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Cardiovascular Research 2001 49(2):253-256; doi:10.1016/S0008-6363(00)00305-9
© 2001 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Reduced abundance of transverse tubules and L-type calcium channels: another cause of defective contractility in failing ventricular myocytes

Steven R Houser*

Cardiovascular Research Group, Department of Physiology, Temple University School of Medicine, 3400 North Broad Street, Philadelphia, PA 19140, USA

* Tel.: +1-215-707-3278; fax: +1-215-707-4003 srhouser@unix.temple.edu

The first 150 words of the full text of this article appear below.

See article by He et al. [1] (pages 298–307) in this issue.


   1 Introduction
 
Congestive heart failure (CHF) is a complex syndrome that is the leading cause of death in Western society. A central feature of this syndrome is reduced cardiac contractility and blunted adrenergic responsiveness that together cause poor pump performance and limit exercise tolerance. Depression of myocyte contractility is thought to be a principle cause of the progressive decline in cardiac function that is a hallmark feature of end-stage CHF. The cellular and molecular basis of dysfunctional myocyte contractility in CHF is currently being studied in many laboratories in the hope that novel therapeutic targets can be identified. The manuscript by He et al. [1] in the current issue of Cardiovascular Research focuses on changes in transverse (T)-tubules and L-type Ca channel abundance in the contractile defects of ventricular myocytes from a canine model of CHF induced by rapid pacing.

. . . [Full Text of this Article]


   2 Do alterations in the structure of failing cardiac myocytes cause abnormal ECC?
 

   3 Do changes in protein abundance cause dysfunctional ECC?
 

   4 Does abnormal protein regulation cause defective ECC?
 

   5 Final considerations
 

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