Types and stages of atherosclerosis and the role of lipoproteins
Fat is deposited in the damaged areas of the arterial walls and then overgrown with fibrous (connective) tissue. Such formations are called atherosclerotic plaques. As a result, the lumen of the vessel Narrows, worsening the blood supply to tissues and organs.
Atherosclerosis is considered a disease that affects only the elderly. Indeed, this pathology in most cases is detected in men aged 40-60 years and women over fifty. But over the years, the number of patients under the age of 40 is increasing. This is due to poor ecology, malnutrition, and a large number of stressful situations.
Lipoproteins and their participation in the development of atherosclerosis
Lipoproteins (lipoproteins) are complex lipoprotein compounds that circulate in the blood plasma. They transport cholesterol in the bloodstream. Lipoproteins are divided into 3 categories:
- HDL (high-density lipoproteins)
- LDL (Lipids with a low density)
- VLDL (extremely low-density lipoproteins).
VLDL and LDL transport cholesterol into the cells and HDL removes excess cholesterol from the body. (In other words, VLDL and LDL can affect the development of the disease, and HDL, on the contrary, helps to avoid it.). In the body of a healthy person, the balance between lipoproteins of all three categories is maintained.
However, if a failure occurs, and there are more low-density and low-density lipoproteins, there is a risk of atherosclerosis-cholesterol accumulating in the cells in excess.
Macrophages (cell-eaters), consisting of monocytes
are also a part of how the condition develops. Monocytes are large leukocytes that carry out specific protection of the body from carcinogens and foreign cells.
Macrophages are found in almost all organs and tissues and are responsible for the destruction of living and non-living foreign particles (bacteria, toxins, dead cells, etc.). If low-density and low-density lipoproteins are retained in the vessels, they are damaged and oxidized over time. Macrophages eat up the products of oxidation. Some of them, after the destruction of foreign particles, turn into foam cells, which are deposited on the walls of blood vessels.
Types and stages of atherosclerosis
Atherosclerosis can affect the arteries of the elastic and muscular-elastic types (large and medium). Elasticity is located near the heart. These include, for example, the aorta, and the pulmonary artery. Muscular-elastic arteries include medium-sized arteries: heart, femoral, brain, and carotid artery. Depending on the localization of the pathological process and the organ that lacks blood circulation.
atherosclerosis can be divided into the following types:
- Atherosclerosis of the aorta (may occur in the chest or abdominal cavity)
- Atherosclerosis of the coronary arteries (heart vessels)
- Cerebral atherosclerosis (vessels of the brain)
- a condition is known as lower extremity artery atherosclerosis.
- Atherosclerosis of the arteries of the upper extremities
- arterial atherosclerosis in the kidneys.
- Hardening of the arteries of the penis (vessels of the penis).
There are three stages in the development of the disease:
The stage of fat strips.
The appearance of small (1-2 mm) yellowish greasy spots on the walls of human vessels is observed after birth. Over time, they increase in size and merge with each other. Macrophages begin to destroy them and turn into foam cells. Later, fatty streaks appear from the smooth muscle cells of the vascular walls and foam cells. The presence of fatty streaks after it does not mean that the pathological process will progress, and fibrous plaques (atherosclerosis) will appear.
The stage of fibrous plaque.
The growth of connective tissue begins in areas with fatty strips. Fibrous plaque consists of connective tissue and fat cells. At first, they are soft, but they can be solved with timely medical intervention. Subsequently, calcium salts are deposited in them and Harden.
The stage of complex violations.
Fibrous plaques are damaged, torn, and ulcers or cracks form on them. This process can be caused by macrophage activity, excess oxidized LDL, or cholesterol accumulation. Platelets (colorless blood cells responsible for blood clotting and the transport of nutrients to the endothelium, the inner layer that covers the walls of blood vessels) are attached to the damaged plaque. As a result, the vessel is partially or completely clogged.
As for the direct manifestations of atherosclerosis, the classification of A.L. Myasnikov.
According to her, atherosclerosis has two stages of development:
Preclinical (the initial period when neurological and metabolic disorders occur, but the disease does not yet manifest itself with clinical signs)
Clinical (symptoms of atherosclerosis are detected).
The clinical period consists of three stages:
- Tell it. Blood vessels narrow, and blood flow to internal organs and tissues deteriorates.
- Coagulation. Thrombosis (blockage) of arteries occurs, accompanied by small or extensive necrosis (tissue death) of internal organs.
- Levi's hardening. In organs with insufficient blood supply, overgrowth of connective tissue occurs. Atrophy of organs can be observed.
Clinical manifestations begin to be detected only after narrowing the lumen of the vessel by 50% or more.
Causes of the development of atherosclerosis
Scientists have not yet come to a consensus on the causes of atherosclerosis. They agree with each other in the following aspects: there is damage to the arterial walls and fat deposition in these areas, which leads to the formation of atherosclerotic plaques. However, the causes of damage (as well as the sequence of operations) are different.
There are quite a few different hypotheses for the development of atherosclerosis, the most common of which are:
The theory of lipids.
Adherents of this hypothesis suggest that low and very low-density lipoproteins, accumulating in the vessels and turning into foam cells, and then fatty slices, cause damage to the endothelium (the upper layer of the vessel walls). As a result of these processes, fats begin to be deposited already in the extracellular space (the environment surrounding the cells). Then atherosclerotic plaques form.
The hypothesis of chronic endothelial damage
Scientists believe that the arterial walls are first damaged (due to impaired blood flow, the activity of bacteria and viruses, an increased concentration of LDL, etc.), and then atherosclerotic processes develop in pathological areas.
The monoclonal hypothesis
According to this theory, one of the genes controlling the cell cycle (cell life from the moment of formation to division or death) turns on, This causes the vascular wall to produce more smooth muscle cells. The pathological process has only started at this point. In this case, the development of atherosclerosis can be compared with the formation of a benign tumor.
A parasitic hypothesis
It is believed that atherosclerosis occurs due to damage to the walls of blood vessels due to chlamydia. This bacterium is found in atherosclerotic plaques. Other studies have shown that chlamydia is found in the blood of 80% of patients with atherosclerosis. In people who do not suffer from this disease, this microorganism is found only in 4% of cases. Therefore, adherents of the parasitic theory believe that atherosclerosis should be treated with antibacterial drugs.
The neuroendocrine hypothesis. According to this theory, atherosclerosis develops due to a failure of neuroendocrine regulation of protein and fat metabolism.
The cholesterol hypothesis is still popular
This theory was put forward by N. Anichkov was born in 1912 and is associated with the intake of excess cholesterol into the body with food. The scientist conducted an experiment in which rabbits were fed food of animal origin. Soon, the test subjects died from blockage of the arteries of the heart.
Even though for herbivorous rabbits the use of food of animal origin is atypical (unlike humans, who are omnivores), which could be the reason for such an end to the experiment, based on the results of this experiment, the cholesterol theory of atherosclerosis. According to them, excess cholesterol from food penetrates the walls of blood vessels and leads to the development of atherosclerosis.
This theory has not been proven.
Moreover, it has been refuted many times. However, many people still believe in it, on which food manufacturers speculate, offering consumers food with low or no cholesterol. In fact, the relationship between the intake of this fat with food and its accumulation in the body has not been proven.
Indeed, patients with high cholesterol in the blood are more likely to develop coronary artery disease (atherosclerosis of the blood vessels of the heart) and other cardiovascular diseases. But with food, a person receives only 20% of cholesterol. Patients with high cholesterol in the blood are more likely to develop coronary artery disease and other cardiovascular diseases.
But with food, a person receives only 20% of cholesterol. Patients with high cholesterol in the blood are more likely to develop coronary artery disease and other cardiovascular diseases. But with food, a person receives only 20% of cholesterol.
The main part of cholesterol
is produced directly by the body itself (liver, intestines, gonads, kidneys, adrenal glands). It is found in the membrane of every cell in the human body. This fat is involved in many important biochemical processes.
Experiments were conducted during which, over several months, people absorbed large amounts of cholesterol-rich food. As a result, none of these people showed an increase in the level of cholesterol in the blood, or signs of atherosclerosis.
It is impossible not to mention the French: their cuisine is very fatty, but at the same time, residents of France suffer from arterial diseases much less often than other Europeans. And the opposite example - atherosclerosis is often diagnosed in patients who adhere to vegetarian diets.
an excess of harmful fats in the blood
is formed as a result of a failure in the synthesis and metabolism of cholesterol in the body. Undoubtedly, you should not consume fats of animal origin in unlimited quantities, but an absolute rejection of them (or severely restricting them) will not benefit a healthy person either. The diet is suitable if the body already has an elevated level of cholesterol. But an absolute rejection of her (or severely restricting her) will also not benefit a healthy person.
The diet is suitable if the body already has an elevated level of cholesterol. But an absolute rejection of her (or severely restricting her) will also not benefit a healthy person. The diet is suitable if the body already has an elevated level of cholesterol.
The risk of atherosclerosis development is influenced by a number of variables. These include:
Paul
In men younger than 50-60 years, atherosclerosis is observed much more often than in women of the same age. This is because estrogens (female sex hormones) have a positive effect on fat metabolism, as well as metabolic processes in the walls of blood vessels, preventing the development of atherosclerosis.
Climax
This factor is similar to the previous one. During menopause, the synthesis of estrogens in the female body decreases, therefore, after 50-55 years, a woman has the same probability of developing atherosclerosis as a man.
Age
Over time, blood vessels wear out, lose their elasticity, and become clogged. Therefore, in people over 40-50 years old, the risk of developing atherosclerosis is much higher than in patients under 40 years of age.
Heredity
Genetic predisposition can be associated with both disorders of fat metabolism and the activity of immunity in the body. If the patient's close relatives suffer from atherosclerosis, then the risk of developing this disease increases even more. Genetic predisposition increases the likelihood of diseases up to 50 years, after 50 years heredity does not really matter, other risk factors are already emerging.
Excess weight with hyperdynamic (decrease in motor activity)
Obesity in itself does not have a special effect on the development of atherosclerosis. But in obese people who lead a sedentary lifestyle, there is often high blood pressure and an increase in blood cholesterol, which can lead to atherosclerosis.
Wrong nutrition
It's not about eating food of animal origin (which adherents of the cholesterol theory refer to), but about an unbalanced diet. The population of the regions where it is customary to eat is diverse, giving preference to fresh and healthy foods (for example, in Japan and the Mediterranean), and atherosclerosis develops much less often than in residents of other countries.
Smoking. This addiction causes vasoconstriction, the intoxication of the body, and increased blood pressure. All this leads to impaired vascular function.
High blood pressure. A chronic increase in blood pressure leads to pathological changes in the vessels.
An alcoholic.
Regular drinking in large doses increases the risk of developing atherosclerosis. Under the influence of alcohol, the vessels First expand, and then narrow backward. Such fluctuations are very harmful to the health of the cardiovascular system. There is a hypothesis (and it is unlikely to have a medical origin) that the daily use of alcohol in small doses is useful even for preventive purposes: it is believed that alcoholic beverages dissolve atherosclerotic plaques.
However, this has not been scientifically proven. Alcohol can break down part of the atherosclerotic plaques (only part!), However, the melted fat is not excreted from the body but is deposited in the internal organs. This causes serious disruption in their work. Daily alcohol consumption, even in small doses, can lead to the development of many diseases.
Diabetes mellitus.
Carbohydrate and fat metabolism are interrelated, so if one of them is disturbed, the other may also suffer.
Stress.
During stress, adrenaline is produced in the body, which leads to a sharp rise in blood pressure and vasoconstriction. It's not just about strong nervous shocks, but also about simple everyday experiences.
The presence of risk factors does not mean that the patient will necessarily develop atherosclerosis. For example, the disease is not observed in all elderly people and not in all hypertensive or diabetic patients. However, for preventive purposes, it is recommended to strive to reduce the number of risk factors to a minimum.
a summary
Atherosclerosis is the accumulation of fatty substances inside the walls of arteries. The three types of atherosclerosis are stable, unstable, and medial. Stable atherosclerosis is the most common and occurs when fatty matter accumulates over a long period. Unstable atherosclerosis is usually faster in progressing and can occur when there is a sudden injury to the artery.
Lipoproteins are the main carrier of cholesterol and other fats in the blood and play a role in the development of atherosclerosis. Lipoprotein molecules can be small, large, or medium in size, they can be either dense or fluffy. Large and dense lipoprotein particles are more likely to form plaque in the arteries, while small and medium-sized particles are more likely to travel through the blood and reach the liver.