Document Detail

Atrial remodeling in an ovine model of anthracycline-induced nonischemic cardiomyopathy: remodeling of the same sort.
MedLine Citation:
PMID:  20662987     Owner:  NLM     Status:  In-Data-Review    
Atrial Remodeling in Doxorubicin Cardiomyopathy. Introduction: All preclinical studies of atrial remodeling in heart failure (HF) have been confined to a single model of rapid ventricular pacing. To evaluate whether the atrial changes were specific to the model or represented an end result of HF, this study aimed to characterize atrial remodeling in an ovine model of doxorubicin-induced cardiomyopathy. Methods and Results: Fourteen sheep, 7 with cardiomyopathy induced by repeated intracoronary doxorubicin infusions and 7 controls, were studied. The development of HF was monitored by cardiac imaging and hemodynamic parameters. Open chest electrophysiological study was performed using custom-made 128-electrode epicardial plaque assessing effective refractory period (ERP) and conduction velocity. Atrial tissues were harvested for structural analysis. The HF group had demonstrable moderate global HF (left ventricular ejection fraction [LVEF]: 37.1 vs 46.4%; P = 0.003) and showed the following compared to controls: left atrial dilatation (P = 0.02) and dysfunction (P = 0.005); longer P-wave duration (P < 0.05); higher ERP at all cycle lengths (P ≤ 0.002) and locations (P < 0.001); slower conduction velocity (P < 0.001); increased conduction heterogeneity index (P < 0.001); increased atrial fibrosis (right atrial [RA]: 5.9 ± 2.6 vs 2.8 ± 0.9%; P < 0.0001, left atrial [LA]: 3.7 ± 2.2 vs 2.4 ± 1.1%; P = 0.002), and longer induced atrial fibrillation (AF) episodes (16 ± 22 vs 2 ± 3 seconds; P = 0.04). Conclusion: In this model of HF, there was significant atrial remodeling characterized by atrial enlargement/dysfunction, increased fibrosis, slowed/heterogeneous conduction, and increased refractoriness associated with more sustained AF. These findings appear the "same sort" to previous models of HF implicating a final common substrate leading to the development of AF in HF. (J Cardiovasc Electrophysiol, Vol. 22, pp. 175-182, February 2011).
Dennis H Lau; Peter J Psaltis; Lorraine Mackenzie; Darren J Kelly; Angelo Carbone; Michael Worthington; Adam J Nelson; Yuan Zhang; Pawel Kuklik; Christopher X Wong; James Edwards; David A Saint; Stephen G Worthley; Prashanthan Sanders
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of cardiovascular electrophysiology     Volume:  22     ISSN:  1540-8167     ISO Abbreviation:  J. Cardiovasc. Electrophysiol.     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-02-14     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9010756     Medline TA:  J Cardiovasc Electrophysiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  175-82     Citation Subset:  IM    
Copyright Information:
© 2010 Wiley Periodicals, Inc.
Cardiovascular Research Centre, Departments of Cardiology and Cardiothoracic Surgery, Royal Adelaide Hospital and the Disciplines of Medicine and Physiology, University of Adelaide, Adelaide, Australia Department of Medicine, St. Vincent's Hospital, University of Melbourne, Melbourne, Australia.
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