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J Am Coll Cardiol, 2001; 37:1403-1407
© 2001 by the American College of Cardiology Foundation
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CLINICAL STUDY

Increased dispersion and shortened refractoriness caused by verapamil in chronic atrial fibrillation

Hemanth Ramanna, MDa, Arif Elvan, MDa, Fred H. M. Wittkampf, PhDa, Jacques M. T. de Bakker, PhD{dagger}, Richard N. W. Hauer, MDa and Etienne O. Robles de Medina, MD, FACCa

a Heart-Lung Institute, University Medical Center, Utrecht, Netherlands
{dagger} Interuniversity Cardiology Institute of The Netherlands, Utrecht, Netherlands. ?1

Manuscript received May 4, 2000; revised manuscript received November 22, 2000, accepted December 21, 2000.

Reprint requests and correspondence: Dr. Hemanth Ramanna, Heart-Lung Institute, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, Netherlands

OBJECTIVES

The objective was to assess the effect of verapamil 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 of verapamil, 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.

Abbreviations and Acronyms
  AF = atrial fibrillation
  APD90 = monophasic action potential duration
  CS = coronary sinus




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