Altered contractile function in heart failure.
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.
de Tombe
P P
PP
Dept. of Physiology and Biophysics M/C 902, University of Illinois at Chicago 60607-7171, USA. pdetombe@uic.edu
D008841:Actin Cytoskeleton / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D006332:Cardiomegaly / Q000378:metabolism / Q000503:physiopathology; D006321:Heart / Q000503:physiopathology*; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D008870:Microtubules / Q000378:metabolism; D009200:Myocardial Contraction; D012508:Sarcolemma / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000378:metabolism
D002118:Calcium