title: Alteration of ventricular fibrillation by flecainide, verapamil, and sotalol: an experimental study.
abstract: BACKGROUND
  The purpose of this study was to determine whether the myocardial electrophysiological properties are useful for predicting changes in the ventricular fibrillatory pattern.
  
  
  RESULTS
  Thirty-two Langendorff-perfused rabbit hearts were used to record ventricular fibrillatory activity with an epicardial multiple electrode. Under control conditions and after flecainide, verapamil, or d,l-sotalol, the dominant frequency (FrD), type of activation maps, conduction velocity, functional refractory period, and wavelength (WL) of excitation were determined during ventricular fibrillation (VF). Flecainide (1.9+/-0.3 versus 2.4+/-0.6 cm, P<0. 05) and sotalol (2.1+/-0.3 versus 2.5+/-0.5 cm, P<0.05) prolonged WL and diminished FrD during VF, whereas verapamil (2.0+/-0.2 versus 1. 7+/-0.2 cm, P<0.001) shortened WL and increased FrD. Simple linear regression revealed an inverse relation between FrD and the functional refractory period (r=0.66, P<0.0001), a direct relation with respect to conduction velocity (r=0.33, P<0.01), and an inverse relation with respect to WL estimated during VF (r=0.49, P<0.0001). By stepwise multiple regression, the functional refractory periods were the only predictors of FrD. Flecainide and sotalol increased the circuit size of the reentrant activations, whereas verapamil decreased it. The 3 drugs significantly reduced the percentages of more complex activation maps during VF.
  
  
  CONCLUSIONS
  The activation frequency is inversely related to WL during VF, although a closer relation is observed with the functional refractory period. Despite the diverging effects of verapamil versus flecainide and sotalol on the activation frequency, WL, and size of the reentrant circuits, all 3 drugs reduce activation pattern complexity during VF.
authors.affiliation: Service of Cardiology, Valencia University Clinic Hospital, Valencia University, Valencia, Spain.
authors.forename: F J
authors.initials: FJ
authors.lastname: Chorro
authors.forename: J
authors.initials: J
authors.lastname: Cánoves
authors.forename: J
authors.initials: J
authors.lastname: Guerrero
authors.forename: L
authors.initials: L
authors.lastname: Mainar
authors.forename: J
authors.initials: J
authors.lastname: Sanchis
authors.forename: L
authors.initials: L
authors.lastname: Such
authors.forename: V
authors.initials: V
authors.lastname: López-Merino
mesh_terms: D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D002304:Cardiac Pacing, Artificial; D004594:Electrophysiology; D005424:Flecainide / Q000627:therapeutic use*; D006329:Heart Conduction System / Q000503:physiopathology; D011817:Rabbits; D012032:Refractory Period, Electrophysiological; D013015:Sotalol / Q000627:therapeutic use*; D014693:Ventricular Fibrillation / Q000188:drug therapy* / Q000503:physiopathology; D014700:Verapamil / Q000627:therapeutic use*
chemical_list: D000889:Anti-Arrhythmia Agents; D013015:Sotalol; D014700:Verapamil; D005424:Flecainide