title: [Mechanism of Formation of Cardiac Arrhythmia Due to Pathological Distribution of Myocardium Conductivity].
abstract: Two mechanisms responsible for the emergence of arrhythmia are known: a change of part of the cells to a self-oscillatory mode and generation of circulating waves. In this paper, we investigate the generation mechanism of the circulating waves using the unidirectional block. One of the variants of its realization is a narrow gap between two non-conducting regions. Implementation of this mechanism in the human heart turns out to be impossible, since in the heart in which the duration of cardiac action potential lasts 0.3 s and the velocity of wave propagation is equal to 33 cm/s, the minimal length of the pathway for wave circulation is approximately 10 cm, while the distance between the ventricular apex and atrioventricular septal is, on the average, 8 cm. Therefore, that inhomogeneity cannot exist at the scale of human heart. To adapt this mechanism to the size of the human heart, we introduce into the scheme the regions with low conductivity, which provide slow propagation of the wave. The value of conductivity is chosen based on the results of evaluation of the "conductivity-wave velocity" correlation. The analysis of wave propagation through the boundary between two regions with different conductivities has shown that the refractory period depends on the conductivity ratio. To minimize this dependence we introduce the transition zone, in which conductivity changes linearly from some normal value to a reduced one. This allowed us to generate a 12-mm inhomogeneity area, provoking the appearance of the circulating wave.
authors.forename: I N
authors.initials: IN
authors.lastname: Vasserman
authors.forename: V P
authors.initials: VP
authors.lastname: Matveenko
authors.forename: I N
authors.initials: IN
authors.lastname: Shardakov
authors.forename: A P
authors.initials: AP
authors.lastname: Shestakov
mesh_terms: D000200:Action Potentials; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000503:physiopathology*; D053840:Brugada Syndrome / Q000209:etiology / Q000503:physiopathology*; D000075224:Cardiac Conduction System Disease; D006352:Heart Ventricles / Q000503:physiopathology*; D006801:Humans; D008962:Models, Theoretical