scholarly journals Linear Catheter Ablation of the Right Atrium for Rapid Atrial Pacing-Induced Sustained Atrial Fibrillation in Dogs

2012 ◽  
Vol 53 (6) ◽  
pp. 375-382 ◽  
Author(s):  
Ichiro Watanabe ◽  
Yasuo Okumura ◽  
Rikitake Kogawa ◽  
Naoko Sasaki ◽  
Kimie Ohkubo ◽  
...  
Circulation ◽  
2002 ◽  
Vol 106 (11) ◽  
pp. 1317-1320 ◽  
Author(s):  
Masahiko Goya ◽  
Feifan Ouyang ◽  
Sabine Ernst ◽  
Marius Volkmer ◽  
Matthias Antz ◽  
...  

2004 ◽  
Vol 287 (5) ◽  
pp. H2324-H2331 ◽  
Author(s):  
Ulrich Schotten ◽  
Sunniva de Haan ◽  
Hans-Ruprecht Neuberger ◽  
Sabine Eijsbouts ◽  
Yuri Blaauw ◽  
...  

Atrial fibrillation (AF) induces a progressive dilatation of the atria which in turn might promote the arrhythmia. The mechanism of atrial dilatation during AF is not known. To test the hypothesis that loss of atrial contractile function is a primary cause of atrial dilatation during the first days of AF, eight goats were chronically instrumented with epicardial electrodes, a pressure transducer in the right atrium, and piezoelectric crystals to measure right atrial diameter. AF was induced with the use of repetitive burst pacing. Atrial contractility was assessed during sinus rhythm, atrial pacing (160-, 300-, and 400-ms cycle length), and electrically induced AF. The compliance of the fibrillating right atrium was measured during unloading the atria with diuretics and loading with 1 liter of saline. All measurements were repeated after 6, 12, and 24 h of AF and then once a day during the first 5 days of AF. Recovery of the observed changes after spontaneous cardioversion was also studied. After 5 days of AF, atrial contractility during sinus rhythm or slow atrial pacing was greatly reduced. During rapid pacing (160 ms) or AF, the amplitude of the atrial pressure waves had declined to 20% of control. The compliance of the fibrillating atria increased twofold, whereas the right atrial pressure was unchanged. As a result, the mean right atrial diameter increased by ∼12%. All changes were reversible within 3 days of sinus rhythm. We conclude that atrial dilatation during the first days of AF is due to an increase in atrial compliance caused by loss of atrial contractility during AF. Atrial compliance and size are restored when atrial contractility recovers after cardioversion of AF.


2019 ◽  
Vol 30 (10) ◽  
pp. 1773-1785 ◽  
Author(s):  
Steven M. Markowitz ◽  
Daniel Y. Choi ◽  
Foysal Daian ◽  
Christopher F. Liu ◽  
Jim W. Cheung ◽  
...  

1994 ◽  
Vol 17 (10) ◽  
pp. 1610-1620 ◽  
Author(s):  
ERIK KONGSGAARD ◽  
ARNOLD FOERSTER ◽  
HALFDAN AASS ◽  
STEINAR MADSEN ◽  
JAN P. AMLIE

1987 ◽  
Vol 253 (4) ◽  
pp. H863-H868 ◽  
Author(s):  
D. E. Euler ◽  
P. J. Scanlon

This study was designed to evaluate the importance of local release of autonomic neuromediators when electrical stimuli are applied to the right atrium to measure the atrial fibrillation threshold (AFT). Experiments were performed in 16 open-chest dogs anesthetized with alpha-chloralose. The dogs were denervated by bilateral transection of the stellates and cervical vagi. The AFT was determined in 11 dogs by delivering either a train of stimuli (14 pulses, 4 ms, 100 Hz) or a single stimulus (10 ms) to the right atrium during its vulnerable period. In eight dogs, beta-adrenergic blockade with timolol (0.1 mg/kg) had no effect on the AFT determined with either method. Atropine (0.2 mg/kg), given after timolol, significantly increased the train-of-pulses AFT from 4.7 +/- 0.4 to 32.3 +/- 4.6 mA (P less than 0.001). The single-pulse AFT increased from 16.5 +/- 1.5 to 17.8 +/- 1.5 mA (P less than 0.05). Atropine had a similar effect on the AFT when it was given in the absence of timolol (n = 3). In five additional dogs, a monophasic action potential was recorded while a 10-mA train was delivered to the atrium during its absolute refractory period. There was marked shortening of the monophasic action potential duration (55 +/- 6 ms) in the first beat after the train. The shortening was totally abolished by atropine (0.2 mg/kg). The results suggest that a train of stimuli liberates local stores of acetylcholine, which cause a shortening of atrial repolarization time and a profound decrease in the current necessary to evoke fibrillation.


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