How to eliminate 50 percent of all coronary events

The European Society of Cardiology estimates a 50 percent reduction of coronary events if you can stabilize soft, vulnerable plaques (1). We are often led to believe that plaques you can see on an angiogram are “killer” plaques. It’s true that if they are large enough to obstruct blood flow, they will decrease oxygen transfer to the heart muscle cells making them more tired with less effort.

This is the definition of stable angina. It simply means it takes less effort to over-exert the heart muscles before they fatigue. However, you need approximately a 90 percent total obstruction of the blood vessel to develop stable angina. These plaques account for most of the plaques you might find in an angiogram. This is why if you take an angiogram, you are often immediately wheeled into the operating room to have a stent put into the artery with the belief you are only seconds away from an immediate heart attack and death.

However, the same angiogram can’t see a few plaques (because they are so small), known as the soft, vulnerable ones. When soft, vulnerable plaques rupture (like a pimple), then you have the death and disability (i.e., damaged heart tissue) that truly characterize heart disease. Technically, this is called an acute coronary event, and it has very little to do with the stable plaques that can cause angina. It is this small number of “rogue” soft, vulnerable plaques that are the true killers in heart disease (2,3).

The ultimate cause of plaque rupture is cellular inflammation inside the plaque. Cellular inflammation degrades the fibrous external coating of the plaque. Usually inside these soft, vulnerable plaques are also a lot of macrophages engorged with lipids. This is called the “necrotic core”. When the plaque bursts, these lipid pools are released into the bloodstream causing platelet aggregation and the rapid blockage of the artery resulting in a complete restriction of blood flow (as opposed to a limited restriction of blood flow with a typical stable plaque that will never rupture). It is estimated that about 75 percent of all coronary events are caused by ruptures of the soft, vulnerable plaques (2).

As I mentioned above, the really scary part of this story is that there is no type of imaging technology that can detect dangerous soft, vulnerable plaques. In essence, you don’t know if you have them or not. This is why the prediction of impeding cardiovascular events remains a guessing game. Even more interesting is that these soft, vulnerable plaques seem to form rather quickly (in about 10 years) as opposed to growing slowly over a lifetime (4). Moreover, the rate of growth of these soft, vulnerable plaques is strongly correlated with increasing insulin levels in the blood (4).

So what does this mean for people who don’t want to die from a sudden rupture of soft, vulnerable plaques that can’t be detected? The first thing is to reduce the inflammation within the plaque. Surprisingly, there is only one clinical study that has ever been published that addressed this question, and it used fish oil (5). This study indicated that if you give patients relatively high doses of fish oil, you could see a definite remodeling of the soft, vulnerable plaques in about 40 days compared to subjects taking a placebo composed of safflower oil. The plaques in the subjects taking the fish oil became less inflamed, had higher levels of omega-3 fatty acids, fewer macrophages and more well-formed fibrous caps compared to those taking the placebo. So taking a therapeutic level of fish oil for a lifetime seems to be a good way to reduce the rupture of these plaques.

Another way to potentially reduce their formation in the first place is lower insulin levels. The reason insulin levels are elevated is because organs, such as the adipose tissue, the liver and the muscles, are also inflamed (6). The best way to reduce that systemic inflammation is to follow the anti-inflammatory diet and take therapeutic levels of fish oil for a lifetime. Your success is best measured by the AA/EPA ratio in the blood. Call me crazy, but I think that’s what I have been recommending for the past 16 years (7).

References

  1. Yia-Herttulala S, Bentzon JF, Daemen M, Falk E, Garcia-Garcia HM, Merrmann J, Hoefer IM, Juekma JW, Krams R, Kwak BR, Marx N, Maruszeqica M, Newby A, Pasterkamp G, Serruys PWJC, Waltenberger J, Weber C, and Tokgozoglu L. “Stabilization of atherosclerotic plaques.” Thomobosis and Haemostasis 106: 1-19 (2011)
  2. Schaar JA, Muller JE, Falk E, Virmani R, Fuster V, Serruys PW, Colombo A, Stefanadis C, Ward Casscells S, Moreno PR, Maseri A, and van der Steen AF. “Terminology for high-risk and vulnerable coronary artery plaques. Report of a meeting on the vulnerable plaque.” Eur Heart J 25: 1077-1082 (2004)
  3. Lloyd-Jones D, Adams R, Carnethon M, De Simone G, Ferguson TB, Flegal K, Ford E, Furie K, Go A, Greenlund K, Haase N, Hailpern S, Ho M, Howard V, Kissela B, Kittner S, Lackland D, Lisabeth L, Marelli A, McDermott M, Meigs J, Mozaffarian D, Nichol G, O’Donnell C, Roger V, Rosamond W, Sacco R, Sorlie P, Stafford R, Steinberger J, Thom T, Wasserthiel-Smoller S, Wong N, Wylie-Rosett J, and Hong Y. “Heart disease and stroke statistics–2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee.” Circulation 119:480-486 (2009)
  4. Hagg S, Salehpour M, Noori P, Lundstrom J, Possnert G, Takolander R, Konrad P, Rosfors S, Ruusalepp A, Skogsberg J, Tegner J, and Bjorkegren J. “Carotid plaque age is a feature of plaque stability inversely related to levels of plasma insulin.” PLoS One 6: e1824 (2011)
  5. Thies F, Garry JM, Yaqoob P, Rerkasem K, Williams J, Shearman CP, Gallagher PJ, Calder PC, and Grimble RF. “Association of n-3 polyunsaturated fatty acids with stability of atherosclerotic plaques: a randomized controlled trial.” Lancet 2003 361: 477-485 (2003)
  6. Sears, B. “Toxic Fat.” Thomas Nelson. Nashville, TN (2008)
  7. Sears B. “The Zone.” Regan Books. New York, NY (1995)

Nothing contained in this blog is intended to be instructional for medial diagnosis or treatment. If you have a medical concern or issue, please consult your personal physician immediately.

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About Dr. Barry Sears

Dr. Barry Sears is a leading authority on the impact of the diet on hormonal response, genetic expression, and inflammation. A former research scientist at the Boston University School of Medicine and the Massachusetts Institute of Technology, Dr. Sears has dedicated his research efforts over the past 30 years to the study of lipids. He has published more than 30 scientific articles and holds 13 U.S. patents in the areas of intravenous drug delivery systems and hormonal regulation for the treatment of cardiovascular disease. He has also written 13 books, including the New York Times #1 best-seller "The Zone". These books have sold more than 5 million copies in the U.S. and have been translated into 22 different languages.

20 thoughts on “How to eliminate 50 percent of all coronary events

  1. Never heard of this, facinating. Thanks, seems like no one sits down to figure this stuff out. Your overview of the physiology, nutrition and bio-chem is extraordinary. Even this Dr. Oz seems to have no organized dietary recommendations-though a Venn diagram of his various recommendations would show significant overlap with your system-most of the effective ones do!

    • Unfortunately that test will not indicate the levels of soft vulnerable plaques. I believe that best prevention for heart disease is the continued reduction of cellular inflammation and that is best measured by the AA/EPA ratio in the blood.

  2. Yes, this is a very interesting article.

    A question: what is a therapeutic level of fish oil?

    An observation:

    The title of the article states that 50% of all coronary events can be eliminated by the recommendations in this article. The article also states at the end of the 4th paragraph that “It is estimated that about 75 percent of all coronary events are caused by ruptures of the soft, vulnerable plaques (2).” Therefore, it implies that taking therapeutic levels of fish oil for a lifetime canl eliminate 2/3 of coronary events caused by soft plaque rupture. Is this the conclusion from the clinic study in reference [5]?

    • The best marker of a therapeutic level of omega-3 fatty acids is the amount required to keep the AA/EPA ratio in the blood between 1.5 and 3. The amount used in the clinical study was 1.4 grams of EPA and DHA per day. That may not be enough to reduce the AA/EPA ratio into the desired zone especially for Americans consuming a pro-inflammatory diet.

  3. If there is no type of imaging technology that can detect soft, vulnerable plaques, what technique did the researchers use to observe how fish oil remodeled these soft, vulnerable plaques? Drawing blood? I suppose measuring the level of soft, vulnerable plaques in the blood is not a way to make a sound prediction if those plaques are obstructing a blood vessel?

    • They did a surgical removal of the artery so they could see the soft plaques visually. Soft vulnerable plaques will not disturb blood flow until they rupture and then can cause a complete block of the arterial blood flow. However, since it was demonstrated that omega-3 fatty acids could reduce the inflammation in the plaques from the dissected tissue, the measurement of the AA/EPA ratio in the blood would be the best diagnostic test of the reduction of the likelihood of their rupture.

  4. Hi, Dr. Sears,
    A couple of questions: I’d heard that Zone Labs was going to get the blood SIP test. Any progress? What do you take for supplements on a daily basis? Is a baby aspirin part of your regime?
    Thanks,
    Joe

    • Hopefully our insurance will be ready in September so we can offer the test. The supplements that I take are high dose fish oil (7.5 grams of EPA and DHA per day) and about 16,000 ORAC units of purified polyphenols in addition to following an anti-inflammatory diet. My AA/EPA remains pretty steady at 1.5. As along as I maintain that AA/EPA ratio, I don’t take a baby aspirin.

  5. What pertinent information does the Berkeley Heart Lab test give in relation to your above article and information?

  6. What pertinent information does the Berkeley Heart Lab test give in relation to your above article and information?

    Thanks

    • The Berkely Heart Lab test gives the size of the LDL particle. The larger the percentage of large LDL particles, the less likely they are to be oxidized leading to the acceleration of soft vulnerable plaques. A better test in my opinion would be the levels of oxidized cholesterol in the blood. We are working on the validation of that test in our clinical laboratory and should be ready by the end of this year.

      • Dr.Sears,

        my girlfriend and me started the zone diet a couple of months ago.

        we started to take fishoil app. 3 weeks ago.

        we feel good but we identified more pimples sometimes on face and cleavage.
        is this possibly coming from the fish oil?
        or is our fat releasing the toxins now?

        thanks

        klaus

        • The fish oil will help reduce the cellular inflammation in the fat cells making them more likely to release stored arachidonic acid (AA). It is the AA that is causing the pimples to form. I would suggest taking more fish oil to counteract the released AA from the fat cells.

          Consider AA to be a very potent toxin. My most recent book, Toxic Fat, describes the reason why in greater detail.

          • thanks,

            for answer, i´m reading toxic fat actual.
            i´ll do a AA/EPA test and you gave me in another articel a dr. in vienna doing the test and i´m unable to find the blog again (i think it was named how to remove super bad cholesterol..)

            can you please repeat the name

            thx´s

  7. Pretty portion of content. I just stumbled upon your weblog and in accession capital to say that I get in fact loved account your blog posts. Anyway I?ll be subscribing to your feeds and even I success you get admission to persistently fast.

  8. question: 1 gram of fish oils would equal to how many DHA and EPA units? So if I want to take high dose like 4 to 7 grams of fish oil per day how many units of EPA and DHA do I take?

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