© 1998 by European Society of Cardiology
Copyright © 1998, European Society of Cardiology
Altered contractile function in heart failure
Dept. of Physiology and Biophysics M/C 902, University of Illinois at Chicago, Chicago, IL 60607-7171, USA
* Tel.: +1 (312) 3550259; fax: +1 (312) 3550261; E-mail: pdetombe@uic.edu
The syndrome of congestive heart failure (CHF) is an entity of ever increasing clinical significance. CHF is characterized by a steady decrease in cardiac pump function which is eventually lethal. The mechanisms that underlie the decline in cardiac function are incompletely understood. End-stage CHF often involves the general loss of functional myocytes, a hyperplasia of the extracellular matrix, ventricular chamber remodeling, and decreased myocyte function. This review article focuses on the latter aspect of CHF, mechanisms of decreased myocyte function. Recent data from studies on human myocardial tissue obtained in the setting of cardiac transplantation or from studies that employed experimental animal models of CHF have suggested depressed myocyte function. The mechanisms that may be involved in the decline of myocyte contractile function include alterations in (i) calcium handling, (ii) myofilament function, and (iii) the cytoskeleton. At present, however, it is not known how or to what degree these alterations in cellular processes contribute to the decline of in vivo cardiac pump function in CHF. Accurate knowledge regarding the cellular processes that participate in the development of CHF is critical to the development of innovative strategies aimed to combat CHF.
KEYWORDS Congestive heart failure; Ventricular hypertrophy; Sarcomere length; Myofibrillar function; Animal models; Calcium handling; Isolated cardiac trabeculae; Isolated cardiocytes
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  D. J. Duncker, N. M. Boontje, D. Merkus, A. Versteilen, J. Krysiak, G. Mearini, A. El-Armouche, V. J. de Beer, J. M.J. Lamers, L. Carrier, et al. Prevention of Myofilament Dysfunction by {beta}-Blocker Therapy in Postinfarct Remodeling Circ Heart Fail, May 1, 2009; 2(3): 233 - 242. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Davis, M. V. Westfall, D. Townsend, M. Blankinship, T. J. Herron, G. Guerrero-Serna, W. Wang, E. Devaney, and J. M. Metzger Designing Heart Performance by Gene Transfer Physiol Rev, October 1, 2008; 88(4): 1567 - 1651. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Hamdani, V. Kooij, S. van Dijk, D. Merkus, W. J. Paulus, C. d. Remedios, D. J. Duncker, G. J.M. Stienen, and J. van der Velden Sarcomeric dysfunction in heart failure Cardiovasc Res, March 1, 2008; 77(4): 649 - 658. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Fuchs, M. F. Muller, H. Oswald, H. Thony, P. Mohacsi, and O. M. Hess Cardiac rotation and relaxation in patients with chronic heart failure Eur J Heart Fail, October 1, 2004; 6(6): 715 - 722. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. J Miller, N. G MacFarlane, and G. Wilson Altered oscillatory work by ventricular myofilaments from a rabbit coronary artery ligation model of heart failure Cardiovasc Res, January 1, 2004; 61(1): 94 - 104. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. van der Velden, J.W. de Jong, V.J. Owen, P.B.J. Burton, and G.J.M. Stienen Effect of protein kinase A on calcium sensitivity of force and its sarcomere length dependence in human cardiomyocytes Cardiovasc Res, June 1, 2000; 46(3): 487 - 495. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
U Ravens and D Dobrev Regulation of sarcoplasmic reticulum Ca2+-ATPase and phospholamban in the failing and nonfailing heart Cardiovasc Res, January 1, 2000; 45(1): 245 - 252. [Full Text] [PDF]
|
|