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1 Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center, and 2 Division of Cardiology, Departments of Medicine and Physiology and Physiological Science, University of California School of Medicine, Los Angeles, California 90048; and 3 Department of Physics and Astronomy, Vanderbilt University, Nashville, Tennessee 37235
Several different patterns of wave
break have been described by mapping of the tissue surface during
fibrillation. However, it is not clear whether these surface patterns
are caused by multiple distinct mechanisms or by a single mechanism. To
determine the mechanism by which wave breaks are generated during
ventricular fibrillation, we conducted optical mapping studies and
single cell transmembrane potential recording in six isolated swine
right ventricles (RV). Among 763 episodes of wave break (0.75 times · s
1 · cm
2), optical
maps showed three patterns: 80% due to a wave front encountering the
refractory wave back of another wave, 11.5% due to wave fronts passing
perpendicular to each other, and 8.5% due to a new (target) wave
arising just beyond the refractory tail of a previous wave. Computer
simulations of scroll waves in three-dimensional tissue showed that
these surface patterns could be attributed to two fundamental
mechanisms: head-tail interactions and filament break. We conclude that
during sustained ventricular fibrillation in swine RV, surface patterns
of wave break are produced by two fundamental mechanisms: head-tail
interaction between waves and filament break.
reentry; mapping; electrophysiology; action potentials; restitution
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