Hyperlipidemia: diagnosis and treatment

Roza Ismailovna Yagudina , Ph.D. Sc., prof., head. Department of Organization of Drug Supply and Pharmacoeconomics and Head. laboratory of pharmacoeconomic research of the First Moscow State Medical University named after. I. M. Sechenov.

Evgenia Evgenievna Arinina , Ph.D., leading researcher at the laboratory of pharmacoeconomic studies of the First Moscow State Medical University named after. I. M. Sechenova

Cardiovascular diseases (CVDs) are the leading cause of death worldwide. WHO estimates that 17.3 million people died from CVDs in 2008, accounting for 30% of all deaths worldwide. Of this number, 7.3 million died from coronary heart disease. According to WHO forecasts, by 2030, approximately 23.3 million people will die from CVDs annually.

The group of cardiovascular diseases includes several nosological units:

coronary heart disease - a disease of the blood vessels that supply blood to the heart muscle;
disease of the blood vessels in the brain that supply it with blood;
disease of the peripheral arteries that supply blood to the arms and legs;
rheumatic carditis - damage to the heart muscle and heart valves as a result of a rheumatic attack caused by streptococcal bacteria;
congenital heart disease - deformations of the structure of the heart existing from birth;
Deep vein thrombosis and pulmonary embolism - the formation of blood clots in the leg veins that can dislodge and move towards the heart and lungs.

One of the most common pathologies in the structure of CVD is coronary heart disease (CHD), to which we will devote a number of articles. IHD, as defined by WHO, is acute or chronic cardiac dysfunction resulting from an absolute or relative decrease in the supply of arterial blood to the myocardium.

In more than 90% of cases, the anatomical basis for the development of coronary artery disease is damage to the coronary arteries of the heart, leading to a decrease in coronary blood flow and an imbalance between the need of the heart muscle for oxygen and nutrients and the blood supply capabilities of the heart. Often this effect is caused by dyslipidemias, leading to the development of atherosclerosis, therefore, in the first article devoted to the problem of pharmacotherapy of IHD, we will dwell in detail on dyslipidemias (hyperlipidemias).

Currently, the following forms of IHD are distinguished:
Sudden cardiac arrest
Angina pectoris
Silent cardiac ischemia
Syndrome X (microvascular angina)
Myocardial infarction
Cardiosclerosis (atherosclerosis)
Heart failure
Heart rhythm disturbances

Why is this dangerous?

Cholesterol is important for our body: being a component of the cell membrane, it is indispensable in the synthesis of hormones and the transport of other molecules. But elevated levels of cholesterol and other fats provoke the development of atherosclerosis, in which plaques form from fats (lipids) circulating in the blood. Over time, there can be so many of them that the lumen of the vessel narrows completely, and life-threatening complications arise, including, for example, myocardial infarction. Please note: you may not know that you have high cholesterol levels in your blood, since hyperlipidemia itself gives virtually no symptoms until it provokes other diseases, such as atherosclerosis. In other words, you can feel great while the pathological process progresses. That's why it's important to check if your cholesterol and other fats are normal. Only a specialist can do this. Therefore, do not delay diagnosis if you want to prevent the development of dangerous diseases in time. Make an appointment now.

What factors accelerate the development of atherosclerosis?

Risk factors predisposing to atherosclerotic damage to elastic and mixed arteries are considered: causes that can be eliminated and independent of the individual.

Eliminated (modified) include:

features of lifestyle, routine, habits - lack of sufficient mobility, smoking, addiction to alcohol, emotionality of experiences and behavior, resistance to stress, work on night shifts are important;
type of diet - in families that accustom the child from childhood to fatty and high-calorie foods, those who like to eat a lot of fried meat, barbecue, there are more cases of acute diseases caused by atherosclerosis;
High blood pressure in hypertensive patients should be monitored and treated;
For patients with diabetes, there are recommendations for correcting blood glucose levels, using hypoglycemic agents, and a specially calculated diet.

Fat deposition in men with a waist size of 102 cm or more is considered critical.

Factors that a person cannot change include:

your gender (men suffer more often);
age (hereditary disorders appear already in children, secondary changes are more often observed after 40 years);
genetic predisposition in cases of familial types of hyperlipidemia;
consequences arising after a stroke or myocardial infarction.

In these cases, patients are prevented from possible or repeated complications of atherosclerosis. When choosing which doctor to treat, patients should not forget that dyslipidemia should be consulted with an endocrinologist.

Elevated blood cholesterol: causes

Elevated blood cholesterol levels are usually the result of a complex of reasons, which usually include:

Hereditary diseases
Kidney disease, such as chronic renal failure
Hypertension
Diabetes
Liver diseases, for example, acute and chronic hepatitis, cirrhosis of the liver
Diseases of the pancreas, such as tumor, acute and chronic pancreatitis
Diabetes
Hypothyroidism
Growth hormone deficiency
Pregnancy – increases the amount of “bad” cholesterol and decreases the level of “good” cholesterol
Alcohol abuse or overt alcoholism
Smoking
Metabolic disorders
Obesity
The use of certain medications, including oral contraceptives, steroid hormones, diuretics and a number of others
Acquired chronic diseases in adulthood and old age

Dyslipidemia in diabetes mellitus

The connection between metabolic disorders simultaneously in carbohydrate and fat metabolism is manifested in diabetes. Detection of dyslipidemia in a patient with diabetes mellitus can seriously worsen the prognosis of the disease.

The reasons are considered:

uncompensated blood glucose levels;
negative effects of certain medications (diuretics, beta blockers, antiviral drugs, antidepressants, cytostatics);
concomitant hypothyroidism and obesity;
hereditary burden.

The disease causes a change in the synthesizing and neutralizing function of liver cells by disrupting the formation of chylomicrons, inhibiting a number of necessary enzyme systems, and activating the supply of free fatty acids from adipose tissue reserves. The production of lipoproteins is very sensitive to the presence of insulin. The forms of dyslipidemia depend on the type of diabetes.

In treatment, endocrinologists must monitor the level of fat metabolism indicators. The prescription of drugs that affect the synthesis and excretion of cholesterol is indicated when the analysis numbers are elevated.

It is preferable to prescribe drugs to patients from the statin group, possibly in combination with fibrates.

Types of hyperlipidemia

Depending on the amount of fat in the blood, there are five types of hyperlipidemia:

The first type is a high level of triglycerides in the blood, which increases the risk of developing pancreatitis.
The second type is an increased content of low-density lipoproteins (LDL), which results in the development of atherosclerotic changes in blood vessels and increases the risk of heart attack.
The third type is a high level of very low density lipoproteins and triglycerides, which also increases the risk of developing atherosclerosis, coronary heart disease and various pathologies of the vessels of the lower extremities.
The fourth type is increased levels of triglycerides and normal or slightly increased levels of cholesterol, which together increase the risk of developing diabetes, obesity and sclerotic changes.
Type five – the body cannot absorb and eliminate triglycerides, which can cause a severe form of pancreatitis. This most often happens when you abuse alcohol and unhealthy fatty foods, such as fast food.

Modern pharmacotherapy of hyperlipidemia: the view of a clinical pharmacologist

Hyperlipidemia (HLP) is a general term that reflects a pathological increase in plasma lipid levels. Human blood plasma lipids - triglycerides, phospholipids and cholesterol - are in a protein-bound state, i.e. in the form of lipoproteins. Different classes of lipoproteins differ in the percentage of protein, TG, cholesterol and its esters, in density and diameter, as well as in clinical significance. Thus, chylomicrons (CM), very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL) and high-density lipoprotein (HDL), as well as lipoprotein (a) are distinguished. Their properties are shown in Table 1. Normal values of lipid content in blood plasma are defined in the European recommendations for the prevention of cardiovascular diseases, III revision (2003) [1]: J Total cholesterol - less than 5 mmol/l; J LDL cholesterol – less than 3 mmol/l; J HDL cholesterol – more than 1 mmol/l in men and more than 1.2 mmol/l in women; J TG – less than 1.77 mmol/l. It is necessary to note that a number of laboratories use lipid spectrum indicators expressed in mg% (or mg/dL). To recalculate cholesterol, the indicator in mg% should be multiplied by 0.0259, and triglycerides by 0.0113. Depending on the predominant increase in one or another component of the lipid spectrum, hypertriglyceridemia, hypercholesterolemia and combined hyperlipidemia are distinguished. WHO experts have proposed a classification of hyperlipidemias, which includes 5 types (Table 2). In addition, from a clinical point of view, it is important to distinguish between primary and secondary hyperlipidemias: Primary HLP: I. Polygenic HLP II. Monogenic HLP Familial hypercholesterolemia J Familial combined hyperlipidemia J Familial dysbetalipoproteinemia J Familial endogenous hypertriglyceridemia J Familial chylomicronemia Secondary HLP: 1. Secondary hypercholesterolemia J For diabetes mellitus J For hypothyroidism J For nephrotic syndrome J For cholestasis J For paraproteinemia (for example, multiple myeloma) 2. Secondary hypertriglyceridemia J With diabetes mellitus J With hypothyroidism J With nephrotic syndrome J With chronic alcoholism J When taking b-blockers, thiazide diuretics. The identification of secondary HLPs that complicate the course of a number of diseases and syndromes or that occur during the use of certain drugs is justified from a practical point of view. In such cases, the leading importance belongs to the diagnosis and treatment of the underlying disease. In some cases, patients with irreversible organic changes (biliary cirrhosis, chronic kidney disease) may require lipid-lowering therapy. The “foundation” in the treatment of any HLP is non-drug recommendations regarding nutrition and lifestyle. Next, the doctor needs to decide on the advisability of prescribing lipid-lowering pharmacotherapy and select a drug, and in some cases, a combination of drugs. Classification of lipid-lowering drugs Hypolipidemic drugs are those drugs that can reduce the level of TG, total cholesterol, LDL cholesterol and VLDL. The ability to increase HDL levels is also beneficial. All lipid-lowering drugs used in clinical practice can be divided into the following groups: 1. Statins - HMG-CoA reductase inhibitors (atorvastatin, lovastatin, pravastatin, simvastatin, fluvastatin, rosuvastatin); 2. Ezetimibe; 3. Fibrates – fibric acid derivatives (clofibrate, gemfibrozil, bezafibrate, fenofibrate, etofibrate); 4. Bile acid sequestrants – anion exchange resins (cholestyramine, colestipol); 5. Nicotinic acid preparations (niacin, enduracin); 6. Omega-3 fatty acid compounds. Representatives of these groups differ from each other not only in their mechanism of action and chemical structure, but also in their ability to predominantly influence different components of the lipid spectrum (Table 3). Statins - HMG-CoA reductase inhibitors Today, statins are the most widely used group of lipid-lowering drugs due to their high effectiveness, rich clinical experience and convincing evidence-based research data. The first representative of this group - lovastatin - was obtained from the fungus Monascus ruber and since 1987 has been used in the treatment of hyperlipidemia, pushing into the background traditional lipid-lowering agents - nicotinic acid, fibrates, anion exchange resins. Other statins were obtained later synthetically (fluvastatin, atorvastatin, rosuvastatin) or semi-synthetically (simvastatin and pravastatin). Mechanism of action. The effect of statins is realized by inhibiting the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase) of hepatocytes, which results in inhibition of the conversion of HMG-CoA to mevalonic acid, an intermediate product in the synthesis of cholesterol. As a result, the activity of LDL receptors in hepatocytes, which capture circulating LDL from the blood, and, to a lesser extent, VLDL and DILI, increases. This leads to a decrease in the concentration of LDL and cholesterol, as well as a moderate decrease in the content of VLDL and TG. At the same time, inhibition of this enzyme leads to a decrease in the synthesis of biologically active substances isoprenoids, which probably underlies the so-called “pleiotropic” effects of statins, namely anti-inflammatory, antiproliferative and the ability to improve endothelial function [6]. It takes 1–2 months for the effect of statins to develop; as a rule, long-term, in most cases lifelong, therapy is carried out [2]. Practical aspects of statin pharmacokinetics. While there are a number of common features in the pharmacokinetics of different statins, it is in this area that there are significant and practically significant differences between the drugs within the group. In particular, the participation of one or another biotransformation enzyme (cytochrome P450 isoenzymes, UDP-glucuronyl transferase) or transporter (glycoprotein P, organic anion transporters) in the kinetic processes of a particular drug will determine possible drug interactions, incl. posing a danger in terms of the development of adverse drug reactions. All statins are characterized by binding to blood proteins of more than 95%, with the exception of pravastatin, which binds to blood proteins by 50%. For most drugs, T1/2 is about 2–3 hours, for atorvastatin – 15 hours. A characteristic feature of the pharmacokinetics of statins is their excretion in bile by 90% or more [3, 4]. Lovastatin is a prodrug; in the liver, under the action of carboxylesterases, it is hydrolyzed to an active b-hydroxy acid metabolite, which actually inhibits HMG-CoA reductase. The b-hydroxy acid metabolite of lovastatin is metabolized by CYP3A4 to low-active metabolites. The partially b-hydroxy acid metabolite of lovastatin undergoes glucuronidation by UGT1A1 and UGT1A3. Lovastatin itself and its metabolites can be actively secreted into bile with the participation of glycoprotein-P. The combined use of CYP3A4 inhibitor drugs (macrolides, azole antimycotics, HIV proteinase inhibitors - indinavir, ritonavir, saquinavir) or P-glycoprotein (verapamil, spironolactone, quinidine, cyclosporine) leads to a clinically significant increase in the blood concentration of lovastatin itself and its metabolites . The reason for the increase in the concentration of the b-hydroxy acid metabolite of lovastatin when used together with gemfibrozil (an inhibitor of UGT1A1 and UGT1A2) is the inhibition of glucuronidation. In all of these cases, the risk of developing rhabdomyolysis increases significantly. Simvastatin, like lovastatin, is a prodrug; in the liver it is converted by hydrolysis under the action of carboxylesterases into an active b-hydroxy acid metabolite. The b-hydroxy acid metabolite of simvastatin is metabolized by CYP3A4, partially by CYP2D6, and to a small extent by CYP2C9 to low-active metabolites, which are mainly excreted in the bile. Part of the b-hydroxy acid metabolite of simvastatin undergoes glucuronidation under the influence of UGT1A1 and UGT1A3. Atorvastatin is an initially active drug. Once absorbed and entering the portal vein, atorvastatin is “absorbed” by hepatocytes with the participation of the organic anion transporter OATP-C. Atorvastatin is metabolized primarily by CYP3A4 to active metabolites. Some of atorvastatin and its metabolites are subject to glucuronidation by UGT1A1 and UGT1A2. In addition, atorvastatin is able to be secreted into bile using glycoprotein-P [5]. Fluvastatin is also an initially active drug. The main enzyme in the metabolism of fluvastatin is CYP2C9. As a result of the oxidation of fluvastatin under the influence of CYP2C9, 2 metabolites are formed that retain their lipid-lowering activity. The inhibitory activity of 5-hydroxyfluvastatin against HMG-CoA reductase is 85% of the activity of fluvastatin, and 6-hydroxyfluvastatin is 45%. The third metabolite of fluvastatin, N-desopropylfluvastatin, is inactive. Pravastatin is “absorbed” by hepatocytes with the participation of OATP-C. Pravastatin does not undergo biotransformation and is actively secreted unchanged into bile using the MRP-2 transporter. Rosuvastatin is also “absorbed” by hepatocytes with the participation of OATP-C. In hepatocytes, 10% of the drug is metabolized by CYP2C9, and, to a lesser extent, by CYP2C19 and carboxylesterases with the formation of low-active metabolites. 90% of rosuvastatin is excreted into bile. Pitavastatin, which is undergoing phase III clinical trials and has not yet been registered in Russia, is transported into hepatocytes via OATP-C. In hepatocytes, pitavastatin is slightly metabolized by CYP3A4, CYP2C9 and carboxylesterases to form inactive metabolites. The differences in the pharmacokinetics of statins are clearly presented in Table 4. Side effects. Among the most important side effects of statins are increased liver enzymes, less commonly hepatitis, myopathy and myositis, and extremely rarely rhabdomyolysis. Muscle toxicity is likely due to increased protein catabolism and is assessed by CPK levels. Statins can cause headaches, abdominal pain, flatulence, constipation, diarrhea, nausea and vomiting. The appearance of rash and allergic reactions (including angioedema and anaphylaxis) is uncommon. In general, severe adverse drug reactions when taking statins are observed infrequently (1 case of rhabdomyolysis per 100 thousand people per year). However, the widespread use of statins in recent years means that a small percentage may represent a large actual number of patients. Therefore, when choosing within a group, preference should be given to the safest and most studied drugs for which sufficient experience in practical use has been accumulated. Thus, according to the FDA, for 2003–2004. The smallest number of cases of rhabdomyolysis was registered with the use of pravastatin and atorvastatin, slightly more with the use of simvastatin and rosuvastatin. Interaction. As mentioned above, a significant contribution to the development of undesirable effects can be made by interaction with other drugs at the level of various pharmacokinetic processes and, as a consequence, an increase in the concentration of statin in the blood. CYP3A4 inhibitors ketoconazole, fluconazole, clarithromycin, azithromycin, cimetidine, HIV proteinase inhibitors increase the risk of side effects of lovastatin, simvastatin, atorvastatin, cerivastatin when used together. P-glycoprotein inhibitors verapamil, dipyridamole, itraconazole, clarithromycin, propafenone, sertraline, spironolactone, fluoxetine, chlorpromazine, quinidine, cyclosporine, erythromycin can increase the toxicity of lovastatin and atorvastatin. The combination of these statins with drugs that simultaneously inhibit CYP3A4 and glycoprotein-P is especially dangerous, which is accompanied by a high risk of developing rhabdomyolysis. Thus, the antifungal agent itraconazole (inhibitor of CYP3A4 and glycoprotein-P) increases the maximum concentration of the b-hydroxy acid metabolite of lovastatin by 10–20 times. A similar phenomenon occurs with the combined use of lovastatin and cyclosporine (an inhibitor of CYP3A4 and glycoprotein-P) in patients with a kidney transplant in combination with hyperlipidemia. The described interactions are not typical for fluvastatin, pravastatin and rosuvastatin, because CYP3A4 and glycoprotein-P do not participate in their pharmacokinetics. However, when pravastatin, rosuvastatin or atorvastatin are combined with gemfibrozil, an OATP-C inhibitor, the maximum concentration of the statin increases and the risk of side effects increases [7]. Contraindications. Absolute contraindications include active liver disease (with a persistent increase in liver enzymes), pregnancy and breastfeeding. Particular caution is required when using statins in patients with a history of liver disease or who frequently drink alcohol. Patients with hypothyroidism should receive adequate appropriate treatment before prescribing statins. Statins should not be used for porphyria, but rosuvastatin has been shown to be safe. Evidence base for statins The first large study examining the effectiveness of statins was the West of Scotland Pravastatin Study in the Primary Prevention of IHD - WOSCOPS. The study involved 6595 patients with hyperlipidemia. It has been shown that taking pravastatin at a dose of 40 mg leads to a decrease in the level of total cholesterol by 20%, LDL cholesterol by 26%, and a reduction in the relative risk of developing coronary artery disease by 31% compared with patients receiving placebo [8]. In addition, the studies PROSPER, CARE, LIPID, in which a total of more than 25 thousand patients took part, were devoted to studying the effectiveness of pravastatin. Simvastatin was studied in the Scandinavian 4S study in 4444 patients, half of whom received simvastatin, the other half received placebo, the drug was highly effective and a relative reduction in the risk of coronary mortality by 42% and total mortality by 30% [9]. Another 25 thousand patients took part in other studies of simvastatin, the Heart Protection Study, A to Z. The use of atorvastatin has also been studied in a convincing number of patients included in the ASCOT, CARDS, PROVE IT, TNT studies. The studies on lovastatin and fluvastatin included fewer than 10 thousand people, while multicenter studies on rosuvastatin and pitavastatin have not yet been completed. In addition, the use of statins in selected conditions has been studied. In particular, in acute coronary syndrome (ACS), both with and without ST-segment elevation, the use of statins is justified for more successful secondary prevention, but should begin after the patient’s condition has stabilized (approximately day 7). Atorvastatin can be considered the drug of choice here, since its effectiveness and safety in ACS was proven in the PROVE-IT study. However, statins cannot be considered a method of treating developed ACS. The CARDS study showed the high efficacy and safety of atorvastatin in diabetes mellitus. Conflicting data have been obtained on the use of statins in patients with CHF and left ventricular (LV) systolic dysfunction, but it is expected that a more definitive answer will be obtained after completion of the CORONA and GISSI-HF studies. A number of reports suggest the potential benefit of statins in CHF with normal LVEF (so-called LV diastolic dysfunction). Ezetimibe Ezetimibe is a relatively new drug used in the treatment of hyperlipidemia in combination with a statin [10]. The mechanism of action is associated with inhibition of the specific transporter NPC1L1 in enterocytes, as a result of which cholesterol absorption is selectively inhibited. Application. Ezetimibe is added to diet and statin treatment for primary hypercholesterolemia. In addition, it can be used independently in patients for whom statins are contraindicated, as well as in cases of familial sitosterolemia. The standard dose of the drug is 10 mg once a day. Side effects may include dyspepsia, headache, weakness, myalgia; hypersensitivity reactions and hepatitis are less commonly described. Pancreatitis, thrombocytopenia, myopathy and rhabdomyolysis can occur extremely rarely. Contraindications. Ezetimibe is not prescribed for breastfeeding and under 10 years of age; special caution should be exercised when prescribed to pregnant women and patients with liver disease. Fibrates are derivatives of fibric acid. Fibrates are derivatives of fibric acid. They are inferior to statins in their ability to reduce total cholesterol and LDL cholesterol, as well as in their evidence base. The advantage of fibrates can be considered their more pronounced effect on triglyceride levels. The first representative was clofibrate, which was used especially successfully in the 60–70s. XX century, but subsequently supplanted by second-generation drugs: gemfibrozil, bezafibrate, ciprofibrate, fenofibrate. The mechanism of action is associated with an activating effect on a special subclass of nuclear receptors - pyroxisome proliferators (PPARs), as a result of which the processes in the cell nucleus that regulate the metabolism of drugs, the synthesis of apoproteins, and the oxidation of fatty acids become more intense. Fibrates are mainly used for isolated hypertriglyceridemia (type IV), as well as combined hyperlipidemia (types IIb and III). Fibrates, as a rule, are well tolerated. Among the side effects of modern fibrates, digestive disorders, headache, dizziness, skin rashes, sometimes flickering atrial, rarely oppressing blood formation, myositis, visual impairment are noted. Fibrates are contraindicated in alcoholism, diseases of the biliary tract, severe liver and kidney lesions, as well as in pregnant and nursing. With joint use with indirect anticoagulants, fibrates can potentiate their effect, therefore, in such cases, it is recommended to reduce the dose of indirect anticoagulant (warfarin) by half. As already indicated, a combination of fibrates with statins is potentially dangerous due to an increase in the risk of myopathy and rabdomyolysis. The HHS and Vahit studies show the ability of hemfibrosil to increase the level of cholesterol LVP, reduce the risk of myocardial infarction, but there was no statistically reliable difference between compared groups in general mortality. The DAIS study evaluated the condition of the coronary arteries in patients with type 2 diabetes against the background of therapy with phenofibrata. Until now, the inconsistency of data on the influence of fibrates on a distant forecast restrains their widespread use for the primary and secondary prevention of coronary heart disease. The results confirming an increase in the survival of patients with coronary heart disease against the background of prolonged use of fibrates have not been obtained. Omega -3 -fatty acid preparations drugs containing omega -3 -fatty acid ethyl esters can be used to reduce triglycerides in the quality of fibrams in a combination of statin in patients with combined hyperlipidemia in cases where it is not possible to control the disease with statin monotherapy. These drugs can cause digestive disorders, less often - taste disorders, dizziness, hypersensitivity reactions, in rare cases, impaired liver function, headache, hyperglycemia, skin rashes, and in extremely rare cases - hypotension, urticaria, and leukocytosis. They are contraindicated in breastfeeding, the use of hemorrhagic diathesis, liver diseases in patients with hemorrhagic diathesis, as well as in pregnant women and patients receiving anticoagulants, requires special caution. In the past, anion exchange resin and nicotinic acid preparations are widespread. At present, their significance in the treatment of hyperlipidemia is reduced due to the appearance of new more effective and safe drugs with proven effect not only on individual lipid spectrum indicators, but also on the survival of patients, on the frequency of development of coronary heart disease and its complications. The choice of a hyopolipidemic drug or a combination of most of patients with hyperlipidemia as a starting treatment method is prescribed a diet with a reduced content of animal fat, recommendations for a change in lifestyle: weight correction, rejection of smoking, increasing physical activity. After 3 months, a re -study of the lipid spectrum is necessary, according to the results of which they solve the issue of the appropriateness of drug therapy. If the target levels of the total cholesterol and cholesterol LNP are not achieved, hypolipidemic drugs are prescribed. In addition, hypolipidemic pharmacotherapy can be prescribed immediately, without a period of non -drug treatment in a certain category of patients, namely in patients with a high risk of cardiovascular complications and initially very high concentrations of LNP cholesterol. As a rule, for the treatment of hypercholesterolemia, statins are the drugs. Treatment can be started with a dose of 10 or 20 mg once in the evening. With insufficient efficiency and good tolerance, the dose can be increased to 40 mg, and up to 80 mg for atorvastatin and simvastatin. In case of insufficient efficiency of monotherapy with statin, a combination with an ezetimib is 10 mg per day. As an alternative to Ezetimib, you can use anionno exchange resins: Coloritypipol or Kholestiramin. With isolated hyperthyglyceridemia that cannot be corrected by a diet, fibrates are most effective. In cases of combined hyperlipidemia, when the concentration of cholesterol and triglycerides is increased, drug treatment also begins with the prescription of statins. If against this background the level of triglycerides remains high, fibrates are added to the treatment, and in some cases nicotinic acid. However, it must be remembered that the combination of statin with fibrate or nicotinic acid increases the risk of undesirable drug reactions, including rabdomyolysis, and can only be used under the supervision of a specialist and under the control of laboratory markers of liver damage and muscle tissue. The combination of hemfibrozil with statin should not be used altogether because of a significant increase in the risk of rabdomyolysis. As an alternative to fibrams and nicotinic acid in the treatment of combined hyperlipidemia, Omega -3 -fatty acids are proposed. In addition, all patients over 40 with diabetes (both 1st and 2nd type) should be prescribed statins to reduce the risk of cardiovascular complications. The target levels of cholesterol and levels for the onset of drug therapy in various groups of patients according to European recommendations for the prevention of cardiovascular diseases of the III review (2003), the following optimal values of the lipid parameters of the population for the population as a whole were adopted: J. General cholesterol - less than 5 mmols/ l; J XC LNP - less than 3 mmol/l; J XC LVP - more than 1 mmol/L in men and more than 1.2 mmol/L in women; J TG - less than 1.77 mmol/l. At the same time, in patients with coronary heart disease or its equivalents, as well as with a high risk of its development, the target level of LNP cholesterol can differ significantly from the specified. In patients without coronary heart disease, the following indicators are used to determine the risk of its development: age (for men for more than 45 years, for women for more than 55 years or early menopause in the absence of hormonal replacement therapy), family history (closest relatives of patients with the early IBS: in men younger 55 years, in women - 65 years), smoking, blood pressure above 140 and 90 mm. Hg Art., low concentration of cholesterol LVP, diabetes. To calculate the risk of IBS development, the Score tables are offered as a percentage. Thus, for patients without coronary heart disease with no more than 1 risk factor, they are focused on indicators developed for the population: the target level of LNP cholesterol is less than 3 mmol/l. Medicine therapy in these patients should be prescribed with the content of LNP cholesterol more than 4 mmol/l. In patients with 2 or more risk factors, one should also strive for the target value of LNP cholesterol less than 3 mmol/l, however, drug therapy is recommended already at the LNP cholesterol 3.5 mmol/l and higher. For patients with IBS or its equivalents, the target level of LNP cholesterol should be less than 2.5 mmol/L, and possibly less than 2 mmol/l, while its concentration of more than 3 mmol/L in such patients serves as an indication for the onset of hypolipidemic pharmacotherapy. IBS equivalents include atherosclerosis of the peripheral arteries, atherosclerosis of the arteries of the brain, aneurysm of the abdominal aorta. Conclusion is a rational approach to the treatment of hyperlipidemia allows you to actually optimize pharmacotherapy of patients with coronary heart disease and its equivalents, reduce the total risk of cardiovascular complications and improve the prognosis. The choice of the drug or their combination should be based on the type of hyperlipidemia, the degree of increase in lipid spectrum indicators, the degree of cardiovascular risk and carried out taking into account the individual characteristics of the patient, including possible contraindications. Hyperlipidemia pharmacotherapy is carried out for a long time, most often for life, and when treatment is stopped in most cases, the indicators of the lipid spectrum are returned to the original ones.

Abbreviations: HLP - hyperlipidemia TG - triglycerides CS - cholesterol CM - chylomicrons LP - lipoproteins HMG - CoA reductase - 3-hydroxy-3-methylglutaryl-coenzyme A reductase

References 1. European guidelines on cardiovascular disease prevention in clinical practice. Third Joint Task Force of European and other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of eight societies and invited experts). Eur Heart J 2003; 24: 1601.10. 2. Aronov D.M. Treatment and prevention of atherosclerosis. M., 2000, 411 pp. 3. Kukes V.G. Metabolism of drugs: clinical and pharmacological aspects. M.: Reafarm, 2004. 4. Garcia MJ, Reinoso RF, Sanchez Navarro A, Prous JR. Clinical pharmacokinetics of statins. Methods Find Exp Clin Pharmacol. 2003 Jul-Aug;25(6):457–81. 5. Lennernas H. Clinical pharmacokinetics of atorvastatin. Clin Pharmacokinet. 2003;42(13):1141–60. 6. Martin G, Duez H, Blanquart C, Berezowski V, Poulain P, Fruchart JC, Najib–Fruchart J, Glineur C, Staels B. Statin-induced inhibition of the Rho-signaling pathway activates PPARalpha and induces HDL apoA-I. J Clin Invest. 2001 Jun;107(11):1423–32. 7. Molecular mechanisms of drug interaction, ed. Paltseva M.A., Kukesa V.G., Fisenko V.P. M., 2004. 224 p. 8. West of Scotland Coronary Prevention Study: implications for clinical practice. The WOSCOPS Study Group. Eur Heart J 1996 Feb;17(2):163–4. 9. Randomized trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S) Lancet. 1994 Nov 19;344(8934):1383–9. 10. Pearson TA, Denke MA, McBride PE, Battisti WP, Brady WE, Palmisano J. A community–based, randomized trial of ezetimibe added to statin therapy to achieve NCEP ATP III goals for LDL cholesterol in hypercholesterolemic patients: the ezetimibe add– on to statin for effectiveness (EASE) trial. Mayo Clin Proc. 2005 May;80(5):587–95.

Diagnosis of hyperlipidemia

A blood test called a lipid profile helps diagnose hyperlipidemia. Do not eat or drink anything for 9-12 hours before your blood draw. The analysis will help assess the level of fats, identify or exclude changes in serum color characteristic of hyperlipidemia. Important: in order to protect your health as much as possible, the lipid profile analysis must be repeated every 5 years. If a blood test shows that you have high levels of cholesterol and other fats, your doctor may prescribe additional diagnostic tests that will help identify or rule out various associated pathological processes:

Doppler ultrasound of blood vessels
CT scan
Angiography
Additional laboratory tests

Prevention

If left untreated, dyslipidemia leads to atherosclerosis with chronic and acute complications. In the first case, chronic ischemia develops in the area of the blood supply where an atherosclerotic plaque has formed. In the second - acute vascular insufficiency due to the closure of the lumen of blood vessels, and then infarction of various organs.

The prognosis depends on the localization of atherosclerosis, the rate of development of changes and provoking factors that can be influenced. It is very important to normalize body weight and adjust your diet, give up bad habits and emotional overload, and switch to a physical activity program on an individual schedule.

Specialists from Professor Gorbakov’s Clinic will talk about these and other preventive methods with which you can maintain your health and prevent serious consequences.

Hyperlipidemia: treatment

The most important thing in the treatment of hyperlipidemia is to find and remove the causes that provoked an increase in the level of fat in the body. Diet and lifestyle correction are one of the key conditions for successful treatment. We will talk about how to eat and what kind of lifestyle is preferable to lead below, but now we’ll talk about drug treatment of hyperlipidemia.

Drug treatment

As a rule, in the early stages of hyperlipidemia, it is enough to adjust your diet and lifestyle to normalize the level of fat in the body. Medicines are usually prescribed to people who have not responded to diet therapy during the first month of treatment. What medications can our specialists prescribe for you:

Statins
Fibrates
Vitamin B5 or niacin
Drugs that bind bile acids

Our specialist will select all medications strictly individually, based solely on your situation. It is important to remember: treating hyperlipidemia is not a one-time measure. If your body has a tendency to this disease, therapy must be carried out constantly: eat right, lead a correct lifestyle and, if necessary, adjust the level of fat in the body with medications. Please note: one of the key reasons to choose treatment for hyperlipidemia in our network of clinics is the opportunity to cleanse blood vessels of excess cholesterol using high-tech methods of gravitational blood surgery.

Causes

Heredity.
Hypothyroidism is a dysfunction of the thyroid gland.
Diabetes.
Obstructive liver diseases.
Taking diuretics, immunosuppressants and other medications.
Increased content of animal fats in food.

Provoking factors include a sedentary lifestyle, cholesterol abuse, alcohol intake, smoking, and a stressful personality type. The sooner a patient at risk contacts a lipidologist, the higher his chances of avoiding complications.

Prevention of high blood cholesterol levels

Proper nutrition and a healthy lifestyle are the main conditions for successful treatment and effective prevention of high cholesterol in particular and hyperlipidemia in general.

Lifestyle

Strictly follow the diet prescribed by our specialists.
Exercise, but avoid excessive exercise. Light fitness or swimming are ideal options.
Never smoke or abuse alcohol again, and best of all, give up alcohol completely, including red wine.
Sleep at least 8 hours a day.
Make sure your blood pressure is normal.
Don't be nervous about trifles, try to enjoy life.
From time to time, cleanse your body of “bad” cholesterol using methods. gravity surgery.

Nutrition

Our specialists will select a diet individually, based on the level of fat in your body, as well as your taste preferences. Here we will give only general recommendations:

Eliminate foods with saturated fats, trans fats and cholesterol from your diet
Give up fast food forever
Eat fruits and vegetables every day
Eat more fish - sardines, salmon, mackerel and salmon. Fish is very healthy as it contains omega-3 fatty acids, which help reduce triglyceride levels

Please note: hyperlipidemia is a common pathology that is diagnosed in many people. If you feel well and do not complain about anything, this does not mean that the level of fat in your body is normal. Therefore, do not hesitate to visit a doctor if you want to avoid serious complications. Make an appointment now.

Should dyslipidemia be treated?

Treatment of secondary dyslipidemia depends on the severity of the underlying pathology, the form of diabetes, and the possibility of drug-free correction of changes.

Hyperlipidemia begins to be treated with a restrictive diet. Animal fats (lard, fatty sour cream, sausages), baked goods, sweets, and high-fat dairy products are excluded from the foods consumed.

What are the symptoms of lipidemia?

This abnormal accumulation of fat can begin during puberty, after pregnancy, or even during menopause.

Patients notice:

Blood cholesterol levels - table by age. Cholesterol in the blood - norms for women, men and children

Soft tissue pain when resting, walking, or touching.
Sudden accumulation of lipid-lowering fat from the waist to the knees or ankles other than the feet.
Fat accumulates in nodules or small pockets that put pressure on the joints until it becomes impossible to walk normally.
The skin loses its elasticity.
Bruising and swelling occur.

A few months after this first stage, patients notice the following symptoms:

Constant feeling of cold.
Fatigue.
The skin takes on a rubbery texture.
Chronic pain and gradual deterioration in mobility.

Combined with an unattractive appearance, these symptoms cause feelings of sensation, anger, and sadness until depression develops.