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Optocardiography and Electrophysiology Studies of Ex Vivo Langendorff-perfused Hearts
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EC-coupling in normal and failing hearts

Jon Arne Birkeland1, Ole M Sejersted, Tore Taraldsen

  • 1Institute for Experimental Medical Research, Ullevål University Hospital, University of Oslo, Oslo, Norway. j.a.birkeland@medisin.uio.no

Scandinavian Cardiovascular Journal : SCJ
|August 16, 2005
PubMed

Insights

Systolic heart failure involves impaired heart cell function, specifically altered calcium (Ca2+) handling. Reduced sarcoplasmic reticulum (SR) Ca2+ load, likely due to impaired SR Ca2+ ATPase (SERCA) function, contributes to this dysfunction.

Area of Science:

  • Cardiology
  • Cellular Biology
  • Biochemistry

Background:

  • Systolic heart failure stems from either reduced cardiomyocyte numbers or impaired contractile function.
  • Myocardial failure, characterized by impaired cellular contractility, has an unknown pathophysiological basis but involves altered calcium (Ca2+) handling.
  • Despite unaltered L-type Ca2+ current, sarcoplasmic reticulum (SR) Ca2+ load is reduced in human heart failure, potentially explaining decreased contractility.

Purpose of the Study:

  • To investigate the underlying mechanisms of reduced SR Ca2+ load in systolic heart failure.
  • To elucidate the role of specific cellular components, including RyR, SERCA, and NCX, in the pathophysiology of myocardial failure.
  • To identify potential therapeutic targets for systolic dysfunction.

Main Methods:

  • Review and synthesis of existing literature on calcium handling in heart failure.
  • Analysis of proposed mechanisms for reduced SR Ca2+ load: RyR leak, SERCA impairment, and NCX upregulation.
  • Consideration of findings from studies involving genetically modified models.

Main Results:

  • Reduced SR Ca2+ load is a key feature of failing hearts, correlating with diminished contractility.
  • Three primary mechanisms for reduced SR Ca2+ load are proposed: RyR leak, impaired SERCA function, and increased NCX function.
  • Evidence suggests impaired SERCA function is a likely primary mechanism, while increased NCX function may be secondary but therapeutically relevant.

Conclusions:

  • Impaired SR Ca2+ ATPase (SERCA) function is a probable primary cause of systolic dysfunction in heart failure.
  • Modulating the Na+/Ca2+-exchanger (NCX) may offer therapeutic benefits.
  • Further research, particularly using genetically modified models, is crucial for a comprehensive understanding of these mechanisms.

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