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Re: Paging Larry Hoover! Can you help here? Thanks

Posted by Larry Hoover on March 15, 2003, at 22:16:36

In reply to Paging Larry Hoover! Can you help here? Thanks (nm), posted by mopey on March 15, 2003, at 18:28:19

I know that there is clear evidence of a preventative effect of omega-3 fatty acids on the incidence of ventricular fibrillation, but I've found no reference to atrial fibrillation and omega-3s. I didn't enter into the discussion as I didn't want to appear to be discounting people's experience. Perhaps the fish oil had a arrhythmogenic effect, but there could be other factors at play.

As far as I can tell, fish oil is being given a green light with respect to cardiac function and health. Here are a couple of reviews giving that position.

Lar

Lipids 2001;36 Suppl:S111-4

Myocardial membrane fatty acids and the antiarrhythmic actions of dietary fish oil in animal models.

McLennan PL.

Smart Foods Centre, Department of Biomedical Science, University of Wollongong, NSW, Australia. petermcl@uow.edu.au

Epidemiologic studies, animal studies, and more recently, clinical intervention trials all suggest a role for regular intake of dietary fish oil in reducing cardiovascular morbidity and mortality. Prevention of cardiac arrhythmias and sudden death is demonstrable at fish or fish oil intakes that have little or no effect on blood pressure or plasma lipids. In animals, dietary intake of fish oil [containing both eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n-3)] selectively increases myocardial membrane phospholipid content of DHA, whereas low dose consumption of purified fatty acids shows antiarrhythmic effects of DHA but not EPA. Ventricular fibrillation induced under many conditions, including ischemia, reperfusion, and electrical stimulation, and even arrhythmias induced in vitro with no circulating fatty acids are prevented by prior dietary consumption of fish oil. The preferential accumulation of DHA in myocardial cell membranes, its association with arrhythmia prevention, and the selective ability of pure DHA to prevent ventricular fibrillation all point to DHA as the active component of fish oil. The antiarrhythmic effect of dietary fish oil appears to depend on the accumulation of DHA in myocardial cell membranes.


Am J Clin Nutr 2000 Jan;71(1 Suppl):202S-7S

Prevention of fatal cardiac arrhythmias by polyunsaturated fatty acids.

Kang JX, Leaf A.

Department of Medicine, Massachusetts General Hospital, Boston, MA 02129, USA.

In animal feeding studies, and probably in humans, n-3 polyunsaturated fatty acids (PUFAs) prevent fatal ischemia-induced cardiac arrhythmias. We showed that n-3 PUFAs also prevented such arrhythmias in surgically prepared, conscious, exercising dogs. The mechanism of the antiarrhythmic action of n-3 PUFAs has been studied in spontaneously contracting cultured cardiac myocytes of neonatal rats. Adding arrhythmogenic toxins (eg, ouabain, high Ca(2+), lysophosphatidylcholine, beta-adrenergic agonist, acylcarnitine, and the Ca(2+) ionophore) to the myocyte perfusate caused tachycardia, contracture, and fibrillation of the cultured myocytes. Adding eicosapentaenoic acid (EPA: 5-15 micromol/L) to the superfusate before adding the toxins prevented the expected tachyarrhythmias. If the arrhythmias were first induced, adding the EPA to the superfusate terminated the arrhythmias. This antiarrhythmic action occurred with dietary n-3 and n-6 PUFAs; saturated fatty acids and the monounsaturated oleic acid induced no such action. Arachidonic acid (AA; 20:4n-6) is anomalous because in one-third of the tests it provoked severe arrhythmias, which were found to result from cyclooxygenase metabolites of AA. When cyclooxygenase inhibitors were added with the AA, the antiarrhythmic effect was like those of EPA and DHA. The action of the n-3 and n-6 PUFAs is to stabilize electrically every myocyte in the heart by increasing the electrical stimulus required to elicit an action potential by approximately 50% and prolonging the relative refractory time by approximately 150%. These electrophysiologic effects result from an action of the free PUFAs to modulate sodium and calcium currents in the myocytes. The PUFAs also modulate sodium and calcium channels and have anticonvulsant activity in brain cells.

Full text of the above report at:
http://www.ajcn.org/cgi/content/full/71/1/202

 

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poster:Larry Hoover thread:208905
URL: http://www.dr-bob.org/babble/20030314/msgs/209553.html