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Mechanistic insight into spontaneous transition from cellular alternans to arrhythmia—A simulation study.

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Title: Mechanistic insight into spontaneous transition from cellular alternans to arrhythmia—A simulation study.
Authors: Wang, Wei1, Zhang, Shanzhuo2, Ni, Haibo1, Garratt, Clifford J.3, Boyett, Mark R.3, Hancox, Jules C.1,4, Zhang, Henggui1,2,5,6 henggui.zhang@manchester.ac.uk
Source: PLoS Computational Biology. 11/30/2018, Vol. 14 Issue 11, p1-27. 27p. 8 Graphs.
Subject Terms: *ARRHYTHMIA, *BIOLOGICAL tags, *HEART diseases, *LABORATORY rabbits, *SUDDEN death
Abstract: Cardiac electrical alternans (CEA), manifested as T-wave alternans in ECG, is a clinical biomarker for predicting cardiac arrhythmias and sudden death. However, the mechanism underlying the spontaneous transition from CEA to arrhythmias remains incompletely elucidated. In this study, multiscale rabbit ventricular models were used to study the transition and a potential role of INa in perpetuating such a transition. It was shown CEA evolved into either concordant or discordant action potential (AP) conduction alternans in a homogeneous one-dimensional tissue model, depending on tissue AP duration and conduction velocity (CV) restitution properties. Discordant alternans was able to cause conduction failure in the model, which was promoted by impaired sodium channel with either a reduced or increased channel current. In a two-dimensional homogeneous tissue model, a combined effect of rate- and curvature-dependent CV broke-up alternating wavefronts at localised points, facilitating a spontaneous transition from CEA to re-entry. Tissue inhomogeneity or anisotropy further promoted break-up of re-entry, leading to multiple wavelets. Similar observations have also been seen in human atrial cellular and tissue models. In conclusion, our results identify a mechanism by which CEA spontaneously evolves into re-entry without a requirement for premature ventricular complexes or pre-existing tissue heterogeneities, and demonstrated the important pro-arrhythmic role of impaired sodium channel activity. These findings are model-independent and have potential human relevance. [ABSTRACT FROM AUTHOR]
Copyright of PLoS Computational Biology is the property of Public Library of Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Mechanistic insight into spontaneous transition from cellular alternans to arrhythmia—A simulation study.
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  Data: <searchLink fieldCode="AR" term="%22Wang%2C+Wei%22">Wang, Wei</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Zhang%2C+Shanzhuo%22">Zhang, Shanzhuo</searchLink><relatesTo>2</relatesTo><br /><searchLink fieldCode="AR" term="%22Ni%2C+Haibo%22">Ni, Haibo</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Garratt%2C+Clifford+J%2E%22">Garratt, Clifford J.</searchLink><relatesTo>3</relatesTo><br /><searchLink fieldCode="AR" term="%22Boyett%2C+Mark+R%2E%22">Boyett, Mark R.</searchLink><relatesTo>3</relatesTo><br /><searchLink fieldCode="AR" term="%22Hancox%2C+Jules+C%2E%22">Hancox, Jules C.</searchLink><relatesTo>1,4</relatesTo><br /><searchLink fieldCode="AR" term="%22Zhang%2C+Henggui%22">Zhang, Henggui</searchLink><relatesTo>1,2,5,6</relatesTo><i> henggui.zhang@manchester.ac.uk</i>
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  Data: <searchLink fieldCode="JN" term="%22PLoS+Computational+Biology%22">PLoS Computational Biology</searchLink>. 11/30/2018, Vol. 14 Issue 11, p1-27. 27p. 8 Graphs.
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  Data: *<searchLink fieldCode="DE" term="%22ARRHYTHMIA%22">ARRHYTHMIA</searchLink><br />*<searchLink fieldCode="DE" term="%22BIOLOGICAL+tags%22">BIOLOGICAL tags</searchLink><br />*<searchLink fieldCode="DE" term="%22HEART+diseases%22">HEART diseases</searchLink><br />*<searchLink fieldCode="DE" term="%22LABORATORY+rabbits%22">LABORATORY rabbits</searchLink><br />*<searchLink fieldCode="DE" term="%22SUDDEN+death%22">SUDDEN death</searchLink>
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  Label: Abstract
  Group: Ab
  Data: Cardiac electrical alternans (CEA), manifested as T-wave alternans in ECG, is a clinical biomarker for predicting cardiac arrhythmias and sudden death. However, the mechanism underlying the spontaneous transition from CEA to arrhythmias remains incompletely elucidated. In this study, multiscale rabbit ventricular models were used to study the transition and a potential role of INa in perpetuating such a transition. It was shown CEA evolved into either concordant or discordant action potential (AP) conduction alternans in a homogeneous one-dimensional tissue model, depending on tissue AP duration and conduction velocity (CV) restitution properties. Discordant alternans was able to cause conduction failure in the model, which was promoted by impaired sodium channel with either a reduced or increased channel current. In a two-dimensional homogeneous tissue model, a combined effect of rate- and curvature-dependent CV broke-up alternating wavefronts at localised points, facilitating a spontaneous transition from CEA to re-entry. Tissue inhomogeneity or anisotropy further promoted break-up of re-entry, leading to multiple wavelets. Similar observations have also been seen in human atrial cellular and tissue models. In conclusion, our results identify a mechanism by which CEA spontaneously evolves into re-entry without a requirement for premature ventricular complexes or pre-existing tissue heterogeneities, and demonstrated the important pro-arrhythmic role of impaired sodium channel activity. These findings are model-independent and have potential human relevance. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of PLoS Computational Biology is the property of Public Library of Science and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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              Text: 11/30/2018
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