Document Detail

Effect of global ischemia and reperfusion during ventricular fibrillation in myopathic human hearts.
MedLine Citation:
PMID:  19820201     Owner:  NLM     Status:  MEDLINE    
The effect of lack of global coronary perfusion on myocardial activation rate, wavebreak, and its temporal progression during human ventricular fibrillation (VF) is not known. We tested the hypothesis that global myocardial ischemia decreases activation rate and spatiotemporal organization during VF in myopathic human hearts, while increasing wavebreak, and that a short duration of reperfusion can restore these spatiotemporal changes to baseline levels. The electrograms were acquired during VF in a human Langendorff model using global mapping consisting of two 112-electrode arrays placed on the epicardium and endocardium simultaneously. We found that global myocardial ischemia results in slowing of the global activation rate (combined endo and epi), from 4.89+/-0.04 Hz. to 3.60+/-0.04 Hz. during the 200 s of global ischemia (no coronary flow) (P<0.01) in eight myopathic hearts. Two minutes of reperfusion contributed to reversal of the slowing with activation rate value increasing close to VF onset (4.72+/-0.04 Hz). In addition, during the period of ischemia, an activation rate gradient between the endocardium (3.76+/-0.06 Hz) and epicardium (3.45+/-0.06 Hz) was observed (P<0.01). There was a concomitant difference in wavebreak index (that provides a normalized parameterization of phase singularities) between the epicardium (11.29+/-2.7) and endocardium (3.25+/-2.7) during the 200 s of ischemia (P=0.02). The activation rate, gradient, and wavebreak changes were reversed by short duration (2 min) of reperfusion. Global myocardial ischemia of 3 min leads to complex spatiotemporal changes during VF in myopathic human hearts; these changes can be reversed by a short duration of reperfusion.
St?phane Mass?; Talha Farid; Paul Dorian; Karthikeyan Umapathy; Krishnakumar Nair; John Asta; Heather Ross; Vivek Rao; Elias Sevaptsidis; Kumaraswamy Nanthakumar
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-10-09
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  297     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-11-25     Completed Date:  2010-02-17     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1984-91     Citation Subset:  IM    
Division of Cardiology, Toronto General Hospital, GW 3-522, 150 Gerrard St. West, Toronto, ON, Canada M5G 2C4.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Action Potentials
Cardiomyopathies / complications*,  physiopathology
Coronary Circulation*
Electrophysiologic Techniques, Cardiac
Endocardium / physiopathology*
Middle Aged
Myocardial Ischemia / complications*,  physiopathology
Myocardial Reperfusion*
Pericardium / physiopathology*
Time Factors
Ventricular Fibrillation / etiology*,  physiopathology
Grant Support
NA 777687//Canadian Institutes of Health Research

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Shear-induced interaction of platelets with von Willebrand factor results in glycoprotein Ib{alpha} ...
Next Document:  Viability Assessment With Global Left Ventricular Longitudinal Strain Predicts Recovery of Left Vent...