Pilsicainide Hydrochloride Hydrate

Early recurrence of atrial tachyarrhythmia (ERAT) after ablation for atrial fibrillation (AF) is common during the blanking period; however, no standardized management approach exists. This study aimed to identify effective antiarrhythmic drugs (AADs) during the blanking period and to examine the association between AAD efficacy and long‐term outcomes.

Initially, 497 patients who underwent catheter ablation for AF between April 2017 and December 2022 were included. Among these, patients who experienced ERAT after their first AF ablation were analyzed for this retrospective study. During the blanking period, the effectiveness of three AAD regimens, pilsicainide, bepridil, and bepridil plus aprindine, was compared. Patients were followed for 2 years after AAD discontinuation and stratified according to late recurrence.

Among the 75 patients analyzed, ERAT was suppressed in 29.6% (8/27) with pilsicainide, 38.1% (8/21) with bepridil, and 77.8% (21/27) with bepridil plus aprindine ( p  = 0.0009). Among patients without late recurrence, ERAT suppression was higher with bepridil‐based regimens: pilsicainide, 27.8% (5/18); bepridil, 66.7% (6/9); and bepridil plus aprindine, 89.5% (17/19) ( p  = 0.0006). Poor response to bepridil‐based therapy was associated with a high late recurrence rate (73.7%, 14/19), whereas lack of response to pilsicainide was not (31.6%, 6/19) ( p  = 0.009).

Bepridil, particularly in combination with aprindine, was effective for managing ERAT after AF ablation. A poor response to bepridil or to bepridil plus aprindine during the blanking period may serve as a marker for identifying patients at higher risk of late recurrence.

Abnormal epicardial potentials in J wave syndrome predominantly involve the right ventricular outflow tract (RVOT), while left ventricular (LV) involvement remains less characterized and associates with increased ventricular fibrillation (VF) risk. We report a case demonstrating an inverted J wave in lead V1, suggesting LV posterior wall substrate rather than typical RVOT involvement.

A 19-year-old man with resuscitated VF received a subcutaneous implantable cardioverter-defibrillator (S-ICD). Despite cilostazol and quinidine therapy, he experienced five appropriate shocks within 6 months. Twelve-lead electrocardiography showed inferior J waves and a negative deflection in V1, suggesting an inverted J wave. Epicardial mapping showed fractionated potentials in both RVOT and LV posterior wall. Pilsicainide administration augmented RVOT potentials while attenuating those in the LV posterior wall. Spontaneous VF was triggered by premature ventricular contractions (PVCs) originating from the LV posterior wall, where prepotentials preceded QRS onset by 50 ms. Radiofrequency applications eliminated the PVCs, followed by anatomical ablation of RVOT fractionated regions. Subsequently, VF was never induced by program stimulation of up to triple extra stimuli. In the post-operative electrocardiogram, inverted J waves in the V1 lead disappeared. At 8 months post-ablation, the patient remained free from VF recurrence without antiarrhythmic medications, and no S-ICD therapies occurred.

This case demonstrates complex electrophysiological manifestations of J wave syndrome, with the inverted J wave in V1 potentially reflecting LV posterior wall substrate. Although the overlapping ablation procedure limited definitive attribution, these findings contribute to understanding the heterogeneous substrates in J wave syndrome.