The concept of atherosclerosis. Etiology and pathogenesis of atherosclerosis

Atherosclerosis of the vessels of the lower extremities is one of the most serious and dangerous diseases of the arteries of the legs. It is characterized by the fact that due to blockage of blood vessels by atherosclerotic plaques or blood clots, there is a partial or complete cessation of blood flow in the lower extremities.

With atherosclerosis, narrowing (stenosis) or complete blockage (occlusion) of the lumen of the vessels that supply blood to the lower extremities occurs, which prevents the normal flow of blood to the tissues. With arterial stenosis of more than 70%, the speed indicators and the nature of blood flow change significantly, there is insufficient blood supply to cells and tissues with oxygen and nutrients, and they cease to function normally.

Damage to the arteries leads to pain in the legs. In case of progression of the disease, as well as with insufficient or incorrect treatment, trophic ulcers or even necrosis of the limbs (gangrene) may appear. Fortunately, this rarely happens.

Obliterating atherosclerosis of the arteries of the lower extremities is a very common disease of the blood vessels of the legs. The largest number of cases is detected in the age group over 60 years - 5-7%, at the age of 50-60 years - 2-3%, 40-50 years - 1%. But atherosclerosis can also be diagnosed in younger people - in 0.3%, people aged 30–40 years get sick with it. It is noteworthy that men suffer from atherosclerosis 8 times more often than women.

Fact: Smoking men over 50 years of age are at the greatest risk of getting atherosclerosis obliterans.

The main causes of atherosclerosis

The main cause of atherosclerosis is smoking. The nicotine contained in tobacco causes the arteries to spasm, thereby preventing blood from moving through the vessels and increasing the risk of blood clots in them.

Additional factors that provoke atherosclerosis of the arteries of the lower extremities and lead to an earlier onset and severe course of the disease:

  • elevated cholesterol levels with frequent consumption of foods rich in animal fats;
  • high blood pressure;
  • excess weight;
  • hereditary predisposition;
  • diabetes;
  • lack of sufficient physical activity;
  • frequent stress.

Symptoms of atherosclerosis of the vessels of the legs

The main symptom to look out for is leg pain. Most often, pain occurs when walking in the calf muscles and thigh muscles. When moving, the muscles of the lower extremities increase the need for arterial blood, which delivers oxygen to the tissues. Narrowed arteries during physical exertion cannot fully satisfy the need of tissues for arterial blood, which is why oxygen starvation begins in them, and it manifests itself in the form of intense pain. At the beginning of the disease, the pain disappears quickly enough when physical activity is stopped, but then returns again when moving. There is a so-called intermittent claudication syndrome, which is one of the main clinical signs of obliterating atherosclerosis of the arteries of the lower extremities. Pain in the muscles of the thighs is called high intermittent claudication pain, and pain in the calves of the legs is called low intermittent claudication pain.

In old age, such pains are easily confused with painful sensations in the joints inherent in arthrosis and other joint diseases. Osteoarthritis is characterized not by muscle, but by joint pains, which are most intense at the beginning of the movement, and then somewhat weaken when the patient “walks around”.

In addition to pain in the muscles of the legs while walking, obliterating atherosclerosis of the arteries of the lower extremities can cause the following symptoms in patients (one of them or several at once):

  1. Chilliness and numbness in the feet, aggravated by climbing stairs, walking, or other exertion.
  2. Temperature differences between the lower extremities (a leg affected by atherosclerosis of the vessels is usually slightly cooler than a healthy one).
  3. Pain in the leg in the absence of physical activity.
  4. Non-healing wounds or sores appear in the area of ​​the foot or lower third of the leg.
  5. Darkened areas form on the toes and feet.
  6. Another symptom of atherosclerosis may be the disappearance of the pulse on the arteries of the lower extremities - behind the inner ankle, in the popliteal fossa, on the thigh.

Stages of the disease

According to the existing classification of arterial insufficiency of the vessels of the legs, the above symptoms can be divided into 4 stages of the development of the disease.

  • Stage I - pain in the legs that appear only after a lot of physical activity, such as walking long distances.
  • Stage IIa - pain when walking over relatively short distances (250-1000 m).
  • Stage IIb - the distance of painless walking is reduced to 50–250 m.
  • Stage III (critical ischemia) - pain in the legs appears when walking at a distance of less than 50 m. At this stage, pain in the muscles of the lower extremities can begin even if the patient is at rest, this is especially evident at night. To relieve pain, patients usually lower their legs from the bed.
  • IV stage - at this stage, the occurrence of trophic ulcers. As a rule, areas of blackening of the skin (necrosis) appear on the fingers or heel areas. In the future, this can lead to gangrene.

In order not to bring obliterating atherosclerosis to an extreme stage, it is important to diagnose it in time and treat it in a medical institution.

Treatment of atherosclerosis of arteries of the lower extremities

This disease requires an individually designed treatment regimen for each individual patient. Treatment of atherosclerosis of the vessels of the lower extremities depends on the stage of the disease, its duration, the level of damage to the blood arteries. In addition, when diagnosing and compiling a clinical picture, the presence of concomitant diseases in the patient is also taken into account.

If obliterating atherosclerosis is detected at the initial stage, it may be sufficient to improve the condition by eliminating risk factors. In this case, help:

  1. Compulsory cessation of smoking and other bad habits.
  2. Compliance with a diet low in animal fats and lowering cholesterol levels in the blood.
  3. With excessive fullness or obesity - weight correction.
  4. Maintaining normal blood pressure at a level not exceeding 140/90 mm Hg. Art.
  5. Regular physical activity (walking, swimming pool, exercise bike, etc.).
  6. For patients with diabetes - control of blood sugar levels.

With vascular atherosclerosis, the use of the following products is strictly prohibited: butter, margarine, lard, margarine, fatty meat, sausages, pates, offal, high-fat dairy products, fried potatoes, ice cream, mayonnaise, flour buns.

Important: A sedentary lifestyle makes blood vessels less elastic and accelerates the progression of the disease.

At other stages, the following methods are used to treat atherosclerosis of the vessels of the lower extremities:

  • Conservative;
  • Endovascular (minimally invasive);
  • Operational.

Conservative treatment

It can also be used at the initial stage of the disease, as well as in cases where the patient's condition does not allow the use of other methods (with complications of concomitant pathology). Conservative treatment involves the use of medications, physiotherapy and includes pneumopressure therapy, dosed walking and exercise therapy.

Unfortunately, there are no medications that completely restore normal blood circulation in a clogged artery and cure atherosclerosis. Drug treatment can only provide support and affect the small vessels that carry blood around the blocked portion of the artery. Drug treatment aims to widen these "detours" and compensate for poor blood circulation.

To relieve spasm from small arterial vessels, thin the blood and protect the walls of the arteries from further damage, special medications are used, some of which need to be drunk in courses, while others should be taken constantly.

In addition to medicines, patients are prescribed pneumopress therapy - massage of the soft tissues of the leg with the help of special equipment. With the help of alternating low and high pressure in the cuff worn on the limb, peripheral arteries expand, blood flow to the skin, muscles and subcutaneous tissue increases, and vessels are stimulated.

Endovascular treatment

The most common methods of treatment for atherosclerosis of the vessels of the legs are endovascular methods - arterial stenting, balloon dilatation, angioplasty. They allow you to restore normal blood circulation through the vessel without surgery.

Such procedures are carried out in the X-ray operating room, on special equipment. At the end, a pressure bandage is applied to the patient's leg, and he must remain in bed for 12-18 hours.

Surgery

If the clogged arteries in the legs are too long for endovascular techniques, one of the following types of surgery is used to restore blood circulation in the legs:

  1. Prosthetics of an artery section with an artificial vessel (alloprosthesis);
  2. Shunting is the restoration of blood flow by redirecting the movement of blood through an artificial vessel (shunt). A segment of the saphenous vein of the patient himself can be used as a shunt;
  3. Thrombendarterectomy is the removal of an atherosclerotic plaque from an affected artery.

Surgical methods can be combined or supplemented with other types of operations. If the operation is performed at the IV stage of the disease, when dead zones have already appeared, these areas are surgically removed and the trophic ulcers are closed with a skin flap.

If obliterating atherosclerosis has passed into the extreme stage, when the patient has developed gangrene of the lower extremities, and it is no longer possible to restore blood flow, amputation of the leg is performed. Sometimes this becomes the only way to save the patient's life.

How to avoid the disease?

Prevention of atherosclerosis includes primarily:

  • To give up smoking.
  • Proper nutrition, cholesterol-free diet.
  • Physical exercise.

These are three whales that will reduce the risk of atherosclerosis of the vessels of the lower extremities. It is not necessary to exhaust yourself with physical exercises, you can just take daily walks and do gymnastics for the legs. In addition, special acupressure and traditional medicine recipes help as a prophylactic.

Read more about the comprehensive prevention of atherosclerosis here.

Video: atherosclerosis of the vessels of the legs, presentation

Step 2: after payment, ask your question in the form below ↓ Step 3: You can additionally thank the specialist with another payment for an arbitrary amount

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Atherosclerosis is a chronic disease of the arteries, accompanied by the formation of single and multiple lipid, mainly cholesterol, deposits or plaques in the inner lining of the arteries.

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Atherosclerosis, or rather, increased blood cholesterol, is one of the main risk factors for the development of cardiovascular diseases ... this is the "RUT OF LIFE"

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The term "atherosclerosis" comes from two Latin words: athere - which means gruel, and sclerosis - hard, dense, which reflects the stages of development of an atherosclerotic plaque. Atherosclerosis occurs in all people. The first signs of atherosclerosis are found at the age of five. "Atherosclerosis is a natural aging process" A. Davydovsky

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Causes of atherosclerosis The causes of atherosclerosis are high blood pressure, smoking, diabetes, high cholesterol. But the main cause of atherosclerosis lies in the violation of cholesterol metabolism.

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Risk factors for atherosclerosis Gender. Men are more prone to developing atherosclerosis than women. The first signs of this pathology can appear already from the age of 45 or even earlier, in women from the age of 55. Perhaps this is due to a more active participation in the exchange of estrogen cholesterol and low and very low density lipoproteins.

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Age. This is a natural risk factor. With age, atherosclerotic manifestations worsen.

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Heredity. This is one of the causes of atherosclerosis. Atherosclerosis is a multi-causal disease. Therefore, the level of hormonal levels, hereditary disorders of the plasma lipid profile, and the activity of the immune system play important roles in accelerating or slowing down the development of atherosclerosis.

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Bad habits. Smoking is a poison to the body. This habit is another reason for the development of atherosclerosis. As for alcohol, there is an interesting relationship: the use of small doses of alcohol daily is an excellent prevention of atherosclerosis. True, the same dose contributes to the development of cirrhosis of the liver. In addition, large doses of alcohol accelerate the development of atherosclerosis.

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Excess weight. This factor has a very negative effect on atherosclerosis. Excess weight can lead to diabetes mellitus, and this pathology is very malignant for the development of atherosclerosis.

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Nutrition. Our future health will depend on how useful our food is, how much it contains the chemical compounds we need. Few people know that no diet, other than therapeutic, is approved by the World Food Hygiene Council. You need to eat rationally and adequately to your needs and energy costs.

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Symptoms of atherosclerosis are often cold, bluish-white extremities; frequent heart problems; memory loss; violation of blood supply; poor concentration; the patient becomes irritable and feels tired. People with high blood pressure, as well as weak kidneys and diabetes, are most susceptible to atherosclerosis.

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Doctors consider atherosclerosis to be the most typical today: aorta, causing angina pectoris; kidneys; limbs; coronary arteries (ischemic heart disease); extracranial vessels, mainly the carotid artery, leading to cerebrovascular disease and cerebral stroke.

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How to treat atherosclerosis? Smoking cessation Physical activity Normalizing body weight Maintaining normal blood pressure Changing dietary habits

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"sclerosis" - solid) is a disease that affects the walls of blood vessels, mainly arteries of the muscular and musculo-elastic type, which is based on disorders of fat and protein metabolism, primarily cholesterol metabolism, manifested by imbibition of the vascular wall by proteins and lipids, followed by development around of these deposits 3. Dynamics of mortality of the population of Russia from diseases of the circulatory system for the period 1980–2002. 4. The dynamics of mortality in Russia for various classes of causes refers to arterial sclerosis, regardless of the cause and mechanism of its development.

Pathophysiology of atherosclerosis - online presentation

"sclerosis" - solid) is a disease,

affecting the walls of blood vessels

way, the arteries of the muscular and musculo-elastic type, which is based on

lie violations of fat and protein

metabolism, especially cholesterol metabolism,

manifested by imbibition of the vascular

walls with proteins and lipids, followed by

development around these deposits

3. Dynamics of mortality of the population of Russia from diseases of the circulatory system for the period 1980–2002.

4. Dynamics of mortality in Russia for various classes of causes

designate arterial sclerosis regardless of cause and mechanism

its development. Atherosclerosis is just a type

arteriosclerosis, reflecting disorders of lipid metabolism

and proteins (metabolic arteriosclerosis). In such an interpretation

The term "atherosclerosis" was introduced in 1904 by Marchand and

substantiated by experimental studies by N.N. Anichkov.

Therefore, atherosclerosis is called Marchand-Anichkov disease.

Depending on the etiological, pathogenetic and

morphological features distinguish types of arteriosclerosis:

1) atherosclerosis (metabolic arteriosclerosis);

2) arteriosclerosis, or hyalinosis (for example, with hypertensive

3) inflammatory arteriolosclerosis (for example, syphilitic,

4) allergic arteriosclerosis (for example, with nodular

5) toxic arteriosclerosis (for example, adrenaline);

6) primary calcification of the middle lining of the arteries

7) age-related (senile) arteriosclerosis.

response to damage (R. Ross, A. Glomset, A. Gotto, R. Jackson, 1976).

macrophages and some lipoproteins occurs

first intracellular and then extracellular accumulation of lipids

(cholesterol). In turn, alteration of the vascular wall

promotes both inflammation and

proliferation of smooth muscle cells and their synthesis of collagen,

glycosaminoglycans that form the tire and other

connective tissue elements of an atherosclerotic plaque. Growth,

development, and subsequently, the rupture of atherosclerotic

plaque contributes to the formation and separation of blood clots, the release

atheromatous masses into the vessel lumen, initiation of thromboembolic

8. Damage to the vascular endothelium - a trigger for the development of atherosclerosis

9. The role of hypertension in damage to the vascular endothelium

endothelial injury factor

vessels, especially in places

their bifurcations. This phenomenon is good

illustrates the following

In section ≪a≫ blood pressure

greatest, shear stress

maximum. Right here

and destruction occurs

endotheliocytes and their desquamation

(peeling) from the surface

vessel. In section ≪b≫ pressure

least blood. Damage

endothelium in these areas

happening. As is known,

hypertension and

atherosclerosis is two

processes that are closely related

themselves, or, more precisely, contributing

each other's development

10. Damage to the vascular endothelium is a trigger for the development of atherosclerosis

20-NETE (20-hydroxyeicosotetraenoic acid)

low density lipoproteins (LDL, β-lipoproteins, β-LP),

very low density lipoproteins (VLDL, pre-β-LP),

HDL-transfer of cholesterol from cells of various organs and tissues to liver cells, where it and

play apoproteins that are embedded in the lipid monolayer of the membrane

lipoprotein micelles. It is the molecules of apoproteins that micelles of lipoproteins are

ligands that bind the corresponding lipoprotein to its receptor. They are in a row

cases also play the role of cofactors for the corresponding enzymes. Currently

Four types of apoproteins have been identified:

Apo-A - provides a connection between HDL and the corresponding receptor apparatus.

Apo-B - provides communication between LDL and the receptor apparatus of liver cells and

Apo-C-II is a cofactor for lipoprotein lipase, due to which triglycerides

removed from chylomicrons and VLDL;

Apo-E - ensures the connection of lipoproteins with the receptor apparatus of hepatocytes.

Another type of apoprotein, the so-called apoprotein (a), has also been described.

attribute the greatest atherogenicity and being a part of LDL. The atherogenicity of this

apoprotein is explained by several of its properties. First, it is easily oxidized and

taken up by macrophages. Secondly, hepatic cells have the least amount

receptors for LDL containing lipoprotein (a). And finally, thirdly, there are data on

that LDL containing lipoprotein (a) have increased

activated platelets stimulate the release of factor from the endothelium

growth. The latter stimulates the proliferation of smooth muscle cells of the arterial

wall, which leads to its thickening and creates conditions for the formation of

further atherosclerotic plaques. activation of leukocytes, which have

increased adhesion to the endothelium, leads to its damage and promotes

penetration of lipids into the vascular wall. increased endothelial permeability

and vascular intima for coarse plasma proteins and lipids. Through the endothelium

through pinocytosis, globulins, albumins, fibrinogen and

lipids. In addition, the permeability of the vascular intima to monocytes increases. When

monocytes penetrate the vascular wall, they are transformed

macrophages, which begin to actively capture lipids and accumulate them in

vascular wall. increased activity of serum hyaluronidase, which leads to

depolymerization of hyaluronic acid contained in the vessel wall, and

increase in vascular tissue permeability. Cholesterol split off in the cell

from LDL by acting on this complex of lysosomal enzymes, through

regulation of the activity of the 3-hydroxy-3-methylglutaryl-coenzyme A-reductase enzyme contained in the cells, which is responsible for controlling the rate

limiting reaction of biosynthesis of endogenous cholesterol, reduces the synthesis

the last one. Hypercholesterolemia in the dolipid period has one important

feature: the chemical structure of cholesterol changes. If in intact

body cholesterol esters contain unsaturated fatty acids and such

cholesterol is easily utilized, then against the background of the development of atherosclerosis in these esters

saturated fatty acids appear. This cholesterol is poorly utilized and

retained in the blood serum.

At this stage of atherosclerosis,

vascular intima appear yellow

spots. Lipolytic Activity

vascular wall is sharply reduced, in

intimacy is delayed a lot

the amount of lipids (result

mechanism), proteins. For these products,

also into decaying acidic

mucopolysaccharides reaction develops

from the side of the vascular wall in the form

proliferation of connective tissue.

In the vascular wall around deposits

proteins and lipids there is a rapid

proliferation of connective tissue. AT

intimacy there is a large number

fat-laden macrophages (so

called xanthoma cells)

which partly go into the lymph, and

partly disintegrate, increasing the

the highest amount of detritus in the vascular

wall, where a dense plaque is formed,

protruding into the lumen of the artery.

in liposclerotic plaque

Two processes run in parallel:

increased sclerosis, that is, growth

connective tissue, and strengthening

breakdown of protein and lipid masses, then

there is detritus formation.

atherosclerotic plaque in this

the period on the cut is

dense connective tissue

capsule containing

masses of detritus and cholesterol crystals.

At this stage, intimacy becomes thinner,

capsule, the plaque adsorbs on itself

calcium salts and

6. Atheromatous ulcer

The plaque shell becomes very

thin, the plaque ulcerates, and

atheromatous masses enter

play the so-called

which are synthesized in

receptors and disrupt

which was already

more foam cell death

spurs inflammation by

(interleukin 1, necrosis factor

tumors, etc.). In the same

period of time is activated

smooth muscle cells. Under

influence of a number of growth

factors and pro-inflammatory

they acquire cytokines

mobility, migrate from the media

into the intima and subendothelial layer and

there they become secretory. Produced

they form collagen

enters its own cycle

PDGF, α-FGF, TGF-β, IGF - growth factors, IL-1 -

22. Mechanisms of atherosclerotic plaque formation

a - elastic "yellow" plaque with a large lipid core and a thin cap; b - rupture of the "yellow" plaque c

detritus falling into the lumen of the vessel (red dots) and the formation of a parietal thrombus; c - the structure of the "white"

fibrous plaque with a relatively small lipid core and a thick, durable fibrous capsule.

MECHANISMS OF ATHEROGENIC ACTION

Hypercholesterolemia, increased cholesterol and LDL

Elevation of cholesterol and LDL levels in the postmenstrual period

Decreased HDL content and increased VLDL

Increase in cholesterol and LDL, decrease in HDL

Decreased HDL, endothelial damage

Genetically determined dyslipidaemias

Endothelial damage, atherogenic changes in lipid

spectrum of blood, disorders of the trophism of the vascular wall

Endothelial damage, increased lipolysis

Atherogenic changes in the blood lipid spectrum, endothelial damage

27. Research on primary prevention of atherosclerosis

primary prevention of atherosclerosis

Primary prevention of atherosclerotic diseases in the population

implies a set of government measures aimed at

prevention of atherosclerosis of vessels of vital organs and complications with

using non-drug methods to combat risk factors (arterial

hypertension, smoking, hyper- and dyslipidemia, overweight,

hypodynamia) and medications (under the secondary

Prevention refers to measures taken to

inhibition of the progression of the disease and the reverse development of the existing

The study was devoted to the study of the possibility of implementing

primary prevention of coronary artery disease with an anti-atherosclerotic diet and

smoking cessation. The research program has been carried out since 1972.

in the city of Oslo (Norway). Of 16,202 apparently healthy men aged 40–49, there were

1232 people were selected with a high risk of coronary artery disease, but with a normal level of blood pressure

Particular importance was attached to the assessment of the actual nutrition of persons in the group

interventions, educating them on an anti-atherosclerotic diet and monitoring it.

compliance. The smoking weaning intervention consisted of conversations about the dangers