Propafenone to Prevent AF Induction During Ablation

Exploratory findings have suggested that ryanodine receptor-driven intracellular calcium leak is a mediator of atrial fibrillation. In a study led by co-first authors, M. Benjamin Shoemaker and Zachary T. Yonenda, researchers investigated whether (R)-propafenone, an antiarrhythmic drug and ryanodine receptor inhibitor, was effective at preventing atrial fibrillation induction during ablation procedures when compared with (S)-propafenone or placebo.

The study’s authors found that there was no difference in atrial fibrillation induction between (R)-propafenone and (S)-propafenone, though they added that their conclusions were subject to limitations. Their results were published in Circulation: Arrhythmia and Electrophysiology.

Propafenone Enantiomers Show Similar Atrial Fibrillation Induction Prevention

The study enrolled 193 patients with atrial fibrillation referred for ablation, of which 165 (median years of age, 63; 58% male, 95% paroxysmal atrial fibrillation) completed the trial. The cohort was randomized 4:4:1 to a single intravenous dose of (R)-propafenone, (S)-propafenone, or placebo administered at the start of ablation procedures with atrial fibrillation induction using rapid atrial pacing. The primary end point of the study was incidence of 30 seconds of atrial fibrillation or atrial flutter.

According to the report, sustained atrial fibrillation and atrial flutter episodes were observed in 60 (80.0%) patients in the (R)-propafenone group, 60 (80.0%) in the (S)-propafenone group, and 12 (63.2%) in the placebo group. Notably, atrial flutter was reported significantly more often in the (R)- (n=23; 32.4%) and (S)-propafenone (n=26; 34.7%) groups compared with placebo (n=1; 5.3%; P=.029)

Overall, the researchers did not find any significant differences in the primary atrial fibrillation and atrial flutter outcomes between the (R)- and (S)-propafenone groups in both univariable (P=.522) and multivariable analysis adjusted for age and serum drug level (P=.199).

The authors ultimately summarized that “there is no difference in AF inducibility between (R)- and (S)-propafenone at clinically relevant concentrations.” They did acknowledge that the results were “confounded by a high rate of inducible atrial flutter due to sodium-channel blockade.”

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