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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Effects of flecainide on ectopic atrial automaticity and conduction.

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.[1]


  1. Effects of flecainide on ectopic atrial automaticity and conduction. Windle, J.R., Witt, R.C., Rozanski, G.J. Circulation (1993) [Pubmed]
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