Articles |
From the Departments of Pediatrics and Cell Biology, Duke University Medical Center, Durham, NC.
Correspondence to Madison S. Spach, MD, Box 3475, Duke University Medical Center, Durham, NC 27710.
Abstract The object of this study is to present evidence
that the myocardial architecture creates inhomogeneities of electrical
load at the cellular level that cause cardiac propagation to be
stochastic in nature; ie, the excitatory events during propagation are
constantly changing and disorderly in the sense of varying
intracellular events and delays between cells. At a macroscopic level,
however, these stochastic events become averaged and appear consistent
with a continuous medium. We examined this concept in a two-dimensional
(2D) model of myocardial architecture by exploring whether
experimentally observed
max variability reflected
different patterns of intracellular excitation events and junctional
delays. The patterns of
max variability at randomly
chosen intracellular sites were similar experimentally and in the 2D
model. The 2D cellular model produced marked variability in gap
junction delays; however, on the average, different gap junctions were
used for cell-to-cell charge flow during conduction in different
directions. During longitudinal propagation (LP), the velocity
increased from the proximal to the distal end of each myocyte, and
max was lowest proximally, increased to a maximum at
the distal fourth of the cell, and decreased distally. Transverse
propagation (TP) produced rapid intracellular conduction with variable
intracellular excitation sequences. TP
max was
greater than LP
max in most subcellular regions, but
near the ends of some myocytes, a reversed "TP>LP
max" relation occurred. Total charge carried by
the sodium current varied inversely with
max,
demonstrating feedback effects of cellular loading on the subcellular
sodium current and the kinetics of the sodium channels. The results
suggest that the stochastic nature of normal propagation at a
microscopic level provides a considerable protective effect against
arrhythmias by reestablishing the general trend of wave-front movement
after small variations in excitation events occur.
Key Words: stochastic propagation myocardial architecture discontinuous propagation gap junction delays intracellular conduction
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