© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
Endovascular stimulation within the left pulmonary artery to induce slowing of heart rate and paroxysmal atrial fibrillation
aCardiac Arrhythmia Research Institute at the University of Oklahoma Health Sciences Center, Department of Veterans Affairs Medical Center, 1200 Everett Drive, Room UH6E103, Oklahoma City, OK 73104, USA
bTechnical University RWTH, Aachen, Germany
cXinjiang Medical University, Urumuqi, PR China
* Corresponding author. Tel.: +1-405-271-9696; fax: +1-405-271-7455 benjamin_scherlag{at}ouhsc.edu
Objective: In recent years there have been many reports dealing with basic models for sustained atrial fibrillation (AF), however few animal models exist for paroxysmal AF which closely simulate that seen clinically. Methods: In 12 dogs, anesthetized with sodium pentobarbital, a right thoracotomy was performed. We stabilized a basket electrode catheter within the left pulmonary artery (LPA) through a purse string suture in the right ventricle. Electrode catheters were sutured to multiple atrial sites including the four pulmonary veins and the right and left atrial appendages, along Bachman's bundle and the coronary sinus. Results: Continuous pulses of electrical stimulation (20 Hz square wave stimuli, each 0.1 ms in duration, voltage range 1–40 V) across adjacent splines of the five arms of the basket induced slow heart rates (at lower voltages) and then initiated atrial premature depolarizations (APDs), atrial tachycardia (AT) and AF (at higher voltages). To avoid possible direct activation of atrial myocardium, we also applied a train (50–100 ms duration) of high frequency stimuli (200 Hz) coupled to each atrial paced beat so that the train fell within the atrial refractory period. Stimulation in the LPA at an average of 14±7 V induced heart rate slowing, APDs were seen followed by AT/AF at a voltage of 20±6 V, P=0.002. Stimulation in the LPA resulted in APDs arising from a variety of sites including the left pulmonary veins (superior or inferior) and the left atrial appendage. After β-blockade (intravenous esmolol or propranolol, 1 mg/kg) the voltage threshold for induction of AF rose from 14±7 to 25±10 V, P=0.02. Upon the addition of intravenous atropine (1–2 mg) the arrhythmic response (AF) to stimulation was completely abolished. Atrial pacing threshold was unchanged after autonomic blockade. Local application of radiofrequency energy (average number=3±2) across the metallic splines of the basket catheter in the LPA (70–80 V for 60 s) caused abolition of both the slowing and the arrhythmic response to LPA stimulation. Conclusion: These data suggest that stimulation of autonomic nerves in the LPA causes slowing of the heart rate followed by paroxysmal APD/AT/AF simulating the spontaneously occurring paroxysmal AF syndrome, associated with bradycardia, reported in patients.
KEYWORDS Ablation; Adrenergic (ant)agonists; Arrhythmia (mechanisms); Autonomic nervous system; Bradycardia; Muscarinic (ant)agonists
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