Atherosclerosis

Factors affecting the development of atherosclerosis are divided into three groups: unavoidable, avoidable and potentially avoidable. The unavoidable factors include those that cannot be excluded with the help of volitional or medical influence. These include:

• Age. With age, the risk of developing atherosclerosis increases. Atherosclerotic vascular changes are more or less observed in all people after 40-50 years.
• Gender. In men, the development of atherosclerosis occurs ten years earlier and exceeds the incidence of atherosclerosis among women by 4 times. After 50-55 years, the incidence of atherosclerosis among women and men is leveled. This is due to a decrease in the production of estrogens and their protective function in menopausal women.
• Burdened family inheritance. Atherosclerosis often develops in patients whose relatives suffer from this disease. It is proved that heredity for atherosclerosis contributes to the early (up to 50 years) development of the disease, while after 50 years genetic factors do not play a leading role in its development.
• Disposable factors of atherosclerosis are those that can be eliminated by the person himself by changing the usual lifestyle. These include:
• Smoking. Its influence on the development of atherosclerosis is explained by the negative effects of nicotine and resins on blood vessels. Long-term smoking increases the risk of hyperlipidemia, arterial hypertension, CHD several times.
• Unbalanced nutrition. Eating a large amount of animal fats accelerates the development of atherosclerotic vascular changes.
• Physical inactivity. Maintaining a sedentary lifestyle contributes to the violation of fat metabolism and the development of obesity, diabetes mellitus, vascular atherosclerosis.

Potentially and partially removable risk factors include those chronic disorders and diseases that can be corrected through prescribed treatment. They include:

• Arterial hypertension. Against the background of high blood pressure, conditions are created for increased impregnation of the vascular wall with fats, which contributes to the formation of atherosclerotic plaque. On the other hand, a decrease in the elasticity of the arteries in atherosclerosis contributes to maintaining high blood pressure.
• Dyslipidemia. Violation of fat metabolism in the body, manifested by an increased content of cholesterol, triglycerides and lipoproteins, plays a leading role in the development of atherosclerosis.
• Obesity and diabetes mellitus. They increase the probability of atherosclerosis by 5-7 times. This is due to a violation of fat metabolism, which is the basis of these diseases and is the trigger mechanism of atherosclerotic vascular damage.
• Infections and intoxication. Infectious and toxic agents have a damaging effect on vascular walls, contributing to their atherosclerotic changes. There are opinions that infectious agents (herpes simplex virus, cytomegalovirus, chlamydia infection, etc.), hereditary diseases accompanied by an increase in cholesterol levels, mutations of vascular wall cells, etc. play a role in the development of atherosclerosis.

Knowledge of the factors contributing to the development of atherosclerosis is especially important for its prevention, because the influence of avoidable and potentially avoidable circumstances can be weakened or completely eliminated. Elimination of adverse factors can significantly slow down and facilitate the development of atherosclerosis.

With atherosclerosis, systemic damage to the arteries occurs as a result of violations of lipid and protein metabolism in the walls of blood vessels. Metabolic disorders are characterized by a change in the ratio between cholesterol, phospholipids and proteins, as well as excessive formation of β-lipoproteins. It is believed that atherosclerosis goes through several stages in its development:

• Stage I - lipid (or fat) spots. Micro-injuries of arterial walls and local slowing of blood flow play an essential role in the deposition of fats in the vascular wall. The areas of vascular branching are most susceptible to atherosclerosis. The vascular wall loosens and swells. The enzymes of the arterial wall tend to dissolve lipids and protect its integrity. When the protective mechanisms are depleted, complex complexes of compounds consisting of lipids (mainly cholesterol), proteins are formed in these areas and their deposition occurs in the intima (inner lining) of the arteries. The duration of the lipid spot stage varies. Such fat spots are visible only under a microscope, they can be detected even in infants.
• Stage II - liposclerosis. It is characterized by an overgrowth in the areas of fatty deposits of young connective tissue. The formation of an atherosclerotic (or atheromatous) plaque, consisting of fats and connective tissue fibers, is gradually underway. At this stage, atherosclerotic plaques are still liquid and can be dissolved. On the other hand, they are dangerous, because their loose surface can rupture, and fragments of plaques can clog the lumen of the arteries. The vessel wall at the place of attachment of the atheromatous plaque loses its elasticity, cracks and ulcerates, leading to the formation of blood clots, which are also a source of potential danger.
• Stage III - atherocalcinosis. Further formation of the plaque is associated with its compaction and deposition of calcium salts in it. An atherosclerotic plaque can behave stably or gradually grow, deforming and narrowing the lumen of the artery, causing a progressive chronic violation of the blood supply to the organ fed by the affected artery. At the same time, there is a high probability of acute blockage (occlusion) of the vessel lumen by a thrombus or fragments of a decayed atherosclerotic plaque with the development of a site of infarction (necrosis) or gangrene in the limb or organ supplied by the artery.

With atherosclerosis, the thoracic and abdominal aorta, coronary, mesenteric, renal vessels, as well as the arteries of the lower extremities and the brain are more often affected. In the development of atherosclerosis, there are preclinical (asymptomatic) and clinical periods. In the asymptomatic period, an increased content of β-lipoproteins or cholesterol is detected in the blood in the absence of symptoms of the disease. Clinically, atherosclerosis begins to manifest itself when there is a narrowing of the arterial lumen by 50% or more. During the clinical period, there are three stages: ischemic, thrombonecrotic and fibrous.

At the stage of ischemia, insufficiency of blood supply to a particular organ develops (for example, myocardial ischemia due to atherosclerosis of the coronary vessels is manifested by angina pectoris).

In the thrombonecrotic stage, thrombosis of altered arteries is joined - atherothrombosis (so, the course of atherosclerosis of coronary vessels can be complicated by myocardial infarction).

At the stage of fibrous changes, connective tissue grows in poorly supplied organs (for example, atherosclerosis of the coronary arteries leads to the development of atherosclerotic cardiosclerosis).

The clinical symptoms of atherosclerosis depend on the type of affected arteries. The manifestations of atherosclerosis of coronary vessels are angina, myocardial infarction and cardiosclerosis, consistently reflecting the stages of circulatory insufficiency of the heart.

The course of aortic atherosclerosis is asymptomatic for a long time, even in severe forms. Clinically, atherosclerosis of the thoracic aorta is manifested by aortalgia - pressing or burning pains behind the sternum, radiating into the arms, back, neck, upper abdomen. Unlike pain with angina, aortalgia can last for several hours and days, periodically weakening or intensifying. A decrease in the elasticity of the aortic walls causes an increase in the work of the heart, leading to left ventricular myocardial hypertrophy.

Atherosclerosis of the abdominal aorta is manifested by abdominal pain of various localization, flatulence, constipation. With atherosclerosis of the abdominal aortic bifurcation, numbness and cold of the legs, swelling and hyperemia of the feet, necrosis and ulcers of the toes, intermittent lameness are observed.

Manifestations of atherosclerosis of the mesenteric arteries are attacks of "abdominal toad" and violation of digestive function due to insufficient blood supply to the intestine. Patients have the appearance of sharp pains a few hours after eating. The pain is localized in the navel or upper abdomen. The duration of the pain attack is from several minutes to 1-3 hours, sometimes the pain syndrome is stopped by taking nitroglycerin. There are bloating, belching, constipation, palpitations, increased blood pressure. Later, fetid diarrhea is joined with fragments of undigested food and undigested fat.

Atherosclerosis of the renal arteries leads to the development of vasorenal symptomatic hypertension. Red blood cells, protein, and cylinders are detected in the urine. With unilateral atherosclerotic lesion of the arteries, there is a slow progression of hypertension, accompanied by persistent changes in urine and persistently high blood pressure. Bilateral damage to the renal arteries causes malignant arterial hypertension.

With atherosclerosis of the cerebral vessels, there is a decrease in memory, mental and physical performance, attention, intelligence, dizziness, sleep disorders. In cases of severe atherosclerosis of the cerebral vessels, the behavior and psyche of the patient changes. Atherosclerosis of the arteries of the brain can be complicated by acute violation of cerebral circulation, thrombosis, hemorrhages.

Manifestations of obliterating atherosclerosis of the arteries of the lower extremities are weakness and pain in the calf muscles of the lower leg, numbness and chilliness of the legs. The development of the syndrome of "intermittent lameness" is characteristic (pain in the calf muscles occurs when walking and subsides at rest). There is a cold snap, pallor of the limbs, trophic disorders (peeling and dry skin, the development of trophic ulcers and dry gangrene).

Complications of atherosclerosis are chronic or acute vascular insufficiency of the blood-supplied organ. The development of chronic vascular insufficiency is associated with a gradual narrowing (stenosis) of the artery lumen by atherosclerotic changes – stenosing atherosclerosis. Chronic insufficiency of blood supply to an organ or part of it leads to ischemia, hypoxia, dystrophic and atrophic changes, proliferation of connective tissue and the development of small-focal sclerosis.

Acute vascular insufficiency is caused by acute blockage of blood vessels by a thrombus or embolus, which is manifested by the clinic of acute ischemia and organ infarction. In some cases, a rupture of an artery aneurysm may occur with a fatal outcome.

Initial data for atherosclerosis are established by clarifying the patient's complaints and risk factors. A cardiologist's consultation is recommended. During a general examination, signs of atherosclerotic lesions of the vessels of internal organs are revealed: edema, trophic disorders, weight loss, multiple fatty spots on the body, etc. Auscultation of the vessels of the heart, aorta reveals systolic murmurs. Atherosclerosis is indicated by a change in arterial pulsation, an increase in blood pressure, etc.

Laboratory data indicate an increased level of blood cholesterol, low-density lipoproteins, triglycerides. Radiographically, aortography reveals signs of atherosclerosis of the aorta: its elongation, compaction, calcification, expansion in the abdominal or thoracic regions, the presence of aneurysms. The condition of the coronary arteries is determined by coronary angiography.

Violations of blood flow through other arteries are determined by angiography - contrast radiography of vessels. With atherosclerosis of the arteries of the lower extremities, according to angiography, their obliteration is recorded. With the help of ultrasound of the renal vessels, atherosclerosis of the renal arteries and corresponding renal dysfunction are detected.

Methods of ultrasound diagnostics of the arteries of the heart, lower extremities, aorta, carotid arteries register a decrease in the main blood flow through them, the presence of atheromatous plaques and blood clots in the vessel lumen. A decrease in blood flow can be diagnosed using rheovasography of the lower extremities.

In the treatment of atherosclerosis , the following principles are adhered to:

• restriction of cholesterol entering the body and reduction of its synthesis by tissue cells;
• increased excretion of cholesterol and its metabolites from the body;
• use of estrogen replacement therapy in menopausal women;
• exposure to infectious pathogens.

The restriction of cholesterol coming from food is made by prescribing a diet that excludes cholesterol-containing products.

The following groups of drugs are used for the medical treatment of atherosclerosis:

• Nicotinic acid and its derivatives - effectively reduce the content of triglycerides and cholesterol in the blood, increase the content of high-density lipoproteins with anti-atherogenic properties. The administration of nicotinic acid preparations is contraindicated in patients suffering from liver diseases.
• Fibrates (clofibrate) - reduce the synthesis of own fats in the body. They can also cause liver disorders and the development of cholelithiasis.
• Bile acid sequestrants (cholestyramine, colestipol) – bind and remove bile acids from the intestine, thereby lowering the amount of fat and cholesterol in cells. When they are used, constipation and flatulence may occur.
• Drugs of the statin group (lovastatin, simvastatin, pravastatin) are the most effective for lowering cholesterol, since they reduce its production in the body itself. Statins are used at night, because cholesterol synthesis increases at night. They can lead to disorders in the liver.

Surgical treatment for atherosclerosis is indicated in cases of high threat or development of arterial occlusion by plaque or thrombus. Both open operations (endarterectomy) and endovascular operations are performed on the arteries - with dilation of the artery using balloon catheters and the installation of a stent at the site of narrowing of the artery, preventing blockage of the vessel.

With severe atherosclerosis of the heart vessels, threatening the development of myocardial infarction, coronary artery bypass surgery is performed.

In many ways, the prognosis of atherosclerosis is determined by the behavior and lifestyle of the patient himself. Elimination of possible risk factors and active drug therapy can delay the development of atherosclerosis and achieve improvement in the patient's condition. With the development of acute circulatory disorders with the formation of foci of necrosis in the organs, the prognosis worsens.

In order to prevent atherosclerosis, it is necessary to give up smoking, eliminate the stress factor, switch to low-fat and cholesterol-poor food, systematic physical activity commensurate with opportunities and age, normalization of weight. It is advisable to include in the diet foods containing fiber, vegetable fats (linseed and olive oils), dissolving cholesterol deposits. The progression of atherosclerosis can be slowed down by taking cholesterol-lowering medications.