title: Purkinje-muscle reentry as a mechanism of polymorphic ventricular arrhythmias in a 3-dimensional model of the ventricles.
abstract: Multiple electrode mapping of the ventricles during complex tachyarrhythmias has revealed focal subendocardial activation whose mechanism remains unexplained. We hypothesized that reentry involving the Purkinje-muscle junctions (PMJs) may be a mechanism for such focal excitations. We have constructed an anatomically appropriate computerized 3-dimensional model of the mammalian ventricles that includes the Purkinje conduction system and 214 PMJs distributed throughout the endocardium. Isochronal maps during normal excitation, as well as during right or left bundle branch block, resembled experimental measurements and compared well with isochronal maps of propagation in the human heart. Activity observed at both sides of a PMJ in the model showed that propagation from Purkinje fibers to muscle was slower than in the opposite direction. Under these realistic and normal conditions, the evolution of reentrant activity involving muscle and the Purkinje network was simulated. The reentry pattern was independent of the initiation site. It evolved with drifting epicardial breakthroughs and transformed on the endocardium from focal activity to figure-of-8 reentry. In addition, the ECG amplitude undulated during the evolution, and decrease in the cycle period, apparent wavelength, and propagation velocity were observed. Finally, the reentry was terminated if the Purkinje system was disconnected from the muscle before it reached a relative steady state. The simulation results suggest the following: (1) Epicardial breakthroughs and endocardial focal activity may originate at the PMJs. (2) The ECG amplitude may decrease as the reentry stabilizes and the excitation wavelength decreases. (3) The Purkinje system may have a double role in the evolution of reentry: first, it is essential to the reentry at the initial stage; second, it may lead to the establishment of intramyocardial reentry, at which time the Purkinje system becomes irrelevant.
authors.affiliation: Department of Pharmacology, SUNY Health Science Center at Syracuse, NY 13210, USA. beren@sundial.pharm.hscsyr.edu
authors.forename: O
authors.initials: O
authors.lastname: Berenfeld
authors.forename: J
authors.initials: J
authors.lastname: Jalife
mesh_terms: D000200:Action Potentials; D002037:Bundle-Branch Block / Q000503:physiopathology; D004562:Electrocardiography; D006352:Heart Ventricles / Q000503:physiopathology*; D006801:Humans; D007700:Kinetics; D008953:Models, Anatomic; D008955:Models, Cardiovascular; D011690:Purkinje Fibers / Q000503:physiopathology*; D014693:Ventricular Fibrillation / Q000503:physiopathology*