Format

Send to

Choose Destination
See comment in PubMed Commons below
Wien Med Wochenschr. 2012 Jul;162(13-14):297-301. Epub 2012 Jun 12.

Calcium handling in human heart failure--abnormalities and target for therapy.

Author information

1
Department of Internal Medicine III, University of Cologne, Kerpener Str. 62, 50937 Cologne, Germany. hannes.reuter@uk-koeln.de

Abstract

The fast cycling of calcium between internal stores and the myofilaments with rapid diffusion down steep concentration gradients provides the cellular basis for cardiac contraction and relaxation. In heart failure, the intracellular Ca(2) (+) dynamics are impaired showing reduced systolic peak Ca(2) (+), elevated diastolic Ca(2) (+) levels, and prolonged diastolic Ca(2) (+) decay. The recognition that defects in the function of Ca(2) (+) handling proteins are central to the pathogenesis of heart failure has attracted attention to these proteins as potential targets for therapy. Besides pharmacologic interventions including digitalis, ranolazine, levosimendan and others, cardiac gene therapy holds great promise and the recent clinical studies have proven the feasibility of this therapeutic approach. In this review, the rationale underlying modern therapies that modulate intracellular Ca(2) (+) handling for the treatment of human heart failure are presented and discussed.

PMID:
22688623
DOI:
10.1007/s10354-012-0117-9
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Support Center