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RANOLAZINE FACILITATES ELECTRICAL CARDIOVERSION IN CARDIOVERSION RESISTANT PATIENTS
A2.E11 JACC March 9, 2010 Volume 55, issue 10A
CARDIAC ARRHYTHMIAS RANOLAZINE FACILITATES ELECTRICAL CARDIOVERSION IN CARDIOVERSION RESISTANT PATIENTS ACC Poster Contributions Georgia World Congress Center, Hall B5 Sunday, March 14, 2010, 9:30 a.m.-10:30 a.m.
Session Title: Clinical Electrophysiology--Supraventricular Arrhythmias Abstract Category: Clinical Electrophysiology--Supraventricular Arrhythmias Presentation Number: 1023-120 Authors: David K. Murdock, Jeffrey W. Kaliebe, Mary Kersten, German Larrain, Cardiovascular Associates of Northern Wisconsin, S.C., Wausau, WI, CaRE Foundation, Inc., Wausau, WI Background: Electrical cardioversion (ECV) is the most effective means of terminating atrial fibrillation (AF). Occasionally AF is resistant to ECV due to complete inability to restore sinus rhythm or to rapid relapse into AF within a few seconds of cardioversion. The mechanism of cardioversion resistance is unknown, but rapidly discharging foci from pulmonary venoatrial junctions has been suggested as a potential cause. Triggered activity from after-depolarizations may serve as the mediator of the arrhythmogenic activity. Ranolazine is an anti-anginal agent, which inhibits abnormal late Na+ channel currents in cardiomyocytes and decreases sodium-calcium overload. Ranolazine is a potent inhibitor of after-depolarizations and triggered activity. Ranolazine has been shown to have beneficial effects in AF and has no known pro-arrhythmic effects. We postulated ranolazine could facilitate ECV in patients resistant to ECV. Methods: Fifteen patients were administered 2,000 mg of oral ranolazine shortly after failing attempted ECV. An anterior-posterior approach was used and up to the maximum output of a biphasic cardioversion device employed. Repeat ECV was planned for 3.5-4 hours later using the same device, sedation, and lead placement. The duration of AF (less than 3 months or duration unknown) was noted. Results: Three patients spontaneously converted to sinus rhythm after oral ranolazine, but before the second attempt at ECV. Each of these patients had AF of less than 48 hours duration. Of the 12 undergoing another attempt at ECV, 8 were successfully converted to sinus rhythm. Each of the 4 patients refractory to repeat ECV despite ranolazine had AF of unknown duration and is now in chronic AF. No adverse effects were noted. Conclusion: Ranolazine shows promise as a safe and convenient agent to facilitate ECV in ECV resistant patients. It appears to be most effective in patients who are in AF known to be less than 3 months in duration.
CARDIAC ARRHYTHMIAS RANOLAZINE FACILITATES ELECTRICAL CARDIOVERSION IN CARDIOVERSION RESISTANT PATIENTS ACC Poster Contributions Georgia World Congress Center, Hall B5 Sunday, March 14, 2010, 9:30 a.m.-10:30 a.m.
Session Title: Clinical Electrophysiology--Supraventricular Arrhythmias Abstract Category: Clinical Electrophysiology--Supraventricular Arrhythmias Presentation Number: 1023-120 Authors: David K. Murdock, Jeffrey W. Kaliebe, Mary Kersten, German Larrain, Cardiovascular Associates of Northern Wisconsin, S.C., Wausau, WI, CaRE Foundation, Inc., Wausau, WI Background: Electrical cardioversion (ECV) is the most effective means of terminating atrial fibrillation (AF). Occasionally AF is resistant to ECV due to complete inability to restore sinus rhythm or to rapid relapse into AF within a few seconds of cardioversion. The mechanism of cardioversion resistance is unknown, but rapidly discharging foci from pulmonary venoatrial junctions has been suggested as a potential cause. Triggered activity from after-depolarizations may serve as the mediator of the arrhythmogenic activity. Ranolazine is an anti-anginal agent, which inhibits abnormal late Na+ channel currents in cardiomyocytes and decreases sodium-calcium overload. Ranolazine is a potent inhibitor of after-depolarizations and triggered activity. Ranolazine has been shown to have beneficial effects in AF and has no known pro-arrhythmic effects. We postulated ranolazine could facilitate ECV in patients resistant to ECV. Methods: Fifteen patients were administered 2,000 mg of oral ranolazine shortly after failing attempted ECV. An anterior-posterior approach was used and up to the maximum output of a biphasic cardioversion device employed. Repeat ECV was planned for 3.5-4 hours later using the same device, sedation, and lead placement. The duration of AF (less than 3 months or duration unknown) was noted. Results: Three patients spontaneously converted to sinus rhythm after oral ranolazine, but before the second attempt at ECV. Each of these patients had AF of less than 48 hours duration. Of the 12 undergoing another attempt at ECV, 8 were successfully converted to sinus rhythm. Each of the 4 patients refractory to repeat ECV despite ranolazine had AF of unknown duration and is now in chronic AF. No adverse effects were noted. Conclusion: Ranolazine shows promise as a safe and convenient agent to facilitate ECV in ECV resistant patients. It appears to be most effective in patients who are in AF known to be less than 3 months in duration.