Propranolol in polymorphic ventricular premature beats

Cornelia Scheurlen (Köln)1, J. Wörmann (Köln)1, J.-H. van den Bruck (Köln)1, K. Filipovic (Köln)1, S. C. R. Erlhöfer (Köln)1, S. Dittrich (Köln)1, J.-H. Schipper (Köln)1, F. Pavel (Köln)1, J. Ackmann (Köln)1, J. Lüker (Köln)1, D. Steven (Köln)1, A. Sultan (Köln)1

1Herzzentrum der Universität zu Köln Elektrophysiologie Köln, Deutschland

 

Background

Therapy of polymorphic premature ventricular contractions (pPVC) is sometimes challenging despite improved catheter ablation options especially in patients suffering from non-ischemic cardiomyopathy. Previous studies have proven the benefit of non-selective ß-blocker such as propranolol in the stetting of electrical storm. Data for the use of propranolol to treat pPVC is sparse.

Aim

We sought to analyze the potential benefit of propranolol in the setting of failed or only partially successful pPVC ablation.

Methods

This retrospective analysis included patients (pts) undergoing catheter ablation (CA) for pPVC or pPVC triggered ventricular tachycardia (VT) at our center between January and October 2023. If ablation was unsuccessful or not all PVCs were completely abolished oral propranolol was started after the procedure. Propranolol replaced selective ß-blocker in case of preexisting medication. The dosage was up titrated to 240mg/d if feasible. No other antiarrhythmic drug was administered simultaneously. Follow-up (FU) was conducted 3 months after ablation. During FU visit at least one 24-48h ecg was obtained to assess PVC burden.

Results

A total of 13 CA in the setting of pPVC with propranolol naive patients were performed (mean age 62.6±10.3 years, 10 pts (77%) male; all suffering from non-ischemic cardiomyopathy). The mean left ventricular ejection fraction (LVEF) was 46.6±14.6%. Five patients had previous catheter ablation. Site of ablation was: 2 left papillary muscle, 2 outflow tract (RVOT), 7 great cardiac vein/ left ventricluar summit, 1 moderator band and 1 lateral mitral valve annulus. In all cases only transient or moderate pPVC supression was achieved by CA.

After a median follow-up (FU) of 113.3±30.2 days a complete 3-month FU was obtained in 11 pts. The preprocedural mean VES burden of 14.0±7.7% was significantly reduced using propranolol to 4.2±7.7%; p=0.003 within three month after CA. No major propranolol complications occurred.

Conclusion

Data on the use of propranolol in the setting of pPVC is sparse. This analysis demonstrates for the first time a significant burden reduction of pPVC after starting propranolol in patients with failed or incomplete CA for pPVCs. Of note, although patients suffering from HFmrEf and HFrEF were included no clinical deterioration of preexisting heart failure was observed. Further comparative studies are needed.

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