title: Effects of propafenone on anisotropic conduction properties within the three-dimensional structure of the canine ventricular wall.
abstract: BACKGROUND
  Structural complexities of the intact ventricular wall cause a very complex spread of activation. The effects of regional tissue damage and of antiarrhythmic drugs on directional differences in activation should help to further elucidate intramural conduction patterns.
  
  
  RESULTS
  In 10 healthy dogs and in 5 dogs with subacute anterior wall infarction, 6 parallel rows of 6 needle electrodes with 4 bipolar electrode pairs per needle were inserted into the left anterior ventricular wall. Using a computerized multiplexer-mapping system, the spread of activation in epi-, endo- and midmyocardial muscle layers and in the surviving epicardium, respectively, was reconstructed. Marked differences in conduction velocities relative to fiber orientation were evident in the surviving epicardium of infarcted hearts. Directional differences in conduction velocities, although less pronounced, were still preserved throughout the intact ventricular wall. Epicardial transverse conduction in intact hearts was significantly faster than transverse conduction in infarcted hearts (0.87 +/- 0.11 m/s vs 0.68 +/- 0.1 m/s). In normal hearts, propafenone (2 mg/kg) decreased conduction velocities primarily in longitudinal directions (-27 +/- 10%), but also moderately in transverse directions (-13 +/- 7 %) of all muscle layers, with no significant effect on straight (-4 +/- 8 %), but on oblique transmural conduction (-33 +/- 18 %). In infarcted hearts propafenone decreased conduction particularly in longitudinal direction (-23 +/- 14 %) without affecting conduction transverse to the fiber orientation (+3 +/- 6%).
  
  
  CONCLUSIONS
  Longitudinal intramural shortcircuits reduce directional differences in activation. Transmural infarction results in a loss of alternative intramural pathways, unmasking marked anisotropy in the surviving epicardium. Conduction delay in intramural pathways explains the effects of propafenone on transverse and oblique transmural conduction. Primarily longitudinal conduction delay results in reduced tissue anisotropy.
authors.affiliation: Abteilung Innere Medizin III, Medizinische Universitätsklinik, Heidelberg, Germany. alexander_bauer@med.uni-heidelberg.de
authors.forename: A
authors.initials: A
authors.lastname: Bauer
authors.forename: P A
authors.initials: PA
authors.lastname: Schnabel
authors.forename: K D
authors.initials: KD
authors.lastname: Schreiner
authors.forename: R
authors.initials: R
authors.lastname: Becker
authors.forename: F
authors.initials: F
authors.lastname: Voss
authors.forename: P
authors.initials: P
authors.lastname: Kraft
authors.forename: J
authors.initials: J
authors.lastname: Senges
authors.forename: M
authors.initials: M
authors.lastname: Licka
authors.forename: W
authors.initials: W
authors.lastname: Kübler
authors.forename: W
authors.initials: W
authors.lastname: Schoels
mesh_terms: D000818:Animals; D016880:Anisotropy; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D004285:Dogs; D006321:Heart / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology*; D011405:Propafenone / Q000494:pharmacology*; D017180:Tachycardia, Ventricular / Q000188:drug therapy / Q000503:physiopathology*
chemical_list: D000889:Anti-Arrhythmia Agents; D011405:Propafenone