of paroxysmal atrial fibrillation and regional sympathetic innervations in the atria and pulmonary veins: experiment with dogs

To test the hypothesis that regional sympathetic innervation in the atria and pulmonary veins are correlated with atrial fibrillation (AF). Sixteen adult mongrel dogs underwent thoracotomy under general anesthesia. Bilateral cervical vagal trunks were decentralized. Multipolar catheters were placed into right atrial appendage (RAA), left atrial appendage (LAA), left atrium (LA), left superior pulmonary vein (LSPV), left inferior pulmonary vein (LIPV), right superior pulmonary vein (RSPV), and left inferior pulmonary vein (LIPV). The bilateral sympathovagal trunks were stimulated, S1S1 burst stimulation and S1S2 stimulation procedure were performed on different points of RAA, LAA, LA, LSPV, LIPV, RSPV, and LIPV. The TF thus induced was monitored. After that, the dogs were killed with their hearts and lungs were taken out. Immunocytochemical staining of cardiac nerves was performed using anti-tyrosine hydroxylase (TH) antibodies. The nerve fiber density was counted manually for each case and expressed as the mean number per slice. Two dogs died during the experiment and the whole procedure was completed on 14 dogs. There was no significant difference in the AF induction rate among the most points, however, the AF induction rate of the RIPV was significantly lower than those of the other points (all P < 0.05). The levels of density of TH-positive nerves in the atria and atrial appendages were significantly higher than those in the pulmonary veins (P = 0.02). The density of TH-positive nerves in the dogs with AF was significantly higher than that in the dog without AF (P < 0.05). The innervation of sympathetic nerves in atria and pulmonary veins was highly correlated to the induction of atrial fibrillation (r = 0.83). Regional sympathetic hyperinnervation plays an important role in atrial fibrillation induction.