© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
Cellular and molecular aspects of contractile dysfunction in heart failure
Abteilung Allgemeine Pharmakologie, Universitäts-Krankenhaus Eppendorf, Martinistrasse 52, D-20246 Hamburg, Germany
* Corresponding author. Tel.: +49 (40) 4717 2786; Fax: +49 (40) 4717 4876; E-mail: mittmann@plexus.uke.uni-hamburg.de
Received 24 December 1997; accepted 24 April 1998
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1 Introduction |
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Heart failure is a syndrome in which dysfunction of the heart causes a mismatch between blood supply and demand of the organs. This activates neurohumoral systems and water and salt retention by the kidneys. These counterregulatory mechanisms in turn influence cardiac function. The pump failure can comprise systolic and diastolic dysfunction that depend on preload, afterload, frequency, and the systolic and diastolic myocardial patterns of contraction, the former often referred to as ‘contractility’. Preload in the intact heart is determined by the enddiastolic ventricular pressure, which, depending on ventricular distensibility, determines enddiastolic volume. On a cellular basis the elongation of the sarcomere (strain) depends on diastolic stress and fiber stiffness [1]. Afterload is defined as the wall stress during contraction and is determined by the forces opposing ventricular ejection, chamber diameter, and the wall thickness. Glower et al. (1985) [2]stated that, in the intact heart in vivo, "no
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2 Cellular and molecular alterations in heart failure |
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2.1 Contractile proteins
2.2 Calcium homeostasis
2.3 Signal transduction
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3 Systolic dysfunction of the failing myocardium |
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3.1 Frank–Starling mechanism
3.2 Force–frequency relationship
3.3 Responsiveness of the failing myocardium to positive inotropic drugs
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4 Diastolic dysfunction in the failing heart |
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5 Summary |
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