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

OBJECTIVES The objective was to assess the effect of verapamil on atrial fi brillation (AF) cycle length and spatial dispersion of refractoriness in pa tients with chronic AF. BACKGROUND Previous studies have suggested that verapamil prevents acute re modeling by AF. The effects of verapamil in chronic AF are unknown. METHODS During electrophysiologic study in 15 patients with chronic AF (dur ation >1 year), 12 unipolar electrograms were recorded from right atrial fr ee wall, right atrial appendage and coronary sinus, along with monophasic a ction potential recordings from the right atrial appendage. The mean fibril latory interval at each atrial recording site was used as an index for loca l refractoriness. Dispersion of refractoriness was calculated as the standa rd deviation of all local mean fibrillatory intervals expressed as a percen tage of the overall mean fibrillatory interval. After baseline measurements , verapamil (0.075 mg/kg intravenous in 10 min) was infused and the measure ments were repeated. RESULTS After administration of verapamil, mean fibrillatory intervals shor tened 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 patien ts from 3.8 +/- 0.8 to 5.1 +/- 1.8 (p < 0.001). A strong correlation betwee n mean fibrillatory intervals and action potential duration was found, both before and after verapamil. CONCLUSIONS Verapamil caused shortening of refractoriness and increase in s patial dispersion of refractoriness in patients with chronic AF. This impli es that verapamil is not useful in reversing the remodeling process in thes e patients. (J Am Coil Cardiol 2001;37:1403-7) (C) 2001 by the American Col lege of Cardiology.