Author + information
- Received August 20, 1999
- Revision received July 6, 2000
- Accepted August 18, 2000
- Published online December 1, 2000.
- Claudio Pandozi, MDa,* (, )
- Leopoldo Bianconi, MDa,
- Leonardo Calò, MDa,
- Antonio Castro, MDa,
- Filippo Lamberti, MDa,
- Maria Carmela Scianaro, MDa,
- Giuseppe Gentilucci, MDa and
- Massimo Santini, MDa
- ↵*Reprint requests and correspondence: Dr. Claudio Pandozi, Via Madonna di Fatima 24, 00147 Rome, Italy
The aim of our study was to verify the effect of oral administration of verapamil on atrial electrophysiologic characteristics after cardioversion of persistent atrial fibrillation (AF) in humans.
Discordant findings have been reported regarding the efficacy of verapamil in preventing the electrical remodeling induced by AF.
We determined the effective refractory periods (ERPs) at five pacing cycle lengths (300 to 700 ms) and in five right atrial sites after internal cardioversion of persistent AF (mean duration 238.1 ± 305.9 days) in 19 patients. Nine patients received oral verapamil (240 mg/day) starting four weeks before the electrophysiologic study, whereas the other 10 patients were in pharmacologic washout.
The mean ERPs were 202.0 ± 22.7 ms in the washout group and 189.3 ± 18.5 ms in the verapamil group (p < 0.0001). The degree of adaptation of refractoriness to rate was similar in the two groups (mean slope value in the washout group and verapamil group: 0.07 ± 0.03 and 0.08 ± 0.05, respectively), showing a normal or nearly normal adaptation to rate in the majority of the paced sites in both groups. The mean ERP was slightly longer in the septum than in the lateral wall and in the roof, both in the washout and verapamil groups.
In patients with persistent AF, long-term administration of verapamil before internal cardioversion resulted in 1) shortening of atrial ERPs; 2) no change in refractoriness dispersion within the right atrium; and 3) no change in atrial ERP adaptation to rate.
- Received August 20, 1999.
- Revision received July 6, 2000.
- Accepted August 18, 2000.
- American College of Cardiology