© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Pacing-induced heart failure: a model to study the mechanism of disease progression and novel therapy in heart failure
aTerrence Donnelly Heart Center, St. Michaels Hospital, 30 Bond Street, University of Toronto, Toronto, Ontario, Canada M5B 7W8
bDivision of Cardiology, Department of Medicine, University of Alberta, Edmonton, Alberta, Canada
moeg@smh.toronto.on.ca
* Corresponding author.
Received 29 October 1998; accepted 28 December 1998
KEYWORDS Heart failure; Cytokines; Endothelins; Natriuretic peptides; Ventricular function
| The first 150 words of the full text of this article appear below. |
| 1. Introduction |
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Congestive heart failure (CHF) is a common clinical problem that confronts physicians and is often the final manifestation of many cardiovascular disorders. The diagnosis of CHF is accompanied by significant mortality and morbidity [1]. The syndrome is characterized by a relentless progressive course that is often manifested as repeated hospital admissions imposing heavy economic burden on the health care delivery system [2,3]. Therefore, basic research into the fundamental mechanisms accounting for the progression of CHF with the hope for developing novel therapeutic approaches to alter the progressive course has become a priority for many researchers. To facilitate these investigations, an animal model that closely mimics human CHF and also exhibits key components of what are now perceived to be important pathogenetic contributors to CHF progression is ideal. It is therefore the objective of this review to highlight how the model of pacing-induced cardiomyopathy has provided insights into the
| 2. Mechanisms of the progression of heart failure: alterations in the biological properties of the failing heart |
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| 3. Pacing-induced cardiomyopathy |
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3.1 Fluid retention in pacing-induced cardiomyopathy
3.2 Myocardial remodeling and dysfunction
3.3 Structural and functional alterations of the myocytes
3.4 Continuing myocyte loss
3.5 Extracellular matrix remodeling
3.6 Neurohormones and cytokines
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