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Effects of class IA antiarrhythmic drugs on the reentrant circuit in common human atrial flutter
1First Department of Internal Medicine, Kobe University School of Medicine, Hyogo, Japan.
Insights
Class IA antiarrhythmic drugs aided rapid pacing to interrupt atrial flutter (AF) by causing conduction block in a slow conduction zone near the coronary sinus. This approach successfully restored normal sinus rhythm in most patients.
Area of Science:
- Cardiology
- Electrophysiology
- Pharmacology
Background:
- Atrial flutter (AF) is a common arrhythmia.
- A specific slow conduction zone near the coronary sinus orifice is implicated in AF maintenance.
- The efficacy of Class IA antiarrhythmic drugs in AF management requires further elucidation.
Purpose of the Study:
- To investigate the effect of Class IA antiarrhythmic drugs on a slow conduction zone in patients with atrial flutter.
- To determine if these drugs facilitate AF termination by rapid atrial pacing.
Main Methods:
- Nine patients with common atrial flutter underwent intravenous administration of Class IA antiarrhythmic drugs.
- Conduction velocity was assessed, particularly within the slow conduction zone.
- Rapid atrial pacing was employed to attempt AF termination.
Main Results:
- Class IA drugs suppressed conduction velocity but did not preferentially affect the slow conduction zone in most patients.
- AF was converted to sinus rhythm in only one patient with drug administration alone.
- Rapid atrial pacing successfully terminated AF in 8 patients, often following conduction block in the slow conduction zone.
Conclusions:
- Class IA antiarrhythmic drugs can facilitate AF interruption by rapid atrial pacing.
- This facilitation occurs through the induction of conduction block in the slow conduction zone.
- Targeting this specific zone may be a strategy for AF management.
Abstract:
In 9 patients with the common type of atrial flutter (AF), a zone of slow conduction was observed proximal to the coronary sinus orifice. Class IA antiarrhythmic drugs were administrated intravenously in all 9 patients. AF was converted to sinus rhythm in only 1 patient. In the remaining 8 patients, although IA drugs suppressed conduction velocity, this effect was not preferential with regard to the zone of slow conduction. Conversion of AF to sinus rhythm by rapid pacing was achieved in these 8 patients. At a critical pacing cycle length, AF was interrupted just after conduction block developed in the zone of slow conduction. A progressive decrease in conduction velocity was observed in the zone of slow conduction for several beats just before the onset of conduction block. In conclusion, class IA drugs facilitate the interruption of AF by rapid atrial pacing by inducing conduction block in the zone of slow conduction.