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Published on: July 29, 2011
Increased dispersion and shortened refractoriness caused by verapamil in chronic atrial fibrillation
H Ramanna1, A Elvan, F H Wittkampf
1Heart-Lung Institute, University Medical Center, Utrecht, Netherlands.
Insights
Verapamil shortened refractoriness but increased spatial dispersion in patients with chronic atrial fibrillation (AF). These findings suggest verapamil is not effective for reversing AF remodeling.
Area of Science:
- Cardiology
- Electrophysiology
- Pharmacology
Background:
- Previous research indicated verapamil may prevent acute atrial fibrillation (AF) remodeling.
- The impact of verapamil on chronic AF remodeling remained uninvestigated.
Purpose of the Study:
- To evaluate verapamil's effects on atrial fibrillation cycle length.
- To assess verapamil's impact on spatial dispersion of refractoriness in chronic AF patients.
Main Methods:
- Electrophysiologic studies were conducted on 15 patients with chronic AF (>1 year).
- Unipolar electrograms and monophasic action potentials were recorded.
- Refractoriness and its spatial dispersion were measured before and after verapamil administration.
Main Results:
- Verapamil significantly shortened mean fibrillatory intervals across multiple atrial sites.
- Monophasic action potential duration decreased post-verapamil.
- A significant increase in spatial dispersion of refractoriness was observed.
Conclusions:
- Verapamil administration led to shortened refractoriness and increased spatial dispersion in chronic AF.
- These results indicate verapamil is unlikely to be beneficial in reversing AF remodeling.
Objectives:
The objective was to assess the effect ofverapamil on atrial fibrillation (AF) cycle length and spatial dispersion of refractoriness in patients with chronic AF.
Background:
Previous studies have suggested that verapamil prevents acute remodeling by AF. The effects of verapamil in chronic AF are unknown.
Methods:
During electrophysiologic study in 15 patients with chronic AF (duration >1 year), 12 unipolar electrograms were recorded from right atrial free wall, right atrial appendage and coronary sinus, along with monophasic action potential recordings from the right atrial appendage. The mean fibrillatory interval at each atrial recording site was used as an index for local refractoriness. Dispersion of refractoriness was calculated as the standard deviation of all local mean fibrillatory intervals expressed as a percentage of the overall mean fibrillatory interval. After baseline measurements, verapamil (0.075 mg/kg intravenous in 10 min) was infused and the measurements were repeated.
Results:
After administration ofverapamil, mean fibrillatory intervals shortened by a mean of 16.6 +/- 3.3 ms (p < 0.001) at the right free wall, 15.0 +/- 3.5 ms (p < 0.001) at the appendage and 17.1 +/- 3.2 ms (p < 0.01) in the coronary sinus. Monophasic action potential duration decreased by 15.9 +/- 4.0 ms (p < 0.01). Dispersion of refractoriness increased in all patients from 3.8 +/- 0.8 to 5.1 +/- 1.8 (p < 0.001). A strong correlation between mean fibrillatory intervals and action potential duration was found, both before and after verapamil.
Conclusions:
Verapamil caused shortening of refractoriness and increase in spatial dispersion of refractoriness in patients with chronic AF. This implies that verapamil is not useful in reversing the remodeling process in these patients.
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