Key result
Propafenone linked to alternating ventricular preexcitation in WPW via prolonged accessory pathway refractory period.
Case Report (n=1)
Propafenone can cause alternating ventricular preexcitation in patients with Wolff-Parkinson-White syndrome by prolonging the antegrade refractory period of the accessory pathway.
May induce alternating preexcitation in WPW; hypothesis-generating and should not yet change practice.
A 45-year-old woman diagnosed with Wolff-Parkinson-White syndrome preferred treatment with propafenone rather than catheter ablation.A 12-lead electrocardiogram (Fig. 1) after the drug administration showed sinus arrhythmia; alternating ventricular preexcitation; and alternating T wave inversion in the inferior leads during normal AV conduction.Ventricular preexcitation may disappear because of decreased conduction delay over the AV node, relative to the accessory pathway; this was similar to that observed on vagal tone withdrawal.However, loss of ventricular preexcitation associated with decreased sinus cycle length was observed, which excluded the first possibility as a mechanism for intermittent preexcitation.The other mechanisms include prolongation of the refractory period (RP) of the accessory pathway (AP) due to increased vagal tone 1) and linking.Linking is defined as repetitive conduction over 1 of 2 potential pathways, with persistent conduction block in the other pathway maintained by concealed retrograde conduction.2)3) However, the alternating preexcitation cannot be attributed to linking and was most probably caused by prolongation of the antegrade RP of the AP by propafenone greater than sinus cycle length (Fig. 2).
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Kim et al. (2012) conducted a case report in Wolff-Parkinson-White syndrome (n=1). Propafenone was evaluated on Electrocardiographic changes. Propafenone administration in a patient with Wolff-Parkinson-White syndrome resulted in alternating ventricular preexcitation, likely caused by prolongation of the antegrade refractory period of the accessory pathway.
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