The electrophysiologic determinants of the pharmacologic conversion and the prevention of
atrial flutter are poorly defined. This study investigated the effects of pharmacologically induced changes in atrial conduction velocity and refractoriness, in the conversion and suppression of
atrial flutter induced in the open-chest anesthetized dog by intercaval crush and rapid atrial pacing. The effects of an
intravenous infusion of the new class III
antiarrhythmic drug N-acetylprocainamide (30 mg/kg over 15 min) and the class Ic
antiarrhythmic drug recainam (10 mg/kg over 20 min followed by 10 mg/kg/h) were evaluated.
N-acetylprocainamide restored sinus rhythm in 10 of 15 (66%) dogs, while
recainam converted only 2 of 10 (20%).
N-acetylprocainamide prevented reinduction in 3 (20%), while
recainam was effective in none. In the atria,
N-acetylprocainamide induced significant increases in effective refractory period (+27%, p less than 0.01), functional refractory period (+22%, p less than 0.01), and in
atrial flutter cycle length (+13%, p less than 0.01).
Recainam increased effective refractory period (+28%, p less than 0.01), functional refractory period (+20%, p less than 0.01), conduction time at atrial paced cycle length of 150 msec (+70%, p less than 0.01) and
atrial flutter cycle length (+56%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)