| Atria are more susceptible to electroporation than ventricles: implications for atrial stunning, shock-induced arrhythmia and defibrillation failure. | |
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MedLine Citation:
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PMID: 18362029 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Vadim V Fedorov; Geran Kostecki; Matt Hemphill; Igor R Efimov |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2008-01-29 |
Journal Detail:
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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:
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Created Date: 2008-03-25 Completed Date: 2008-06-13 Revised Date: 2011-04-26 |
Medline Journal Info:
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Nlm Unique ID: 101200317 Medline TA: Heart Rhythm Country: United States |
Other Details:
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Languages: eng Pagination: 593-604 Citation Subset: IM |
Affiliation:
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Department of Biomedical Engineering, Washington University, St. Louis, Missouri 63130-4899. USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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
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