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Title:
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Conduction Alternans in the Ischemic Border Zone as a Precursor of
Reentrant Arrhythmias
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Keywords:
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Arrhythmias,Ischemia
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Author Block:
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Olivier Bernus, Christian W Zemlin, Sergey F Mironov, Arkady M
Pertsov, SUNY Upstate Med Univ, Syracuse, NY
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Disclosure Block:
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O. Bernus, None; C.W. Zemlin, None; S.F.
Mironov, None; A.M. Pertsov, None.
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Unlabeled/unapproved:
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There are no unlabeled/unapproved uses of drugs or products
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Alternans has been shown to occur during ischemia and is known to
precede the onset of ventricular arrhythmias and fibrillation. Various
types of alternans have been identified, however, their role in the
initiation of arrhythmias remains unclear. We investigated the formation of
alternans and reentry at early stages of acute regional ischemia (0-15
min), using the dynamic Luo-Rudy model (2000). We studied propagation in
three-dimensional slabs of ventricular tissue with realistic fiber
organization, during S1-S2 and incremental pacing protocols. Different
phases of ischemia were modeled by varying the levels of hyperkalemia,
acidosis and anoxia following Shaw & Rudy (1997). For comparison with
experiments, we simulated pseudo-electrograms and optical recordings from
the epicardial surface using the diffusion equation for light. Computations
were performed on a parallel cluster consisting of 32 processors.
Simulations predict two different mechanisms for the initiation of reentry
(scroll waves) at early stages of acute ischemia. The first mechanism
(<10 min) involves slow propagation and unidirectional blocks due to
post-repolarization refractoriness in the ischemic core. The second
mechanism (>10 min) was observed after the ischemic core became
non-conductive: scroll waves occurred due to conduction alternans in the
border zone. The amplitude of the alternans increased near the ischemic
core and led to 2:1 conduction blocks in its vicinity. As the pacing
frequency increased, the area in the border zone showing APD alternans and
conduction blocks expanded. This led to wave breaks and reentry. We found
that hyperkalemia was the main component of ischemia leading to conduction
alternans.
The alternans was unrelated to the restitution hypothesis, as it was not
seen in single cell simulations. However, simulated electrograms and
optical signals were reminiscent of concordant APD alternans due to a steep
APD restitution curve. The lifetime of the resulting reentrant patterns was
highly sensitive to the local fiber orientation.
In conclusion, we identify post-repolarization refractoriness and
conduction alternans in the ischemic border zone, causing wave breaks and
reentry during acute regional ischemia, at different times after its onset.
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