| Tunnel propagation of postshock activations as a hypothesis for fibrillation induction and isoelectric window. | |
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MedLine Citation:
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PMID: 18218982 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Comprehensive understanding of the ventricular response to shocks is the approach most likely to succeed in reducing defibrillation threshold. We propose a new theory of shock-induced arrhythmogenesis that unifies all known aspects of the response of the heart to monophasic (MS) and biphasic (BS) shocks. The central hypothesis is that submerged "tunnel" propagation of postshock activations through shock-induced intramural excitable areas underlies fibrillation induction and the existence of isoelectric window. We conducted simulations of fibrillation induction using a realistic bidomain model of rabbit ventricles. Following pacing, MS and BS of various strengths/timings were delivered. The results demonstrated that, during the isoelectric window, an activation originated deep within the ventricular wall, arising from virtual electrodes; it then propagated fully intramurally through an excitable tunnel induced by the shock, until it emerged onto the epicardium, becoming the earliest-propagated postshock activation. Differences in shock outcomes for MS and BS were found to stem from the narrower BS intramural postshock excitable area, often resulting in conduction block, and the difference in the mechanisms of origin of the postshock activations, namely intramural virtual electrode-induced phase singularity for MS and virtual electrode-induced propagated graded response for BS. This study provides a novel analysis of the 3D mechanisms underlying the origin of postshock activations in the process of fibrillation induction by MS and BS and the existence of isoelectric window. The tunnel propagation hypothesis could open a new avenue for interventions exploration to achieve significantly lower defibrillation threshold. |
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Authors:
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Takashi Ashihara; Jason Constantino; Natalia A Trayanova |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2008-01-24 |
Journal Detail:
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Title: Circulation research Volume: 102 ISSN: 1524-4571 ISO Abbreviation: Circ. Res. Publication Date: 2008 Mar |
Date Detail:
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Created Date: 2008-03-28 Completed Date: 2008-04-10 Revised Date: 2011-09-26 |
Medline Journal Info:
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Nlm Unique ID: 0047103 Medline TA: Circ Res Country: United States |
Other Details:
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Languages: eng Pagination: 737-45 Citation Subset: IM |
Affiliation:
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Department of Cardiovascular Medicine, Shiga University of Medical Science, Otsu, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Action Potentials Animals Cardiac Pacing, Artificial Computer Simulation Electric Countershock / adverse effects* Electric Stimulation / methods Heart Conduction System / physiopathology* Imaging, Three-Dimensional Kinetics Models, Cardiovascular Rabbits Research Design Signal Processing, Computer-Assisted Treatment Failure Ventricular Fibrillation / etiology*, physiopathology |
| Grant Support | |
ID/Acronym/Agency:
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HL-063195/HL/NHLBI NIH HHS; HL-067322/HL/NHLBI NIH HHS; HL-082729/HL/NHLBI NIH HHS; R01 HL063195-08/HL/NHLBI NIH HHS; R01 HL082729-02/HL/NHLBI NIH HHS |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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