The cardiac antiarrhythmic effects of polyunsaturated fatty acid
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Published on: July 7, 2016
Insights
Fish oil
Area of Science:
- Cardiovascular Science
- Molecular Cardiology
- Pharmacology
Background:
- Acute myocardial infarction leads to over 250,000 deaths annually in the US.
- Ischemia-induced ventricular arrhythmias, particularly ventricular fibrillation (VF), are the primary cause of these sudden deaths.
- Preventing these arrhythmias offers significant public health benefits.
Purpose of the Study:
- To investigate the antiarrhythmic effects of n-3 polyunsaturated fatty acids (PUFA).
- To determine the electrophysiological mechanisms underlying PUFA's protective action against ischemia-induced ventricular arrhythmias.
Main Methods:
- Intravenous infusion of n-3 PUFA in non-anesthetized, exercising dogs experiencing myocardial ischemia.
- Electrophysiological studies on isolated cardiac myocytes.
- Analysis of sodium channel function and interaction with PUFA.
Main Results:
- n-3 PUFA infusion prevented ischemia-induced ventricular fibrillation in dogs.
- PUFA stabilizes cardiac myocytes by altering their electrophysiology.
- PUFA directly blocks fast voltage-dependent sodium channels, prolonging their inactivated state.
Conclusions:
- n-3 PUFA possesses significant antiarrhythmic properties.
- The mechanism involves direct modulation of cardiac sodium channels.
- These findings support the potential of n-3 PUFA for preventing sudden cardiac death.
Abstract:
Each year in the United States alone some 250,000 persons die within one hour of an acute myocardial infarction. These deaths are largely due to ischemia-induced ventricular arrhythmias, primarily ventricular fibrillation (VF). Thus a safe, simple means of preventing such arrhythmias has considerable public health benefit potential. We have demonstrated that the intravenous infusion of n-3 polyunsaturated fatty acids (PUFA) from fish oils will prevent ischemia-induced VF in prepared, nonanesthetized, exercising dogs, confirming earlier feeding studies in rats. We show that this protective effect is due to an action of the free acidic form of the PUFA to alter the electrophysiology of individual cardiac myocyte so that the cells are electrically more stable. The electrophysiologic effects, in turn, result from direct and specific effects of the PUFA to block the fast voltage-dependent sodium channels. The binding of the free fatty acids is directly to the protein of the sodium channels and results in prolongation of the inactivated state of these channels. Other ion channels are also affected by the PUFA. Two clinical trials with n-3 PUFA are mentioned which inadvertently support the antiarrhythmic potential of PUFA ingestion.
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