Flecainide reduced PVC burden by 80.1% in patients with prior beta-blocker therapy compared to 69.0% in beta-blocker-naive patients (p=0.029).
Cohort (n=88)
Does slow-release flecainide reduce PVC burden in patients with idiopathic PVCs and prior beta-blocker failure compared to beta-blocker-naïve patients?
Flecainide provides substantial and safe PVC suppression in patients with idiopathic PVCs without structural heart disease, particularly those who have failed prior beta-blocker therapy.
Absolute Event Rate: 80.1% vs 69%
p-value: p=0.029
Abstract Background Persistent high-burden of premature ventricular contractions (PVCs) is associated with an increased risk of PVC-induced cardiomyopathy. β-blockers are recommended as first-line pharmacologic therapy in the current ESC guidelines; however, their efficacy is frequently limited. Flecainide, a class IC antiarrhythmic agent, is indicated (Class IIa) in selected patients without structural heart disease and may offer superior suppression in cases of β-blocker failure. Purpose To assess the efficacy of flecainide in patients with high PVC burden and prior β-blocker therapy, and to compare outcomes with β-blocker–naïve patients, as well as evaluate whether concomitant β-blocker use influences therapeutic response. Methods This subanalysis included patients with idiopathic PVCs enrolled in the prospective UNIFLECA study. All had a PVC burden ≥5% on two Holter recordings, no evidence of structural or coronary heart disease and declined catheter ablation. Slow-release Flecainide (100,150,200 mg/day) was administered, and follow-up 24-hour Holter monitoring was performed at one and 6 month. Patients were categorized by prior β-blocker exposure and by concomitant β-blocker use during therapy. Response was defined as a ≥80% or ≥90% reduction in PVC burden. Results Among patients with prior β-blocker therapy (n=32), flecainide reduced PVC burden by 80.1% on average; 71.9% achieved ≥80% and 65.6%, ≥90% reduction, respectively. In β-blocker-naïve patients (n=56), mean reduction was 69.0%, with 60.7% and 53.6% meeting ≥80% and ≥90% thresholds. The mean reduction was greater after prior β-blocker therapy (p=0.029). Failed use of β-blocker prior to flecainide treatment initiation is associated with increased PVC burden. Concomitant β-blocker during flecainide (n=4) was associated with a 49.8% mean reduction with no apparent advantage. No major adverse events occurred. Conclusions Flecainide achieved substantial PVC suppression after β-blocker failure, independent of concomitant β-blockade. These results support flecainide as a safe and effective therapeutic option when β-blockers are insufficient in patients declining catheter ablation.Flecainide with b-blockade response
Kotoulas et al. (Mon,) conducted a cohort in High premature ventricular contractions (PVC) burden (n=88). Flecainide in patients with prior beta-blocker therapy vs. Flecainide in beta-blocker-naive patients was evaluated on Mean reduction in PVC burden (p=0.029). Flecainide reduced PVC burden by 80.1% in patients with prior beta-blocker therapy compared to 69.0% in beta-blocker-naive patients (p=0.029).