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Video: Do You Really Need To Forget About Cholesterol And Statins? Russian Expert Commentary
Do you really need to forget about cholesterol and statins? Russian expert commentary
MedNovosti recently published the news of a major scientific review, the authors of which made a loud statement that the role of cholesterol in the development of cardiovascular disease is insufficiently proven, and the benefits of statins are questionable. We present a commentary by a cardiologist, Ph.D. Yaroslava Ashikhmina, who will help you sort out this controversial issue.
Yaroslav Ashikhmin /
We recently published the news of a major scientific review, the authors of which stated that the role of cholesterol in the development of cardiovascular disease is insufficiently proven, and the benefits of statins, which lower its levels in the blood, are highly questionable.
The authors of this study have been known for their "anti-cholesterol" position for many years, and their high-profile claims can confuse thousands of patients. The XXI CENTURY edition asked to comment on this work of a cardiologist, candidate of medical sciences, a researcher of the research department of cardiology of the First Moscow State Medical University. I.M.Sechenov Yaroslav Ashikhmin. MedNews cites this comment uncut.
- It is necessary to very clearly distinguish between statins in primary prevention and in secondary prevention. Secondary prevention is a situation where a person has already had a stroke or heart attack, or at least has confirmed coronary artery disease. There is no doubt that statins are the most effective means of preventing recurrent heart attacks and strokes. If a person has already had a heart attack or stroke, they do not need to measure any cholesterol to decide on statins. These patients should receive them automatically.
As for primary prevention, when it comes to prescribing statins for people who have not had heart attacks or strokes, there was no surprise for me personally in the results of this review. The position of statins in primary prevention has never been strong. And this is easily explained: for a statin to work, a person must have a formed atherosclerotic plaque (or there must be a very high risk that it will grow very quickly). Statins do not work by "lowering cholesterol", but by strengthening the fibrous cap of the atherosclerotic plaque. After using statins, it becomes less prone to rupture and more dense.
How did we decide in the past to prescribe statins for primary prevention? Apart from specific cases, for example, the presence of a family heterozygous form of hypercholesterolemia in a person, we previously assessed the patient's risks using special calculators. The risk of developing a heart attack and stroke, that is, diseases based on the risk of rupture of an atherosclerotic plaque. The models that these calculators work on include gender, age, smoking habits, blood pressure and cholesterol levels. If the risk - according to the analysis of these factors - was assessed as high, then the person was prescribed statins. We then had a large population of a wide variety of patients who could develop plaque. But they might not have grown.
It can be assumed that the higher the risk of plaque formation, and then the risk of plaque rupture, the higher the statin effectiveness. But in the modern world, many people are committed to a healthy lifestyle, and many are receiving drugs to lower blood pressure. Therefore, it may turn out that the model does not work very well, because plaques do not develop very often in this population for some reason. And the point of application of statins simply will not be.
Now - literally in the period from 2016 to 2018. - there has been a paradigm shift in prevention. We try to prescribe statins in primary prevention, not to those patients who have high-risk calculators, but to those who have benefited most from statins in clinical trials. And it turned out that there are not so many such patients. These are mainly patients with diabetes mellitus and patients with high levels of C-reactive protein (JUPITER study). That being said, interestingly, they can have fairly low levels of low density lipoprotein and cholesterol. In this case, systemic inflammation can play a significantly larger role in the formation of atherosclerotic plaques and create a substrate, a "field of action" for statins.
But we go further, and my scientific work is about the prevention concept 3.0. Even if we take and prescribe statins to those patient populations that have definitely benefited from statin prescriptions, on the one hand we can still prescribe statins unnecessarily. The fact is that in this situation we still use a population-based, not an individualized approach - and a particular patient may not have a substrate. On the other hand, risk models do not include important factors associated with rapid plaque growth, such as an early family history of heart attack, high levels of social stress, the presence of rheumatological diseases, and so on. That is, this approach is also imperfect.
But within the framework of the 3.0 concept, it is possible to make the prescription of statins truly individualized - for this it is necessary to see if a person has developed plaques against the background of all the risk factors that he had. It is one thing to count virtual risks, and another to do a low-dose computed tomography scan of the heart and assess the presence of plaque. With such a study (the assessment of the calcium index is implied), the radiation exposure is comparable to mammography, but it allows you to find out if there are atherosclerotic plaques.
The MESA study gave us the basis to use computed tomography when deciding whether to prescribe statins to patients in moderate and low risk groups. In the presence of additional factors that are not considered in the risk model, the appointment of statins may be appropriate.
Thus, statins are one of the tools for reducing cardiovascular mortality. But this tool only works by strengthening the lining of the atherosclerotic plaque. If we know for sure that there is a plaque, statins should be prescribed, especially if the plaque has already ruptured. If there is no plaque, then it should be understood that prescribing statins - and they are used throughout life - is an extremely serious decision, which requires deep reflection to make. I have no reason to believe that statins will be effective in large populations of patients without heart disease. These patients may have a higher chance of dying from injury or cancer than from heart attack or stroke. Or from heart failure not associated with atherosclerosis: for example, due to ventricular tachycardia (athletes), alcoholic heart disease (our compatriots),heart failure associated with hypertension. In these diseases, there is also no point for statin administration.
Another problem is that reading such articles, people often decide that statins are not useful for them personally. But we have a catastrophe in our country with the fact that statins are not prescribed to those patients who have already suffered a heart attack or stroke. Target cholesterol levels are not reached (those who have had a stroke or heart attack need to go on the most aggressive therapy to reach the recommended LDL levels, less than 1.5 - 1.8 mmol / L). These numbers indicate that the dose of statin is sufficient to stabilize the plaque, and cholesterol lowering itself is not an end in itself, that is, cholesterol is just a marker. If any "plaque strength indicator" emerges, there will be no need to measure cholesterol in this context. But it is very important that people do not cancel statins, because in our country these drugs are often not prescribed when it is necessary, and not vice versa.
It can be expanded by saying that the body is so complex that there is huge skepticism about medical effects in order to prolong life (I am talking, of course, about cases when there are no diseases). Aspirin “failed” as a primary prevention tool, and many other drugs failed. There is no reason to believe that the so-called mythical "geroprotectors" will also show effectiveness. I suggest that people come to terms with the fact that now we do not have - and, most likely, in the near future will not have - medical measures for effective prevention of death in people who feel healthy and without an obvious significant genetic substrate that provides early QT interval or familial heterozygous hypercholesterolemia). But drugs can, of course, significantly improve the quality of life.