SIMULATION OF 2-DIMENSIONAL ANISOTROPIC CARDIAC REENTRY - EFFECTS OF THE WAVELENGTH ON THE REENTRY CHARACTERISTICS

Citation
Lj. Leon et al., SIMULATION OF 2-DIMENSIONAL ANISOTROPIC CARDIAC REENTRY - EFFECTS OF THE WAVELENGTH ON THE REENTRY CHARACTERISTICS, Annals of biomedical engineering, 22(6), 1994, pp. 592-609
Citations number
34
Categorie Soggetti
Engineering, Biomedical
ISSN journal
00906964
Volume
22
Issue
6
Year of publication
1994
Pages
592 - 609
Database
ISI
SICI code
0090-6964(1994)22:6<592:SO2ACR>2.0.ZU;2-I
Abstract
A two-dimensional sheet model was used to study the dynamics of reentr y around a zone of functional block. The sheet is a set of parallel, c ontinuous, and uniform cables, transversely interconnected by a brick- wall arrangement of fixed resisters. In accord with experimental obser vations on cardiac tissue, longitudinal propagation is continuous, whe reas transverse propagation exhibits discontinuous features. The width and length of the sheet are 1.5 and 5 cm, respectively, and the aniso tropy ratio is fixed at approximately 4:1. The membrane model is a mod ified Beeler-Reuter formulation incorporating faster sodium current dy namics. We fixed the basic wavelength and action potential duration of the propagating impulse by dividing the time constants of the seconda ry inward current by an integer K. Reentry was initiated by a standard cross-shock protocol, and the rotating activity appeared as curling p atterns around the point of junction (the q-point) of the activation ( A) and recovery (R) fronts. The curling R front always precedes the A front and is separated from it by the excitable gap. In addition, the R front is occasionally shifted abruptly through a merging with a slow -moving triggered secondary recovery front that is dissociated from th e A front and q-point. Sustained irregular reentry associated with sub stantial excitable gap variations was simulated with short wavelengths (K = 8 and K = 4). Unsustained reentry was obtained with a longer wav elength (K = 2), leading to a breakup of the q-point locus and the tri ggering of new activation fronts.