Copyright © 2005, European Society of Cardiology
Something old, something new: Changing views on the cellular mechanisms of heart failure
aLaboratory of Experimental Cardiology, University of Leuven, KUL, Campus Gasthuisberg O/N 7th floor, Herestraat 49, B-3000 Leuven, Belgium
bUnit of Cardiac Physiology, University of Manchester, Manchester, UK
* Corresponding author. Tel.: +32 16 347153; fax: +32 16 345844. Email address: Karin.Sipido@med.kuleuven.be
Received 17 August 2005; accepted 31 August 2005
| The first 150 words of the full text of this article appear below. |
See article by Fauconnier et al. [84] (pages 204–212) in this issue.
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1. Introduction |
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Despite improvements in therapy, mortality in heart failure (HF) remains high, and there is a need for alternative and additional approaches [1,2]. The possibility of replacement and/or supporting the failing heart with new cardiomyocytes from stem cells, implanted or recruited locally, is one of the exciting possibilities under investigation [3]. Other approaches aim at improving the function of the failing myocytes. Although the temporal and causal relationship between the development of chronic HF and myocyte dysfunction remains unclear [4], there is little doubt that at the time of advanced HF, the isolated myocytes have reduced contractility, in particular under normal physiological stress, i.e. at physiological heart rates and in the response to adrenergic stimulation. The first trials with chronic inotropic therapy, however, had a very poor outcome, and the idea was abandoned for quite a
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2. Excitation–contraction coupling in the normal heart |
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3. Global changes of contractile function in HF |
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4. Regulation of sarcoplasmic reticulum Ca2+ release in HF |
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4.1 Triggers for activation of the RyR
4.2 Properties of the RyR
4.3 Ca2+ availability in the SR and the role of SERCA–not only the numbers count
4.4 Na/Ca exchange–interaction with SERCA
4.5 The Ca2+–arrhythmia connection
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5. Emphasis on modulated activity of Ca2+ transporters, not expression |
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6. Conclusions |
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