Canine model of paroxysmal atrial fibrillation and paroxysmal atrial tachycardia

• Published in: American journal of physiology. Heart and circulatory physiology 2005-11, Vol.289 (5), p.H1851-H1857
• Main Authors: Swissa, Moshe, Zhou, Shengmei, Paz, Offir, Fishbein, Michael C, Chen, Lan S, Chen, Peng-Sheng
• Format: Article
• Language: English
• Subjects: Animals; Atrial Fibrillation - physiopathology; Disease Models, Animal; Dogs; Electrocardiography; Electrophysiology; Heart - innervation; Heart Block; Immunohistochemistry; Myocardial Infarction - physiopathology; Myocardium - metabolism; Stellate Ganglion - physiopathology; Sympathetic Nervous System - physiopathology; Tachycardia, Paroxysmal - physiopathology
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.00083.2005

1 Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center; 2 Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, California; and 3 Department of Neurology, Childrens Hospital Los Angeles and Keck School of Medicine of the University of Southern California, Los Angeles, California Submitted 27 January 2005 ; accepted in final form 21 June 2005 Both autonomic nerve activity and electrical remodeling are important in atrial arrhythmogenesis. Therefore, dogs with sympathetic hyperinnervation, myocardial infarction (MI), and complete atrioventricular block (CAVB) may have a high incidence of atrial arrhythmias. We studied eight dogs (experimental group) with MI, CAVB, and sympathetic hyperinnervation induced either by nerve growth factor infusion ( n = 4 dogs) or subthreshold electrical stimulation ( n = 4 dogs) of the left stellate ganglion. Cardiac rhythm was continuously monitored by a Data Sciences International transmitter for 48 (SD 27) days. Three normal control dogs were also monitored. Six additional normal dogs were used for histology control. Paroxysmal atrial fibrillation (PAF) and paroxysmal atrial tachycardia (PAT) were documented in all dogs in the experimental group, with an average of 3.8 (SD 3) episodes/day, including 1.3 (SD 1.6) episodes of PAF and 2.5 (SD 2.2) episodes of PAT. The duration averaged 298 (SD 745) s (range, 7–4,000 s). There was a circadian pattern of arrhythmia onset ( P < 0.01). Of 576 episodes of PAF and PAT, 236 (41%) episodes occurred during either sustained or nonsustained ventricular tachycardia (VT). Among these 236 episodes, 53% started before VT, whereas 47% started after the onset of VT. Normal dogs did not have either PAF or PAT. The hearts from the experimental group had a higher density of nerve structures immunopositive ( P < 0.01) for three different nerve specific markers in both right and left atria than those of the control dogs. We conclude that the induction of nerve sprouting and sympathetic hyperinnervation in dogs with CAVB and MI creates a high yield model of PAF and PAT. electrophysiology; stellate ganglion; atrial arrhythmia; pathology Address for reprint requests and other correspondence: P.-S. Chen, Rm. 5342, CSMC, 8700 Beverly Blvd., Los Angeles, CA 90048-1865 (e-mail: chenp{at}cshs.org )