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Altered contractile function in heart failure
1Dept. of Physiology and Biophysics M/C 902, University of Illinois at Chicago 60607-7171, USA. pdetombe@uic.edu
Insights
Congestive heart failure (CHF) involves decreased cardiac pump function due to reduced myocyte function. Understanding cellular changes like calcium handling and cytoskeleton alterations is key to developing new CHF treatments.
Area of Science:
- Cardiology
- Cellular Biology
- Pathophysiology
Background:
- Congestive heart failure (CHF) is a progressive, lethal condition marked by declining cardiac pump function.
- End-stage CHF involves myocyte loss, extracellular matrix changes, ventricular remodeling, and impaired myocyte function.
- Mechanisms driving decreased myocyte function in CHF remain incompletely understood.
Purpose of the Study:
- This review focuses on the cellular mechanisms underlying decreased myocyte function in congestive heart failure.
- To elucidate the specific cellular processes contributing to diminished cardiac contractility in CHF.
Main Methods:
- Review of recent studies utilizing human myocardial tissue from cardiac transplantation.
- Analysis of data from experimental animal models of congestive heart failure.
- Examination of alterations in cellular processes within myocytes.
Main Results:
- Studies suggest depressed myocyte function in CHF.
- Potential mechanisms include alterations in intracellular calcium handling.
- Other implicated factors are changes in myofilament function and the cytoskeleton.
Conclusions:
- The precise contribution of altered cellular processes to in vivo cardiac pump dysfunction in CHF is not yet established.
- Further research into these cellular mechanisms is critical for developing novel therapeutic strategies against CHF.
Abstract:
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.