Document Detail


Reversal of repolarization gradient does not reverse the chirality of shock-induced reentry in the rabbit heart.
MedLine Citation:
PMID:  11021470     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
INTRODUCTION: Two hypotheses have been proposed to explain the mechanisms of vulnerability and related failure of defibrillation therapy: the cross-field-induced critical point hypothesis and the virtual electrode-induced phase singularity hypothesis. These two hypotheses predict the opposite effect of preshock repolarization on the chirality (direction of rotation) of shock-induced reentry. The former suggests its reversal upon reversal of repolarization, whereas the latter suggests its preservation. The aim of this study was to determine, by reversing the repolarization sequence, which of the mechanisms is responsible for internal shock-induced arrhythmia in the Langendorff-perfused rabbit heart. METHODS AND RESULTS: We used high-resolution optical mapping to assess the chirality of postshock reentry in 11 hearts. Hearts were paced at a coupling interval of 300 msec at various sites around the field of view (13.5 x 13.5 to 16.5 x 16.5 mm). Cathodal monophasic implantable cardioverter defibrillator shocks (-100 V, 8 msec) were applied during the T wave from a 10-mm coil electrode placed into the right ventricular cavity. We used 3.5 +/- 0.8 different pacing sites per heart. Change in direction of repolarization did not result in change of chirality. Chirality was constant in all 11 hearts despite the complete reversal of activation and repolarization patterns. However, the position of resulting vortices depended on transmembrane polarization gradient inverted delta Vm and amplitude of negative polarization Vm (deexcitation). Stronger gradients and deexcitation produced earlier epicardial break excitation (P = 0.04 and P < 0.0001, respectively). CONCLUSION: Virtual electrode-induced phase singularity mechanism underlies internal shock-induced arrhythmia in this model.
Authors:
Y Cheng; V Nikolski; I R Efimov
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of cardiovascular electrophysiology     Volume:  11     ISSN:  1045-3873     ISO Abbreviation:  J. Cardiovasc. Electrophysiol.     Publication Date:  2000 Sep 
Date Detail:
Created Date:  2001-02-05     Completed Date:  2001-02-08     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9010756     Medline TA:  J Cardiovasc Electrophysiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  998-1007     Citation Subset:  IM    
Affiliation:
Department of Cardiology, Cleveland Clinic Foundation, Ohio, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arrhythmias, Cardiac / physiopathology
Cardiac Pacing, Artificial
Electric Countershock*
Electric Stimulation
Heart Conduction System / physiology*
Rabbits
Rotation
Grant Support
ID/Acronym/Agency:
R01-HL59464/HL/NHLBI NIH HHS
Comments/Corrections
Comment In:
J Cardiovasc Electrophysiol. 2000 Sep;11(9):1008-13   [PMID:  11021471 ]

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