Document Detail


Contribution of fibrosis and the autonomic nervous system to atrial fibrillation electrograms in heart failure.
MedLine Citation:
PMID:  22722658     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Fibrotic and autonomic remodeling in heart failure (HF) increase vulnerability to atrial fibrillation (AF). Because AF electrograms (EGMs) are thought to reflect the underlying structural substrate, we sought to (1) determine the differences in AF EGMs in normal versus HF atria and (2) assess how fibrosis and nerve-rich fat contribute to AF EGM characteristics in HF.
METHODS AND RESULTS: AF was induced in 20 normal dogs by vagal stimulation and in 21 HF dogs (subjected to 3 weeks of rapid ventricular pacing at 240 beats per minute). AF EGMs were analyzed for dominant frequency (DF), organization index, fractionation intervals (FIs), and Shannon entropy. In 8 HF dogs, AF EGM correlation with underlying fibrosis/fat/nerves was assessed. In HF compared with normal dogs, DF was lower and organization index/FI/Shannon entropy were greater. DF/FI were more heterogeneous in HF. Percentage fat was greater, and fibrosis and fat were more heterogeneously distributed in the posterior left atrium than in the left atrial appendage. DF/organization index correlated closely with %fibrosis. Heterogeneity of DF/FI correlated with the heterogeneity of fibrosis. Autonomic blockade caused a greater change in DF/FI/Shannon entropy in the posterior left atrium than left atrial appendage, with the decrease in Shannon entropy correlating with %fat.
CONCLUSIONS: The amount and distribution of fibrosis in the HF atrium seems to contribute to slowing and increased organization of AF EGMs, whereas the nerve-rich fat in the HF posterior left atrium is positively correlated with AF EGM entropy. By allowing for improved detection of regions of dense fibrosis and high autonomic nerve density in the HF atrium, these findings may help enhance the precision and success of substrate-guided ablation for AF.
Authors:
Hemantha Koduri; Jason Ng; Ivan Cokic; Gary L Aistrup; David Gordon; J Andrew Wasserstrom; Alan H Kadish; Richard Lee; Rod Passman; Bradley P Knight; Jeffrey J Goldberger; Rishi Arora
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-06-21
Journal Detail:
Title:  Circulation. Arrhythmia and electrophysiology     Volume:  5     ISSN:  1941-3084     ISO Abbreviation:  Circ Arrhythm Electrophysiol     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-08-16     Completed Date:  2012-10-26     Revised Date:  2013-08-13    
Medline Journal Info:
Nlm Unique ID:  101474365     Medline TA:  Circ Arrhythm Electrophysiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  640-9     Citation Subset:  IM    
Affiliation:
Feinberg Cardiovascular Research Institute, Division of Cardiology, Department of Medicine, Northwestern University-Feinberg School of Medicine, Chicago, IL 60611, USA.
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MeSH Terms
Descriptor/Qualifier:
Adipose Tissue / pathology
Adrenergic Antagonists / pharmacology
Animals
Atrial Appendage / innervation,  pathology
Atrial Fibrillation / diagnosis*,  etiology,  pathology,  physiopathology
Atrial Function* / drug effects
Autonomic Denervation / methods
Autonomic Nervous System / drug effects,  physiopathology*
Cardiac Pacing, Artificial
Disease Models, Animal
Dogs
Electrophysiologic Techniques, Cardiac*
Fibrosis
Heart Atria / innervation,  pathology
Heart Failure / complications*,  diagnosis,  pathology,  physiopathology
Muscarinic Antagonists / pharmacology
Predictive Value of Tests
Grant Support
ID/Acronym/Agency:
1R01HL093490/HL/NHLBI NIH HHS; 3R01HL093490-01S1/HL/NHLBI NIH HHS; R01 HL093490/HL/NHLBI NIH HHS; R21 HL088304/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Adrenergic Antagonists; 0/Muscarinic Antagonists
Comments/Corrections

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


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