Effects of N-Acetylprocainamide and Recainam in the Pharmacologic Conversion and Suppression of Experimental Canine Atrial Flutter

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 < 0.01), functional refractory period (+22%, p < 0.01), and in atrial flutter cycle length (+13%, p < 0.01). Recainam increased effective refractory period (+28%, p < 0.01), functional refractory period (+20%, p < 0.01), conduction time at sinus cycle length (+50%, p < 0.01), conduction time at atrial paced cycle length of 150 msec (+ 70%, p < 0.01) and atrial flutter cycle length (+ 56%, p < 0.01). Conversion of atrial flutter correlated with the degree of drug-induced changes in atrial refractoriness; with N-acetylprocainamide the effective refractory period increased +30% versus +21% (p = NS), and the functional refractory period +25% versus +17% (p = NS), in converters compared with nonconverters and for recainam the effective refractory period increased + 46% versus +24% (p = NS) and the functional refractory period +43% versus + 14% (p < 0.05). A similar correlation was observed for reinducibility of atrial flutter; with N-acetylprocainamide the effective refractory period increased +51% versus +21%, and the functional refractory period +40% versus + 18% in those not reinducible compared with those reinducible (p < 0.01, respectively). In contrast, the lack of conversion or suppression of atrial flutter, correlated with greater increases in atrial flutter cycle length in those reinducible versus those not reinducible. It is concluded that selective prolongation of atrial refractoriness, rather than the depression of conduction and slowing of the tachycardia, is more likely to result in conversion and suppression of atrial flutter in this canine experimental model.