Flecainide acetate caused exit conduction slowing and block between transitional and atrial muscle fibers in isolated rabbit tricuspid valves, with little direct effect on ectopic atrial automaticity.
Does flecainide alter ectopic atrial automaticity and conduction in isolated rabbit tricuspid valves?
Flecainide suppresses ectopic atrial rhythms primarily by causing exit conduction block between transitional and atrial muscle fibers due to decreased atrial excitability, rather than directly affecting automaticity.
BACKGROUND: Previous studies have shown that class Ic antiarrhythmic agents are effective in suppressing ectopic atrial rhythms and accessory pathway conduction. METHODS AND RESULTS: To explore the potential mechanisms for their effectiveness, we investigated the concentration-dependent effects of the Ic agent flecainide acetate (0.5 to 10 micrograms/mL) on atrial ectopic automaticity and exit conduction in isolated rabbit tricuspid valves. This experimental model consists of three major cell types as defined anatomically and by intracellular recordings: pacemaker, transitional, and working atrial muscle. Simultaneous recordings from these cell types before and during flecainide superfusion (n = 7) showed that the drug produced a slight, concentration-dependent slowing of pacemaker-transitional conduction but elicited third-degree transitional-working atrial muscle block in six of seven preparations at 10 micrograms/mL. Flecainide caused a significant dose-dependent reduction in the initial phase of diastolic depolarization of pacemaker cells but produced only a small, biphasic change in spontaneous pacemaker cycle length. It also caused a significant prolongation in action potential duration in pacemaker and transitional cells and reduction in upstroke velocity in atrial cells. Of note in four additional preparations, flecainide caused a concentration-dependent upward shift in the strength-duration curve for atrial fibers. CONCLUSIONS: These data suggest that flecainide has little direct effect on ectopic atrial automaticity but rather causes exit conduction slowing and block between transitional and atrial muscle fibers. The mechanism for the induction of block is likely due to a decrease in atrial excitability creating a greater electrical load on generated impulses.
Windle et al. (1993) studied Ectopic atrial automaticity and conduction (n=11). Flecainide acetate vs. Baseline (before flecainide superfusion) was evaluated on Atrial ectopic automaticity and exit conduction. Flecainide acetate caused exit conduction slowing and block between transitional and atrial muscle fibers in isolated rabbit tricuspid valves, with little direct effect on ectopic atrial automaticity.