A COMPUTER HEART MODEL INCORPORATING ANISOTROPIC PROPAGATION .1. MODEL CONSTRUCTION AND SIMULATION OF NORMAL ACTIVATION

Citation
M. Lorange et Rm. Gulrajani, A COMPUTER HEART MODEL INCORPORATING ANISOTROPIC PROPAGATION .1. MODEL CONSTRUCTION AND SIMULATION OF NORMAL ACTIVATION, Journal of electrocardiology, 26(4), 1993, pp. 245-261
Citations number
54
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
00220736
Volume
26
Issue
4
Year of publication
1993
Pages
245 - 261
Database
ISI
SICI code
0022-0736(1993)26:4<245:ACHMIA>2.0.ZU;2-#
Abstract
Present-day computer models of the entire heart, capable of simulating the activation isochrones and subsequently the body surface potential s, focus on considerations of myocardial anisotropy. Myocardial anisot ropy enters into play at two levels, first by affecting the spatial pa ttern of activation owing to faster propagation along cardiac fibers a nd second by altering the equivalent dipole sources used to calculate the surface potentials. The construction of a new and detailed model o f the human heart is described, based on 132 transverse sections obtai ned following a computed tomography scan of a frozen human heart whose chambers were inflated with pressurized air. The entire heart anatomy was reconstructed as a three-dimensional array of approximately 250,0 00 points spaced 1 mm apart. Conduction in the thin-walled atria was a ssumed isotropic from the sinus node region to the atrioventricular no de, where it was subject to a 50 ms delay. A two-tier representation o f the specialized conduction system was used, with the initial segment s of the left and right bundles represented by a system of cables that feeds to the second tier, which is a sheet of conduction tissue repre senting the distal Purkinje system. Approximately 1, 120 ''Purkinje-my ocardium'' junctions present at the terminations of the cables and spr inkled uniformly over the sheet, transmit the excitation to the ventri cles. A stylized representation of myocardial fiber rotation was incor porated into the ventricles and the local fiber direction at each mode l point used to compute the velocity of propagation to its nearest nei ghbors. Accordingly, the activation times of the entire ventricular my ocardium could be determined using the 1,120 or so Purkinje-myocardium junctions as start points. While myocardial anisotropy was considered in the ventricular propagation process, it was ignored in the computa tion of the equivalent dipole sources. Nevertheless, the computed elec trocardiogram, vectorcardiogram, and body surface potential maps obtai ned with the new heart model properly positioned inside an inhomogeneo us torso model were all within normal limits.