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LDL Cholesterol & Heart Health

The National Cholesterol Education Program’s (NCEP’s) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults creates updated clinical guidelines for testing and management of cholesterol. NCEP periodically updates existing recommendations based on new research. The third version, Adult Treatment Panel III or ATPIII, was published in 2001. In 2004, updates were added based on several clinical trials of statin therapy.

The fact is, elevated low-density lipoprotein (LDL), the bad cholesterol, is a major cause of heart disease. LDL causes the build-up of fatty deposits within your arteries, reducing or blocking the flow of blood and oxygen your heart needs. This can lead to chest pain and heart attack. (Atherosclerosis, the medical term for “hardening of the arteries,” is not limited to heart arteries, though. It also occurs in arteries elsewhere in your body, causing problems such as stroke, kidney failure and poor circulation. ). In addition, studies show that lowering LDL cholesterol reduces risk for coronary heart disease. For this reason, ATPIII continues to focus goals of initiating treatment based on LDL.

It is extremely important for everyone — men and women of every age, with or without known heart disease — to have a low LDL cholesterol level. The optimal guideline level of LDL cholesterol is less than 100 mg/dl. Research from the Cleveland Clinic (REVERSAL study) compared two cholesterol lowering drugs (pravastatin and atorvastatin) and found that lower levels of LDL, as low as 60 mg/dl had better outcomes. A second study called PROVE-IT also found that the lower the LDL cholesterol the better – the PROVE-IT study results stated – “These findings indicate that patients who have recently had an acute coronary syndrome benefit from early and continued lowering of LDL cholesterol to levels substantially below current target levels.” TNT, Treating to New Targets also found that “intensive Atorvastatin therapy to achieve LDL cholesterol concentrations well below recommended target levels provides an incremental clinical benefit in patients with stable coronary artery disease. ” These studies have impacted LDL goals and have provided now options as to when to initiate drug therapy — as seen in the new updates.

Additional research has shown that statins, drugs used to treat high LDL cholesterol appear to also protect the heart in other ways. These drugs also reduce the progression of plaque buildup in the coronary arteries by reducing C-reactive protein, a measure of inflammation in the arteries. Therefore, it seems the lower the LDL cholesterol the better, and how you get there may be important as well.

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Measure your LDL and other blood lipids

Everyone age 20 and older should have their cholesterol checked at least every five years through a blood test. The guidelines recommend you have a complete “lipoprotein profile” that measures total cholesterol, LDL cholesterol, high-density lipoprotein (HDL, the good cholesterol that may help prevent heart disease), and triglycerides, another type of fat in the blood stream. The test should be performed after fasting.

Low density lipoprotein (LDL cholesterol) goal values:

  • Less than 70 mg/dL for those with heart or blood vessel disease and for other patients at very high risk of heart disease (those with metabolic syndrome)
  • Less than 100 mg/dL for high risk patients (for example: some patients who have diabetes or multiple heart disease risk factors)
  • Less than 130 mg/dL otherwise

Total cholesterol (TC) goal values:

  • 75-169 mg/dL for those age 20 and younger
  • 100-199 mg/dL for those over age 21

High density lipoprotein (HDL) goal value:

  • Greater than 45 mg/dl (the higher the better)

Triglyceride (TG) goal value:

Learn more about these tests

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Determine your other risk factors for heart disease

If you have already diagnosed coronary heart disease, atherosclerosis, or diabetes, the guidelines would place you into the high risk category, even if you have no symptoms of heart disease.

In addition to high LDL, atherosclerosis or diabetes, other important risk factors for heart disease are:

  • Cigarette smoking
  • High blood pressure (140/90 mm Hg and above or on blood pressure medication)
  • low HDL cholesterol
  • family history of early coronary heart disease
  • age (for men, age 45 or older; for women, age 55 or older)

For people who do not have coronary disease, but who have two or more risk factors, doctors may use a risk-factor chart* plus your LDL level to calculate your 10-year risk of developing disease and determine whether intensive cholesterol lowering is warranted.

With this risk-factor information, your doctor will place you in one of four categories of risk for heart disease. The higher your risk, the lower your LDL cholesterol goal will be:

If you have heart disease, diabetes, other forms of atherosclerosis and multiple risk factors listed above (andrisk score*greater than 20%), you are in Category: I. Highest Risk

  • LDL Goal: less than 100 mg/dl with a therapeutic option of treating to under 70 mg/dL. For very high-risk patients whose LDL levels are already below 100 mg/dL, there is also an option to use drug therapy to reach the less than 70 mg/dL goal.

If you have 2 or more risk factors listed above (and risk score* 10 – 20%), you are in Category II. Next Highest Risk

  • LDL Goal: less than 100mg/dl with option for drug therapy for those high-risk patients whose LDL is 100 to 129 mg/dL

If you have 2 or more risk factors (andrisk score* less than 10%) you are in Category III. Moderate Risk

  • LDL Goal: less than 130 mg/dl

If you have 0 or 1 risk factor, you are in Category IV. Low-to-Moderate Risk

  • LDL Goal: less than 160 mg/dl

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Improve your cholesterol numbers

The new guidelines emphasize preventing heart disease in the short- and long-term, and recommend “therapeutic lifestyle changes (TLC)” to lower LDL. These involve:

  • Reducing saturated fat and cholesterol intake
  • Increasing intake of soluble fiber
  • Reducing weight if you are overweight – especially if you have metabolic syndrome (see below)
  • Increasing physical activity – regular physical activity is recommended for everyone.
  • Controlling high blood pressure
  • Quitting smoking

Working with a dietitian or nutritionist is extremely helpful.

Should I take cholesterol-lowering medication?

Drugs to reduce LDL include the “statins,” bile acid sequestrants, nicotinic acid and fibric acid. If your LDL and heart-disease risk are both high, doctors may prescribe medications at the same time as lifestyle changes. For others, medication may be added if six to 12 weeks on the TLC plan fail to adequately reduce LDL. Those who are started on a cholesterol-lowering medication will need to continue lifestyle changes.

Identifying those with metabolic syndrome

A group of specific risk factors, known as the metabolic syndrome, raise your risk for coronary disease at any LDL cholesterol level. If you have three of the following risk factors, you may have metabolic syndrome, and need more rigorous cholesterol lowering:

  • Abdominal obesity (a waistline over 35 inches in women and 40 inches in men)
  • Triglycerides of 150 of higher
  • Low HDL (lower than 40 in men and lower than 50 in women)
  • Blood pressure of 130/85 mm Hg or higher
  • Fasting glucose of 110 mg/dL or higher

Middle-aged men (age 35 – 65) are predisposed to abdominal obesity and the metabolic syndrome. As a result, they carry a relatively high risk for heart disease. For those with high risk, intensive LDL reducing strategies should be followed.

See your doctor!

See your doctor. Ask for a complete lipoprotein profile. With results in hand and with your doctor’s help, determine your risk for heart disease. If your cholesterol levels are not optimal, ask for a referral to a nutritionist, and begin your heart-healthy lifestyle right away.

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To make an appointment:

You do not need a referral to make an appointment in the Preventive Cardiology Programs. For more information about cardiac risk factors and controlling high cholesterol, please contact the Preventive Cardiology and Rehabilitation Program at 216.444.9353 or toll-free 1-800-223-2273, extension 49353 to schedule a consultation.

For more information on implementing a low cholesterol diet, contact Preventive Cardiology Nutrition Program at 216.444.9353 or toll-free 1-800-223-2273, extension 49353 to schedule a consultation or utilize our remote Nutrition Counseling service*

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Know the Cholesterol Level That’s Right for You – And Stick to It

The National Lipid Association’s recommendations for how clinicians can help patients control their cholesterol levels focus on setting a personal goal based on your overall risk for cardiovascular disease.

Heart disease is the number one killer in the United States, and lipids — fats that circulate in your blood — are the primary cause. Recommendations published in the September 2014 issue of the Journal of Clinical Lipidology outline patient-specific ways to lower specific risks for potentially fatal cardiovascular events.

We spoke with NYU Langone Medical Center’s James A. Underberg, MD, director of the Bellevue Hospital Lipid Clinic in New York City and president of the National Lipid Association (NLA), about what the recommendations mean for patients and their families.

Everyday Health: According to the latest from the NLA, how often should you have your blood levels of cholesterol checked?

Dr. Underberg: For adults 20 or older, a good rule of thumb is every five years.

Everyday Health: When the blood test results come back, if your doctor tells you that you have dyslipidemia, what does that mean for your future?

Dr. Underberg: The way to understand it is as an abnormality in the lipid profile that puts you at risk for vascular disease or stroke. It can be abnormal triglycerides, not just cholesterol. The first step is to find out that there’s a problem. The second is to find the cause.

Everyday Health: What are the cutoff numbers that are considered normal for lipids?

Dr. Underberg: We describe these as desirable, rather than normal. Desirable levels of LDL cholesterol are under 100 milligrams per deciliter (mg/dL), and non-HDL cholesterol of under 130 mg/dL. These are the numbers to aim for.

In addition, HDL should be above 40 mg/dL for men, and above 50 mg/dL for women. And triglycerides should be below 150 mg/dL.

Everyday Health: Does a particular level mean you might have inherited high cholesterol, also known as familial hypercholesterolemia (FH)?

Dr. Underberg: The number that the NLA uses is an LDL cholesterol level above 190 mg/dL. This is in agreement with the American Heart Association and the American College of Cardiology. If your LDL is over 190, you need to be concerned about FH.

Everyday Health: Does this mean the other members of your family should get checked, too?

Dr. Underberg: Indeed, family members should get checked. Obviously your kids should get checked. Just as important, your siblings and your parents should, too. Call them up and get them checked. Ask them to get tested by someone who knows about FH. I say that screening should be north and south, east and west — across the family tree and across the United States.

Everyday Health: Why might your blood cholesterol target number, or goal, be a different number than another person’s?

Dr. Underberg: We decide based on two things. One, the inherent level of risk; and two, what the blood cholesterol level is. If cholesterol is low, but you have many risk factors — like smoking, diabetes, high blood pressure, or other heart disease — then your cholesterol goal is lower. On the other hand, if you have high cholesterol but fewer risk factors, your goal may be higher. It is not just putting the information into a calculator, but making it personal.

Everyday Health: If cholesterol levels don’t reach the goal, how do you know when it’s the right time to give medication a try — and what do you start with?

Dr. Underberg: We always like to give lifestyle interventions a really good try. Not for a few weeks, but for several months. If after three to four months the goal isn’t met, it may take reinforcement. See what’s working and make some changes. But if after one or two attempts you’re still not at goal and cholesterol is significantly above where it needs to be, then we recommend medication.

Statins are the first line of therapy. But not everyone can take a statin.

A woman thinking of getting pregnant would not want to be on a statin. And a person who had side effects from statins in the past also wouldn’t. But in some cases, you may require more than a statin, and may need another medication added to control cholesterol.

RELATED: 9 Hidden Heart Toxins and How to Avoid Them

Everyday Health: What are the risk factors within our control that, together with fat in the blood, increase the chances of having a heart attack or stroke?

Dr. Underberg: Some things we can’t control, like our age and our family medical history of heart disease. But the ones we can control include inactivity, smoking, obesity, and poor diet. These are in our own control. Sometimes treating other conditions may be helpful, too — for example if you have diabetes or high blood pressure. We need to think about the entire patient.

Everyday Health: What are the lifestyle changes NLA recommends to keep cholesterol levels down?

Dr. Underberg: We really focus on lifestyle, and have a second document coming out on diet. In the current recommendations, we focus on those interventions that have been shown to lower cholesterol. These are a diet restricted in saturated fat (found in butter, lard, meat, full-fat dairy, and coconut oil), weight loss, and referral to a registered dietician. If you also have diabetes, you’ll do better with a low-carb diet than a low-fat one.

Remember that clinical treatment guidelines are based on large groups of patients in clinical trials. But I still see patients one at a time who may not be the same as the people in those groups. That’s why personalization is so important.

Why Cholesterol Matters for Women

Ah, cholesterol and triglycerides. We hear about them all the time. Even foods that might seem good for you on the surface, like fruit-filled yogurt or bran muffins, can contribute to abnormal levels if they contain too much saturated fat or refined sugar, says Erin Michos, M.D., associate director of preventive cardiology at the Ciccarone Center for the Prevention of Heart Disease.

What’s more, many women are at risk for high cholesterol and don’t realize it. “Approximately 45 percent of women over the age of 20 have a total cholesterol of 200 mg/dl and above, which is considered elevated — but a survey by the American Heart Association found that 76 percent of women say they don’t even know what their cholesterol values are,” Michos says.

Scarier still: Triglycerides, a type of blood fat typically measured alongside cholesterol, are even more risky in women compared with men. This is a problem because women’s cholesterol levels can fluctuate quite a bit after menopause and tend to increase with age, putting us at greater risk of heart disease and stroke. Knowing your cholesterol numbers and how to control them is a big step toward staying healthy.

Understanding the Highs and Lows of Cholesterol

You know that too much is dangerous. But what is cholesterol, anyway? Where does it come from? And is it all bad?

Cholesterol is a waxy substance that is found in every cell in the body. It’s either made by the body or absorbed from food. Your body needs cholesterol to make important steroid hormones such as estrogen, progesterone and vitamin D. It’s also used to make bile acids in the liver; these absorb fat during digestion.

So some cholesterol is necessary — but bad cholesterol is something you can do without. Excess bad cholesterol in the bloodstream can deposit into the body’s arteries. These deposits are called plaques and result in atherosclerosis, or hardening of the arteries. This is the major cause of heart attacks, strokes and other vascular problems.

Your total cholesterol level is a measure of the total amount of cholesterol circulating in your bloodstream, which includes several components:

  • LDL cholesterol: LDL stands for “low-density lipoprotein.” This is known as the “bad” cholesterol, which directly contributes to plaque buildup in the arteries. Very low density lipoprotein, or VLDL cholesterol, is another type, which is a precursor to LDL.
  • Total cholesterol is VLDL cholesterol plus LDL cholesterol plus HDL cholesterol.
  • HDL cholesterol: HDL stands for “high-density lipoprotein.” Experts think at optimal levels (around 50 mg/dl) it might help the body get rid of LDL cholesterol.

So bits of this stuff circulate through your system, and here’s what happens: The bad parts – the LDL particles – like to stick to the lining of your arteries, like soap scum in pipes. As it sticks there, it generates an inflammatory response and your body starts converting it into plaque. Plaque in your blood vessels makes them stiffer and narrower, restricting blood flow to vital organs such as your brain and heart muscle, leading to high blood pressure. Additionally, chunks can break off and cause a heart attack or a stroke.

And guess what? This buildup can start as early as your 20s.

What to Know About Triglycerides

In addition to cholesterol, you might hear about your triglycerides, another kind of fat found in the bloodstream. Women should pay particular attention to this. “A high level of triglycerides seems to predict an even greater risk for heart disease in women compared with men,” says Michos.

When you take in more calories than you need, your body converts the extra calories into triglycerides, which are then stored in fat cells. Triglycerides are used by the body for energy, but people with excess triglycerides have higher risk of medical problems, including cardiovascular disease. Drinking a lot of alcohol and eating foods containing simple carbohydrates (sugary and starchy foods), saturated fats and trans fats contributes to high triglycerides. High levels may also be caused by health conditions such as diabetes, an underactive thyroid, obesity, polycystic ovary syndrome or kidney disease.

Triglycerides also circulate in the bloodstream on particles that may contribute to plaque formation. Many people with high triglycerides have other risk factors for atherosclerosis, including high LDL levels or low HDL levels, or abnormal blood sugar (glucose) levels. Genetic studies have also shown some association between triglycerides and cardiovascular disease.

What’s your cholesterol level, anyway?

A standard lipid blood test usually measures the concentration of total cholesterol, HDL cholesterol, and triglycerides levels. The LDL-cholesterol level is typically estimated from these numbers using a well-established formula that has been more recently revised and improved by researchers at Johns Hopkins.

So what are your target numbers? According to Michos, an ideal LDL cholesterol level should be less than 70 mg/dl, and a woman’s HDL cholesterol level ideally should be close to 50 mg/dl. Triglycerides should be less than 150 mg/dl. As Michos notes, total cholesterol levels well below 200 mg/dl are best.

Why Cholesterol Affects Women Differently

In general, women have higher levels of HDL cholesterol than men because the female sex hormone estrogen seems to boost this good cholesterol. But, like so much else, everything changes at menopause. At this point, many women experience a change in their cholesterol levels — total and LDL cholesterol rise and HDL cholesterol falls. This is why women who had favorable cholesterol values during their childbearing years might end up with elevated cholesterol later in life. Of course, genetics and lifestyle factors can play big roles, too.

How to Lower Your Cholesterol

If you’ve been told that you have high cholesterol — or you just want to prevent it — what can you do?

There are several ways to manage it, including:

Medication: Depending on your overall cardiovascular disease risk, you might be treated with a cholesterol-lowering medication, such as a statin. The decision to use a statin is based on a woman’s overall risk for heart attack and stroke including all these factors and the LDL cholesterol value.

If you already have vascular disease or evidence of atherosclerosis, or if you are at high risk for cardiovascular disease, a statin for prevention is strongly recommended because this treats the plaque in the arteries, and lowers LDL cholesterol, Michos says.

Diet and lifestyle: “Diet and lifestyle are very important to help maintain healthy cholesterol levels. Even for women who are recommended to take cholesterol-lowering medications, a healthy lifestyle helps these drugs work better,” says Michos.

Here’s how to maintain a lifestyle that promotes healthy cholesterol levels:

  • Maintain a healthy body weight
  • Don’t smoke.
  • Exercise for at least 30 minutes five or more days per week.
  • Eat a diet rich in fruits, vegetables, lean protein and high amounts of soluble fiber such as beans and oats, which can reduce LDL.
  • Avoid sugar-sweetened drinks and fruit juices — opt for water and unsweetened tea instead — and minimize your intake of other simple carbohydrates like baked goods and candy.
  • Drink alcohol in moderation, especially if you have elevated triglycerides.
  • Consider the Mediterranean diet, which is rich in fruits, vegetables, grainy breads and fish. Use olive oil (instead of butter) and spices (instead of salt).
  • Eat monounsaturated and polyunsaturated fats — such as those found in olive oil, nuts and fatty fish like salmon. They can actually have a positive effect on cholesterol, Michos says, by reducing the amount of LDL in the blood and reducing inflammation in the arteries, especially when they replace saturated fats in the diet.

Add these to your shopping list:

  • Fatty fish such as salmon, trout, mackerel, sardines and albacore tuna
  • Nuts, including walnuts, pecans, almonds and hazelnuts
  • Olive oil to drizzle lightly over your salads and vegetables

While nobody wants to have high cholesterol, there are plenty of ways to keep it in check.  “With regular checkups and attention to what you eat, it’s possible to manage your cholesterol and blood fats to keep your heart healthy,” says Michos.

What Your Cholesterol Levels Mean

Understanding your cholesterol levels

Maintaining healthy cholesterol levels is a great way to keep your heart healthy. It can lower your chances of getting heart disease or having a stroke.

But first, you have to know your cholesterol numbers.

The American Heart Association recommends

All adults age 20 or older should have their cholesterol (and other traditional risk factors) checked every four to six years. If certain factors put you at high risk, or if you already have heart disease, your doctor may ask you to check it more often. Work with your doctor to determine your risk for cardiovascular disease and stroke and create a plan to reduce your risk.

Learn how to get your cholesterol tested

Your test results: A preview

Your test results will show your cholesterol levels in milligrams per deciliter of blood (mg/dL). Your total cholesterol and HDL (good) cholesterol are among numerous factors your doctor can use to predict your lifetime or 10-year risk for a heart attack or stroke. Your doctor will also consider other risk factors, such as age, family history, smoking status, diabetes and high blood pressure.

Lipid profile or lipid panel is a blood test that will give you results for your HDL (good) cholesterol, LDL (bad) cholesterol, triglycerides and total blood (or serum) cholesterol.

Watch an animation about cholesterol score.

HDL (good) cholesterol

HDL cholesterol is called “good” cholesterol. A healthy HDL-cholesterol level may protect against heart attack and stroke. Your doctor will evaluate your HDL and other cholesterol levels and other factors to assess your risk for heart attack or stroke.

People with high blood triglycerides usually also have lower levels of HDL. Genetic factors, Type 2 diabetes, smoking, being overweight and being sedentary can all lower HDL cholesterol.
Women tend to have higher levels of HDL cholesterol than men do, but this can change after menopause.

LDL (bad) cholesterol

Since LDL is the bad kind of cholesterol, a low LDL level is considered good for your heart health.

LDL levels are one factor among many to consider when evaluating cardiovascular risk. Talk to your doctor about your LDL cholesterol level as well as other factors that impact your cardiovascular health.

A diet high in saturated and trans fat is unhealthy because it tends to raise LDL cholesterol levels.

Triglycerides

Triglycerides are the most common type of fat in your body. They come from food, and your body also makes them.

Normal triglyceride levels vary by age and sex. People with high triglycerides often have a high total cholesterol level, including a high LDL (bad) cholesterol level and a low HDL (good) cholesterol level. Many people with metabolic syndrome or diabetes also have high triglyceride levels.

Factors that can contribute to elevated triglyceride levels:

  • Overweight or obesity
  • Insulin resistance or metabolic syndrome
  • Diabetes mellitus, especially with poor glucose control
  • Alcohol consumption, especially in excess
  • Excess sugar intake, especially from processed foods
  • High saturated fat intake
  • Hypothyroidism
  • Chronic kidney disease
  • Physical inactivity
  • Pregnancy (especially in the third trimester)
  • Inflammatory diseases (such as rheumatoid arthritis, systemic lupus erythematosus

Some medications may also increase triglycerides.

Total blood (or serum) cholesterol

This part of your test results is a composite of different measurements. Your total blood cholesterol is calculated by adding your HDL and LDL cholesterol levels, plus 20% of your triglyceride level.

“Normal ranges” are less important than your overall cardiovascular risk. Like HDL and LDL cholesterol levels, your total blood cholesterol level should be considered in context with your other known risk factors.

Your doctor can recommend treatment approaches accordingly.

LDL Cholesterol | Lab Tests Online

Sources

American College of Cardiology. Understanding strengths and limitations of different methods of LDL-C estimation. Updated April 2, 2019. Accessed June 13, 2021. https://www.acc.org/latest-in-cardiology/articles/2019/04/02/13/21/understanding-strengths-and-limitations-of-different-methods-of-ldl-c-estimation

A.D.A.M. Medical Encyclopedia. Cholesterol testing and results. Updated January 27, 2020.. Accessed June 3, 2021. https://medlineplus.gov/ency/patientinstructions/000386.htm

A.D.A.M. Medical Encyclopedia. Venipuncture. Updated April 26,/2019. Accessed June 12, 2021. https://medlineplus.gov/ency/article/003423.htm

American Family Physician. Cholesterol Management: ACC/AHA Updates Guideline. Published May 1, 2019. Accessed July 5, 2021. https://www.aafp.org/afp/2019/0501/p589.html

ARUP Consult. Atherosclerotic cardiovascular disease risk markers. Updated April 2021. Accessed June 13, 2021. https://arupconsult.com/content/cardiovascular-disease-traditional-risk-markers

Centers for Disease Control and Prevention. Getting your cholesterol checked. Updated September 8, 2020. Accessed June 3, 2021. https://www.cdc.gov/cholesterol/cholesterol_screening.htm

Centers for Disease Control and Prevention. How and when to have your cholesterol checked. Updated April 15, 2021. Accessed June 3, 2021. https://www.cdc.gov/cholesterol/checked.htm

MedlinePlus: National LIbrary of Medicine. Cholesterol. Updated February 20, 2021. Accessed June 3, 2021.  https://medlineplus.gov/cholesterol.html

MedlinePlus: National Library of Medicine. Cholesterol levels. Updated July 30, 2020. Accessed June 3, 2021.  https://medlineplus.gov/lab-tests/cholesterol-levels/

MedlinePlus: National LIbrary of Medicine. Cholesterol levels: What you need to know. Updated December 4, 2017. Accessed June 3, 2021. https://medlineplus.gov/cholesterollevelswhatyouneedtoknow.html

MedlinePlus: National Library of Medicine. Fasting for a blood test. Updated March 3, 2021. Accessed June 13, 2021. https://medlineplus.gov/lab-tests/fasting-for-a-blood-test/

MedlinePlus: National LIbrary of Medicine. LDL: The bad cholesterol. Updated December 4, 2017. Accessed June 3, 2021.  https://medlineplus.gov/ldlthebadcholesterol.html

MedlinePlus: National Library of Medicine. What you need to know about blood testing. Updated March 9, 2021. Accessed June 12, 2021. https://medlineplus.gov/lab-tests/what-you-need-to-know-about-blood-testing/

MedlinePlus: National Library of Medicine. Triglycerides. Updated January 23, 2017. Accessed June 19, 2021. https://medlineplus.gov/triglycerides.html

National Heart, Lung, and Blood Institute. Blood cholesterol. Date unknown. Accessed June 3, 2021.  https://www.nhlbi.nih.gov/health-topics/blood-cholesterol

Rosenson RS. Measurement of blood lipids and lipoproteins. In: Freeman MW, ed. UpToDate. January 16, 2020. Accessed July 5, 2021. https://www.uptodate.com/contents/measurement-of-blood-lipids-and-lipoproteins

US Food and Drug Administration. Home use tests: Cholesterol. Updated February 4, 2018. Accessed June 3, 2021. https://www.fda.gov/medical-devices/home-use-tests/cholesterol

[Achieving optimal cholesterol levels in patients with chronic ischemic heart disease: from guidelines to the real world]


Background:

It is known that less than half of patients with coronary heart disease reaches the target of LDL cholesterol (LDL-C) <100 mg/dl. According to the latest international guidelines, this target has been lowered to <70 mg/dl in very high-risk patients.


Methods:

From November 1, 2009 to December 31, 2012, 4953 patients with coronary heart disease were enrolled in the Cardiovascular Registry of Trieste (Italy). We assessed clinical data, LDL-C levels, statin prescription and medium-term outcome in patients with coronary heart disease.


Results:

At first clinical evaluation, LDL-C values were available for only 61.5% of patients. The target level of LDL-C <70 mg/dl was reached in 17% of cases and LDL-C <100 mg/dl in 53%. Patients with lower LDL-C levels were more frequently males, with higher cardiovascular risk profile, more comorbidity and more frequent polypharmacy. LDL-C levels influenced statin prescription: in patients with LDL-C ≥ 100 mg/dl, cardiologists started or modified the dosage of statin therapy twice more than in patients with LDL-C <100 mg/dl, even if only in less than 20% of cases. Patients with LDL-C <100 mg/dl in statin therapy had better prognosis, whereas patients with low LDL-C levels without statin therapy had the worst prognosis. Other prognostic factors in this population with LDL-C <100 mg/dl were age, presence of heart failure, comorbidities (evaluated with Charlson index) and polypharmacy.


Conclusions:

In our population of outpatients with coronary heart disease, the target of LDL-C <100 mg/dl was reached in 53% of cases. LDL-C levels influenced statin prescription and modification of dosages. The medium-term outcome is closely influenced by the achievement of target LDL-C levels and statin prescription.

Cholesterol test – Mayo Clinic

Overview

A complete cholesterol test — also called a lipid panel or lipid profile — is a blood test that can measure the amount of cholesterol and triglycerides in your blood.

A cholesterol test can help determine your risk of the buildup of fatty deposits (plaques) in your arteries that can lead to narrowed or blocked arteries throughout your body (atherosclerosis).

A cholesterol test is an important tool. High cholesterol levels often are a significant risk factor for coronary artery disease.

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Why it’s done

High cholesterol usually causes no signs or symptoms. A complete cholesterol test is done to determine whether your cholesterol is high and to estimate your risk of heart attacks and other forms of heart disease and diseases of the blood vessels.

A complete cholesterol test includes the calculation of four types of fats in your blood:

  • Total cholesterol. This is a sum of your blood’s cholesterol content.
  • Low-density lipoprotein (LDL) cholesterol. This is called the “bad” cholesterol. Too much of it in your blood causes the buildup of fatty deposits (plaques) in your arteries (atherosclerosis), which reduces blood flow. These plaques sometimes rupture and can lead to a heart attack or stroke.
  • High-density lipoprotein (HDL) cholesterol. This is called the “good” cholesterol because it helps carry away LDL cholesterol, thus keeping arteries open and your blood flowing more freely.
  • Triglycerides. Triglycerides are a type of fat in the blood. When you eat, your body converts calories it doesn’t need into triglycerides, which are stored in fat cells. High triglyceride levels are associated with several factors, including being overweight, eating too many sweets or drinking too much alcohol, smoking, being sedentary, or having diabetes with elevated blood sugar levels.

Who should get a cholesterol test?

According to the National Heart, Lung and Blood Institute (NHLBI), a person’s first cholesterol screening should occur between the ages of 9 and 11 and then be repeated every five years after that.

The NHLBI recommends that cholesterol screenings occur every 1 to 2 years for men ages 45 to 65 and for women ages 55 to 65. People over 65 should receive cholesterol tests annually.

More-frequent testing might be needed if your initial test results were abnormal or if you already have coronary artery disease, you’re taking cholesterol-lowering medications or you’re at higher risk of coronary artery disease because you:

  • Have a family history of high cholesterol or heart attacks
  • Are overweight
  • Are physically inactive
  • Have diabetes
  • Eat an unhealthy diet
  • Smoke cigarettes

People undergoing treatment for high cholesterol require regular cholesterol testing to monitor the effectiveness of their treatments.

More Information

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Risks

There’s little risk in getting a cholesterol test. You might have soreness or tenderness around the site where your blood is drawn. Rarely, the site can become infected.

How you prepare

You’re generally required to fast, consuming no food or liquids other than water, for nine to 12 hours before the test. Some cholesterol tests don’t require fasting, so follow your doctor’s instructions.

What you can expect

During the procedure

A cholesterol test is a blood test, usually done in the morning if you fast overnight. Blood is drawn from a vein, usually from your arm.

Before the needle is inserted, the puncture site is cleaned with antiseptic and an elastic band is wrapped around your upper arm. This causes the veins in your arm to fill with blood.

After the needle is inserted, a small amount of blood is collected into a vial or syringe. The band is then removed to restore circulation, and blood continues to flow into the vial. Once enough blood is collected, the needle is removed and the puncture site is covered with a bandage.

The procedure will likely take a couple of minutes. It’s relatively painless.

After the procedure

There are no precautions you need to take after your cholesterol test. You should be able to drive yourself home and do all your normal activities. If you’ve been fasting, you might want to bring a snack to eat after your cholesterol test is done.

Results

In the United States, cholesterol levels are measured in milligrams (mg) of cholesterol per deciliter (dL) of blood. In Canada and many European countries, cholesterol levels are measured in millimoles per liter (mmol/L). To interpret your test results, use these general guidelines.

Total cholesterol(U.S. and some other countries)Total cholesterol*(Canada and most of Europe)
Below 200 mg/dLBelow 5.18 mmol/LDesirable
200-239 mg/dL5.18-6.18 mmol/LBorderline high
240 mg/dL and aboveAbove 6.18 mmol/LHigh
LDL cholesterol(U.S. and some other countries)LDL cholesterol*(Canada and most of Europe)
Below 70 mg/dLBelow 1.8 mmol/LBest for people who have coronary artery disease — including a history of heart attacks, angina, stents or coronary bypass.
Below 100 mg/dLBelow 2.6 mmol/LOptimal for people at risk of coronary artery disease or who have a history of diabetes. Near optimal for people with uncomplicated coronary artery disease.
100-129 mg/dL2.6-3.3 mmol/LNear optimal if there is no coronary artery disease. High if there is coronary artery disease.
130-159 mg/dL3.4-4.1 mmol/LBorderline high if there is no coronary artery disease. High if there is coronary artery disease.
160-189 mg/dL4.1-4.9 mmol/LHigh if there is no coronary artery disease. Very high if there is coronary artery disease.
190 mg/dL and aboveAbove 4.9 mmol/LVery high.
HDL cholesterol(U.S. and some other countries)HDL cholesterol*(Canada and most of Europe)
Below 40 mg/dL, men
Below 50 mg/dL, women
Below 1 mmol/L, men
Below 1.3 mmol/L, women
Poor
40-59 mg/dL, men
50-59 mg/dL, women
1-1.5 mmol/L, men
1.3-1.5 mmol/L, women
Better
60 mg/dL and aboveAbove 1.5 mmol/LBest
Triglycerides(U.S. and some other countries)Triglycerides*(Canada and most of Europe)
Below 150 mg/dLBelow 1.7 mmol/LDesirable
150-199 mg/dL1.7-2.2 mmol/LBorderline high
200-499 mg/dL2.3-5.6 mmol/LHigh
500 mg/dL and aboveAbove 5.6 mmol/LVery high

*Canadian and European guidelines differ slightly from U.S. guidelines. These conversions are based on U.S. guidelines.

If your results show that your cholesterol level is high, don’t get discouraged. You might be able to lower your cholesterol with lifestyle changes, such as quitting smoking, exercising and eating a healthy diet.

If lifestyle changes aren’t enough, cholesterol-lowering medications also might help. Talk to your doctor about the best way for you to lower your cholesterol.

90,000 Reaching the Target Level of Low Density Lipoprotein Cholesterol: Current Opportunities | Kotovskaya Yu.V., Eruslanova E.A.

The review provides an analysis of the main characteristics, clinical efficacy and safety of fixed combinations of modern lipid-lowering drugs, shows the prospects for combination therapy using ezetimibe

Target LDL-C levels in current guidelines

Cardiovascular diseases (CVD) rank first among the causes of morbidity and mortality worldwide [1].Reducing the level of low-density lipoprotein cholesterol (LDL-C) with the use of HMG-CoA reductase inhibitors is the cornerstone of primary and secondary prevention of adverse cardiovascular outcomes [2–8]. According to the 2019 European Society of Cardiology guidelines, patients with dyslipidemia are advised to prescribe a high-intensity statin (for example, atorvastatin or rosuvastatin), which provides the necessary reduction in LDL-C levels, and to increase the dose to the maximum tolerated level in order to achieve the target LDL-C levels established depending on risk groups (tab.12). Target LDL-C levels depending on cardiovascular risk and the algorithm for achieving them are presented in Figures 1 and 2. In some patients, despite the use of high doses of even high-intensity statins, it is not possible to achieve target LDL-C levels during monotherapy. Even with the proof of the thesis “the lower the level of LDL-C, the lower the risk of cardiovascular morbidity and mortality”, despite the existence of clear clinical recommendations, the indicators of achieving the target LDL-C among patients taking statins are 33.7%, while among those receiving statins for secondary prevention, 58% [10], and they require combination therapy with ezetimibe [11-15].Taking a fixed combination of a statin and ezetimibe increases the effectiveness of each drug in a pair (due to a synergistic effect), increases adherence to therapy and, in some cases, may be more economically beneficial for the patient [16]. The purpose of this review is to analyze the main characteristics, clinical efficacy and safety of fixed combinations of modern lipid-lowering drugs to increase the ability to achieve the target LDL-C level in accordance with current recommendations.

Simvastatin and ezetimibe

The first fixed combination of a statin and ezetimibe was a simvastatin-based combination. Simvastatin 10–40 mg / day reduces LDL-C levels by 18–41% less than atorvastatin or rosuvastatin [17], which limits its use in cases where it is required to achieve modern target LDL-C values.The bioavailability of simvastatin is about 5%, the half-life is about 1-3 hours [18]. In general, the drug is well tolerated, an increase in the level of hepatic transaminases occurs in 1% of patients [19].

Ezetimibe lowers LDL-C levels by blocking the absorption of cholesterol in the small intestine and increasing the excretion of cholesterol in the bile. Many studies have repeatedly demonstrated the synergistic effect of prescribing drugs from the class of statins and ezetimibe [22-24].

The effectiveness of ezetimibe and simvastatin therapy was shown in the randomized, double-blind, placebo-controlled study IMProved Reduction of Outcomes: Vytorin Efficacy International Trial (IMPROVE-IT).The study design was based on a comparison of simvastatin monotherapy (40 mg) and combination therapy with simvastatin and ezetimibe (40 + 10 mg) in patients after myocardial infarction. In the combination therapy group, the achieved LDL-C level was significantly lower (53.7 mg / dL versus 69.5 mg / dL in the monotherapy group). A decrease in the number of heart attacks and strokes was also demonstrated in the combination therapy group (p <0.05) [25]. Also interesting are the results of a 2017 study, which showed that the protective effect of combination therapy was higher in the group with GFR less than 45 ml / min / 1.73m 2 [26].

The simultaneous administration of simvastatin and ezetimibe did not increase the risk of developing side effects of statins – myopathy and increased levels of hepatic transaminases [27]. Moreover, it has been shown that the combination does not increase the risk of developing type 2 diabetes mellitus, which is sometimes observed with therapy with high doses of statins [28, 29].

Atorvastatin and ezetimibe

Atorvastatin at a dose of 10–80 mg / day reduces the level of LDL-C by 37–51%, reduces the risk of developing cardiovascular and cerebrovascular complications, has demonstrated its effectiveness in conducting both primary and secondary prevention in a series of clinical studies and meta-analyzes [30 ].

A meta-analysis that included 17 studies showed that combination therapy with atorvastatin and ezetimibe reduced LDL-C and triglycerides and increased HDL-C (p <0.05) [31]. Combination therapy has demonstrated a decrease in coronary atherosclerosis, as measured by intravascular ultrasound, compared with atorvastatin alone [32]. Studies have shown a comparable incidence of adverse reactions in combination therapy with atorvastatin and ezetimibe and monotherapy with atorvastatin or ezetimibe, with isolated cases of increased hepatic transaminase levels, the development of myopathy or intestinal irritation [33].

Rosuvastatin and ezetimibe

Rosuvastatin at a dose of 5-40 mg / day lowers the level of LDL-C by 46-55%, the average decrease in cholesterol and LDL-C is higher than that of other drugs from this group in an equivalent dosage. The bioavailability of rosuvastatin is 20% (comparable to the bioavailability of atorvastatin), the half-life is 19 hours. Most of the drug is excreted in the bile (72%), the remainder in the urine. The drug is not metabolized by the liver cytochrome system, and therefore practically does not interact with other drugs.Side effects such as myopathy and rhabdomyolysis are rare (less than 0.1% and less than 0.01%, respectively) [19].

The efficacy and safety of rosuvastatin was demonstrated in the study The Justification for the Use of statins in Prevention: an International Trial Evaluating Rosuvastatin (JUPITER) trial [33]. The appointment of rosuvastatin reduced the risk of heart attack, stroke, the need for revascularization and hospitalization for unstable angina pectoris, as well as the risk of death from all causes by 44% compared with placebo (p <0.00001).The results of the HOPE-3 (Heart Outcomes Prevention Evaluation 3) study showed that treatment with rosuvastatin compared with placebo reduced the risk of cardiovascular complications in patients from the middle risk group, while only antihypertensive therapy (candesartan) compared with placebo did not lead to risk reduction [35]. Compared with simvastatin and atorvastatin, the use of rosuvastatin already at a dose of 10 mg is superior to simvastatin at a maximum dose of 40 mg and is equivalent to the use of atorvastatin 40 mg in its ability to reduce LDL-C [1].

The effectiveness of the combination of rosuvastatin with ezetimibe was demonstrated in a study that included 469 patients at high risk of CVD, who for 6 weeks. received either monotherapy with rosuvastatin (40 mg) or combined therapy with rosuvastatin and ezetimibe (40 + 10 mg). Combination therapy showed an additional 12% reduction in LDL-C levels compared to monotherapy (-69.8% versus -57.1%). Moreover, patients in the combination therapy group were more likely to achieve target LDL-C levels.For example, in the very high-risk group, 79.6% of participants achieved the target values ​​(LDL-C less than 70 mg / dL), while in the monotherapy group it was possible only in 35% of cases [36].

The safety and efficacy of the combination drug (ezetimibe 10 mg and rosuvastatin 5, 10 or 20 mg) was demonstrated in The Multiceneter Randomized Study of Rosuvastatin and Ezetimibe (MRS-ROSE). The study compared the efficacy of the combined drug with the efficacy of rosuvastatin monotherapy for 8 weeks.Depending on the dose of rosuvastatin in the combined preparation, the level of LDL-C decreased by 56–63%, which exceeded the effectiveness of rosuvastatin monotherapy at the same dosage. In addition, in patients with diabetes mellitus or metabolic syndrome, there was a more significant reduction in LDL-C, triglycerides and total cholesterol levels among those receiving therapy with the combination drug [37].

The Ildong Rosuvastatin & Ezetimibe for Hypercholestelomia (I-ROSETTE) study showed that the safety and tolerability of the combination therapy were comparable to those of rosuvastatin monotherapy [38].

Higher efficacy and favorable safety profile of combination therapy with rosuvastatin and ezetimibe compared with increasing the dose of rosuvastatin were shown in a multicenter, randomized, double-blind study conducted in the Americas and Europe. 440 study participants were divided into 2 parallel groups (depending on the dosage of rosuvastatin), each of which, in turn, was also divided into 2 groups: taking the combined drug or increasing the dose of rosuvastatin (from 5 to 10 mg or from 10 to 20 mg , and in combination therapy, the statin dose remained the same).The target level of LDL-C from 70 to 100 mg / dL was reached by 59.4% of patients receiving combination therapy, and only 30.9% with an increase in the dose of rosuvastatin [39].

In January 2019, the first fixed combination drug of rosuvastatin and ezetimibe Rosulip® Plus was registered in Russia. Rosulip® Plus is indicated in addition to the diet of patients with primary hypercholesterolemia (with the exception of heterozygous familial hypercholesterolemia). Rosulip Plus is prescribed as a substitution therapy for patients whose lipid profile was adequately controlled by the simultaneous use of separate preparations of rosuvastatin and ezetimibe in doses equivalent to the corresponding doses in a fixed combination.

Prospects for combination therapy with ezetimibe

Bempedoic acid is a new generation lipid-lowering drug that can lower LDL-C levels by 40%. Bempedoic acid is a prodrug that is converted in the liver to bempedoic acetyl coenzyme A, which is an inhibitor of the enzyme ATP citrate lipase. In accordance with its mechanism of action, this drug not only lowers the level of LDL-C, but also blocks the synthesis of fatty acids [40–42].

The combination of bempedoic acid (120 or 180 mg / day) and ezetimibe (10 mg / day) in patients with statin intolerance and in those who could receive statin therapy led to a decrease in LDL-C levels by 43.1% and 47.7 %, respectively, depending on the dosage of the drug. Bempedoic acid monotherapy reduces LDL-C levels by 27.5% and 30.1% (corresponding to the indicated dose) and is well tolerated [43]. In a phase III clinical trial, the addition of this drug to statin and ezetimibe therapy in patients with high and very high CVD risk reduced LDL-C levels by 28% and the CVD risk by 33% [44].The combination of bempedoic acid and ezetimibe continues to be explored as a promising combination.

Conclusion

Ezetimibe is often used as a second drug to achieve target LDL-C levels. The combination of statins and ezetimibe has been conclusively proven to be effective and safe. In the light of the updated recommendations of the European Society of Cardiology 2019, combination therapy with rosuvastatin and ezetimibe is receiving special attention due to the decrease in the recommended target values ​​of LDL-C in patients with a very high risk of less than 1.4 mmol / L and a decrease in the level of LDL-C by 50% or more …Studies have shown that the combination of a high-intensity statin (such as rosuvastatin) and ezetimibe reduces LDL levels by an average of 65% from baseline [9]. Achieving the target LDL values ​​will reduce the risk of developing cardiovascular complications, and the visible result will increase patient adherence to therapy.

New generation drugs based on bempedoic acid show promising results in lowering LDL-C levels both in monotherapy and in combination with other drugs (for example, with ezetimibe) and are interesting from the point of view of expanding the possibilities of achieving target LDL-C in patients who are not can take statins for a variety of reasons.Fixed combinations of lipid-lowering drugs can reduce the frequency of undesirable side reactions (for example, it has already been proven that when ezetimibe is taken together with statins, the risk of developing diabetes mellitus is reduced), due to the synergistic effect, a more significant decrease in LDL-C and the risk of cardiovascular complications is noted, moreover, adherence to long-term lipid-lowering therapy is significantly increased.

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90,000 often patients accidentally find out about an increased level of cholesterol in the blood – FSBI “NMITs TPM” of the Ministry of Health of Russia

Alexander Vladimirovich Yemelyanov, a cardiologist, deputy chief physician of the CDC FSBI “NMITs TPM” of the Ministry of Health of the Russian Federation, spoke about the danger of cholesterol, from what age it is necessary to control its level and what hereditary hypercholesterolemia is.

Alexander Vladimirovich, what is the danger of an increase in the level of cholesterol in the blood?

The most common cause of cardiovascular disease is atherosclerosis, a chronic disease of the arteries. And the main cause of atherosclerosis is cholesterol, which accumulates in plaques and clogs blood vessels. Cholesterol for the time being does not manifest itself in any way. It “doesn’t hurt.” A common situation: a patient accidentally finds out that his cholesterol level is higher than normal, or even goes to the doctor, having a serious cardiovascular pathology.Therefore, cardiologists, and the entire medical community, have an important task – to identify patients with a risk group, achieve target cholesterol and blood pressure levels and thereby prevent or, at least, significantly reduce cardiovascular accidents.

What is the survey? Do you need to regularly donate blood for cholesterol?

A blood test for total cholesterol must be taken without fail. But this study may not be enough.It is also recommended to check the level of low-density lipoprotein (the so-called “bad” cholesterol) and lipoprotein (a), which are risk factors for atherosclerosis, coronary heart disease and other cardiovascular diseases. Lipid screening is recommended for all people over 40 years of age. But you need to start doing it even in adolescence.

Can teenagers have high cholesterol?

In adolescence, lipid metabolism disorders can already be recorded, when the receptors that remove cholesterol from the body do not function sufficiently.This means that in 15-20 years these patients will develop vascular problems. Therefore, if there are cardiovascular diseases in the family history, then such a patient should begin to be examined by a pediatric cardiologist.

Are these disorders at a young age associated with heredity?

Yes, in most cases these patients have hereditary, or familial, hypercholesterolemia – a genetically determined condition characterized by lipid metabolism disorders.If parents, grandparents and other close relatives had heart attacks and strokes, then the patient is at risk. Such patients need to be provided with qualified assistance on time, otherwise in the future they are threatened with neglected atherosclerosis with subsequent heart attacks, strokes … Moreover, traditional treatment in this case is ineffective.

It is hereditary factors that lead to early – at 35-45 years old – cardiovascular disasters. In addition, high cholesterol levels are still not widely accepted as a dangerous symptom.

What should the doctor do in this case?

It is necessary to change the patient’s attitude to his health, identify hereditary factors and correct the acquired risks, including normalizing cholesterol levels and blood pressure, motivating the patient to quit smoking, exercise and revise eating habits. Primary prevention and early diagnosis will help not to miss specialized patients, correct their condition and prevent cardiovascular risks.

We invite you for a professional examination by a cardiologist at the Federal State Budgetary Institution “NMITs TPM” of the Ministry of Health of Russia. You can sign up by calling 8 (495) 790-71-72.

Laboratory assessment of lipid metabolism parameters in INVITRO

Since 01.07.2019, the INVITRO laboratory has switched to a new format for providing the results of lipid profile tests for adults.

Earlier, on the INVITRO results forms for a number of lipid profile tests, we gave both the reference limits (reference boundaries of the population interval in apparently healthy people) and additionally the recommendations of the NCEP / ATPIII (National Cholesterol Education Program Adult Treatment Panel III) program according to their desired values ​​with preventive point of view.From 01.07.2019, when issuing the results of a lipid profile study, only comments will be provided containing thresholds of the desired level in terms of preventing cardiovascular risks, updated in accordance with current clinical guidelines

Cardiovascular diseases associated with atherosclerotic vascular changes, and their complications (heart attack, stroke) remain the leading cause of death of the population both in our country and throughout the world. To date, prevention is considered the main approach to reducing mortality due to these causes – measures aimed at reducing the impact of risk factors for the development of cardiovascular diseases.Some of the increased risk factors are related to the so-called. not modifiable (male, older). Others (smoking, blood pressure, cholesterol levels) can be manipulated to effectively reduce the risk of death from complications of cardiovascular disease. To choose an effective prevention strategy, you first need to determine the degree of risk for a particular person, taking into account individual factors. To do this, use the SCORE scale (Systematic COronary Risk Evaluation), which allows you to calculate the individual risk of complications of cardiovascular diseases in the next 10 years.Some patients can be immediately categorized as high or very high cardiovascular risk in accordance with the existing cardiac diagnosis. Among the risk factors for this calculation, the level of total cholesterol and its fractions is taken into account.

Result interpretation: reference interval or target values ​​

Any laboratory test result should be interpreted depending on the purpose of the examination and the specific clinical situation, in conjunction with the data of the clinical examination and the results of other studies.

The patient’s result can be assessed either relative to reference values ​​(limits within which the values ​​for 95% of conventionally healthy people of the corresponding sex and age fit), or relative to clinical thresholds established as a result of medical research for certain purposes (including to confirm the probable diagnosis, while the diagnostic threshold of the indicator may be different depending on the suspected disease, assessment of the potential risk of pathology development, prognosis, control of the effectiveness of targeted therapy, etc.). These thresholds for metric values ​​used for certain clinical judgments and medical decision making may not coincide with statistically established reference limits.

Reference intervals and target thresholds are reference values ​​for the interpretation of the result, but they reveal it from different perspectives. So, a result that fits into the statistically accepted reference interval may answer the question: “Is the patient healthy, does his result fit into the usual population interval, does it differ from the expected result?”An assessment of the result in this format is used in the initial examination if there are no generally accepted clinical thresholds. Clinical thresholds, as the name suggests, provide an answer to another question: “Does the patient have a risk / suspected disease, what is the likelihood of developing this disease, based on the threshold?” By setting clinical thresholds, we clearly answer the medical question: if the result exceeds the threshold, it can serve as a marker of a specific disease or pathological condition.Moreover, one and the same test can have several clinical thresholds, based on the tasks of interpretation.

For lipid profile indicators, it is now recommended to indicate on the score sheet expertly established desirable thresholds for the prevention of cardiovascular disease. These thresholds can be considered as the boundaries of the likely increase in cardiac risk or as targets to be achieved during lipid-lowering therapy.

The INVITRO laboratory since 01.07.2019 has expanded the range of studies performed within the lipid profile:

  • Calculation of non-HDL cholesterol (the sum of all atherogenic cholesterol fractions)

The spectrum of studies of the lipid profile in INVITRO currently includes (see Fig. 1):

  1. Total cholesterol – used for an individual assessment of cardiac risk, the indicator is recommended to be used in combination with measuring the level of HDL cholesterol and in combination with other factors, in T.h. using tables SCORE (see below). Desirable values ​​for apparently healthy individuals in the absence of additional risk factors are defined in the interpretation notes. It is advisable to strive to achieve them by practicing a healthy lifestyle and proper nutrition, this reduces the risk of heart attack and stroke.
  2. LDL cholesterol is an atherogenic fraction of cholesterol in the blood. Desirable LDL values ​​for apparently healthy individuals in the absence of additional risk factors are defined in the interpretation notes.Target values ​​of LDL in treatment for individuals of high and very high risk groups are specified by the attending physician. Monitoring the patient’s LDL cholesterol concentration before and during treatment (measured or calculated) should ideally be performed using the same test method.
  3. HDL cholesterol – “antiatherogenic” fraction of cholesterol, “good cholesterol”. A low value of this fraction of cholesterol is considered as an unfavorable factor in assessing cardiac risk, which is recommended to be taken into account in a comprehensive assessment of individual risks (see.LDL-based refinements to the SCORE tables).
  4. Non-HDL cholesterol – all cholesterol minus HDL cholesterol (the concept includes cholesterol of atherogenic fractions: low, very low and intermediate density lipoproteins – LDL, VLDL, LDL, LP (a)). Non-HDL cholesterol should be the target of secondary therapy in patients with mild to moderate hypertriglyceridemia, for whom LDL cholesterol measurements or calculations are less accurate.
  5. Triglycerides – Elevated triglyceride levels in cardiac risk assessment indicate the need for a comprehensive analysis of other risk factors.An increase in triglyceride levels has been associated with an increase in heart rate.
  6. Apolipoprotein A1 (apoA1) is a protein that is part of high density lipoproteins. As with the interpretation of HDL cholesterol results, a low apoA1 value indicates a high cardiac risk.
  7. Apolipoprotein B (apoB) is a protein associated with low, intermediate, very low density lipoproteins and LP (a). A high concentration of this protein indicates an increase in the number of particles that contain atherogenic cholesterol, and can be considered an independent factor of cardiopathic risk.Measurement of apoB, the main protein component of LDL, can also be used to estimate the amount of LDL particles. However, apoB measurement also includes VLDL, LDL, LP (a), and chylomicron residues.
  8. Lipoprotein (a) (LP (a)) – atherogenic particles similar to LDL. A high level may indicate a hereditary disorder of lipid metabolism.
  9. VLDL cholesterol – very low density lipoprotein cholesterol – particles enriched in triglycerides. A calculated indicator is used based on the measurement of triglycerides and the known ratio of triglycerides to cholesterol in VLDL.In assessing cardiac risk, a high level indicates an increased risk.
  10. The atherogenic index is the ratio of non-HDL cholesterol to HDL cholesterol. In assessing cardiac risk, an increased atherogenic index indicates an increased risk.
  11. apoA1 / apoB is the ratio of apoA1 to apoB. In the assessment of cardiac risk, a decrease in this ratio indicates an increased risk.

The current clinical guidelines of the professional communities, adopted as a basis by the INVITRO laboratory, on the interpretation of the results of lipid profile tests

Recommendations for determining the risk category using lipid profile indicators (including SCORE tables), goals and strategies for lipid-lowering therapy for patients in high and very high risk groups can be found in detail here:

  1. Russian Society of Cardiology (RSC).National Society for the Study of Atherosclerosis (NOA). Russian Society for Cardiac Rehabilitation and Secondary Prevention (RosOKR) M.V. Yezhov and other Diagnostics and correction of lipid metabolism disorders for the prevention and treatment of atherosclerosis. Russian recommendations VI revision. Atherosclerosis and dyslipidemia. 2017; 3: 5-22.
  2. European Society of Cardiology / European Atherosclerosis Society (ESC / EAS) Catapano A.L. et al. 2016 ESC / EAS guidelines for the management of dyslipidaemias.European heart journal. 2016; 37 (39): 2999-3058.
  3. 2018 AHA / ACC / AACVPR / AAPA / ABC / ACPM / ADA / AGS / APhA / ASPC / NLA / PCNA
    American College of Cardiology Clinical Policy Approval Committee, American Heart Association Science Advisory and Coordinating Committee, American Association of Cardiovascular and Pulmonary Rehabilitation, American Academy of Physician Assistants, Association of Black Cardiologists, American College of Preventive Medicine, American Diabetes Association, American Geriatrics Society , American Pharmacists Association, American Society for Preventive Cardiology, National Lipid Association, and Preventive Cardiovascular Nurses Association
    Grundy S.M. et al. Guideline on the Management of Blood Cholesterol. Journal of the American College of Cardiology. 2018: 121. doi: https://doi.org/10.1016/j.jacc.2018.11.003.

Some relevant aspects of laboratory assessment of lipid metabolism

As part of modern strategies to reduce mortality from cardiovascular diseases, for the active detection of diseases and their risk factors, screening of the population is carried out, including the assessment of lipid profile indicators.A comprehensive analysis of the survey results allows you to assess the individual risk (low, moderate, high or very high) and apply effective preventive measures to reduce it.

Fig. 1. Characterization of lipoproteins depending on size and density and their laboratory markers

Source: Langlois, Michel R., et al. “Quantifying atherogenic lipoproteins: current and future challenges in the era of personalized medicine and very low concentrations of LDL cholesterol.A consensus statement from EAS and EFLM. “Clinical chemistry 64.7 (2018): 1006-1033.

LDL cholesterol as the main parameter in assessing atherogenic plasma potential and determining the goals of lipid-lowering therapy

Low-density lipoprotein cholesterol (LDL-C) is a significant risk factor for the development of atherosclerosis and complications of cardiovascular diseases. It can be regulated by the use of lipid-lowering drug therapy, in part by diet.Individual, target values ​​of this indicator indicate as the goal of therapy. The assignment of patients to a particular risk group affects the choice of individual goals for LDL cholesterol in lipid-lowering therapy: patients at high risk need more intensive therapy and achieve lower LDL cholesterol targets.

For dynamic control of the effectiveness of lipid-lowering therapy, in accordance with the current recommendations, both a routine lipid profile with the calculation of LDL cholesterol according to the Friedwald formula (using the results of measuring total cholesterol, HDL cholesterol and triglycerides) and methods of direct measurement of LDL cholesterol can be used.

When calculating LDL cholesterol using the Friedwald formula, data on the average ratio of triglycerides / cholesterol in residual lipoproteins are used. Since this ratio gradually increases in VLDL and chylomicrons as the severity of hypertriglyceridemia and chylomicronemia increases, at some of their levels the equation overestimates VLDL cholesterol and, consequently, underestimates LDL cholesterol. Friedwald’s formula becomes increasingly inaccurate with triglyceride concentrations between 2.3 and 4.5 mmol / L and is considered invalid if the triglyceride level exceeds 4.5 mmol / L.

An alternative to the Friedwald formula for assessing LDL cholesterol is the study of the concentration of LDL cholesterol by direct determination, which does not require additional tests for calculation. Currently, there is a wide range of reagents on the market for direct determination, however, the lack of standardization of methods leads to the appearance of reagent-dependent differences in the results obtained. Depending on the method used, different treatment decisions or inconsistencies may arise if monitoring samples are tested in several laboratories using different methods or when changing methods.If the assessment of the effectiveness of therapy is carried out according to the results of the analysis of LDL cholesterol, performed by direct determination, then the observation of the patient from the initial examination to the examination in the process of lipid-lowering therapy should ideally be carried out by the same method (preferably in the same laboratory using the same equipment) to minimize misclassifications of cardiovascular risk.

At the moment, a significant advantage of determining LDL cholesterol by a direct method compared to determining LDL cholesterol according to the Friedwald formula in blood samples with a triglyceride concentration of <4.5 mmol / l has not been established.At the same time, in most clinical trials demonstrating the evidence base for reducing LDL cholesterol with statin therapy, the Friedwald equation was used.

The historically developed concept of “classical” lipid profile indicators, their assessment and interpretation have undergone significant changes in modern lipidology. Fasting blood samples were the standard for lipid determination. Taking blood on an empty stomach reduces the concentration of triglycerides, which makes it possible to more accurately estimate the content of LDL cholesterol using the Friedwald equation.It should be noted that the initially developed clinical thresholds for LDL cholesterol were determined in population studies using fasting samples and LDL cholesterol calculations using the Friedwald formula.

Role of non-HDL cholesterol and lipoprotein (a) in cardiovascular risk assessment and therapy control

The first indicator that was used as a criterion for choosing therapy and monitoring its effectiveness was LDL cholesterol. However, evidence is accumulating that the use of LDL cholesterol alone as a measure of the effectiveness of lipid-lowering therapy is not an effective strategy for all patients, in part because there is evidence that VLDL, remnant cholesterol and lipoprotein (a) levels are also associated with risk development of cardiovascular diseases.

The current evidence base of recommendations considers the target therapeutic values ​​of LDL cholesterol depending on the degree of risk of complications of cardiovascular diseases. Patients with a history of high-risk patients require greater reductions in LDL cholesterol levels. However, often in individual practice and in patients who reached the target values ​​of LDL cholesterol and even had a concentration of <1.8 mmol / L, complications of cardiovascular diseases developed or progression of atherosclerosis was noted.This is due to the presence of other atherogenic lipoprotein fractions containing remnant (residual) cholesterol. The accumulation of triglyceride-rich remnant particles in the blood after a meal is an important factor in atherogenesis. Remnant cholesterol corresponds to cholesterol that is not found in LDL and HDL. In the fasting state, it is VLDL and LDD cholesterol, and in the non-fasting state it is part of the remnant chylomicrons. Fractions containing remnant cholesterol have a residual or "latent" risk that is not determined in the study of LDL cholesterol, which makes a significant contribution to mortality from cardiovascular diseases and emphasizes the need for a personalized medical approach using additional markers.

It is possible to identify the hidden risk using the calculated indicator “non-HDL cholesterol”. This indicator combines all cholesterol, with the exception of HDL cholesterol, that is, in total all atherogenic lipoproteins: low (LDL), very low (VLDL), intermediate density (IDL), chylomicrons and LP (a). Unlike LDL cholesterol, non-HDL cholesterol takes into account the atherogenic potential of remnant lipoproteins. Therefore, non-HDL cholesterol provides a more complete risk assessment than LDL cholesterol in patients with hypertriglyceridemia.

Modern laboratory lipid profile assessment faces two important challenges. The increasing number of people with obesity, metabolic syndrome, insulin resistance and diabetes mellitus is increasing the number of patients with elevated triglyceride concentrations, even on an empty stomach. In samples with a pronounced increase in triglyceride levels, the correlation between non-HDL cholesterol and LDL cholesterol is significantly reduced. In patients with moderate hypertriglyceridemia in the range of 2.3-4.5 mmol / L, non-HDL cholesterol shows much better agreement with the classification of cardiovascular risk.

Another, no less important problem of the calculation method for assessing LDL cholesterol is the low concentration of LDL cholesterol in the process of lipid-lowering therapy. Both the inaccuracy and the bias of the LDL cholesterol from the true value increase at lower LDL cholesterol concentrations – an aspect that is more relevant, since highly effective methods for lowering the LDL concentration are available, including combination therapies (for example, inhibitors of the PCSK9 protein (proprotein convertase subtilisin / kexin type nine)).The original Friedwald equation in 1972 was not intended for patients receiving such treatment.

In patients with high triglycerides and / or low LDL-C, there are differences in risk stratification between LDL-C and non-HDL-C. Taking into account that non-HDL cholesterol includes remnant cholesterol, in the case of discrepancies between the indicators of non-HDL cholesterol, it more reliably predicts the risk in such patients.

LDL cholesterol + apolipoprotein B – additional informative value

Determination of the content of cholesterol in LDL was the first criterion for assessing the risk and effectiveness of therapy.However, evidence is emerging that not only cholesterol content, but also the number and size of LDL particles and their size can influence the risk of complications of cardiovascular disease. All LDL particles are highly atherogenic, but their content is not always reflected in the measurements of LDL cholesterol, especially in patients with hypertriglyceridemia. The concentration of cholesterol in the LDL fraction does not always reflect the number of LDL particles, since the cholesterol content of the particles and their amount can vary widely between individuals.The LDL particle count is superior to the LDL cholesterol study in predicting cardiovascular disease, which is consistent with the fact that many people with atherogenic dyslipidemia have increased LDL particle counts without increasing LDL cholesterol concentration (see explanation in Figure 2).

Fig. 2. Relative size and number of LDL and remnant cholesterol in three patients with achieved low LDL cholesterol level (1.8 mmol / L), but with different values ​​of non-HDL cholesterol and apoV

Patient 1 achieved the goal on all three indicators (predominantly larger LDL).Patient 2 with moderate hypertriglyceridemia has non-HDL cholesterol higher than the target value (2.6 mmol / L) due to an increased level of remnant cholesterol. Patient 3 also has moderate hypertriglyceridemia and increased remnant cholesterol, but at the same time a higher apoB concentration than patient 2, due to the large number of small dense LDL particles not detected by standard LDL cholesterol measurement.

Source: Langlois, Michel R., et al. “Quantifying atherogenic lipoproteins: current and future challenges in the era of personalized medicine and very low concentrations of LDL cholesterol.A consensus statement from EAS and EFLM. “Clinical chemistry 64.7 (2018): 1006-1033.

Apolipoprotein B is part of atherogenic lipoproteins, forming the protein parts of the molecules. This indicator can be used to estimate the number of LDL, VLDL and LDL (a) particles, since one apoB molecule is associated with one LDL particle. Consistent with this view, the risk of cardiovascular complications is directly related to the number of particles containing apoB rather than LDL cholesterol.

Differences between the determination of LDL cholesterol and the number of their particles are reflected in the interpretation of the results when conducting lipid-lowering therapy. Statins reduce the level of LDL cholesterol and non-HDL cholesterol significantly more than the level of apoB. This is due to the fact that statins significantly reduce the concentration of larger LDL particles, rich in cholesterol, than smaller particles with low cholesterol. The increased concentration of apoB when the LDL-C target is reached helps to identify high-risk patients who would otherwise be overlooked, i.e.because optimal values ​​of LDL cholesterol have been achieved. This discrepancy determines the residual risk in patients on statins and affects the potential for additional benefit from lipid-lowering therapy, which is lost if apoB is not measured.

These data indicate that for the majority of patients, the clinical efficacy of target values ​​for habitual LDL cholesterol and alternative non-HDL cholesterol and apoB cholesterol is similar. However, among a subgroup of patients (up to 25% of the population) with a mismatch between LDL cholesterol and non-HDL cholesterol and apoB, the risk may be overestimated or underestimated if only the measurement of LDL cholesterol is relied upon.

The current expert recommendations for patients with hypertriglyceridemia and low LDL cholesterol concentration propose to change the focus of markers of lipid-lowering therapy efficacy and to determine non-HDL cholesterol and apoB, since they are more accurate for risk assessment than directly measured or calculated using the Friedwald’s formula. LDL.

Recommended thresholds for the interpretation of lipid profile indicators in prophylactic screening of individuals with no additional risk factors

  • Total cholesterol.ESC / EAS / RCO recommendation *: Desired level <5.0 mmol / L. Cholesterol should be used in conjunction with other factors in an individual assessment of cardiac risk (see SCORE tables).

  • Triglycerides. ESC / EAS / RCO Cardiac Risk Assessment Guideline: A level <1.7 mmol / L indicates low risk.

  • HDL cholesterol. ESC / EAS / RCO Cardiology Guideline:> 1.2 mmol / L for women and> 1.0 mmol / L for men indicates low risk.

  • LDL cholesterol. ESC / EAS / RCO Recommendations: In the absence of additional cardiac factors, the desired level is <3.0 mmol / L.

  • Non-HDL cholesterol. ESC / EAS / RCO Recommendations: In the absence of additional cardiac factors, the desired level is <3.8 mmol / L.

  • Apolipoprotein A. ESC / EAS Cardiology Guideline: A level> 1.25 g / L indicates low risk.

  • Apolipoprotein B. ESC / EAS recommendation: in the absence of additional cardiac factors, the desired level is <1.0 g / L.

  • Lipoprotein (a). ESC / EAS Cardiology Guideline: A level> 0.5 g / L indicates a high risk.

  • VLDL cholesterol. ESC / EAS Cardiology Guideline: <0.8 mmol / L indicates low risk.

Note:

* Recommendations ESC / EAS / RKO – recommendations of European societies of cardiology, atherosclerosis, Russian Society of Cardiology.

The above thresholds used for the interpretation of lipid profile indicators are aimed at assessing the risk of developing cardiovascular diseases and their complications for patients who undergo an initial examination and have not previously been assigned to any category of risk of developing cardiovascular diseases.

Pronounced shifts in the results of these studies may indicate possible genetically determined diseases, which are manifested by an abnormal increase or decrease in indicators.

Abnormal results requiring in-depth examination

Test Threshold A comment
No. 30 Triglycerides > 10 mmol / L Hyperchylomicronemia syndrome with high risk of acute pancreatitis
No. 33 LDL Cholesterol <0.3 mmol / L Hereditary alpha-beta lipoproteinemia
No. 33 LDL Cholesterol (adults) > 5 mmol / L Familial hypercholesterolemia with high cardiac risk (heterozygous mutation)
No. 33 LDL Cholesterol (children) > 4 mmol / L Familial hypercholesterolemia with high cardiac risk (heterozygous mutation)
No. 32 HDL cholesterol <0.2 mmol / L Hereditary hypo-alpha lipoproteinemia
No. 1071 Lipoprotein (a) > 1.50 g / l High risk of cardiovascular disease (incl.including myocardial infarction and aortic valve stenosis)
No. 220 Apolipoprotein B <0.1 g / l Hereditary alpha-beta lipoproteinemia
No. 219 Apolipoprotein A1 <0.1 g / l Hereditary hypo-alpha lipoproteinemia

Applications:

  1. Appendix 1
  2. Data on population variation in lipid profile and NCEP / ATPIII lipid thresholds (National Cholesterol Education Program, 2001).

Official documents

  1. Boytsov S.A. et al. Cardiovascular prophylaxis 2017. Russian national guidelines. Russian Society of Cardiology, National Society for Preventive Cardiology, Russian Society for the Prevention of Noncommunicable Diseases. Russian journal of cardiology. 2018; 23 (6): 7-122.
  2. Ezhov M.V. and other Diagnostics and correction of lipid metabolism disorders for the prevention and treatment of atherosclerosis. Russian recommendations VI revision.Atherosclerosis and dyslipidemia. 2017; 3: 5-22.
  3. Catapano A.L. et al. 2016 ESC / EAS guidelines for the management of dyslipidaemias. European heart journal. 2016; 37 (39): 2999-3058.
  4. Grundy S.M. et al. 2018 AHA / ACC / AACVPR / AAPA / ABC / ACPM / ADA / AGS / APhA / ASPC / NLA / PCNA Guideline on the Management of Blood Cholesterol, Journal of the American College of Cardiology. 2018: 121. doi: https://doi.org/10.1016/j.jacc.2018.11.003.
  5. Nordestgaard B.G. et al.Fasting is not routinely required for determination of a lipid profile: clinical and laboratory implications including flagging at desirable concentration cut-points — a joint consensus statement from the European Atherosclerosis Society and European Federation of Clinical Chemistry and Laboratory Medicine. European heart journal. 2016: 37 (25): 1944-1958.

Cholesterol – low density lipoprotein (LDL)

Low density lipoproteins are the main carriers of cholesterol (cholesterol) in the body.Cholesterol, which is part of them, is considered “harmful”, because if it is in excess, the risk of plaque in the arteries increases, which can lead to blockage and cause a heart attack or stroke.

Synonyms Russian

LDL, low density lipoproteins, LDL, LDL cholesterol, low density lipoprotein cholesterol, beta-lipoprotein cholesterol, beta-lipoproteins, beta-LP.

Synonyms English

LDL, LDL-C, low density lipoprotein cholesterol, Low density lipoprotein.

Research method

Colorimetric photometric method.

Units

Mmol / L (millimol per liter).

Which biomaterial can be used for research?

Venous blood.

How to properly prepare for the study?

  1. Do not eat within 12 hours prior to examination.
  2. Eliminate physical and emotional stress and do not smoke for 30 minutes before the study.

General information about the study

Cholesterol (cholesterol, cholesterol) is a fat-like substance vital for the body. The correct scientific name for this substance is “cholesterol” (the ending -ol indicates that it belongs to alcohols), however, the name “cholesterol” has become widespread in the mass literature, which we will use later in this article. Cholesterol is involved in the formation of cell membranes in all organs and tissues of the body.On the basis of cholesterol, hormones are created that are necessary for the development of the body and the implementation of the reproduction function. Bile acids are formed from cholesterol, with the help of which fats are absorbed in the intestines.

Cholesterol is insoluble in water, therefore, to move through the body, it is “packed” in a protein shell, consisting of apolipoproteins. The resulting complex (cholesterol + apolipoprotein) is called lipoprotein. Several types of lipoproteins circulate in the blood, differing in the proportions of their constituent components:

  • very low density lipoprotein (VLDL),
  • low density lipoprotein (LDL),
  • high density lipoprotein (HDL).

LDL cholesterol is considered “bad”, because when it is in excess, plaques form in the walls of blood vessels, which can restrict the movement of blood through the vessel, which threatens atherosclerosis and significantly increases the risk of heart disease (coronary disease, heart attack) and stroke.

The liver produces a sufficient amount of cholesterol for the needs of the body, but part of it comes from food, mainly from fatty meat and fatty dairy products. If a person has a hereditary predisposition to high cholesterol or eats too much animal fat, then the level of LDL in the blood can rise to dangerous levels.

What is the research used for?

  • To assess the likelihood of atherosclerosis and heart problems (this is the most important indicator of the risk of coronary artery disease).
  • For monitoring the effectiveness of a diet with a reduced amount of animal fat.
  • For monitoring lipid levels after taking cholesterol-lowering drugs.

When is the study scheduled?

Analysis for LDL is usually part of the lipid profile, which also includes the determination of total cholesterol, VLDL cholesterol, HDL cholesterol, triglycerides and the atherogenic coefficient.A lipidogram can be prescribed during routine preventive examinations or with an increase in the concentration of total cholesterol, in order to find out due to which fraction it is increased.

In general, a lipid profile is recommended for all people over 20 years of age at least once every 5 years, but in some cases even more often (several times a year). First, if the patient is on a diet that restricts animal fats and / or is on cholesterol-lowering medications, then they are tested to see if they are meeting their LDL and total cholesterol targets and, therefore, have a reduced risk of cardiovascular diseases.And, secondly, if one or more risk factors for the development of cardiovascular diseases are present in the patient’s life:

  • smoking,
  • certain age (men over 45, women over 55),
  • high blood pressure (from 140/90 mm Hg),
  • high cholesterol or cardiovascular disease in family members (heart attack or stroke in the closest male relative under 55 years of age or female under 65),
  • ischemic heart disease, previous heart attack or stroke,
  • diabetes mellitus,
  • overweight,
  • alcohol abuse,
  • eating large amounts of food containing animal fats
  • low physical activity.

If a child in the family has had cases of high cholesterol or heart disease at a young age, then for the first time he is recommended to take a lipid profile at the age of 2 to 10 years.

What do the results mean?

Reference values:

The concept of “norm” is not quite applicable in relation to the level of LDL cholesterol. Different people, in whose life there are a different number of risk factors, the LDL norm will be different. An LDL cholesterol test is used to determine the risk of cardiovascular disease, however, in order to accurately determine it for a person, all factors must be taken into account.

An increase in LDL cholesterol may be the result of a hereditary predisposition (familial hypercholesterolemia) or excessive ingestion of animal fats. In most people with high cholesterol, both factors are involved to some extent.

According to clinical guidelines 1 , level

“Diagnostics and correction of lipid metabolism disorders for the prevention and treatment of atherosclerosis. Russian recommendations, VII revision.2020 “.

“2019 ESC / EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk”.

Possible causes of an increase in LDL cholesterol:

  • cholestasis – stagnation of bile, which can be caused by liver disease (hepatitis, cirrhosis) or gallstones,
  • chronic kidney inflammation leading to nephrotic syndrome,
  • chronic renal failure,
  • decreased thyroid function (hypothyroidism),
  • poorly cured diabetes mellitus,
  • alcoholism,
  • obesity,
  • cancer of the prostate or pancreas.

The lowered level of LDL cholesterol is not used in diagnostics due to low specificity. However, its causes may be:

  • hereditary hypocholesterolemia,
  • severe liver disease,
  • oncological diseases of the bone marrow,
  • increased thyroid function (hyperthyroidism),
  • inflammatory diseases of the joints,
  • B 12 – or folate deficiency anemia,
  • common burns,
  • acute diseases, acute infections,
  • chronic obstructive pulmonary disease.

What can influence the result?

The cholesterol concentration may change from time to time, this is normal. A single measurement does not always reflect the usual level, therefore, it may sometimes be necessary to retake the analysis after 1-3 months.

Increase the level of very low density lipoprotein cholesterol (VLDL cholesterol):

  • pregnancy (lipid profile should be done at least 6 weeks after childbirth),
  • prolonged fasting,
  • standing blood donation,
  • anabolic steroids, androgens, corticosteroids,
  • smoking,
  • intake of food containing animal fats.

Reduce the level of VLDL cholesterol:

  • lying down,
  • allopurinol, clofibrate, colchicine, antifungal drugs, statins, cholestyramine, erythromycin, estrogens,
  • intense physical activity,
  • a diet low in cholesterol and saturated fatty acids and, conversely, high in polyunsaturated fatty acids.

Download an example of the result

Important notes

  • A lipidogram must be taken when the person is relatively healthy.After an acute illness, heart attack, surgery, you should wait at least 6 weeks before measuring cholesterol.
  • LDL is usually calculated using the following formula: LDL cholesterol = total cholesterol – (HDL cholesterol – TG (triglycerides) / 2.2).
  • In the United States, lipids are measured in milligrams per deciliter, in Russia and in Europe, in millimoles per liter. The recalculation is carried out according to the formula XC (mg / dl) = XC (mmol / L) × 88.5 or XC (mmol / L) = XC (mg / dL) x 0.0113.
  • LDL cholesterol is usually calculated based on the results of other analyzes included in the lipid profile: total cholesterol, HDL cholesterol and triglycerides – another type of lipids that make up lipoproteins.More often, a fairly accurate indicator is achieved, however, if the triglyceride level is significantly increased (> 10 mmol / l) or a person has eaten a lot of fatty foods before taking the test, the result may not be entirely correct. In this case, LDL is measured directly.

Also recommended

Who orders the study?

General practitioner, therapist, cardiologist.

90,000 Indicators of lipid metabolism. Total cholesterol

Cholesterol is a fat-like substance that is vital for the body.The correct scientific naming of this
substances – “cholesterol” (the ending “-ol” indicates belonging
to alcohols), however, the name
“cholesterol”.

About 80-85% of all cholesterol is synthesized by the human body (liver, intestines, kidneys,
adrenal glands,
sexually
glands), the remaining 15-20% come from food of animal origin (primarily meat,
dairy
products, eggs).

Cholesterol is involved in the formation of cell membranes in all organs and tissues of the body. The largest number
cholesterol is involved in the formation of erythrocyte cell membranes (about 24%), liver cell membranes
make up 17%, the brain (white matter) – 15%, the gray matter of the brain – 5-7%.

On the basis of cholesterol, hormones are created that are involved in the growth, development of the body and implementation
breeding functions. Bile acids are formed from cholesterol, which are part of bile, thanks to
it absorbs fats in the intestines.

Total cholesterol is an indicator reflecting the totality of all circulating cholesterol fractions
in blood.
Cholesterol itself is insoluble in water, therefore, for the transport of cholesterol in the body,
complex compounds due to binding to protein molecules. Such complexes are called lipoproteins.

Several types of lipoproteins circulate in the blood, differing in the proportions of their constituents.
components.Depending on the size of the particles and their functions, they release high lipoproteins
density
(HDL), low density lipoprotein (LDL), very low density lipoprotein (VLDL), cholesterol,
unrelated
with high density lipoproteins (non-HDL), and a number of other substances. LDL and VLDL are considered
“Bad” cholesterol, as they contribute to the formation of plaque in the arteries. HDL,
against,
called “good”, since the composition of HDL is removed from the vessels of excess cholesterol.

The content of cholesterol in the blood is highly dependent on age. Its level at birth
is less than 3.0 mmol / l, then gradually increases. Emerging differences in its concentration
connected
with gender. In men, the concentration of cholesterol in the blood rises in the early
and middle age and decreases with old age. In women, cholesterol levels with age
increases more slowly, up to menopause; may later exceed cholesterol levels
in men.The described age-related changes in the content of cholesterol in the blood are associated with the action of genital
hormones: estrogens lower and androgens raise total cholesterol. During pregnancy
there is a physiological increase in total cholesterol levels.

Increased cholesterol levels are one of the main causes of atherosclerotic vascular disease. Level
total cholesterol in combination with data on existing diseases, family history, age,
field,
the level of blood pressure, the fact of smoking are taken into account when assessing the individual risk of developing severe complications
cardiovascular diseases (myocardial infarction or stroke) on the SCORE scale
(SystematicCOronaryRiskEvaluation)
in primary prevention.

Based on the degree of risk, targets for total cholesterol and other lipid fractions are calculated,
which you need to strive for by practicing a healthy lifestyle and proper nutrition. Diet change
can
reduce blood cholesterol levels by 10-15%, although sensitivity to changes in content
cholesterol
in food and the effect of diet on cholesterol levels can be different. If the target figures are not reached
drug therapy is prescribed by non-drug methods.

How to properly prepare for the study?

  1. Do not eat for 8 hours before testing.
  2. Eliminate physical and emotional stress 30 minutes before the study.
  3. Do not smoke within 30 minutes prior to examination.

What can influence the result?

Raise the level of total cholesterol:

  • intake of food containing animal fats.
  • pregnancy (a cholesterol test must be taken at least 6 weeks after delivery),
  • prolonged fasting,
  • blood donation while standing,
  • taking anabolic steroids, androgens, corticosteroids,
  • smoking,
  • cholestasis (bile stasis),
  • chronic kidney inflammation leading to nephrotic syndrome,
  • chronic renal failure,
  • decreased thyroid function (hypothyroidism),
  • uncompensated diabetes mellitus,
  • obesity,
  • cancer of the prostate or pancreas.
  • gout.

Reduces total cholesterol level:

  • blood donation while lying down,
  • taking a number of drugs (allopurinol, clofibrate, colchicine, antifungal drugs, statins,
  • cholestyramine, erythromycin, estrogens),

  • intense physical activity,
  • diet high in polyunsaturated fatty acids,
  • liver disease,
  • bone marrow diseases,
  • increased thyroid function (hyperthyroidism),
  • disorders of absorption processes in the intestine,
  • folate or B12 deficiency anemia,
  • common burns,
  • tuberculosis,
  • acute diseases, acute infections,
  • chronic obstructive pulmonary disease.

CLINICAL OUTCOMES OF PATIENTS WITH STABLE SENOCARDIA AFTER ROUTINE PERCUTANEOUS CORONARY INTERVENTION WITH A COATING STENT | Tomilova

1. Bibek S, Xie Y, Gao J et al. Role of Pre-procedural C-reactive Protein Level in the Prediction of Major Adverse Cardiac Events in Patients Undergoing Percutaneous Coronary Intervention: a Meta-analysis of Longitudinal Studies.Inflammation 2015; 38 (1): 159-169.

2. Chazov EI, Karpov YuA. Rationale Pharmacotherapy For Cardiovascular Diseases. A guidebook for medical practitioners. Moscow Litterra Publishers 2014; 1056 p. Russian (Chazov E.I., Karpov Yu.A. Rational pharmacotherapy of cardiovascular diseases. A guide for practicing physicians. Moscow: Litterra 2014; 1056 p).

3.Cholesterol Treatment Trialists’ (CTT) Collaborators, Mihaylova B, Emberson J et al. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomized trials. Lancet 2012; 380: 581-590.

4. ESC / EAS Guidelines for the management of dyslipidaemias. European Heart Journal 2011; 32: 1769-1818.

5.Kukharchuk VV, Konovalov GA, Susekov AV et al. Diagnostics and correction of lipid metabolism disorders in order to prevent and treat atherosclerosis. Russian recommendations V revision. Atherosclerosis 2012; 2 (8): 61-94.

6. Stone NJ, Robinson J, Lichtenstein AH et al. 2013 ACC / AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology / American Heart Association Task Force on Practice Guidelines.Circulation 2013; 00: 000–000.

7. Di Sciascio G, Patti G, Pasceri V et al. Atorvastatin for Reduction of Myocardial Damage During Angioplasty (Efficacy of atorvastatin reload in patients on chronic statin therapy undergoing percutaneous coronary intervention: results of the ARMYDA RECAPTURE (Atorvastatin for Reduction of Myocardial Damage During Angioplasty) Randomized Trial. J Am Coll Cardiol 2009; 54: 54: 558-565.

8. Ndrepepa G, Braun S, Tada T et al. Comparative prognostic value of low-density lipoprotein cholesterol and C-reactive protein in patients with stable coronary artery disease treated with percutaneous coronary intervention and chronic statin therapy. Cardiovasc Revasc Med. 2014; 15 (3): 131-136.

9. Puri R, Nissen SE, Libby P et al.C-reactive protein, but not low-density lipoprotein cholesterol levels, associate with coronary atheroma regression and cardiovascular events after maximally intensive statin therapy. Circulation 2013; 128 (22): 2395-2403.

10. Boytsov SA, Khomitskaya YuV. Centralised Survey on the Undertreatment of the Hypercholesterolemia in Russia (CEPHEUS). Cardiovascular Therapy and Prevention 2013; 12 (4): 67–74 (Boytsov SA, Khomitskaya SE.Centralized study to evaluate the effectiveness of treatment of hypercholesterolemia in Russia (CEPHEUS). Cardiovascular therapy and prevention, 2013; 12 (4): 67-74).

11. Yao HM, Wan YD, Zhang XJ et al. Long-term follow-up results in patients undergoing percutaneous coronary intervention (PCI) with drug-eluting stents: results from a single high-volume PCI center. BMJ Open 2014; 4: e004892.

12.Zahn R, Neumann FJ, Buttner HJ et al. Long-term follow-up after coronary stenting with the sirolimus-eluting stent in clinical practice: results from the prospective multi-center German Cypher Stent Registry. Clin Res Cardiol 2012; 101: 709-716.

13. Akhmedzhanov NM, Nebieridze DV, Safaryan AS et al. Analysis of hypercholesterolemia prevalence in the outpatient practice (according to the ARGO study): Part I. Rational Pharmacotherapy in Cardiology 2015; 11 (3): 253-260 (Akhmedzhanov NM, Nebieridze DV, Safaryan AS et al.Analysis of the prevalence of hypercholesterolemia in outpatient practice (according to the ARGO study): part I. Rational Pharmacotherapy in Cardiology 2015; 11 (3): 253-260).

14. Goodman SG, Langer A, Bastien NR et al. Prevalence of dyslipidemia in statin-treated patients in Canada: results of the DYSlipidemia International Study (DYSIS). Can J Cardiol 2010; 26 (9): 330-335.

15.Gitt AK, Junger C, Smolka W et al. Prevalence and overlap of different lipid abnormalities in statin-treated patients at high cardiovascular risk in clinical practice in Germany. Clin Res Cardiol 2010; 99 (11): 723-733.

INFORMATION AND PECULIARITIES OF STATIN THERAPY IN PERSONS WITH DIFFERENT CARDIOVASCULAR RISK: STUDY BY ESSE-RF | Shalnova

Authors

S.A. Shalnova

State Research Center for Preventive Medicine, Ministry of Health of Russia, Moscow

Russia

Doctor of Medical Sciences, Professor, Head of the Department of Epidemiology of Chronic Noncommunicable Diseases.

Tel .: 8 (499) 553-69-65, e-mail: [email protected]; [email protected]

A.D. Deev

State Research Center for Preventive Medicine, Ministry of Health of Russia, Moscow

Russia

Candidate of Physical and Mathematical Sciences, Head of the Laboratory of Medical Biostatistics

V.A. Metelskaya

State Research Center for Preventive Medicine, Ministry of Health of Russia, Moscow

Russia

Doctor of Biological Sciences, Professor, Head of the Department for the Study of Biochemical Markers of Risk of Chronic Noncommunicable Diseases

S. E. Evstifeeva

State Research Center for Preventive Medicine, Ministry of Health of Russia, Moscow

Russia

Candidate of Medical Sciences, Senior Researcher, Department of Epidemiology of Chronic Noncommunicable Diseases

O.P. Rotar

Almazov North-West Federal Medical Research Center, Ministry of Health of Russia, St. Petersburg

Russia

Candidate of Medical Sciences, Head. laboratory of epidemiology of arterial hypertension

Yu.V. Zhernakova

Russian Cardiology Research and Production Complex, Ministry of Health of Russia, Moscow

Russia

Doctor of Medical Sciences, Senior Researcher of the Department for Coordination and Monitoring of Scientific Programs

S.A. Boytsov

State Research Center for Preventive Medicine, Ministry of Health of Russia, Moscow

Russia

Doctor of Medical Sciences, Professor, Director, Head of the Department of Clinical Cardiology and Molecular Genetics.

The author of the article on behalf of the research participants ESSE-RF

Yu. A. Balanova

State Research Center for Preventive Medicine

Russia

Department of Epidemiology of Chronic Noncommunicable Diseases,

101990, Moscow, Petroverigsky per., 10, building 3

N.V. Gomyranova

State Research Center for Preventive Medicine

Russia

101990, Moscow, Petroverigsky per., 10, building 3

A.E. Imaeva

State Research Center for Preventive Medicine

Russia

Department of Epidemiology of Chronic Noncommunicable Diseases,

101990, Moscow, Petroverigsky per., 10, building 3

A.V. Kapustina

State Research Center for Preventive Medicine

Russia

Department of Epidemiology of Noncommunicable Diseases,

101990, Moscow, Petroverigsky per., 10, building 3

A.V. End

State Research Center for Preventive Medicine

Russia

Department of Epidemiology of Chronic Noncommunicable Diseases, Laboratory for Economic Analysis of Epidemiological Research and Preventive Technologies,

101990, Moscow, Petroverigsky per., 10, building 3

O. A. Litinskaya

State Research Center for Preventive Medicine

Russia

Department for the Study of Biochemical Markers of Risk of Chronic Noncommunicable Diseases,

101990, Moscow, Petroverigsky per., 10, p. 3

M.N. Mamedov

State Research Center for Preventive Medicine

Russia

Department of Comorbidity in Cardiology,

101990, Moscow, Petroverigsky per., 10, building 3

G. A. Muromtseva

State Research Center for Preventive Medicine

Russia

Department of Epidemiology of Chronic Noncommunicable Diseases,

101990, Moscow, Petroverigsky per., 10, p. 3

R. G. Oganov

State Research Center for Preventive Medicine

Russia

Department of Prevention of Metabolic Disorders,

101990, Moscow, Petroverigsky per., 10, building 3

E. I. Suvorova

State Research Center for Preventive Medicine

Russia

Department of Epidemiology of Chronic Noncommunicable Diseases, Laboratory for Economic Analysis of Epidemiological Research and Preventive Technologies,

101990, Moscow, Petroverigsky per., 10, p. 3

M.B. Khudyakov

State Research Center for Preventive Medicine

Russia

101990, Moscow, Petroverigsky per., 10, building 3

E. I. Baranova

First Saint Petersburg State Medical University named after I.I. acad. I.P. Pavlova

Russia

Department of Faculty Therapy,

St. Petersburg

A.O. Konradi

Northwestern Federal Medical Research Center named after V.I. V.A. Almazova

Russia

Research Institute of Arterial Hypertension,

197341, St. Petersburg, st. Akkuratova, 2

E. V. Shlyakhto

Northwestern Federal Medical Research Center named after V.I. V.A. Almazova

Russia

administrative and managerial staff,

197341, g.St. Petersburg, st. Akkuratova, 2

V.A.Ilyin

Vologda Scientific Center of the Russian Academy of Sciences

Russia

Directorate,

Vologda

R. A. Kasimov

Yaroslavl State Pedagogical University named after K. D. Ushinsky

Russia

Yaroslavl

A.A. Shabunova

Vologda Scientific Center of the Russian Academy of Sciences

Russia

Department of research of the level and lifestyle of the population,

Vologda

K. N. Kalashnikov

Vologda Scientific Center of the Russian Academy of Sciences

Russia

department of standard and lifestyle,

Vologda

O.N. Kalachikova

Vologda Scientific Center of the Russian Academy of Sciences

Russia

Department of Living Standards and Lifestyle Research,

Vologda

O. A. Kondakova

Russia

A.V. Popov

Vologda Scientific Center of the Russian Academy of Sciences

Russia

Department of research of the level and lifestyle of the population,

Vologda

N.A. Ustinova

Russia

O. G. Azarin

Russia

N. I. Babenko

Voronezh State Medical University N.N. Burdenko

Russia

Department of Hospital Therapy,

Voronezh

L.V. Bondartsov

Voronezh State Medical University N.N. Burdenko

Russia

Department of Hospital Therapy,

Voronezh

E. V. Minakov

Voronezh State Medical University N.N. Burdenko

Russia

Department of Hospital Therapy,

Voronezh

A.E. Khvostikova

Russia

G. I. Furmenko

Voronezh State Medical University N.N. Burdenko

Russia

Department of Hospital Therapy,

Voronezh

S.V. Nedogoda

Volgograd State Medical University

Russia

Faculty of advanced training for doctors,

Volgograd

A.A. Ledyaeva

Volgograd State Medical University

Russia

Department of Therapy and Endocrinology FUV,

Volgograd

E.V. Chumachek

Volgograd State Medical University

Russia

Department of Therapy and Endocrinology FUV,

Volgograd

N.V. Kulakova

Russia

M.V. Mokshina

Russia

V. A. Nevzorova

Pacific State Medical University

Russia

Department of Therapy, Functional and Ultrasound Diagnostics of FPC and PPS, Head of Department,

Vladivostok

L.V. Rodionova

Russia

N.V. Shestakova

All-Union. cardiol. scientific. center of AMS SS. Institute wedge. cardiology them. A. L. Myasnikova

Russia

Moscow

O. A. Belova

Russia

O.A. Nazarova

Ivanovo State Medical Academy

Russia

Department of Therapy and General Medical Practice,

Ivanovo

S. V. Romanchuk

Scientific Research Institute of Physics and Chemistry L. Ya. Karpova

Russia

Moscow

O.A. Shutemova

Ivanovo State Medical Academy

Russia

Department of Therapy FDPPO, Cardiological Dispensary,

Ivanovo

V.S.Kaveshnikov

Tomsk National Research Medical Center of the Russian Academy of Sciences

Russia

Department of Population Cardiology with the Group of Scientific and Medical Information of Patent Science and International Relations,

Tomsk

R.S. Karpov

Tomsk National Research Medical Center of the Russian Academy of Sciences, Scientific Research Institute of Cardiology

Russia

Tomsk

V. N. Serebryakova

Tomsk National Research Medical Center of the Russian Academy of Sciences, Scientific Research Institute of Cardiology

Russia

Tomsk

I.A. Trubacheva

Tomsk National Research Medical Center of the Russian Academy of Sciences, Scientific Research Institute of Cardiology

Russia

Tomsk

A.I. Aristov

Krasnoyarsk State Medical University named after prof. V.F. Voino-Yasenetsky

Russia

Department of Therapy, Institute of Postgraduate Education,

Krasnoyarsk

Yu.I. Grinshtein

Krasnoyarsk State Medical University named after prof. V.F. Voino-Yasenetsky

Russia

Department of Therapy IPO,

Krasnoyarsk

L. K. Danilova

Krasnoyarsk State Medical University named after prof. V.F. Voino-Yasenetsky

Russia

Department of Therapy IPO,

Krasnoyarsk

A.A. Evsyukov

Krasnoyarsk State Medical University named after prof. V.F. Voino-Yasenetsky

Russia

Department of Outpatient Therapy, Family Medicine and Healthy Lifestyle with the Course of PO,

Krasnoyarsk

D. S. Kaskaeva

Krasnoyarsk State Medical University named after prof. V.F. Voino-Yasenetsky

Russia

Department of Outpatient Therapy, Family Medicine and Healthy Lifestyle with the Course of PO,

Krasnoyarsk

A.A. Kosinova

Krasnoyarsk State Medical University named after prof. V.F. Voino-Yasenetsky

Russia

Department of Therapy IPO,

Krasnoyarsk

M. M. Petrova

Krasnoyarsk State Medical University named after prof. V.F. Voino-Yasenetsky

Russia

Department of Outpatient Therapy, Family Medicine and Healthy Lifestyle with the Course of PO,

Krasnoyarsk

R.R. Roof

Krasnoyarsk State Medical University named after prof. V.F. Voino-Yasenetsky

Russia

Department of Therapy IPO,

Krasnoyarsk

N.V. Topolskaya

Russia

V. V. Shabalin

Krasnoyarsk State Medical University named afterprof. V.F. Voino-Yasenetsky

Russia

Department of Therapy, Institute of Postgraduate Education,

Krasnoyarsk

E. N. Shmatova

Volgograd State Medical University

Russia

Department of Pharmaceutical and Toxicological Chemistry,

Volgograd

O.L. Barbarash

Research Institute for Complex Issues of Cardiovascular Diseases

Russia

administration,

Kemerovo

G. V. Artamonova

Research Institute for Complex Issues of Cardiovascular Diseases

Russia

Department of Optimization of Medical Care in Cardiovascular Diseases,

Kemerovo

A.E. Skripchenko

Research Institute for Complex Issues of Cardiovascular Diseases

Russia

Department of Optimization of Medical Care in Cardiovascular Diseases, Laboratory of Epidemiology of Cardiovascular Diseases,

Novokuznetsk

E. V. Indukaeva

Research Institute for Complex Issues of Cardiovascular Diseases

Russia

Department of Optimization of Medical Care for CVD, Laboratory of Epidemiology of CVD,

Kemerovo

T.A. Mulerova

Research Institute for Complex Issues of Cardiovascular Diseases

Russia

Laboratory of Epidemiology of Cardiovascular Diseases,

Novokuznetsk

S. A. Maksimov

Research Institute for Complex Issues of Cardiovascular Diseases

Russia

Laboratory of Epidemiology of Cardiovascular Diseases,

Kemerovo

N.V. Cherkassy

Research Institute for Complex Issues of Cardiovascular Diseases

Russia

Laboratory for Modeling Management Technologies,

Kemerovo

M.V. Tabakaev

Research Institute for Complex Issues of Cardiovascular Diseases

Russia

Laboratory for Modeling Management Technologies,

Kemerovo

Y.V. Danilchenko

Research Institute for Complex Issues of Cardiovascular Diseases

Russia

Department of Optimization of Medical Care in Cardiovascular Diseases, Laboratory for Modeling Management Technologies,

Kemerovo

I.R.Basyrova

Orenburg State Medical University

Russia

Department of Hospital Therapy,

Orenburg

E.N. Isaeva

Interregional Clinical and Diagnostic Center

Russia

cardiology,

Kazan

V. Yu. Kondratenko

Russia

R. A. Libis

Orenburg State Medical University

Russia

Department of Hospital Therapy,

Orenburg

E.A. Lopina

Orenburg State Medical University

Russia

Department of Hospital Therapy named after R.G. Mezhebovsky,

Orenburg

D. V. Safonova

Orenburg State Medical University

Russia

Department of Hospital Therapy. R.G. Mezhebovskogo,

Orenburg

S. K. Gutnova

North Ossetian State Medical Academy

Russia

Vladikavkaz

T. M. Gatagonova

North Ossetian State Medical Academy

Russia

Administration,

Vladikavkaz

G.V. Tolparov

North Ossetian State Medical Academy

Russia

Department of Internal Medicine No. 4,

Vladikavkaz

S. A. Gudkova

Russian Scientific Center for Surgery named after acad. B.V. Petrovsky

Russia

Department of Surgical Treatment of Complex Cardiac Arrhythmias and Electrocardiostimulation,

Moscow

D.V. Duplyakov

Samara State Medical University

Russia

administration,

Samara

N. A. Cherepanova

Russian Chemical-Technological University named after DI. Mendeleev

Russia

Moscow

A.Y. Efanov

Tyumen State Medical University

Russia

Faculty of General Medicine, Department of Hospital Therapy with the Course of Endocrinology and Clinical Pharmacology,

Tyumen

I. V. Medvedeva

Tyumen State Medical University

Russia

Department of Hospital Therapy,

Tyumen

M.A. Watchman

Tyumen State Medical University

Russia

Faculty of General Medicine, Department of Hospital Therapy with the Course of Endocrinology and Clinical Pharmacology,

Tyumen

V.P. Shava

Tyumen Department of the South Ural Scientific Center of the Russian Academy of Medical Sciences

Russia

management,

Tyumen

S.V. Shalaev

Tyumen State Medical University

Russia

Department of Cardiology FPK and PPS,

Tyumen

.