title: Determination of refractory periods and conduction velocity during atrial fibrillation using atrial capture in dogs: direct assessment of the wavelength and its modulation by a sodium channel blocker, pilsicainide.
abstract: OBJECTIVE
  The purposes of this study were to measure the atrial refractory period and the conduction velocity (CV) during atrial fibrillation (AF) and to explore the antiarrhythmic mechanism of a sodium channel blocker, pilsicainide, during AF.
  
  
  BACKGROUND
  Sodium channel blockers not only decrease the CV, but also prolong the atrial refractory period, particularly during rapid excitation. Because these effects on the wavelength are counteractive and rate dependent, it is critical to measure these parameters during AF.
  
  
  METHODS
  In eight dogs, after AF was induced under vagal stimulation, a single extra-stimulus was repeatedly introduced from the left atrium and its capture was statistically determined for each coupling interval. The local CV was also measured during constant capture of the fibrillating atrium by rapid pacing. The same procedure was repeated after pilsicainide administration.
  
  
  RESULTS
  Pilsicainide significantly increased the mode of AF intervals from 81 +/- 10 to 107 +/- 16 ms (p < 0.01). While the CV was decreased from 0.9 +/- 0.1 to 0.7 +/- 0.1 m/s (p < 0.02), the effective refractory period during AF was increased from 69 +/- 11 ms to 99 +/- 17 ms (p < 0.01). As a result, the wavelength was significantly increased by pilsicainide from 6.6 +/- 0.9 to 7.6 +/- 1.2 cm (p < 0.05).
  
  
  CONCLUSIONS
  During AF, whereas the sodium channel blocker pilsicainide decreases CV, it lengthens the wavelength by increasing the refractory period, an action that is likely to contribute to the drug's ability to terminate the arrhythmia. The direct measurement of refractoriness and CV during AF may provide new insights into the determinations of the arrhythmia and antiarrhythmic drug action.
authors.affiliation: Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Shinagawa
authors.forename: H
authors.initials: H
authors.lastname: Mitamura
authors.forename: A
authors.initials: A
authors.lastname: Takeshita
authors.forename: T
authors.initials: T
authors.lastname: Sato
authors.forename: H
authors.initials: H
authors.lastname: Kanki
authors.forename: S
authors.initials: S
authors.lastname: Takatsuki
authors.forename: S
authors.initials: S
authors.lastname: Ogawa
mesh_terms: D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D001281:Atrial Fibrillation / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D004285:Dogs; D004562:Electrocardiography / Q000187:drug effects; D005260:Female; D008012:Lidocaine / Q000031:analogs & derivatives / Q000494:pharmacology; D008297:Male; D012815:Signal Processing, Computer-Assisted; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology
chemical_list: D000889:Anti-Arrhythmia Agents; D015222:Sodium Channels; D008012:Lidocaine; C042288:pilsicainide