Induction of atrial fibrillation in mice by rapid transesophageal atrial pacing

• Published in: Basic research in cardiology 2002-11, Vol.97 (6), p.452-460
• Main Authors: Schrickel, Jan Wilko, Bielik, Helga, Yang, Alexander, Schimpf, Rainer, Shlevkov, Nikolay, Burkhardt, Dietmar, Meyer, Rainer, Grohé, Christian, Fink, Klaus, Tiemann, Klaus, Lüderitz, Berndt, Lewalter, Thorsten
• Format: Article
• Language: English
• Subjects: Animals; Arrhythmias, Cardiac - etiology; Atrial Fibrillation - etiology; Atrial Fibrillation - physiopathology; Cardiac Pacing, Artificial; Electric Stimulation; Electrocardiography; Electrophysiology; Female; Heart Atria; Heart Rate; Male; Mice; Mice, Inbred C57BL; Reproducibility of Results
• ISSN: 0300-8428; 1435-1803
• DOI: 10.1007/s003950200052

Atrial fibrillation (AF) as an "indicator arrhythmia" for enhanced atrial vulnerability in mouse hearts has not yet been systematically examined. We therefore evaluated a transesophageal rapid atrial stimulation protocol for the induction of AF in C57Bl/6 mice. 40 C57Bl/6 mice (19 female and 21 male; 5.2 +/- 2.1 months; 18 - 27 g) were examined by closed chest transesophageal atrial stimulation. Baseline ECG and electrophysiological parameters, AF-inducing stimulation cycle length (CL) and AF duration were analyzed. The surface ECG demonstrated a significantly faster heart rate in female mice (R-R: 138.7 +/- 19.9 ms versus 150.5 +/- 15.7 ms, P < 0.05). AF was inducible in 90 % of the population and not inducible in 4 mice, all female (21 % in this subgroup). Mean induction CL was 27.4 +/- 7.3 ms. Mean AF duration was 26.9 +/- 42.6 s before spontaneous termination. In a subgroup of 4 female and 4 male mice (mean age 7.5 months), successive testing of AF induction showed a range of higher susceptibility to AF at stimulus amplitudes of 3.0 - 4.0 mA and stimulation CLs between 15 - 25 ms. AF induction was observed to be constantly reproducible in the individual animals. No correlation to pacing stimulus length and amplitude was found. This study demonstrates that it is possible to reproducibly induce self-terminating AF and supraventricular arrhythmias in mice by transesophageal atrial burst stimulation. The presented method allowing serial testings of the same animal can be a useful tool in further investigations with transgenic mice and might be helpful in the characterization of underlying genetic or molecular mechanisms of AF.