© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
The failing human heart
Department of Molecular Physiology and Biophysics, University of Vermont College of Medicine, Burlington, VT 05405, USA
* Corresponding author. Fax: +1-807-656-747
Received 24 December 2001; accepted 27 December 2001
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1 Introduction |
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Heart failure remains a significant public health problem with an unacceptably high morbidity and mortality affecting about three persons per thousand per year [1]. The percent survival following diagnosis decreases significantly as a function of the severity of the disease with survival rates for NYHA (New York Heart Association) I–II being 65% at the end of 4 years, for NYHA III it is 50% at the 4-year period and for NYHA IV it is 50% after only 1 year [2,3]1. In the patients with heart failure, there is a significant correlation between survivability and ejection fraction [4]. The deficits in ventricular function in failing human hearts led us to examine the contributions of the contractile (acto–myosin interaction) and excitation–contraction–coupling (EC) (calcium cycling) systems to that insufficiency.
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2 The contractile system |
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2.1 Myofibrillar ATPase activity and velocity of shortening
The first demonstration of a molecular alteration in the contractile system of human failing hearts was found in studies carried out
2.2 Protection of human left ventricular myocardium during dissection and transport
2.3 Mechanical studies on human heart tissue
2.4 Thermo–mechanical studies of human heart tissue
2.5 Determination of the average cross-bridge force–time integral from the tension dependent heat during the isometric contraction–relaxation
2.6 The average cross-bridge force–time integral in failing hearts
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3 The excitation–contraction coupling system |
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3.1 Calcium cycling
3.2 The force–frequency relationship
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4 Familial hypertrophic cardiomyopathy |
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4.1 Background
4.2 R403Q and L908V mutations in familial hypertrophic cardiomyopathy
4.3 The mechanical performance of R403Q and L908V myosin
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5 Heart failure: summary and conclusions |
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