title: Effects of procainamide on wave-front dynamics during ventricular fibrillation in open-chest dogs.
abstract: BACKGROUND
  There is increasing evidence that both functional reentrant wave fronts and multiple wavelets are present during ventricular fibrillation (VF). However, the effects of procainamide on the characteristics of activation waves during VF are poorly understood.
  
  
  RESULTS
  Seven dogs were studied; six underwent subendocardial chemical ablation procedures. A plaque with 317 to 480 bipolar electrodes was sutured to the right ventricular free wall, and the patterns of activation were registered with a computerized mapping system. VF was electrically induced, and the patterns of activation were registered at baseline and during procainamide infusion (serum concentration, 9.3+/-1.9 microg/mL). Among the six dogs that had their subendocardium ablated, reentrant wave fronts were present in 6 of the 108 runs of VF at baseline and in 6 of the 100 runs of VF during procainamide infusion. By analyzing the wave fronts, we found that the cycle length, refractory period, conduction velocity, and wavelength at baseline were 101+/-9 ms, 54+/-5 ms, 0.93+/-0.21 mm/ms, and 51+/-16 mm, respectively, and during procainamide infusion, values became 125+/-11 ms (P<.001), 119+/-7 ms (P<.001), 0.42+/-0.02 mm/ms (P<.001), and 50+/-4 mm (P=.8), respectively. The vast majority of the activation waves do not form organized reentry. These activation waves broke up more frequently at baseline than during procainamide administration. The number of activation waves was 7.25+/-1.39 s(-1) x cm(-2) at baseline and 4.45+/-1.80 s(-1) x cm(-2) during procainamide administration (P<.001). The dog without subendocardial ablation had similar results.
  
  
  CONCLUSIONS
  Procainamide decreases the number of wavelets during VF by preventing spontaneous wave breaks. This represents a novel mechanism of antiarrhythmic drug action.
authors.affiliation: Department of Medicine, Cedars-Sinai Medical Center and University of California, Los Angeles, School of Medicine, 90048, USA.
authors.forename: Y Y
authors.initials: YY
authors.lastname: Kwan
authors.forename: W
authors.initials: W
authors.lastname: Fan
authors.forename: D
authors.initials: D
authors.lastname: Hough
authors.forename: J J
authors.initials: JJ
authors.lastname: Lee
authors.forename: M C
authors.initials: MC
authors.lastname: Fishbein
authors.forename: H S
authors.initials: HS
authors.lastname: Karagueuzian
authors.forename: P S
authors.initials: PS
authors.lastname: Chen
mesh_terms: D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology* / Q000627:therapeutic use; D002304:Cardiac Pacing, Artificial; D004285:Dogs; D004554:Electric Countershock; D004562:Electrocardiography; D006329:Heart Conduction System / Q000187:drug effects*; D006352:Heart Ventricles / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D011342:Procainamide / Q000494:pharmacology* / Q000627:therapeutic use; D014693:Ventricular Fibrillation / Q000188:drug therapy / Q000503:physiopathology* / Q000628:therapy
chemical_list: D000889:Anti-Arrhythmia Agents; D011342:Procainamide