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Effects of procainamide on the excitable gap composition in common human atrial flutter
E Jalil1, P Le Franc, R Lebeau
1Research Center Hôpital du Sacré-Coeur de Montréal, Québec, Canada.
Pacing and Clinical Electrophysiology : PACE
|April 29, 1998
Summary
Procainamide prolonged atrial flutter cycle length and refractoriness but did not alter the excitable gap proportion. The persistent excitable tissue explains procainamide
Area of Science:
- Electrophysiology
- Cardiac Arrhythmias
- Pharmacology
Background:
- Common atrial flutter (AF1) is a significant arrhythmia.
- Understanding the electrophysiological properties of AF1 is crucial for developing effective treatments.
- The role of the excitable gap (EG) in AF1 maintenance and termination is an area of ongoing research.
Purpose of the Study:
- To determine the composition of the excitable gap (EG) in common atrial flutter (AF1) before and during procainamide (PA) infusion.
- To investigate the electrophysiological effects of procainamide on AF1 maintenance.
- To elucidate the mechanisms underlying procainamide's efficacy or inefficacy in terminating AF1.
Main Methods:
- Utilized a quadripolar electrode catheter to assess EG in 9 AF1 patients.
- Introduced premature stimuli to determine the atrial effective refractory period (ERP) and reset-response curves (RRC).
- Administered procainamide (15 mg/kg) and repeated electrophysiological measurements to evaluate its effects.
Main Results:
- Procainamide significantly prolonged AF1 cycle length (CL) and ERP.
- The absolute duration of the excitable gap (EG) increased with procainamide, but its proportion of the AF1 CL remained unchanged.
- Procainamide did not alter the duration of the fully excitable tissue within the EG.
Conclusions:
- Procainamide prolongs AF1 cycle length and refractoriness but does not terminate the arrhythmia.
- The persistence of fully excitable tissue at the wavefront's leading edge, despite procainamide, likely explains its limited efficacy in acute AF1 termination.
- These findings highlight the importance of the excitable gap's composition in guiding antiarrhythmic drug therapy for atrial flutter.