title: Acute ischemia of canine interventricular septum produces asymmetric suppression of conduction.
abstract: BACKGROUND
  Acute ischemia depresses tissue excitability more rapidly in the epicardium than in the endocardium of the canine left ventricular (LV) free wall. However, the effects of acute ischemia on conduction in the interventricular septum (IVS), which is composed of right ventricular (RV) and LV endocardium and midmyocardium without epicardium, are less known.
  
  
  OBJECTIVE
  The purpose of this study was to evaluate the hypothesis that the IVS exhibits transseptal differences in local tissue response to acute ischemia.
  
  
  METHODS
  Isolated canine IVS preparations were perfused through the septal branch of the anterior descending coronary artery, and conduction on the cut-exposed transseptal surfaces was optically mapped before and after two sequential episodes of 8 minutes of global ischemia (separated by >60 minutes of reperfusion). The preparations were paced alternately between the RV endocardium and LV endocardium at cycle lengths of 250, 300, and 1,500 ms.
  
  
  RESULTS
  Prior to ischemia, transseptal conduction was radial and symmetric during either RV endocardial or LV endocardial pacing at all cycle lengths. Eight minutes of ischemia depressed conduction velocity more in the RV half than in the LV half of the IVS and caused local conduction block in the sub-RV endocardium, especially during rapid pacing. The K(ATP) channel blocker glibenclamide (10 micromol/L) prevented development of this transseptal asymmetry and conduction block during ischemia.
  
  
  CONCLUSIONS
  Acute global ischemia increased transseptal heterogeneity and induced sub-RV endocardial block of conduction via activation of the ATP-sensitive potassium current. Such changes could contribute to initiation of arrhythmia in patients with septal infarction.
authors.affiliation: Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
authors.forename: Shiho T
authors.initials: ST
authors.lastname: Morita
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Morita
authors.forename: Douglas P
authors.initials: DP
authors.lastname: Zipes
authors.forename: Jiashin
authors.initials: J
authors.lastname: Wu
mesh_terms: D000200:Action Potentials; D000818:Animals; D018780:Body Surface Potential Mapping; D004285:Dogs; D004699:Endocardium / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology*; D017202:Myocardial Ischemia / Q000503:physiopathology*; D054088:Ventricular Septum / Q000503:physiopathology*