title: A model study of intramural dispersion of action potential duration in the canine pulmonary conus.
abstract: Regional gradients of action potential duration (APD) due to electrophysiological differences between endocardial, midmyocardial, and epicardial myocytes may exist across the ventricular wall. In addition, activation sequence-induced gradients of APD may occur if intramural fiber rotation accelerates or decelerates the depolarization wave front. To investigate relative contributions of regional and activation sequence-induced gradients to intramural APD dispersion, we simulated action potential propagation in two-dimensional models with idealized geometries representing the canine pulmonary conus. Ionic currents for endocardial myocytes were described using the Luo-Rudy membrane equations. Modifications to I(Ks) approximated action potentials of epicardial and midmyocardial cells. Spatial coupling was modeled with a bidomain representation of tissue structure that included unequal anisotropic conductivity ratios. Activation sequence-induced gradients reached 69 ms cm(-1) during a nonuniform activation sequence where the change in orientation between endocardial and epicardial fibers accelerated the depolarization wave front. Regional gradients reached 133 ms cm(-1) at the boundary between endocardial and midmyocardial cells. When regional and activation sequence-induced gradients were oriented in opposite directions, overall APD dispersion decreased. When the gradients were oriented in the same direction, overall dispersion measured as high as 202 ms cm(-1). This gradient exceeded values previously estimated as sufficient to induce cardiac arrhythmia during premature stimulation and suggests that regional and activation sequence-induced gradients increase arrhythmia vulnerability in the presence of other arrhythmogenic conditions.
authors.affiliation: Department of Biomedical Engineering, Tulane University, New Orleans, LA, USA. awc@crml.uab.edu
authors.forename: A W
authors.initials: AW
authors.lastname: Cates
authors.forename: A E
authors.initials: AE
authors.lastname: Pollard
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000503:physiopathology; D001698:Biomedical Engineering; D004285:Dogs; D004594:Electrophysiology; D004699:Endocardium / Q000166:cytology / Q000502:physiology; D006321:Heart / Q000033:anatomy & histology / Q000502:physiology*; D006352:Heart Ventricles / Q000033:anatomy & histology; D008955:Models, Cardiovascular; D009206:Myocardium / Q000166:cytology; D010496:Pericardium / Q000166:cytology / Q000502:physiology; D016276:Ventricular Function