Document Detail


Atria are more susceptible to electroporation than ventricles: implications for atrial stunning, shock-induced arrhythmia and defibrillation failure.
MedLine Citation:
PMID:  18362029     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Defibrillation shock is known to induce atrial stunning, which is electrical and mechanical dysfunction.
OBJECTIVE: We hypothesized that atrial stunning is caused by higher atrial susceptibility to electroporation vs ventricles. We also hypothesize that electroporation may be responsible for early recurrence of atrial fibrillation.
METHODS: We investigated electroporation induced by 10-ms epicardial high-intensity shocks applied locally in atria and ventricles of Langendorff-perfused rabbit hearts (n = 12) using optical mapping.
RESULTS: Electroporation was centered at the electrode and was evident from transient diastolic depolarization and reduction of action potential amplitude and maximum upstroke derivative. Electroporation was voltage-dependent and polarity-dependent and was significantly more pronounced in the atria vs ventricles (P <.01), with a summary 50% of Effective Dose (ED50) for main measured parameters of 9.2 +/- 3.6 V/cm and 13.6 +/- 3.2 V/cm in the atria vs 37.4 +/- 1.5 V/cm and 48.4 +/- 2.8 V/cm in the ventricles, for anodal and cathodal stimuli, respectively. In atria (n = 5), shocks of both polarities (27.2 +/- 1.1 V/cm) transiently induced conduction block and reentry around the inexcitable area. Electroporation-induced ectopic activity was a possible trigger for reentry. However, in the thicker ventricles, electroporation and resulting conduction slowing and block were restricted to the surface only, preventing complete block and arrhythmia. The upstroke morphology revealed that the wave front dived below the electroporated region and resurfaced into unaffected epicardial tissue.
CONCLUSION: We showed that the atria are more vulnerable to electroporation and resulting block and arrhythmia than the ventricles.
Authors:
Vadim V Fedorov; Geran Kostecki; Matt Hemphill; Igor R Efimov
Related Documents :
9244209 - In-hospital outcome of elderly patients with acute inferior myocardial infarction and r...
6375989 - Renin and the complications of acute myocardial infarction.
19468019 - Intractable cardiogenic shock in stress cardiomyopathy with left ventricular outflow tr...
12860479 - Type ii nitric oxide synthase activity is cardio-protective in experimental sepsis.
15642569 - Design of the shock inhibition evaluation with azimilide (shield) study: a novel method...
3407699 - Septic shock during pregnancy.
11238289 - High-sensitivity c-reactive protein: a novel and promising marker of coronary heart dis...
18375589 - Discovering regulators of the drosophila cardiac hypoxia response using automated pheno...
629279 - Mid-systolic click and mitral valve prolapse following mitral commissurotomy.
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2008-01-29
Journal Detail:
Title:  Heart rhythm : the official journal of the Heart Rhythm Society     Volume:  5     ISSN:  1556-3871     ISO Abbreviation:  Heart Rhythm     Publication Date:  2008 Apr 
Date Detail:
Created Date:  2008-03-25     Completed Date:  2008-06-13     Revised Date:  2011-04-26    
Medline Journal Info:
Nlm Unique ID:  101200317     Medline TA:  Heart Rhythm     Country:  United States    
Other Details:
Languages:  eng     Pagination:  593-604     Citation Subset:  IM    
Affiliation:
Department of Biomedical Engineering, Washington University, St. Louis, Missouri 63130-4899. USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Action Potentials
Animals
Atrial Fibrillation / etiology*,  physiopathology
Diastole
Electric Countershock / adverse effects*
Electrodes
Electroporation*
Heart Atria / innervation*
Heart Ventricles / innervation
Models, Animal
Pericardium
Rabbits
Recurrence
Risk Factors
Tachycardia, Ventricular / etiology,  physiopathology
Treatment Failure
Grant Support
ID/Acronym/Agency:
R01 HL074283-03/HL/NHLBI NIH HHS; R01HL074283/HL/NHLBI NIH HHS
Comments/Corrections

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


Previous Document:  Cellular basis for arrhythmogenesis in an experimental model of the SQT1 form of the short QT syndro...
Next Document:  Immunotoxicity of the xenoestrogen 4-nonylphenol to the cockle Cerastoderma glaucum.