| TITLE |
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Mechanistic enquiry into the
effect of pre-fibrillatory conditions on the upper limit of vulnerability |
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| AUTHORS |
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David Bourn, Mary Maleckar, Blanca Rodriguez,
and
Natalia
Trayanova |
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| ABSTRACT |
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This study investigates the mechanisms responsible for
the increase in the upper limit of vulnerability (highest shock
strength that induces arrhythmia) following the increase in the
number of simultaneous wavefronts present in the tissue, representative
of pre-fibrillatory conditions. To accomplish this, the study
employs a three-dimensional bidomain model of a slice through the
canine ventricles. The preparation, of significantly decreased
action potential duration, was paced at a basic cycle length (BCL)
of either 80 or 150ms to elicit different numbers of simultaneous
wavefronts. Shocks of various strengths and timings were
delivered. Our results demonstrate that the shock strength which
induced an arrhythmia 50% of the time increased 20% when BCL
decreased from 150 to 80ms. Analysis of the mechanisms underlying
the increased vulnerability revealed that delayed post-shock
activations originating in the tissue depths appeared as
breakthrough activations on the slice surfaces following an
isoelectric window. However, isoelectric window duration was shorter
for the 80ms BCL case; breakthrough activations appeared when the tissue was
less recovered, resulting in higher probability of unidirectional
block and reentry. This explains why same strength shocks were more
likely to result in arrhythmia induction when delivered to a
preparation that has a larger number of simultaneous wavefronts.
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| FIGURES |
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© CCEL 2005
Johns Hopkins University
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< < Click on the image to enlarge! |
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Vulnerability curves for the two pre-shock basic cycle length (BCL) cases, 150ms (solid line), and 80ms (dashed line). Actual data points are denoted by the symbols X and O, respectively. Values of the strength at which a shock resulted in 50% probability of non-induction, ULV_50, are marked by *. |
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