Fractionation of Electrograms and Linking of Activation During Pharmacologic Cardioversion of Persistent Atrial Fibrillation in the Goat

• Published in: Journal of cardiovascular electrophysiology 2004-05, Vol.15 (5), p.572-580
• Main Authors: SHAN, ZHAOLIANG, VAN DER VOORT, PEPIJN H., BLAAUW, YURI, DUYTSCHAEVER, MATTIAS, ALLESSIE, MAURITS A.
• Format: Article
• Language: English
• Subjects: Animals; Anti-Arrhythmia Agents - administration & dosage; antiarrhythmic drugs; atrial fibrillation; Atrial Fibrillation - drug therapy; Atrial Fibrillation - physiopathology; Body Surface Potential Mapping - drug effects; cardioversion; fractionated electrograms; Goats; Heart Atria - drug effects; Heart Atria - physiopathology; Heart Conduction System - drug effects; Heart Conduction System - physiopathology; Imidazoles - administration & dosage; Infusions, Intravenous; mapping
• ISSN: 1045-3873; 1540-8167
• DOI: 10.1046/j.1540-8167.2004.03402.x

Introduction: During atrial fibrillation (AF), there is fractionation of extracellular potentials due to head‐to‐tail interaction and slow conduction of fibrillation waves. We hypothesized that slowing of the rate of AF by infusion of a Class I drug would increase the degree of organization of AF. Methods and Results: Seven goats were instrumented with 83 epicardial electrodes on the left atrium, left atrial appendage, Bachmann's bundle, right atrium, and right atrial appendage. AF was induced and maintained by an automatic atrial fibrillator. After AF had persisted for 4 weeks, the Class IC drug cibenzoline was infused at a rate of 0.1 mg/kg/min. AF cycle length (AFCL), the percentage of fractionated potentials, conduction velocity (CV), and direction of propagation of the fibrillation waves were measured during baseline, after AFCL was increased by 20, 40, 60, and 80 ms, and shortly before cardioversion. Infusion of cibenzoline increased the mean of the median AFCLs from 96 ± 6 ms to 207 ± 43 ms (P < 0.0001). The temporal variation in AFCL in different parts of the atria was 8% to 20% during control and, with the exception of Bachmann's bundle, was not significantly reduced during cibenzoline infusion. CV decreased from 76 ± 14 ms to 52 ± 9 cm/s (P < 0.01). Cibenzoline increased the percentage of single potentials from 81%± 4% to 91%± 4% (P < 0.01) and decreased the incidence of double potentials from 14%± 4% to 7 ± 5% (P < 0.01) and multiple potentials from 5%±% to 1%± 2% (P < 0.001). Whereas during control, linking (consecutive waves propagating in the same direction) during seven or more beats occurred in 9%± 15% of the cycles, after cibenzoline the degree of linking had increased to 40%± 33% (P < 0.05). During the last two beats before cardioversion, there was a sudden prolongation in AFCL from 209 ± 37 ms to 284 ± 92 ms (P < 0.01) and a strong reduction in fractionated potentials (from 22%± 12% to 6%± 5%, P < 0.05). Conclusion: The Class IC drug cibenzoline causes a decrease in fractionation of fibrillation electrograms and an increase in the degree of linking during AF. This supports the observation that Class I drugs widen the excitable gap during AF. (J Cardiovasc Electrophysiol, Vol. 15, pp. 572‐580, May 2004)