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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes

Published on: September 18, 2017

Myocardial calcium signalling and arrhythmia pathogenesis

Mark Scoote1, Alan J Williams

  • 1Department of Cardiac Medicine, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, Dovehouse Street, London SW3 6LY, UK. mark.scoote@imperial.ac.uk

Biochemical and Biophysical Research Communications
|September 1, 2004
PubMed

Insights

Defects in heart calcium signalling cause contractile dysfunction and arrhythmias. Understanding these defects offers new therapeutic strategies for inherited and acquired heart conditions.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Physiology

Background:

  • Myocardial calcium signalling is crucial for normal heart function, particularly in excitation-contraction coupling.
  • Defective calcium handling in cardiomyocytes is linked to heart failure and cardiac arrhythmias.
  • Abnormal calcium homeostasis is implicated in both inherited and acquired heart disease.

Purpose of the Study:

  • To review defects in cardiomyocyte calcium homeostasis leading to pro-arrhythmogenic phenomena.
  • To discuss recent insights into inherited and acquired arrhythmia syndromes involving defective calcium signalling.
  • To explore potential new anti-arrhythmic therapeutic strategies.

Main Methods:

  • Literature review of studies on myocardial calcium signalling.
  • Analysis of defects in excitation-contraction coupling components.
  • Examination of calcium homeostasis in cardiac disease contexts.

Main Results:

  • Abnormalities in calcium handling are central to contractile dysfunction in heart failure.
  • Defective calcium signalling contributes to various forms of cardiac arrhythmias, including inherited sudden death syndromes.
  • Both inherited and acquired cardiac diseases show a dependence on disrupted calcium homeostasis.

Conclusions:

  • Defective cardiomyocyte calcium signalling is a key patho-physiological mechanism in heart failure and arrhythmias.
  • Insights into calcium signalling defects provide a basis for developing novel anti-arrhythmic therapies.
  • Targeting calcium handling pathways may offer new treatment avenues for cardiac arrhythmias.

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