Abstract 2849: Verapamil Remodels Paroxysmal Atrial Fibrillation via Acceleration of Fibrillatory Frequency in the Atria and Elimination of Pulmonary Vein-to-Atrial Frequency Gradient
Background: Growing evidence suggests that high-frequency excitation in the pulmonary vein (PV) plays a crucial role in the maintenance of paroxysmal atrial fibrillation (PAF), showing the presence of a PV-to-atrial frequency gradient during PAF. Verapamil (VER), a blocker of L-type Ca2+channel, is commonly used to control ventricular response during AF; however, previous studies have demonstrated that this drug promotes the sustenance of PAF. We hypothesized that VER might produce this adverse effect through the acceleration of excitation frequencies in the PVs, enhancing the PV-to-atrial frequency gradient.
Methods: The present study included 25 patients with PAF. Bipolar electrograms were recorded simultaneously during AF from the right atrial free wall (RAFW), coronary sinus (CS) and three PVs in 11 patients (Group I) or two PVs and the left atrial appendage (LAA) in the remaining 14 (Group II). Dominant frequency (DF) for each recording site was obtained by FFT analysis of the bipolar signals. After the baseline recordings, VER was administered as a bolus of 0.1 mg/kg over 5 min.
Results: At baseline, highest DF among the 3 PVs (Group I) or 2 PVs (Group II) (PV-DFmax) was higher than the DF in the RAFW (P<0.05), CS (P<0.0001), or LAA (P<0.001). No significant differences were recognized in the DFs among the 3 atrial regions. VER increased the DF in the RAFW (P<0.0001), CS (P<0.0001), and LAA (P<0.0001), whereas PV-DFmax was unaffected (P=0.11). VER-induced increase in the atrial DF was highest in the LAA, intermediate in the CS, and lowest in the RAFW (Table⇓). PV-to-atrial DF gradient was decreased from 0.6±0.8 to 0.1±0.8 Hz (P<0.0001) in the RAFW, from 1.0±0.8 to 0.4±0.7 Hz (P<0.0001) in the CS, and from 0.6±0.7 to −0.5±0.9 Hz (P<0.0001) in the LAA after VER.
Conclusion: Contrary to our expectation, VER accelerated PAF through the increase in fibrillatory frequency in the atria, but not in the PV, eliminating the PV-to-atrial DF gradient as observed in persistent AF.