Abstract

Both animal and clinical studies have demonstrated that omega-3 fatty acids have anti-arrhythmic properties. It has been suggested that these anti-arrhythmic effects are due to modulation of the activity of various myocardial calcium handling proteins such as ryanodine receptor (RyR), L-type calcium current and sodium/calcium exchanger. In this article, we review all the data available on the effects of omega-3 fatty acids on ventricular myocardial calcium handling. In addition we highlight some unanswered questions and discuss possible therapeutic benefits of omega-3 fatty acids.

Highlights

  • Omega-3 poly-unsaturated fatty acids (PUFA) have generated considerable interest as well as controversy regarding their role as anti-arrhythmic agents

  • We rapidly summarize normal myocardial calcium handling and the alteration in calcium handling that lead to delayed after-depolarization (DAD) and triggered activity (TA)

  • Similar to what was previously described by Leifert et al in rat cardiac myocytes, the Coronel group demonstrated that incorporation of Docosahexaenoic acid (DHA) and Eicosapentaenoic acid (EPA) in the membrane of pig ventricular myocytes reduced the incidence of calcium waves and DADs during challenge with norepinephrine (Berecki et al, 2007)

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Summary

Introduction

Omega-3 poly-unsaturated fatty acids (PUFA) have generated considerable interest as well as controversy regarding their role as anti-arrhythmic agents. Rat - or DHA up to 7.5 μM caused AP prolongation Guinea pig—AP shortening was observed already at lower concentrations such as around 5 μM Inhibition of calcium current and the RyR and the shortening of the AP produce marked reduction in calcium transient amplitude and cell shortening 1.

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Conclusion
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