Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/88856
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Type: Journal article
Title: Atrial remodeling in an ovine model of anthracycline-induced nonischemic cardiomyopathy: remodeling of the same sort
Author: Lau, D.
Psaltis, P.
Mackenzie, L.
Kelly, D.
Carbone, A.
Worthington, M.
Nelson, A.
Zhang, Y.
Kuklik, P.
Wong, C.
Edwards, J.
Saint, D.
Worthley, S.
Sanders, P.
Citation: Journal of Cardiovascular Electrophysiology, 2011; 22(2):175-182
Publisher: Wiley
Issue Date: 2011
ISSN: 1045-3873
1540-8167
Statement of
Responsibility: 
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, and Prashanthan Sanders
Abstract: 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.
Keywords: heart failure; atrial fibrillation; remodeling; cardiomyopathy; electrophysiology
Rights: © 2010 Wiley Periodicals, Inc.
RMID: 0020107244
DOI: 10.1111/j.1540-8167.2010.01851.x
Appears in Collections:Medicine publications

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