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

Hemanth Ramanna, MD^a, Arif Elvan, MD^a, Fred H. M. Wittkampf, PhD^a, Jacques M. T. de Bakker, PhD, Richard N. W. Hauer, MD^a and Etienne O. Robles de Medina, MD, FACC^a

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

View larger version (45K): [in a new window]   Figure 1 Electrogram recordings before (left) and after (right) verapamil administration. The electrograms from the decapolar catheter at the right atrial free wall are designated E1 to E10; those from the coronary sinus CS1 to CS4 and the monophasic action potential recording MAP. The mean fibrillatory interval shortened at each recording site. The signal quality in E1 was inadequate for measurement of fibrillatory intervals. This recording site was excluded from the analysis.

View larger version (15K): [in a new window]   Figure 2 Histograms of fibrillatory intervals before and after verapamil administration at a single atrial recording site. The administration of verapamil caused shortening of fibrillatory intervals without changing the distribution of these fibrillatory intervals. Black bar = control; white bar = verapamil.

View larger version (11K): [in a new window]   Figure 3 Mean fibrillatory interval and action potential duration (APD90) were measured in the right atrial appendage in seven patients. For each of these patients, mean fibrillatory interval (x-axis) and APD90 (y-axis) are plotted both before (black boxes) and after (white boxes) verapamil. Both mean fibrillatory intervals as well as APD90 shortened significantly in each patient. The relationship between mean fibrillatory interval and APD90 is linear both before and after verapamil administration, and the relationship between both parameters remains unchanged.