STORY OF THE WEEK
Published in Primary Care and
Journal Scan / Research · August 09, 2016
- In this multicenter, double-blind trial, patients who suffered an acute MI were randomly assigned to 6 months of high-dose omega-3 fatty acids (n = 180) or placebo (n = 178). Significant reductions in left ventricular systolic volume index (−5.8%l; P = .017), non-infarct myocardial fibrosis (−5.6%; P = .026), and serum biomarkers of inflammation and myocardial fibrosis were observed in the omega-3 fatty acids group compared with the placebo group. In addition, increases in red blood cell omega-3 fatty acid correlated with decreases in left ventricular systolic volume index.
- Following acute MI, high-dose omega-3 fatty acids had a beneficial effect on left ventricular remodeling, non-infarct myocardial fibrosis, and biomarkers of inflammation beyond standard-of-care therapy.
Benefits of Omega-3 Fatty Acids From Fish Oil After Acute MI (Heart Attack) was last modified: July 3rd, 2017 by asmithers
Written By-Paul D Thompson MD
Writen By-Peter LIn MD CCFP
What is the deal with omega-3 supplements?
Omega-3 fatty acid has been shown to reduce death post-MI in some studies; but, yet, in other studies, it has no effect. So does it work or not?
In this study, instead of looking at hard endpoints like death or MI, the researchers used cardiac MRI to look for subtle changes in the myocardium. It was a small study of 358 post-MI patients. Half of the participants received 4 gm of omega-3 supplements, and, after 6 months, these patients had less non–infarct related myocardial fibrosis. They also had a reduced left ventricular systolic volume index by 5.8%. They had lower inflammatory markers in their blood, and the higher the levels of omega-3, the better the results; so, the effect seen with omega-3 seemed to be dose-dependent.
Now, before we go betting the farm on omega-3 supplements, let’s go back to some basics of what omega-3 fatty acids really are.
Fatty acids are long chains of carbons with hydrogens attached to them. The tail is referred to as the omega end. These fatty acids are named by where the first double bond is between the carbons. So, omega-3 means that the first double bond is at the third carbon counted from the tail end, the omega end. Omega-6 is a fatty acid that has the first double bond at the sixth carbon.
Both omega-3 and -6 are essential fatty acids, meaning that our bodies cannot make them so we need to eat them in our diet. Many chemicals needed by the body are made from both omega-3 and -6. However, one family of chemicals that can be produced from them is called eicosanoids. This family includes some very familiar chemicals like leukotrienes (inflammation), thromboxane (blood clots), and prostaglandins, which cause inflammation and other effects in the body.
Omega-6 is processed in the body much faster than omega-3, and so it creates more “bad” chemicals. A lot of omega-6 produces a lot of bad chemicals, but more omega-3 counterbalances this, which is why we think of omega-3 as good. In reality, however, omega-3 is simply not as bad as omega-6. Experts believe that we should be eating at a 1:1 ratio of omega-6 to omega-3.
Unfortunately, our western diet is more like 10:1 to 30:1 of omega-6 to omega-3. Too much omega-6 means we make a lot of inflammatory and thrombotic chemicals. Our diet has evolved to higher omega-6 content over the years. For example, corn oil is 46:1 omega-6 to omega-3. The ratio in grass-fed cows is 2:1, but it is more like 4:1 in grain-fed cows. There is less omega-3 in grains than in grass, and so grain-fed cows have less omega-3.
Perhaps to make sense of these studies we need to look at the omega-6 to omega-3 ratios. In the old studies, 1 gm of omega-3 was given to the participants, but if the participants had ratios of 30:1 then that 1 gm would not have had any impact. So, perhaps using the ratio to separate out the patients may give us more consistent outcomes.
For now, how should we improve the ratio? Omega-3 is made in plants, seaweed, and algae. So we can eat more plant-based foods and seaweed. Fish eat the algae, which is how they become rich in omega-3, so we can eat fish. Some estimates put omega-3 at seven times the level of omega-6 in fish; but, remember, that the larger the fish, the greater the amounts of heavy metals they accumulate. So, we should not eat too much of the big fish like tuna but perhaps should focus more on the small, oily fish, which have not lived long enough to accumulate these toxins. For meat, we should try for that from grass-fed livestock.
Perhaps the key is to balance our omega-3 and -6. Maybe it’s simpler to just take a supplement as was done by participants in this study; but, for the majority of us, perhaps we should choose foods that have a better ratio of omega-3 to omega-6. Remember, we can’t make these so our bodies will have to use what we eat. So choose wisely.
This abstract is available on the publisher’s site.
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Omega-3 fatty acids from fish oil have been associated with beneficial cardiovascular effects, but their role in modifying cardiac structures and tissue characteristics in patients who have had an acute myocardial infarction while receiving current guideline-based therapy remains unknown.
In a multicenter, double-blind, placebo-controlled trial, participants presenting with an acute myocardial infarction were randomly assigned 1:1 to 6 months of high-dose omega-3 fatty acids (n=180) or placebo (n=178). Cardiac magnetic resonance imaging was used to assess cardiac structure and tissue characteristics at baseline and after study therapy. The primary study endpoint was change in left ventricular systolic volume index. Secondary endpoints included change in noninfarct myocardial fibrosis, left ventricular ejection fraction, and infarct size.
By intention-to-treat analysis, patients randomly assigned to omega-3 fatty acids experienced a significant reduction of left ventricular systolic volume index (–5.8%, P=0.017), and noninfarct myocardial fibrosis (–5.6%, P=0.026) in comparison with placebo. Per-protocol analysis revealed that those patients who achieved the highest quartile increase in red blood cell omega-3 index experienced a 13% reduction in left ventricular systolic volume index in comparison with the lowest quartile. In addition, patients in the omega-3 fatty acid arm underwent significant reductions in serum biomarkers of systemic and vascular inflammation and myocardial fibrosis. There were no adverse events associated with highdose omega-3 fatty acid therapy.
Treatment of patients with acute myocardial infarction with high-dose omega-3 fatty acids was associated with reduction of adverse left ventricular remodeling, noninfarct myocardial fibrosis, and serum biomarkers of systemic inflammation beyond current guidelinebased standard of care.