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Review
. 2009 Aug;2(4):460-9.
doi: 10.1161/CIRCEP.109.880773.

Impact of dietary fatty acids on cardiac arrhythmogenesis

Julie H Rennison  1 , David R Van Wagoner
Affiliations
Review

Impact of dietary fatty acids on cardiac arrhythmogenesis

Julie H Rennison et al. Circ Arrhythm Electrophysiol. 2009 Aug.
No abstract available

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Figures

Figure 1
Figure 1
Chemical structure of saturated, monounsaturated, and polyunsaturated fatty acids. Fatty acids are straight chains of carbon atoms with a carboxylic end (COOH) and a methyl, or omega, end (CH3). Saturated fatty acids, such as palmitic acid (16:0), have no double bonds. Oleic acid (18:1n9), an 18-carbon monounsaturated fatty acid, has 1 double bond on the ninth carbon when counting from the omega end. ω6-polyunsaturated fatty acids, such as linoleic acid (18:2n6) and arachidonic acid (20:4n6), have the first double bond at the sixth carbon from the omega end. Similarly, ω3-polyunsaturated fatty acids, such as α-linolenic acid (18:3n3), eicosapentaenoic acid (20:5n3), and docosahexaenoic acid (22:6n3), have the first double bond at the third carbon from the omega end.
Figure 2
Figure 2
Pathways underlying lipid modulation of cardiac arrhythmogenesis. Lipids can promote cell injury and inflammation, which can increase lysophospholipids (lysoPL) through enhanced phospholipase A2 (PLA2) activity. Dyslipidemia also leads to loss of vagal tone and sympathetic dominance, resulting in decreased heart rate variability and increased heart rate. These effects promote myocyte calcium overload, which amplifies cellular injury. Calcium overload also promotes oxidative stress and inhibition of mitochondrial oxidative phosphorylation.
Figure 3
Figure 3
Antiarrhythmic effects of dietary ω3 PUFA. ω3 PUFAs decrease fibrosis by inhibiting cytokine production and systemic inflammation (PDGF, platelet-derived growth factor; CRP, C-reactive protein; TNF-α, tumor necrosis factor-α; and IL-6, interleukin-6). Inhibition of cytokine production and antioxidant effects minimize reactive oxygen (ROS) and reactive nitrogen (RNS) production, resulting in decreased post-translational modification of ion channels and preservation of a reduced redox state. Decreased ROS production improves ATP production by oxidative phosphorylation, limiting sodium loading, calcium overload, and ectopic activity. Finally, ω3 PUFA can prevent apoptosis induced by mitochondrial calcium overload
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