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

• Published in: Journal of the American College of Cardiology 2001-04, Vol.37 (5), p.1403-1407
• Main Authors: Ramanna, Hemanth, Elvan, Arif, Wittkampf, Fred H.M, de Bakker, Jacques M.T, Hauer, Richard N.W, Robles de Medina, Etienne O
• Format: Article
• Language: English
• Subjects: Aged; Antiarythmic agents; Atrial Fibrillation - drug therapy; Atrial Fibrillation - physiopathology; Biological and medical sciences; Cardiovascular system; Chronic Disease; Electrocardiography - drug effects; Female; Heart Atria - drug effects; Heart Atria - physiopathology; Humans; Infusions, Intravenous; Male; Medical sciences; Middle Aged; Pharmacology. Drug treatments; Treatment Failure; Verapamil - adverse effects; Verapamil - therapeutic use
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/S0735-1097(01)01132-9

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.