Icosapent Ethyl: Exploring the Remarkable Benefits of the...
Icosapent Ethyl: Exploring the Remarkable Benefits of the REDUCE-IT Trial for Patients with Recent ACS Prof Philippe Steg
By Professor Philippe Steg
That may be the most difficult question because, a clinical trial doesn't study this. A clinical trial tests, whether it's efficacious and whether it's safe and well tolerated, and those are the answers we have from REDUCE-IT. Outside of REDUCE-IT from prior experience and from studies that have been done since, there is evidence that, Icosapent Ethyl is efficacious in lowering triglycerides, reducing CRP to a moderate extent, improving endothelial function, probably has some genuine antiplatelet effects and increases the serum level of EPA. Efficacy appears to be quite correlated to the increase in EPA that's measured in the bloodstream of patients after a year.
Can the benefits of EPA be generalized to other patient populations beyond these included in the reduce it trial?
I think it's a tantalizing question. We don't have a good answer to this until we've tested it. I think until we test it, the safest bet is to use the drug in the population in which it was proven to be efficacious. So I would advise to stick to the REDUCE-IT patient population with the Icosapent Ethyl, although, I think it's a very reasonable proposition to test it in patients, for instance, who have high cardiovascular risk or established cardiovascular disease and do not have elevated triglycerides.
How does the use of EPA impact the incidents of fatal cardiovascular events in patients with recent ACS?
So in the overall REDUCE-IT trial, which enrolled patients who were adults on statins with triglycerides between 135 and 500, were either in secondary prevention or diabetics with at least one additional risk factor. There was a marked and robust cardiovascular event prevention effect with Icosapent Ethyl, compared to placebo, approximately a 25% reduction in cardiovascular events. That reduction included the primary outcome, which was a quintal composite. But also the key secondary outcome, which was CVS, MI and stroke, the conventional triple composite MACE outcome. It included total events, it included a significant reduction in mi, a reduction in stroke, and a reduction in cardiovascular mortality. So there were really substantial and robust benefits overall in the trial. Now, we wondered whether the efficacy and safety would be different in patients with recent ACS, and there were a number of reasons to look at this. First the recent ACS patient population is a high risk patient population in whom thrombosis may play a more important role in inflammation and atherosclerosis in determining risk and benefit of interventions, and therefore we were not sure that the treatment would be as beneficial. On the flip side of the equation, we were also concerned that there might be more safety concerns with Icosapent Ethyl in that specific population who is often receiving intensive antithrombotic therapy and dual antiplatelet therapy than in the overall trial population. And what we found is actually the reverse. What we found is that this group of patients with recent ACS. Approximately 1500 patients with a median time since the index ACS of approximately 5 months had tremendous benefit from Icosapent Ethyl, in terms of reducing the primary outcome, they had a 37% ACS risk reduction, a 9%, 9.3% absolute risk reduction, and a number needed to treat to avoid one primary outcome event of only 11. So this is the population that has the highest risk and the greatest benefit from treatment. And in terms of safety, we were concerned with bleeding, in fact, there was no increase in bleeding, in that population with Icosapent Ethyl. Numerically, if anything, there were fewer bleeds with Icosapent Ethyl with placebo, and that was also true in the subset of patients who were recent ACS on dual antiplatelet therapy, a population of particular concern.
Finally, as in the overall trial, there was a statistically significant increase in the risk of atrial fibrillation or flutter with Icosapent Ethyl. But I would like to point out that despite this increase, there were fewer strokes with Icosapent Ethyl, and fewer, CV deaths in the Icosapent Ethyl arm. So it seems to really that this is a high risk patient population that rise particular benefit. There is no reason to withhold treatment or deny treatment to these patients due to concerns of bleeding.
How does the efficacy of EPA compared to other medications commonly used in the management of ACS, such as aspirin and beta blockers?
Well, we had a medium follow up, which I think was a little over 4 years. But when we look at the outcome event rates, in the REDUCE-IT trial, there are really straight lines. And so it seems that the longer you treat, the greater the benefit. And I don't see any particular reason why we would want to discontinue a therapy that is so effective. So I think we should, once we institute therapy on those patients who are eligible and if they tolerate it, I would continue it long term because probably, as with most secondary prevention therapies, they only work if you take them.
What is the recommended duration of treatment with EPA following ACS, and are there any considerations for discontinuing or tapering medications?
Well, it's really hard to give a formal answer to this because we haven't done the permutation trials that would really address this scientifically. Historically aspirin was tested, on its own Beta blockers quite a while ago then statins were introduced, ACE inhibitors in ARBs and more recently novel agents to lower LDL cholesterol, and then Icosapent Ethyl for hypertriglyceridemia patients. I think when we look at the magnitude of the benefit, this is one of the most potent preventive interventions we can use in patients with established thrombosis. The 25% relative risk reduction favorably compares with most interventions for secondary prevent.
What is the role of EPA and secondary prevention of ACS? And can it be used in combination with other preventative therapies?
I think it has a strong role for patients who are eligible, which I'll remind our audience, our patients with a prior cardiovascular event or patients in primary prevention who have a another risk factor. But if we're talking about post ACS, so there are patients who've had an event and who have received statins, have LDL cholesterol that's reasonably controlled with statins and triglycerides between 135 and 500. I think this is the eligible patient population to which we should stick. Now, not only do I think that it should be used in combination, with other preventive measures, I think it's really important that patients receive full-fledged secondary prevention treatment. In fact, in REDUCE-IT, the rates of uses of evidence-based secondary prevention treatments was very high. This was a well-treated population as would be demand. By regulators and third party payers to evaluate properly this therapy and in REDUCE-IT, we were careful to enforce high rates of uses of secondary prevention treatments.
What are the potential cost savings associated with the use of EPA in the management of ACS?
So, as you know, cost effectiveness studies are quite tricky, and they're largely based on modeling and hypotheses. We have done within the trial using trial data, a cost effectiveness study by Dr. Weintraub, which was published, I think last year, which showed that Icosapent Ethyl was quite cost effective, which isn't surprising given that, it's not that expensive and it's extremely effective. So when you have such a strong treatment effect, usually most treatments are gonna be cost effective and it is cost effective. But I will acknowledge that this is modeling and there's always an element of judgment in how you select the model and whether you believe the models or not, I think it's an extremely effective therapy and it's not a very expensive therapy.
What patient characteristics such as age or comorbidities, should be considered when determining the appropriate use of EPA in the management of ACS?
Well, you know, again, I, I think we have to come back to the inclusion criteria. I think that's the best way to apply the evidence is to use the treatment in the population that, which it was exactly tested, that was statin treated adult men and women, with established cardiovascular disease or diabetes mellitis, and at least one other risk factors with TGS between 135 and 500 and an LDL cholesterol between 40 and a 100 on a statin. So that's the target population. When we model how many patients with cardio coronary artery disease, that would represent, we found in several large scale registries that it represented approximately 15% of the patients, so 1 out of 8 coronary artery disease patients is eligible for Icosapent Ethyl.
Can you achieve the same benefit with diet enriched in fish or with over the calendar supplements?
One last point I'd like to point out to our audience is that Icosapent Ethyl was remarkably effective in the REDUCE-IT trial. This corresponds to highly purified high dose EPA, eicosapentaenoic acid . Now, other combinations of omega-3 fatty acids haven't shown the same efficacy, whether it's combination of EPNDHA or lower dose EPA. I will also point out that supplements that can be routinely found over the counter and are widely used in certain countries, including the United States, omega-3 fatty acid acid supplements should not be used in substitution for EPA or Icosapent Ethyl because when we test them and there are labs such as Preston Mason's lab in Harvard that have tested them. What we find is that their content is unpredictable and can often be not as rich in omega-3. Fatty acid as expected, contained a variety of omega-3 fatty acid acids and contained oxidized omega-3 fatty acids, which are probably not beneficial and likely detrimental. Finally, although diet is important, if we wanted to reach the levels of plasma or serum EPA that are achieved with Icosapent Ethyl, we would need to eat, an enormous amount of fish, every day long term, which is probably not feasible. So I think it's good to eat some fish but I don't think that we can reasonably expect to achieve the same clinical benefits with the amount of EPA that is in a fish rich diet.
In closing, what message would you like to convey to our cardiology viewers as a physician?
I think we have now one more tool in our preventive armamentarium. In addition to the existing, important therapies such as antiplatelet agents antianginal agents, ACE inhibitors. And statins, ezetimibe, and the like. We now have an agent to address the residual risk that's related to elevate triglycerides in that population. And given the magnitude of the benefit and the relative safety of the treatment, we should leverage this and use it widely in the eligible patients. We don't often have therapies that have established reductions in cardiovascular mortality and Icosapent Ethyl does have that. And I think it's important, and our most recent analysis in recent ACS patients found that the recent ACS patient population appears to be the one that derived the greatest benefit and no particular harm. So I think that's a good target audience for our treatment.
What is Icosapent Ethyl and how is it used in Cardiology?
Icosapent ethyl is a prescription medication used to treat high triglyceride levels in the blood. It is a type of omega-3 fatty acid that is derived from fish oil. Specifically, icosapent ethyl is a purified form of eicosapentaenoic acid (EPA), which is one of the main types of omega-3 fatty acids found in fish oil.
High levels of triglycerides in the blood can increase the risk of heart disease, stroke, and other related health problems. Icosapent ethyl works by reducing the production and storage of triglycerides in the liver, which helps to lower triglyceride levels in the blood. It is usually taken orally as a capsule, and the dosage and length of treatment may vary depending on the individual's medical history and condition.
10 Key Takeaways from the REDUCE-IT trail on Icosapent Ethyl
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The REDUCE-IT trial found that icosapent ethyl reduced the risk of major adverse cardiovascular events (MACE) by 25% compared to placebo.
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MACE includes cardiovascular death, non-fatal myocardial infarction, non-fatal stroke, coronary revascularization, and hospitalization for unstable angina.
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The benefit of icosapent ethyl was observed in patients who had elevated triglyceride levels (≥150 mg/dL) and were receiving statin therapy.
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Icosapent ethyl was associated with a 20% reduction in the risk of cardiovascular death compared to placebo.
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The trial also found that icosapent ethyl reduced the risk of myocardial infarction by 31% compared to placebo.
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Icosapent ethyl was generally well-tolerated by patients in the trial, with no significant safety concerns identified.
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The results of the REDUCE-IT trial suggest that icosapent ethyl has a different mechanism of action compared to other omega-3 fatty acid supplements.
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The trial demonstrated that icosapent ethyl has significant anti-inflammatory effects, which may contribute to its cardioprotective effects.
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The REDUCE-IT trial was a randomized, double-blind, placebo-controlled trial, which is considered the gold standard for clinical trials.
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The results of the REDUCE-IT trial have been incorporated into clinical guidelines, and icosapent ethyl is now recommended as an adjunct therapy for patients with elevated triglyceride levels who are receiving statin therapy.
Professor Philippe Steg - About The Author, Credentials, and Affiliations
Professor Philippe Gabriel Steg is a renowned cardiologist and academic who has made significant contributions to the field of cardiovascular medicine. He was born on February 10, 1958, in Paris, France, and obtained his medical degree from the University of Paris.
Professor Steg is currently a professor of cardiology at the Université Paris-Diderot and the Head of the Cardiology Department at Hôpital Bichat in Paris. He is also a Senior Consultant at the Cardiology Department of the Hôpital Européen Georges Pompidou in Paris.
Throughout his career, Professor Steg has been at the forefront of research in the field of cardiovascular medicine, with a focus on the prevention and treatment of atherosclerosis and acute coronary syndrome. He has authored or co-authored over 700 scientific papers, and his research has been published in leading medical journals such as The Lancet, the New England Journal of Medicine, and Circulation.
Professor Steg has received numerous awards and honors for his contributions to cardiology, including the Grand Prix Scientifique of the French Academy of Medicine, the European Society of Cardiology Gold Medal, and the International Atherosclerosis Society Distinguished Leadership Award. He is also a Fellow of the European Society of Cardiology, the American College of Cardiology, and the American Heart Association.
In addition to his research and clinical work, Professor Steg is a dedicated teacher and mentor to many young cardiologists. He has supervised numerous doctoral theses and has served on the editorial boards of several medical journals, including the European Heart Journal and the Journal of the American College of Cardiology.
Overall, Professor Philippe Gabriel Steg is a highly respected and accomplished cardiologist who has made significant contributions to the field of cardiovascular medicine. His work has helped to improve our understanding of the prevention and treatment of heart disease, and his research continues to inspire and inform medical professionals around the world.
Atherosclerosis Model: Comparing Mineral Oil, Corn Oil, E...
Atherosclerosis Model: Comparing Mineral Oil, Corn Oil, EPA, and DHA in Vitro: Phospholipid Membrane Oxidation Rates Preston Mason PhD
By Preston Mason, PhD, MBA
I'd like to discuss with you two presentations I recently gave at the American College of Cardiology meetings in New Orleans. They both have a similar theme and they both looked at the effects of pharmaceutical grade, mineral oil, and corn. And compared to Eicosapentaenoic Acid and Docosahexaenoic Acid in lipoproteins as well as in membranes. Now, omega-3 fatty acids are, the two primary ones are Eicosapentaenoic Acid or EPA and Docosahexaenoic Acid, or DHA. In clinical trials there have been discordant outcomes depending on the formulation used in trials using a highly purified formulation of EPA, known as icosapent ethyl. There have been significant reductions in cardiovascular events, most notably the REDUCE-IT trial. This was a trial using patients followed over time, and there was a resulting 25% relative risk reduction among patients randomized to icosapent ethyl, or IPE compared to placebo, and this includes a 31% reduction in myocardial infarction, stroke, and cardiovascular death. By contrast trials using mixed omega-3 fatty acids. That is EPA plus DHA. Have failed to show benefit in a consistent basis.
Most notably, or most recently was a STRENGTH trial, which used a identical dose, 4 grams per day of, in this case, a combination of EPA and DHA, like REDUCE-IT there were high risk patients and like REDUCE-IT they looked at a composite of cardiovascular events, but unlike REDUCE-IT, the trial was stopped early due to futility. So there have been a lot of questions about why such different outcomes in these two trials. Well, the obvious point is that these are two different medications. One is a highly purified EPA in the form of icosapent ethyl. The other was a mixed omega-3 fatty acid in the form of free carboxylic acids. And yet still people have asked other questions, well maybe it could be due to the different placebo. One was a mineral oil, which is commonly used in trials involving omega-3 fatty acids, the other was corn oil. Now corn oil is highly enriched with linoleic acid, which is an Omega-6 fatty acid, whereas mineral oil is made up of mixture of aliphatic chains, generally C16 to C24, and they're used again at relatively low doses, 2 grams, BID. Now in this study, we wanted to evaluate what potential effects of these different oils might have on a key pathway of atherosclerosis, namely lipoprotein and membrane oxidation. So when lipoproteins become oxidized, they undergo, they become highly atherogenic. They trigger inflammation, endothelial dysfunction, foam cell formation, and a number of other important pathways leading to atherosclerosis. Now when membranes become oxidized, there's also significant damage to the cell, leading ultimately to cell death by apoptosis or necrosis. It also triggers inflammation, damages proteins leading to alterations of signal transduction, and a number of other changes associated with atherosclerosis. So agents that interfere with lipoprotein and membrane oxidation would be considered atheroprotective.
Now we, in this study, compared these oils on this process now we found very consistent results in these two different lipid fraction. We found that both the pharmaceutical grade mineral oil and corn oil failed to have any effect pro or antioxidant in both the membranes and in the lipoprotein particles. So even at very high doses, even higher than would be seen in clinical trials, these placebo oils had a neutral effect on atherosclerosis. Now by contrast, EPA had very potent antioxidant or AFA protective effects. It inhibited oxidation of both lipoproteins, and this included two different fractions, small dense LDL as well as VLDL and membranes in a highly consistent and reproducible fashion, inhibiting oxidation by as much as 90% up to 4 hours. By contrast, DHA had only limited antioxidant effects that were lost after just a few hours.
So in conclusion, we see very different effects of these different oils on this process of atherosclerosis. Specifically, EPA had potent and reproducible antioxidant effects, which be seen as atheroprotective, that were sustained over time compared to DHA and these two different placebo oils. We also believe that this atheroprotective benefit or antioxidant benefit may be part of the explanation for why formulations using EPA alone may result in the benefits seen in outcome trials compared to mixture of EPA with DHA. I'd like to acknowledge again my co-authors and, this was independently funded study. Thank you very much.
What is Atherosclerosis Model, and how is it used in Cardiology?
Atherosclerosis is a medical condition in which plaques build up inside the arteries, leading to a narrowing of the arteries and reduced blood flow. The development of atherosclerosis is a complex process that involves multiple factors, including inflammation, oxidative stress, and lipid metabolism.
The atherosclerosis model is a way of understanding how this disease progresses and how it can be treated. In this model, the development of atherosclerosis is divided into several stages:
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Endothelial dysfunction: The inner lining of the arteries (endothelium) becomes damaged, often due to factors like high blood pressure, smoking, or high cholesterol.
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Fatty streaks: Fatty deposits (lipids) begin to accumulate in the damaged area of the artery, leading to the formation of a fatty streak.
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Fibrous plaque: The fatty streak can become more advanced and develop into a fibrous plaque, which contains smooth muscle cells, collagen, and other substances.
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Complicated plaque: In some cases, the fibrous plaque can rupture, leading to the formation of a blood clot that can block the artery and cause a heart attack or stroke.
Understanding the atherosclerosis model is important in cardiology because it helps doctors to identify patients who are at risk of developing the disease and to develop appropriate treatment plans. Treatment options for atherosclerosis include lifestyle changes (such as exercise and a healthy diet), medication to control risk factors like high blood pressure and cholesterol, and in some cases, surgery to open blocked arteries.
10 Key Takeaways from these Clinical trials about the Atherosclerosis Model
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Omega-3 fatty acids have a protective effect against oxidative stress-induced damage to cell membranes.
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Pharmaceutical grade mineral oil and corn oil do not provide any significant protective effect against oxidative stress-induced damage to cell membranes.
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The results of this trial suggest that omega-3 fatty acids may play an important role in maintaining the integrity of cell membranes.
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The protective effect of omega-3 fatty acids on cell membranes may contribute to their beneficial effects on cardiovascular health.
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The trial provides further evidence for the importance of a diet that includes a sufficient amount of omega-3 fatty acids.
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The results of this trial support previous studies that have demonstrated the beneficial effects of omega-3 fatty acids on cardiovascular health.
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The study suggests that the protective effect of omega-3 fatty acids on cell membranes may be due to their ability to reduce oxidative stress.
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The trial highlights the potential limitations of using mineral oil and corn oil as control substances in studies examining the effects of dietary interventions.
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The results of this trial may have implications for the development of novel therapies for cardiovascular diseases.
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The study provides valuable insights into the mechanisms underlying the protective effects of omega-3 fatty acids on cardiovascular health.
R. Preston Mason, PhD, MBA - About The Author, Credentials, and Affiliations
R. Preston Mason, PhD, MBA, is a renowned scientist and entrepreneur who has made significant contributions to the fields of biochemistry, cardiovascular disease, and translational medicine. He is currently an Associate Professor of Medicine at Harvard Medical School, where he leads a research laboratory focused on developing novel therapeutic approaches for cardiovascular disease.
Dr. Mason earned his Bachelor of Science degree in chemistry from Tuskegee University, followed by a PhD in biochemistry from Emory University. He then pursued an MBA from the Wharton School at the University of Pennsylvania, where he developed his business acumen and honed his skills as an entrepreneur.
Throughout his career, Dr. Mason has held various academic and industry positions, including serving as a faculty member at the University of Connecticut School of Pharmacy and as a senior scientist at Pfizer, Inc. He has also founded several companies, including Elucida Research, LLC, which develops drug delivery technologies for various therapeutic applications.
Dr. Mason's research has led to over 150 peer-reviewed publications and numerous patents. His work has been recognized with several awards, including the American Chemical Society's Heroes of Chemistry Award and the Black Engineer of the Year Award. He is also a Fellow of the American Heart Association.
In addition to his research and entrepreneurial pursuits, Dr. Mason is dedicated to mentoring the next generation of scientists and entrepreneurs. He has served as a mentor to numerous graduate students, postdoctoral fellows, and young professionals, and he is committed to promoting diversity and inclusion in science and entrepreneurship.
Overall, Dr. R. Preston Mason's interdisciplinary background and expertise have enabled him to make significant contributions to the fields of biochemistry and cardiovascular disease, while also serving as a role model and mentor for future generations of scientists and entrepreneurs.
Eicosapentaenoic Acid: Modulated Platelet Activation and ...
Eicosapentaenoic Acid: Modulated Platelet Activation and Thrombosis Proteins in Vascular Endothelial Cells During Inflammation Preston Mason PhD
By Preston Mason, PhD, MBA
Hello, my name is Preston Mason, and I'm here to discuss research. I recently presented at the American College of Cardiology in New Orleans. The title of my presentation that was given there is Eicosapentaenoic Acid or EPA modulates the expression or proteins linked to platelet activation and thrombosis in vascular endothelial cells during inflammation. My co-investigators are Sam Sherratt, Peter Libby, and Deepak Bhatt. They're from, in the case of myself, from Brigham and Women's Hospital and affiliated with Harvard Medical School and Deepak Bott is with Mount Sinai, in New York. So the objective of our study was to evaluate the effect of inflammation on the expression of proteins in human endothelial cells. This was an in vitro laboratory study, so we had very well controlled conditions to study the effects of inflammation on these cells. We then wanted to see what effect EPA, which is an omega-3 fatty acid had on the expression of these protein. Now just as way of background, we all know that platelet activation is essential to thrombus formation during atherosclerosis. So anything that promotes, platelet activation such as inflammatory stimuli like angiotensin II and cytokines like IL-6, they'll trigger that condition leading to thrombus formation and ischemic events. So the healthy endothelium preserves not only normal vasodilation, but interferes with platelet activation and thrombus formation by releasing a variety of proteins and signaling molecules, such as nitric oxide. One of the more important proteins that it releases, it's called tissue factor pathway inhibitor, or TFPI, that in particular is important in inhibiting early phases of the procoagulant process. Now by way of background also Eicosapentaenoic Acid is a highly purified form of EPA.
So this formulation of this particular omega-3 fatty acid has been associated with reduced risk in large clinical outcome trials, such as REDUCE-IT trial in the REDUCE-IT trial high-risk patients, or randomized at the to placebo or to Icosapent Ethyl and followed over almost 5 years and over 8,000 patients. And during that time, there was a 25% relative risk reduction among those patients randomized to Icosapent Ethyl, this was a composite or mace of cardiovascular events. And in addition, there was a 31% relative risk reduction in ischemic events including stroke, MI, and cardiac death. So this was very successful in terms of showing a signal for having a anti-ischemic benefit, but the mechanism is not fully understood. There in general, we know that omega-3 fatty acids and EPA in particular may have an anti-thrombotic event, but the specific mechanisms are not well understood. So that was the purpose of this study is to specifically look at how EPA modulates expression of proteins from endothelial cells given their central role in regulating both platelets and thrombus formation.
The way we measured protein expression was using, advanced mass spectroscopy that enables us to measure the expression of hundreds of proteins simultaneously taking advantage of their unique molecular weight. And under conditions of inflammation triggered by either angiotensin II or IL-6, we measured the effect of EPA on expression. And what we saw was hundreds of proteins significantly modulated by at least a hundred, full a hundred percent or twofold. And those are the proteins we focused on, and I'd like to just share a few of them that are particularly of interest. One protein that was upregulated specifically by EPA was TFPI or tissue factor pathway inhibitor. So that was an important finding of, the ability of EPA to stimulate the production of this agent that interferes with thrombus formation under conditions of inflammation, particularly with an angiotensin II. We also saw an increase in expression of thrombospondin 1 also interferes with thrombus formation, and we saw decrease expression in proteins that promote platelet activation, including CD109 and Thbs1. So we saw both increase in decreases in expression of proteins that modulate favorably thrombosis in the presence of EPA.
In conclusion, EPA affected expression of proteins involved in platelet activation and thrombosis under inflammatory conditions, including in increased levels of tissue factor platelet in, tissue factor pathway inhibitor, or TFPI. And other proteins that modulate thrombosis. These findings represent a potential antithrombotic mechanism for EPA that may contribute to reduce ischemic events beyond the ability of EPA to lower triglycerides. So in further studies, we'll be moving into in-vivo models of atherosclerosis and then further characterizing these important anti-platelet and antithrombotic properties of EPA. Now, what are potential downsides? Well, anything that interferes with platelet activation and thrombosis may lead to increased bleeding and in REDUCE-IT. There was a small but significant increase in bleeding among patients randomized to IPE, but there was no fatal bleeding, and again, the clinical benefits were very impressive, including, like I said, a more than 30% reduction in ischemic events and cardiac death. So in light of that, we believe this could represent a novel benefit of EPA to help explain its benefit in clinical outcome trials. Thank you very much.
What is Eicosapentaenoic Acid and how is it used in Cardiology?
Eicosapentaenoic Acid (EPA) is an omega-3 fatty acid found in fish oil. It is a type of polyunsaturated fatty acid that is essential for human health but cannot be synthesized by the body and must be obtained from the diet or supplements.
In cardiology, EPA has been shown to have a number of beneficial effects, including:
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Lowering triglyceride levels: EPA has been shown to lower triglyceride levels, which are a type of fat found in the blood that can increase the risk of heart disease.
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Reducing inflammation: EPA has anti-inflammatory effects, which can help reduce the inflammation that can contribute to the development of heart disease.
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Improving endothelial function: EPA can improve the function of the endothelium, the layer of cells that lines the inside of blood vessels, which can help improve blood flow and reduce the risk of cardiovascular events.
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Decreasing platelet aggregation: EPA has been shown to decrease platelet aggregation, which can help reduce the risk of blood clots that can lead to heart attacks and strokes.
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Lowering blood pressure: EPA may help lower blood pressure, which is a major risk factor for heart disease.
As a result of these effects, EPA is often used in the treatment of cardiovascular disease, particularly in patients with high triglyceride levels or those at high risk of cardiovascular events. It is available as a dietary supplement and is also found in prescription medications for the treatment of high triglycerides, such as icosapent ethyl.
10 Key Takeaways about the Eicosapentaenoic Acid REDUCE-IT Clinical Trial
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Eicosapentaenoic acid (EPA) is a type of omega-3 fatty acid that is found in fish oil and has been shown to have anti-inflammatory properties.
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Vascular endothelial cells play a key role in the development of thrombosis (blood clots) and are also involved in the inflammatory response.
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Inflammation can cause changes in the expression of proteins in vascular endothelial cells that contribute to thrombosis.
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EPA has been shown to modulate the expression of proteins in vascular endothelial cells that are linked to platelet activation and thrombosis.
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Platelet activation is a key step in the formation of blood clots.
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EPA has been shown to inhibit platelet activation by reducing the expression of proteins involved in platelet activation.
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EPA has also been shown to reduce the expression of proteins involved in the coagulation cascade, which is another key step in the formation of blood clots.
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EPA may have a protective effect against thrombosis by reducing platelet activation and the coagulation cascade.
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The anti-inflammatory properties of EPA may also contribute to its protective effect against thrombosis.
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These findings suggest that EPA may have potential as a therapeutic agent for the prevention and treatment of thrombotic disorders.
R. Preston Mason, PhD, MBA - About The Author, Credentials, and Affiliations
R. Preston Mason, PhD, MBA, is a renowned scientist and entrepreneur who has made significant contributions to the fields of biochemistry, cardiovascular disease, and translational medicine. He is currently an Associate Professor of Medicine at Harvard Medical School, where he leads a research laboratory focused on developing novel therapeutic approaches for cardiovascular disease.
Dr. Mason earned his Bachelor of Science degree in chemistry from Tuskegee University, followed by a PhD in biochemistry from Emory University. He then pursued an MBA from the Wharton School at the University of Pennsylvania, where he developed his business acumen and honed his skills as an entrepreneur.
Throughout his career, Dr. Mason has held various academic and industry positions, including serving as a faculty member at the University of Connecticut School of Pharmacy and as a senior scientist at Pfizer, Inc. He has also founded several companies, including Elucida Research, LLC, which develops drug delivery technologies for various therapeutic applications.
Dr. Mason's research has led to over 150 peer-reviewed publications and numerous patents. His work has been recognized with several awards, including the American Chemical Society's Heroes of Chemistry Award and the Black Engineer of the Year Award. He is also a Fellow of the American Heart Association.
In addition to his research and entrepreneurial pursuits, Dr. Mason is dedicated to mentoring the next generation of scientists and entrepreneurs. He has served as a mentor to numerous graduate students, postdoctoral fellows, and young professionals, and he is committed to promoting diversity and inclusion in science and entrepreneurship.
Overall, Dr. R. Preston Mason's interdisciplinary background and expertise have enabled him to make significant contributions to the fields of biochemistry and cardiovascular disease, while also serving as a role model and mentor for future generations of scientists and entrepreneurs.
Vascular Medicine
Description
Vascular Medicine