title: Preferential depression of conduction around a pivot point in rabbit ventricular myocardium by potassium and flecainide.
abstract: BACKGROUND
  During reentrant arrhythmias, the circulating wavefront often makes a sharp turn around a functional or anatomic barrier. We tested the hypothesis that lowering the safety factor for conduction by high K+ or flecainide preferentially depresses conduction of sharply turning wavefronts.
  
  
  RESULTS
  In 16 Langendorff-perfused rabbit hearts, a thin layer of anisotropic ventricular myocardium was made using a cryoprocedure. In this layer, a linear radiofrequency lesion was made parallel to the fiber orientation. The tip of the lesion was extended by a short incision. U-turning wavefronts were initiated by pacing at one side of the lesion. A mapping electrode (240 electrodes, resolution 350 to 700 microm) was used to measure conduction times and velocity of planar waves (longitudinal and transverse) and U-turning wavefronts. The safety factor for conduction was lowered by high potassium (8, 10, and 12 mmol/L) and flecainide (1 and 2 mg/L). On average, high potassium and flecainide increased the conduction times of U-turning wavefronts 1.6 times more than longitudinal or transverse planar wavefronts (P < 0.01). At a critical lowering of the excitatory current, functional conduction block occurred at the pivot point, which forced the wavefront to make a longer U-turn. In these cases, the total U-turn conduction time increased from 27+/-9 msec to 75+/-37 msec. About 40% of this delay was caused by a shift of the pivot point and consequent lengthening of the returning pathway.
  
  
  CONCLUSIONS
  Lowering the amount of excitatory current by potassium or flecainide preferentially impairs U-turn conduction. The occurrence of long delays and conduction block at pivot points may explain the mode of action of Class I drugs.
authors.affiliation: Department of Physiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, The Netherlands.
authors.forename: P W
authors.initials: PW
authors.lastname: Danse
authors.forename: C J
authors.initials: CJ
authors.lastname: Garratt
authors.forename: F
authors.initials: F
authors.lastname: Mast
authors.forename: M A
authors.initials: MA
authors.lastname: Allessie
mesh_terms: D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D018780:Body Surface Potential Mapping / Q000187:drug effects; D002304:Cardiac Pacing, Artificial; D017115:Catheter Ablation / Q000009:adverse effects; D004195:Disease Models, Animal; D005260:Female; D005424:Flecainide / Q000627:therapeutic use*; D006329:Heart Conduction System / Q000187:drug effects* / Q000503:physiopathology; D006352:Heart Ventricles / Q000187:drug effects / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D011188:Potassium / Q000627:therapeutic use*; D011817:Rabbits; D013611:Tachycardia, Atrioventricular Nodal Reentry / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy
chemical_list: D000889:Anti-Arrhythmia Agents; D005424:Flecainide; D011188:Potassium