Mitochondria and Cardiac Dysrhythmias

  • José Marín-García
Chapter

Abstract

Ventricular dysrhythmias represent the most predominant etiology of sudden cardiac death throughout the world. However, the mechanisms underlying fatal ventricular dysrhythmias are not fully understood. Over the last two decades, a growing body of evidence supports the concept that cardiac mitochondria may be involved at least in part in the genesis of cardiac dysrhythmia. The principal objective of this chapter is to describe the role that mitochondria play in altering the heart’s electrical function by introducing heterogeneity into the cardiac action potential. A focus will be placed on how the energetic status of the mitochondrial network can alter sarcolemmal potassium fluxes through ATP-sensitive potassium channels, thereby creating a “metabolic sink” for depolarizing wave fronts and introducing conditions that favor generation of fatal dysrhythmia. Mechanisms by which mitochondria depolarize under conditions of oxidative stress are characterized, and the contributions of several mitochondrial ion channels to mitochondrial depolarization are reviewed. The inner membrane anion channel in particular opens upstream of other inner membrane channels during metabolic stress and may constitute an effective target to prevent the metabolic oscillations that enhance action potential lability. Finally, therapeutic strategies that may prevent dysrhythmias by preserving mitochondrial membrane potential in the face of oxidative stress will be discussed, supporting a concept that treatments aimed at cardiac mitochondria may have the potential in attenuating electrical dysfunction in the heart.

Keywords

Estrogen Glutathione Respiration Adenosine Folic Acid 

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Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  • José Marín-García
    • 1
  1. 1.The Molecular Cardiology and Neuromuscular InstituteHighland ParkUSA

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