Coronary heart failure. Overview of Acute Coronary Insufficiency: Causes and Treatment

Normally, the cardiovascular system optimally provides the current needs of organs and tissues for blood supply. Impaired cardiac function, vascular tone, or changes in the blood system can lead to circulatory failure. The most common cause of circulatory failure is a disorder of the functions of the cardiovascular system.

Despite the trend towards a decrease in mortality rates from cardiovascular diseases, which has emerged in recent years, they still occupy the first place among the causes of disability and death. The reason is the wide prevalence of various forms of heart pathology and, above all, coronary artery disease (CHD). In industrialized countries, 15-20% of the adult population suffers from coronary artery disease. It is the cause of sudden death in 60% of patients who die from cardiovascular diseases. The morbidity and mortality from coronary artery disease is constantly increasing among the young population (under 35 years old), as well as residents of rural areas.

Among the main factors that determine the high incidence of cardiovascular pathology include frequent, repeated stressful episodes with emotionally negative "coloration", chronic physical inactivity, alcohol intoxication, smoking, consumption of excess tea, coffee and other "household doping", poor nutrition and binge eating.

Most of the various diseases and pathological processes can be attributed to three groups of typical forms of pathology: coronary insufficiency, heart failure, arrhythmias.

coronary insufficiency

Coronary insufficiency (CI) is a typical form of heart pathology, characterized by an excess of myocardial demand for oxygen and metabolic substrates over their inflow through the coronary arteries, as well as a violation of the outflow of biologically active substances, metabolites and ions from the myocardium.

Types of KN. All types of KN can be differentiated into two groups: 1) reversible(transient); 2) irreversible.

Reversible disorders are clinically manifested by various variants of angina pectoris of a stable or unstable course. In addition, due to the intensive introduction into cardiology of various methods for restoring blood perfusion of a previously ischemic area of ​​the heart, conditions after myocardial reperfusion (revascularization) in patients with chronic CI are highlighted. An irreversible cessation or a long-term significant decrease in blood flow through the coronary artery in any region of the heart ends, as a rule, with its death - a heart attack. If this does not lead to the death of the patient, then the dead part of the heart is replaced by connective tissue. Large-focal cardiosclerosis develops.

<Таблица название>Types, clinical forms and outcomes of coronary insufficiency

Etiology KN. The causative factors of CI are divided into two groups:

1. Coronarogenic- causing a decrease or complete closure of the lumen of the coronary arteries and, consequently, a decrease in arterial blood flow to the myocardium. They cause the development of the so-called absolute CI (caused by an "absolute" decrease in blood delivery to the myocardium).

2. Non-coronary- causing a significant increase in myocardial consumption of oxygen and metabolic substrates in comparison with the level of their inflow. The CI caused by them is referred to as relative (it can also develop at a normal level of blood flow to the myocardium).

The most common coronarogenic factors (causing an absolute decrease in blood delivery) are:

1) Atherosclerotic lesions of the coronary arteries. The first signs of atherosclerosis of the heart vessels are detected at 11–15 years of age. In those who accidentally died at the age of 35–40, atherosclerotic changes in the arteries were noted in 66% of cases. It has been proven that with a 50% narrowing of the lumen of the artery, a decrease in its outer diameter by only 9–10% (with contraction of muscle fibers) causes occlusion of the vessel and cessation of blood flow to the myocardium.

2) Aggregation of blood cells(erythrocytes and platelets) and the formation of blood clots in the coronary arteries of the heart. This is facilitated by atherosclerotic changes in the walls of blood vessels.

3) Spasm of the coronary arteries. It is believed that catecholamines are of decisive importance in the development of coronary spasm. A significant increase in their content in the blood, or an increase in the adrenoreactive properties of myocardial vessels, is accompanied by all the clinical, electrocardiographic and biochemical changes characteristic of angina pectoris. However, now more and more scientists believe that in real life, CI is the result of not only “pure” vascular spasm. Apparently, a long and significant narrowing of the lumen of the coronary artery is the result of a complex of such interdependent factors as: a) contraction of the muscles of the coronary arteries under the influence of catecholamines, thromboxane A 2 , prostaglandins; b) a decrease in the internal diameter of the arteries as a result of thickening of its wall; c) narrowing or closure of the vessel by a thrombus ("dynamic" stenosis of the coronary arteries).

4) Decreased blood flow to the myocardium, i.e., a decrease in perfusion pressure in the coronary arteries (with arrhythmias, aortic valve insufficiency, acute hypotension, etc.).

A significant increase in myocardial consumption of oxygen and metabolic substrates (non-coronary causes of CI) is most often caused by the following factors:

1) An increase in the level of catecholamines in the blood and myocardium (with stress, pheochromocytoma, etc.). An excess of catecholamines in the myocardium causes the development of a cardiotoxic effect (an excessive increase in the consumption of oxygen and metabolic substrates by the myocardium, a decrease in the efficiency of energy-producing processes, damage to membranes and enzymes by free radicals and products of lipid peroxidation (LPO), the formation of which is stimulated by catecholamines, etc.). d.).

2) A significant increase in the work of the heart. This may be due to excessive physical activity, prolonged tachycardia, acute arterial hypertension, etc. It is important that these causes lead, as a rule, to the activation of the sympathoadrenal system.

Mechanisms of myocardial damage in CI

1. Disorder of the processes of energy supply of cardiocytes- initial and one of the main factors of cell damage in CI. At the same time, energy supply reactions are disrupted at its main stages: ATP resynthesis; transport of its energy to the effector structures of cells (myofibrils, ion "pumps", etc.), utilization of ATP energy. Under conditions of ischemia, the reserve of oxygen associated with myoglobin is rapidly depleted, and the intensity of oxidative phosphorylation in mitochondria is significantly reduced. Due to the low concentration of O 2 - an acceptor of protons and electrons - their transport by the components of the respiratory chain and the coupling with ADP phosphorylation are disturbed. This causes a decrease in the concentration of ADP and CP in cardiomyocytes.

Violation of aerobic ATP synthesis causes the activation of glycolysis, resulting in the accumulation of lactate, and this is accompanied by the development of acidosis. Intra- and extracellular acidosis significantly changes the permeability of membranes for metabolites and ions, inhibits the activity of energy supply enzymes (including enzymes of glycolytic ATP production), and the synthesis of cellular structures.

These mechanisms operate mainly in the ischemic zone. In areas remote from it, the process of ATP resynthesis suffers less.

It is known that the main share of ATP energy (up to 90%) is consumed in reactions that ensure the contractile process, therefore, an energy supply disorder is manifested primarily by a violation of the contractile function of the heart, and hence a violation of blood circulation in organs and tissues.

2. Damage to the membrane apparatus and enzyme systems of cardiocytes. Under conditions of coronary insufficiency, their damage is a consequence of the action of general mechanisms: intensification of free radical reactions and lipid peroxidation; activation of lysosomal and membrane-bound hydrolases; violations of the conformation of molecules of proteins and lipoproteins; microruptures of membranes as a result of swelling of myocardial cells, etc.

3. Imbalance of ions and liquid. As a rule, dysionia develops "after" or simultaneously with disorders of the reactions of the energy supply of cardiocytes, as well as with damage to their membranes and enzymes. The essence of the changes is the release of potassium ions from ischemic cardiocytes, the accumulation of sodium, calcium and fluid in them. The leading causes of K + -Na + imbalance in CI are ATP deficiency, increased permeability of the sarcolemma and inhibition of the activity of K + - Na + - dependent ATP-ase, which creates the possibility of passive exit of K + from the cell and entry of Na + into it along the gradient concentration. KN is also accompanied by the release of large amounts of potassium and calcium from the mitochondria. The loss of potassium by cardiomyocytes is accompanied by an increase in its content in the interstitial fluid and blood. Concerning hyperkalemia is one of the characteristic signs of coronary insufficiency, especially in myocardial infarction. Hyperkalemia is one of the main causes of ST segment elevation in ischemia and myocardial infarction. An imbalance of ions and fluid causes a violation of electrogenesis and contractile characteristics of myocardial cells. In connection with deviations of transmembrane electrogenesis, cardiac arrhythmias develop.

4. Disorder of the mechanisms of regulation of the heart. For example, CI is characterized by phase changes in the activity of regulatory mechanisms, including sympathetic and parasympathetic ones. At the initial stage of myocardial ischemia, as a rule, there is a significant activation of the sympathoadrenal system. This is accompanied by an increase in the content of norepinephrine and especially adrenaline in the myocardium. As a result, tachycardia develops, the value of cardiac output increases (decreasing immediately after the onset of an episode of CI). In parallel, parasympathetic influences also increase, but to a lesser extent. In the later stages of CI, a decrease in the content of norepinephrine in the myocardium and the preservation of an elevated level of acetylcholine are recorded. As a result, there is the development of bradycardia, a decrease in cardiac output, the rate of contraction and relaxation of the myocardium.

Coronary insufficiency is a condition in which blood flow through coronary-type blood vessels is reduced.

The pathology is chronic. Unlike the acute form of the disease, it will develop gradually. Usually it is a consequence of hypertension, atherosclerosis and other diseases that increase the rate of blood density (for example, diabetes mellitus). All chronic forms of coronary insufficiency are combined as ischemic heart disease or coronary heart disease.

Main reasons

There are various reasons that can provoke coronary syndrome. Consider the following:

Narrowing of the lumen of blood vessels

1. The lumen of the blood vessels narrows. This happens with atherosclerosis. Elastic and muscular-elastic arteries are predominantly affected. Lipoproteins accumulate on the walls of blood vessels. This is a separate class of proteins that transport fats in the human body. There are several classes of such substances, but those that have a low density are considered the most dangerous. They are able to seep into the tissue of the walls of blood vessels and cause certain reactions. In the future, a substance of a pro-inflammatory type is produced, and then connective tissues. Gradually, the lumen of the vessel narrows, its walls lose their elasticity.
2. Formation of atherosclerotic plaques. They are formed due to cholesterol and lipoproteins, interfere with blood circulation. They are formed on the wall and have a conical shape. Under certain conditions provoke the development of inflammatory processes.
3. Inflammatory processes on the walls of blood vessels. Such a factor is quite rare. It occurs when viruses and bacteria enter the bloodstream, and the walls of blood vessels become inflamed due to the action of autoantibodies. This is typical of the autoimmune reaction of the body.
4. Spasm of blood vessels. The walls of the coronary arteries have a certain number of cellular structures of the smooth muscle type. Under the influence of impulses of the nervous system, they are reduced. With spasms, the lumen narrows, but the volume of blood entering it does not decrease. Usually such an attack stops quickly, but sometimes the vessel is completely blocked, which leads to the death of cardiomyocytes due to lack of oxygen.
5. Clogging of blood vessels with blood clots.
6. The need for oxygen increases. Usually, in a normal state, the vessels adjust to the needs of the heart for oxygen and nutrients. They start to expand. But if the coronary arteries are affected by atherosclerosis or other diseases, then this cannot be done, which leads to hypoxia.
7. Lack of oxygen in the blood. This reason is quite rare. It manifests itself in some diseases. Oxygen starvation will be aggravated along with the weakening of blood flow in the coronary arteries.

Available factors

The following factors contribute to the appearance of atherosclerosis of the coronary vessels:

In addition, non-atherosclerotic factors that contribute to the development of coronary insufficiency include the following:

1. Arteritis is an inflammation of the walls of the coronary arteries, which leads to their thickening.
2. Deformations of blood vessels of the coronary type. This usually occurs with postirradiation fibrosis, Fabry syndrome, or mucopolysaccharidosis.
3. Congenital pathologies.
4. Injuries.
5. Irradiation in the region of the heart.
6. Embolism of coronary arteries. For example, this happens with blood clots after surgery or the installation of a catheter, due to defects in the heart valves, thromboendocaritis or endocarditis of bacterial origin.
7. Thyrotoxicosis is a condition in which the concentration of hormonal substances that are synthesized by the thyroid gland increases in the blood.
8. Increasing the level of blood clotting.

Symptoms of the disease

If the patient has coronary insufficiency, the symptoms will not be pronounced, unlike other heart diseases.

This is usually the clinical picture.

1. Painful sensations. This symptom in coronary insufficiency is one of the most important. Often it is the only manifestation of a pathological condition in a patient. Painful sensations have a different character and intensity. Allocate paroxysmal. Often appear after heavy physical exertion, but they can occur when the patient is in a calm state. The reason is the lack of oxygen. In other words, the lumen of the vessel narrows (the cause is an atherosclerotic plaque), the flow of blood with oxygen particles to the heart is limited. During intense exercise, the heart works harder, so it needs more oxygen, but due to limited blood flow, it does not receive it. Arteries narrow and nerve fibers are irritated. Spasms appear. But painful sensations can also be squeezing, cutting, stabbing. Their intensity is usually weak or moderate. Often, with constant pain, the patient tries to take a comfortable position, but this does not work out, since the pathology is chronic, and the pain becomes permanent. Periodically, they can fade. If the patient has angina pectoris, then usually there are several attacks, between which there are small intervals. The duration of the attack is approximately 5 minutes. Painful sensations are localized on the left side of the sternum or behind it. Sometimes the pain in the region of the heart goes to the right side of the chest. In this case, it is difficult for the patient to indicate that the intensity of pain will be the strongest. Quite often, pain passes to the neck, lower jaw, ear, arm, the area between the shoulder blades, much less often - to the groin, lower back.
2. Increases sweating. Usually this symptom occurs abruptly. The patient turns pale during the first attack. Beads of sweat stand out on the forehead. This is due to the acute reaction of the autonomic nervous system to pain.
3. Shortness of breath and cough. Such signs usually occur due to irritation of pain receptors. Shortness of breath is associated with a violation of the respiratory rhythm. Then there are problems with blood flow if arrhythmia or necrosis of the heart tissue develops. Cough is considered to be a rare symptom. It may last for a short period of time without sputum being produced, so that the cough is not productive. Usually the appearance of this symptom is associated with stagnant processes in the pulmonary circulation. As a rule, both cough and shortness of breath appear in parallel.
4. Paleness of the skin. This is due to disturbances in blood circulation, the response of the autonomic nervous system and an increase in the intensity of sweating.
5. Fainting. Fainting is also called syncope. It occurs infrequently. Caused by fainting attacks of arrhythmias or problems with blood circulation. The brain tissue temporarily does not receive useful substances and oxygen, so that it cannot control the entire body.
6. Fear of death. This subjective feeling is temporary. It appears due to interruptions in the work of the respiratory system or with severe pain, heart rhythm disturbances.

Forms of coronary insufficiency

Coronary heart failure can take various forms:

1. Abdominal. Usually areas with tissue necrosis are located on the posterior lower surface of the heart muscle. This form occurs in 3% of people with coronary insufficiency. Due to the fact that the nerve fibers in this place are irritated, symptoms appear that are associated with the digestive tract. For this reason, it is quite difficult to establish a diagnosis. Main symptoms: nausea, vomiting, belching, flatulence, hiccups, abdominal pain under the ribs, tension in the abdominal region, diarrhea.
2. Asthmatic. This form occurs in 20% of patients with coronary insufficiency, so it is quite common. The main factor is a violation of blood circulation. ventricular failure develops. Due to stagnant processes in the pulmonary circulation, symptoms appear that resemble bronchial asthma. A person takes a forced position, there is suffocation, shortness of breath, cyanosis increases. Wheezing is heard in the lungs, the cough is wet. Pain in the region of the heart is weak or completely absent.
3. Painless. This form is considered the rarest, but very dangerous. This is due to the fact that the symptoms that are typical for such a disease are very mild. Because of this, the patient goes to the hospital very rarely. He does not feel pain, but a slight discomfort behind the sternum is felt, while it quickly disappears. Sometimes the rhythm of the heart beats or breathing is disturbed, but everyone recovers quickly.
4. Cerebral. This form is most often characteristic of older people who have problems with blood circulation in the blood vessels of the brain. Usually such difficulties are associated with atherosclerosis. Suddenly there is dizziness, headaches, tinnitus, nausea, darkening of the eyes, fainting.
5. Collaptoid. With this form, there are serious violations of the systemic blood flow. Blood pressure drops sharply. The person is disoriented, but does not lose consciousness. There are attacks with sweating. Sometimes a person falls because control over the limbs is lost. The pulse in patients with this pathology is rapid, but it is mild. Painful sensations in the region of the heart are weak.
6. Edema. This form is characterized by an extensive violation of systemic blood flow and heart failure. The rhythm of the heartbeat is disturbed, shortness of breath, muscle weakness, dizziness appear. Gradually edema of the heart is formed. They spread to the legs, ankles, feet. Fluid may also accumulate in the abdominal cavity.
7. Arrhythmic. One of the constant symptoms is a violation in the rhythm of the heart. The patient does not often complain of shortness of breath or pain, but at the same time notices unevenness in the rhythm of the heart. This form is very rare and occurs in only 2% of patients with coronary syndrome.

Medical therapy

Coronary insufficiency syndrome is treated with medications - this is the main method of dealing with the disease. Therapy is aimed at eliminating the root cause of the disease and the main symptoms. It is required to restore the supply of oxygen to the tissues of the heart. The choice of therapy is carried out by the doctor depending on the patient's condition. These drugs are prescribed.

I. For emergency care.

Usually such means are used as first aid in case of exacerbation of the patient's condition:

1. Nitroglycerine. Helps in supplying the cells of the heart with oxygen. Blood circulation in this place gradually improves, the process of death of cardiomyocytes slows down.
2. Isosorbide dinitrate. This tool is an analogue of nitroglycerin. The coronary vessels dilate, so that the flow of blood with oxygen to the myocardium increases. Tension in the walls of the ventricles decreases.
3. Oxygen. The blood is filled with oxygen, the nutrition of the tissues of the heart muscle improves, and the death of cellular structures slows down.
4. Aspirin. This remedy prevents the formation of blood clots, and also helps to thin the blood. As a result, even with the narrowing of the coronary vessels, blood will pass through them more easily.
5. Clopidogrel. Changes platelet receptors and affects their enzymatic system so that blood clots do not form.
6. Ticlopidin. Does not allow platelets to stick together. The viscosity of the blood decreases. Prevents the formation of blood clots.

II. Beta-blockers.

This is another group of medicines that are prescribed for coronary syndrome. Usually they are used by patients who have high blood pressure and at the same time develop tachycardia.

Propranolol, Atenolol, Esmolol, Iteprolol are prescribed. They block the work of beta-adrenergic receptors in the region of the heart. The contraction force of the organ decreases, so that the myocardium requires less oxygen.

III. Painkillers.

The main symptom of coronary insufficiency is a feeling of pain in the region of the heart. If its intensity increases, then medicines with analgesic properties are prescribed.

They eliminate the feeling of anxiety, fear. The following medicines are used:

1. Morphine. This medicine belongs to strong narcotic opioid substances.
2. Fentanyl. It is an analogue of morphine.
3. Droperidol. This tool blocks dopamine receptors in the brain. Has a sedative effect.
4. diazepam. It belongs to the group of benzodiazepines. It is a sedative and sedative.
5. Promedol. Has a strong analgesic effect. The muscles relax so that the spasms go away. It also has a sedative effect.

IV. Thrombolytic drugs.

Such medicines are used to dissolve blood clots. For example, Streptokinase, Alteplase, Urokinase, Tenecteplase are prescribed. If possible, the dissolution of the neoplasm in the blood is carried out locally. In this case, the drug is administered through a special catheter. In this case, the risk of side effects is reduced.

Traditional medicine recipes

Traditional medicine will not get rid of a disease such as chronic coronary insufficiency, but the patient's condition is gradually improving. Such therapy is only auxiliary.

To improve the nutrition of the muscle tissue of the heart, the following recipes are used:

1. Oat grains. On their basis, an infusion is prepared. You will need to take 1 part of the grains and pour 10 parts of boiling water. Then the remedy will be infused for a day. Then it should be taken three times a day for 0.5 cups before meals. The therapy lasts for several days until the pain in the heart area subsides.
2. Nettle. Raw materials must be collected before flowering. Grind leaves, 5 tbsp. raw materials pour 0.5 liters of boiling water. Boil the mixture for 5 minutes over low heat. When the liquid has cooled, strain it and take it three times a day. A single dosage is 50-100 ml. It is allowed to add a little honey.
3. Centaury. To prepare the infusion, you need 1 tbsp. dry chopped herbs pour two cups of boiling water. The liquid should be put in a dark place for 2 hours. Then divide the infusion into 3 equal parts and take them during the day half an hour before meals. The course takes several weeks.
4. Feverweed. Collect the plant during its flowering, dry for several days. 1 tbsp pour a spoonful of raw materials with 1 glass of boiling water and boil over low heat for 7 minutes, strain and take 5 times a day for 1 tbsp.

Such prescriptions will not completely eliminate the problem, but will help improve the patient's condition.

Surgery for coronary insufficiency

Surgical therapy is required in the acute form of the coronary syndrome. Such treatment is aimed at restoring blood circulation in the coronary-type arteries, as well as providing the tissues of the heart with arterial blood in sufficient volume. Two methods are used - stenting and shunting.

1. Shunting. This technique lies in the fact that for arterial blood new paths are created that will bypass those places where there is a narrowing of the lumen of the vessel or its blockage. To do this, the doctor cuts out a small piece of the vein (usually material is used on the lower leg), and then uses it as a shunt. The new tissue is sutured on one side from the coronary artery and on the other side to the aorta. The advantages of this method are as follows: normal blood flow to the heart is ensured, while there is a low likelihood of infectious agents or autoimmune processes. the risk of complications in the lower leg is very low, since in this place the circulatory system is very branched. The likelihood of developing atherosclerosis on the new tissue is minimal, since veins and arteries have a slightly different structure at the cellular level.
2. Stenting differs in technique from shunting. The essence of the operation is that a lumen is established in the vessel in the form of a metal frame. It is introduced into the artery compressed, but then straightened out and stored in an expanded form. To enter such a device, a special catheter is used. It is usually given through an artery in the thigh. The process is controlled by fluoroscopy.

The advantage is that there is no need to use a machine for artificial circulation of blood. After the operation, only a small scar will remain. There are no allergic reactions to the metal frame. The likelihood of complications is very low.

Conclusion

What is coronary insufficiency, every person who has a predisposition to diseases of the heart and blood vessels should know. With this disease, blood flow in the coronary blood vessels decreases. This pathology is chronic. It can be triggered by various factors. In this case, the patient develops symptoms characteristic of heart failure. Treatment is usually with medication, but in severe cases, surgery is performed. Traditional medicine recipes are used as adjunctive therapy.

Video

Coronary circulation disorders on the ECG can manifest themselves as signs of ischemia, damage, necrosis, and their combinations.

With focal ischemic lesions of the myocardium, it is customary to talk about direct and reciprocal signs of the latter.

Direct signs appear in leads where the active electrode is located above the affected area. Reciprocal signs are recorded in leads from the opposite (unaffected) side.

Changes in the shape and polarity of the T wave.

The nature of the changes is determined by the localization of ischemia in the subendocardial or subepicardial regions of the myocardium. A direct sign of subendocardial ischemia is a high, positive, wide T wave at the base. A reciprocal sign is characterized by a decrease in the amplitude of the T wave. In subepicardial ischemia, a direct sign is the presence of a negative equilateral T wave. Reciprocal changes are manifested by an increase in the amplitude of the T wave.

2. Damage

It manifests itself by changes in the ST segment (displacement of the segment above or below the isoline).

With subendocardial injury, a direct symptom is ST segment depression. A typical reciprocal change is ST segment elevation in lead aVR. With subepicardial and transmural lesions, ST segment elevation (direct sign) occurs with a reciprocal sign in the form of ST segment depression.

It is reflected on the ECG by a change in the QRS complex.

Transmural necrosis is characterized by the appearance of a QS complex;

Subendocardial necrosis is characterized by a pathological Q wave - a QRS complex such as QR, Qr;

Intramural necrosis manifests itself as a decrease in the amplitude of the R wave. The reciprocal sign of any necrosis is an increase in the amplitude of the R wave.

More on the topic ELECTROCARDIOGRAM FOR CORONARY CIRCULATION DISORDERS:

1. ELECTROCARDIOGRAM IN DISORDERS OF INTRACARDIAC CONDUCTIVITY
2. CORONARY INSUFFICIENCY, CORONARY HEART DISEASE AND ACUTE MIOCARDIAC INFARCTION.

75-85 ml of blood per 100 g of heart weight (about 5% of the value of the minute volume of the heart) flows through the coronary vessels in a person at muscle rest in 1 minute, which significantly exceeds the amount of blood flow per unit weight of other organs (except for the brain, lungs and kidneys). ). With significant muscular work, the value of coronary blood flow increases in proportion to the increase in cardiac output.

The amount of coronary blood flow depends on the tone of the coronary vessels. Irritation of the vagus nerve usually causes a decrease in coronary blood flow, which, apparently, depends on a slowing of the heart rate (bradycardia) and a decrease in mean pressure in the aorta, as well as a decrease in the heart's need for oxygen. Excitation of the sympathetic nerves leads to an increase in coronary blood flow, which is obviously due to an increase in blood pressure and an increase in oxygen consumption, which occurs under the influence of norepinephrine released in the heart and adrenaline brought in by the blood. Catecholamines significantly increase myocardial oxygen consumption, so an increase in blood flow may not be adequate to increase the heart's need for oxygen. With a decrease in oxygen tension in the tissues of the heart, the coronary vessels expand and the blood flow through them sometimes increases by 2-3 times, which leads to the elimination of the lack of oxygen in the heart muscle.

Acute coronary insufficiency (angina pectoris)

Acute coronary insufficiency is characterized by a mismatch between the need of the heart for oxygen and its delivery with blood. Most often, insufficiency occurs with atherosclerosis of the arteries, spasm of the coronary (mainly sclerotic) arteries, blockage of the coronary arteries by a thrombus, rarely an embolus. Insufficiency of coronary blood flow can sometimes be observed with a sharp increase in heart rate (atrial fibrillation), a sharp decrease in diastolic pressure. Spasm of unchanged coronary arteries is extremely rare. Atherosclerosis of the coronary vessels, in addition to reducing their lumen, also causes an increased tendency of the coronary arteries to spasm.

The result of acute coronary insufficiency is myocardial ischemia, causing a violation of oxidative processes in the myocardium and excessive accumulation of under-oxidized metabolic products (milk, pyruvic, etc.) in it. At the same time, the myocardium is not sufficiently supplied with energy resources (glucose, fatty acids), its contractility decreases. The outflow of metabolic products is also difficult. With an excess content, the products of interstitial metabolism cause irritation of the receptors of the myocardium and coronary vessels. The resulting impulses pass mainly through the left middle and lower cardiac nerves, the left middle and lower cervical and upper thoracic sympathetic nodes, and through the 5 upper thoracic connecting branches ( rami communicantes) enter the spinal cord. Having reached the subcortical centers, mainly the hypothalamus, and the cerebral cortex, these impulses cause pain sensations characteristic of angina pectoris (Fig. 89).

myocardial infarction

Myocardial infarction - focal ischemia and necrosis of the heart muscle that occurs after a prolonged spasm or blockage of the coronary artery (or its branches). The coronary arteries are terminal, therefore, after the closure of one of the large branches of the coronary vessels, the blood flow in the myocardium supplied by it decreases tenfold and recovers much more slowly than in any other tissue in a similar situation. The contractility of the affected area of ​​the myocardium drops sharply and then completely stops. The phase of isometric contraction of the heart and especially the phase of exile are accompanied by passive stretching of the affected area of ​​the heart muscle, which can later lead to its rupture at the site of a fresh infarction or to stretching and the formation of an aneurysm at the site of scarring of the infarction (Fig. 90). Under these conditions, the pumping force of the heart as a whole decreases, since part of the contractile tissue is turned off; in addition, a certain fraction of the energy of the intact myocardium is wasted, on stretching inactive areas. The contractility of intact areas of the myocardium also decreases as a result of a violation of their blood supply, caused either by compression or by reflex spasm of the vessels of intact areas (the so-called intercoronary reflex).

Mechanisms of weakening myocardial contractility in a heart attack were studied in detail in the experiment.

Experimental myocardial infarctions. Focal myocardial ischemia with subsequent necrosis is most easily reproduced in experimental animals by ligation of one of the branches of the coronary artery of the heart. After ligation of the coronary artery in the myocardium, the content of coenzyme A, which is necessary for the synthesis of acetylcholine, decreases; along with this, the flow of catecholamines - norepinephrine and adrenaline, to the heart, increases, which significantly increase the consumption of oxygen by the heart muscle, regardless of the work it performs. Due to the impossibility of adequate blood flow to the needs of the heart, the degree of hypoxia in the myocardium increases dramatically. Under anaerobic conditions, carbohydrate metabolism is disturbed - glycogen stores are depleted, the content of lactic and pyruvic acids increases, and acidosis develops.

The disintegration of cells is accompanied by the release of K + ions from them. Released in the infarction zone, potassium is mainly concentrated in the perifocal zone. From the damaged cells of the necrotic area, enzymes and other biologically active substances are released that can further aggravate myocardial damage. In some cases, the result of damage to the protein structures of the myocardium is the formation of autoallergens and the subsequent development of specific autoantibodies against them. Fixation of the latter on intact areas of the myocardium can cause subsequent damage to it.

Myocardial necrosis, similar in metabolic disorders to human infarction, can be obtained in laboratory animals by exposure to certain drugs and chemicals (for example, the administration of adrenaline, foxglove extract, irradiated ergosterol preparations, etc.). Selye reproduced myocardial necrosis in rats treated with corticoid preparations, provided that an excess of sodium salts was introduced into their diet. In his opinion, some sodium salts "sensitize" the heart muscle to the damaging effects of corticosteroids.

Electrocardiogram changes in myocardial infarction. Myocardial infarction is characterized by a heart rhythm disorder that appears from the very beginning of the development of a heart attack. The most characteristic changes in the electrocardiogram are a shift in the RST segment and a change in the QRS complex and the T wave. They can be the result of ischemia extending to the conduction system of the heart, as well as influences emanating from the site of necrosis.

The entire area of ​​damage in myocardial infarction can be divided into three zones: the central zone of necrosis, the zone of "damage" surrounding it, and the most peripheral - the zone of ischemia. The presence of a zone of necrosis, and subsequently a scar, explains the change in the QRS complex and, in particular, the appearance of a deep Q wave.

The zone of "damage" causes the shift of the RST segment, and the zone of ischemia leads to a change in the G wave. Different ratios of the values ​​of these zones in different phases of the disease explain the complex dynamics of changes in the electrocardiogram during myocardial infarction (Fig. 91).

Cardiogenic shock. It is a syndrome of acute cardiovascular insufficiency, which develops as a complication of myocardial infarction. Clinically, it manifests itself as a sudden sharp weakness, blanching of the skin with a cyanotic tint, cold sticky sweat, a drop in blood pressure, a small frequent pulse, lethargy of the patient, and sometimes a short-term impairment of consciousness.

In the pathogenesis of hemodynamic disorders in cardiogenic shock, three links are essential:

• 1) decrease in stroke and minute volume of the heart (cardiac index below 2.5 l / min / m 2);
• 2) a significant increase in peripheral arterial resistance (more than 1800 dynes / sec· cm +5);
• 3) violation of microcirculation.

Decreased cardiac output and stroke volume is determined in myocardial infarction by a sharp decrease in the contractility of the heart muscle due to necrosis of a more or less extensive area of ​​it. The result of a decrease in cardiac output is a decrease in blood pressure.

Increased peripheral arterial resistance due to the fact that with a sudden decrease in cardiac output and a decrease in blood pressure, carotid and aortic baroreceptors are activated, a large amount of adrenergic substances are reflexively released into the blood, causing widespread vasoconstriction. However, different vascular regions respond differently to adrenergic substances, which leads to a different degree of increase in vascular resistance. As a result, blood is redistributed: blood flow in vital organs is maintained by contraction of blood vessels in other areas.

However, prolonged and excessive peripheral vasoconstriction in clinical conditions acquires pathological significance, contributing to the disruption of the complex mechanism of microcirculation with impaired peripheral blood flow and the development of a number of severe, sometimes irreversible, changes in vital organs.

Microcirculation disorders in cardiogenic shock manifest as vasomotor and intravascular (rheographic) disorders. Vasomotor disorders of microcirculation are associated with systemic spasm of arterioles and precapillary sphincters, leading to the transfer of blood from arterioles to venules through anastomoses, bypassing the capillaries. In this case, the blood supply to the tissues is sharply disturbed and the phenomena of hypoxia and acidosis develop. Violations of tissue metabolism and acidosis lead to relaxation of the precapillary sphincters; postcapillary sphincters, less sensitive to acidosis, remain in a state of spasm. As a result of this, blood accumulates in the capillaries, part of which is turned off from the circulation; hydrostatic pressure in the capillaries increases, fluid begins to transudate into the surrounding tissues. As a result, the volume of circulating blood decreases. At the same time, changes in the rheological properties of the blood occur - intravascular aggregation of erythrocytes occurs, associated with a decrease in blood flow velocity and a change in the protein fractions of the blood, as well as the charge of erythrocytes.

The accumulation of erythrocytes slows down the blood flow even more and contributes to the closure of the lumen of the capillaries. Due to the slowdown in blood flow, blood viscosity increases and prerequisites for the formation of microthrombi are created, which is also facilitated by an increase in the activity of the blood coagulation system in patients with myocardial infarction complicated by shock.

Violation of peripheral blood flow with pronounced intravascular aggregation of erythrocytes, deposition of blood in the capillaries leads to certain consequences:

• a) the venous return of blood to the heart decreases, which leads to a further decrease in the minute volume of the heart and an even more pronounced violation of the blood supply to the tissues;
• b) oxygen starvation of tissues deepens due to the exclusion of erythrocytes from circulation.

In severe shock, a vicious circle occurs: metabolic disorders in tissues cause the appearance of a number of vasoactive substances that contribute to the development of vascular disorders and erythrocyte aggregation, which in turn support and deepen existing disorders of tissue metabolism. As tissue acidosis increases, deep violations of enzyme systems occur, which leads to the death of cellular elements and the development of small necrosis in the myocardium, liver, and kidneys.

The heart is the central "pumping station" of the circulation. The cessation of heart activity even for a few tens of seconds can lead to serious consequences. Day and night, week after week, month after month and year after year, the heart pumps blood continuously. With each stroke, 50-70 ml of blood (a quarter or a third of a glass) is ejected into the aorta. With 70 beats per minute, this will be 4-5 liters (at rest). Get up, walk, climb the stairs - and the figure will double or triple. Start running - and it will increase by 4 or even 5 times. On average, the heart pumps up to 10 tons of blood per day, even with a lifestyle that is not associated with hard work, and 3650 tons per year. During the life of the heart - this little worker, whose size does not exceed the size of a fist - pumps 300 thousand tons blood, working continuously, without stopping even for a few seconds. The work that the human heart performs throughout life is sufficient to lift a loaded railway car to the height of Elbrus.

To ensure this gigantic work, the heart needs a continuous supply of energetic and plastic materials and oxygen. The energy that the heart muscle (myocardium) develops during the day is approximately 20 thousand kgm. Energy intake is usually calculated in calories. It is known that 1 kcal is equivalent to 427 kgm. The efficiency of the heart and other muscles is approximately 25%. In order to develop energy equal to 20 thousand kgm, the heart must expend approximately 190 kcal per day.

Energy source - the process of oxidation of sugar or fats, which requires oxygen. When consuming 1 liter of oxygen, 5 kcal is released; with an energy expenditure of 190 kcal per day, the heart muscle must absorb 38 liters of oxygen. From 100 ml of flowing blood, the heart absorbs 12-15 ml of oxygen (other organs absorb 6-8 ml.). To deliver the necessary 38-40 liters of oxygen, about 300 liters of blood must flow through the heart muscle per day.

The heart muscle is supplied with blood through the coronary, or coronary, arteries. Coronary circulation has a number of features that distinguish it from blood circulation in other organs and tissues. It is known that in the arterial system there is a pulsating blood pressure: it increases during the contraction of the heart and decreases during its relaxation. An increase in pressure in the arteries with a contraction of the heart increases blood flow through organs and tissues. In the vessels of the heart, the opposite ratio is observed. With the contraction of the heart muscle, intramuscular pressure increases to 130-150 mm, which significantly exceeds the blood pressure in the capillaries. As a result, the capillaries shrink. Unlike blood flow in other organs and tissues, increased blood flow through the coronary vessels is observed not during contraction, but during relaxation of the heart.

With a rarer heart rate, the duration of periods of relaxation (diastole) of the heart increases, which naturally improves coronary blood flow, facilitating the nutrition of the heart muscle. With a rare rhythm, the heart works more economically and productively.

Interruptions in the supply of blood to the heart muscle reduce energy production and immediately affect the work of the heart. It is this condition that occurs in cases of coronary circulation disorders that are not accompanied by more serious consequences.

Disturbances in the blood supply to the heart muscle can occur with a sharp increase in the demand of the heart muscle for oxygen if the body does not have the ability to adequately increase the coronary blood flow when the vessel is clogged with a blood clot, impaired patency, and atherosclerosis. In all these cases, there is a decrease in blood delivery to the heart muscle and a significant weakening of the function of the heart (despite the fact that the heart has some reserve devices for emergency supply of its energy). Such reserves in the heart muscle are the reserves of oxygen bound by the pigment - myoglobin, as well as the ability of the heart muscle to produce energy even without oxygen consumption (due to anaerobic glycolysis). However, these reserves are weak. They can provide energy to the myocardium only for a short time. Therefore, the heart can perform its function only if there is an uninterrupted supply of blood to the heart muscle (the amount of blood supply must correspond to the intensity of work).

In the process of evolution, nature has created a complex, “multi-storied” system of regulation of coronary blood flow. The vascular muscles of the coronary arteries are innervated by fibers of the sympathetic and parasympathetic nervous systems. Sympathetic fibers cause constriction of the coronary vessels, and parasympathetic - expansion. However, such reactions are observed only in the conditions of experiments on the vessels of a stopped heart. In cases where the heart continues to work, irritation of the sympathetic and parasympathetic fibers causes other reactions.

Under the influence of impulses coming through the sympathetic nerves, the work of the heart muscle increases sharply, the strength of each contraction increases, the amount of blood ejected by the heart into the vascular system and the frequency of contractions increase. All this leads to a significant increase in the energy consumption of the heart muscle and to the accumulation of a large amount of certain metabolic products, which, as we already know, have a local vasodilating effect. Therefore, in a beating heart, irritation of the sympathetic nervous system leads not to narrowing, but to expansion of the coronary vessels. The parasympathetic system causes opposite shifts.

It has been established that the heart has its own mechanism of nervous regulation - the intracardiac nervous system, which continues to function even after the organ's connections with the brain and spinal cord are completely turned off. The fibers of the intracardiac nervous system innervate not only the heart muscle, but also the muscles of the coronary vessels. The regulation of coronary circulation can be carried out both by mechanisms functioning in the organ itself, and by a complex interaction of nerve signals that arise in the heart with impulses coming to the heart from the central nervous system.

Numerous, often duplicating each other, regulatory mechanisms ensure that the level of coronary blood flow is adapted to the energy needs of the heart muscle at rest, during physical exertion, emotional and mental stress.

The amount of coronary blood flow increases dramatically during intense physical activity, in which increased activity of the heart muscle causes an increase in its oxygen demand. The resulting expansion of the coronary vessels leads to a significant increase in the amount of blood flowing through the myocardium.

A similar effect is exerted by some adverse effects on the body associated with oxygen starvation or the accumulation of the main "slag" of life - carbon dioxide. The mechanisms of regulation of coronary blood flow in a healthy body quickly and accurately respond to changes in the needs of the heart muscle for oxygen or the conditions for its delivery.

Therefore, systematic physical activity, as well as a number of seemingly unfavorable factors and conditions that contribute to the development of oxygen starvation (stay in the mountains, at high altitudes, breathing gas mixtures with a low oxygen content and an increased carbon dioxide content, etc.) In reality, mechanisms are constantly trained that provide enhanced delivery of blood and oxygen to the heart muscle. The reserve capacity of these mechanisms increases and, consequently, increases the resistance of the heart and the body to the action of adverse factors.

This circumstance is of particular importance. It is possible to improve the state and capabilities of any regulatory mechanism only when increased demands are placed on the body. Not rest, namely increased activity, systematic training, i.e. periodic loads alternating with rest, is the only way to strengthen the mechanisms that regulate blood pressure, heart function and coronary blood flow.

Violation of the activity of the regulatory mechanisms described above can cause disorders in the blood supply to the heart muscle, sometimes leading to the appearance of necrosis foci in it - myocardial infarction.

The possibility of the occurrence of neurogenic lesions of the heart in the experiment was proved by the prominent Russian pathologist A. B. Fokht. He discovered that when the vagus nerves are stimulated, areas of necrosis of the heart muscle appear. When a drop of turpentine is injected into the trunk of the vagus or sympathetic nerve that innervates the heart, an electrocardiogram is recorded, which is characteristic of coronary circulation disorders. The degeneration and death of the myocardium occurred after mechanical damage to the fibers of the cardiac nerves, as well as with chronic irritation or damage to parts of the central nervous system that are in charge of regulating the function of the heart and blood vessels.

Myocardial injury can be reproduced in animal experiments with electrical stimulation of the vagus nerve, using stimuli weaker than those that can slow the heart rate.

When probing the coronary vessels by inserting a thin and flexible polyethylene catheter into the arterial system (if its coccyx touches the mouth of the coronary artery), a spasm of the coronary arteries, clearly visible on x-ray, develops, as well as changes in the electrocardiogram typical of coronary circulation disorders. Irritation of certain areas of the brain stem causes an increase in blood pressure and shifts in the electrocardiogram, which are characteristic of coronary blood flow disorders.

Clinical experience also indicates the possibility of acute coronary insufficiency when exposed to the central nervous system. Thus, for example, lesions of the base of the brain caused by acute disorders of cerebral circulation, as well as lesions of the interstitial brain or brain stem, are often accompanied by a disorder of the coronary circulation.

It was found that emotional and mental stress is accompanied by an increase in the amount of adrenaline, noradrenaline and related products (catecholamines) in the heart muscle, which leads to a significant increase in the energy of contractions and an increase in the heart's need for oxygen. But if the heart and its coronary vessels are not sufficiently trained, they cannot provide a sharp increase in myocardial blood supply. In this case, phenomena of oxygen starvation of the heart muscle, i.e., coronary insufficiency, may occur. There is a disproportion between the needs of the myocardium for oxygen and its supply to the heart with blood. This leads to the so-called "angina pectoris". In a practically healthy person, at the time of sudden physical or emotional stress, pain behind the sternum may occur. In addition, some researchers admit the possibility of direct neurogenic spasm of the coronary vessels.
G. N. Aronova in the laboratory studied the magnitude of the coronary circulation, using electronic sensors implanted in the dog's heart. In unanesthetized animals, with a sudden action of stimuli that cause pain reactions and negative emotions (the appearance of fear), a decrease in the amount of coronary blood flow and signs of coronary insufficiency were often noted.

At the Institute of Experimental Pathology and Therapy, they evoked negative emotions in male monkeys. For this, the male was separated from the female, with whom he had previously been together for a long time. The female was transferred to an adjacent cage, where another male was placed. All this caused the animal, which remained alone, to scream, worry, fits of rage, the desire to break the barrier. However, all attempts to connect with the female were in vain. The animal left alone witnessed the intimacy that arises between a former girlfriend and a new cohabitant. The electrocardiogram showed signs of acute coronary insufficiency. Attacks of violent rage and sharp emotional reactions were replaced by periods of deep depression. The state of oxygen starvation of the heart muscle increased, and in a number of experiments the animals died from acute myocardial infarction. An autopsy confirmed the diagnosis. These cruel experiments are necessary in order to understand the mechanisms of a heart attack in humans. Doesn't life sometimes bring us similar surprises? Are some situations that lead a person to a heart attack less ruthless, hopeless, tragic?

It has also been found experimentally that experimental neuroses in monkeys, arising under other circumstances, sometimes cause severe disturbances in the coronary circulation. Neuroses were reproduced according to the classical Pavlovian method, similar to that used by M.K. Petrova in the experiments described above on dogs (by overstraining the processes of excitation or inhibition, or by “collising” these processes). Such injury to the higher parts of the brain was accompanied by the appearance on the electrocardiogram of changes characteristic of coronary insufficiency and myocardial infarction.

A similar state arose even with changes in the usual daily rhythm of life, for example, with a shift in daytime and nighttime regimes, when at night the monkeys were exposed to influences characteristic of daytime - feeding, exposure to light stimuli, etc., and left in silence and darkness during the day .

The same effect was caused by the regime in which the day was compacted to 12 hours with a 6-hour change of "day" and "night", as well as the regime in which lighting and other stimuli characteristic of daytime affected animals continuously day and night. for many days. If such types of regimens continuously and randomly replaced each other - so that the animal did not have time to adapt to each of them, then after a few months a breakdown of higher nervous activity occurred, often accompanied by violations of the coronary circulation. In some cases, myocardial infarction was detected.

In experiments on animals, it was found that disorders of the coronary circulation sometimes appeared with injuries of the skull and even with the introduction of air into the ventricles of the brain.

It is known that coronary circulation is affected by signals acting through the higher parts of the brain (cerebral cortex) by the mechanism of conditioned reflexes. Changes in blood flow in the heart muscle usually occur not only immediately at the moment of an increase in heart function with an increased load, but also in advance, adapting the heart to the work ahead. However, conditioned signals can not only increase but also decrease coronary blood flow, which sometimes leads to acute coronary circulation disorders.

For remote control of coronary blood flow, a special device was developed, which was applied to one of the coronary arteries of the heart during a preliminary surgical operation. The device was a loop controlled by nylon threads, brought through the chest wall to the surface of the animal's body. A few days after the operation, when the wound healed and the animal became practically healthy, it was possible, by tightening the loop, to cause a sudden cessation of blood flow in one of the coronary arteries, and by loosening the loop, to restore coronary blood flow.

This technique was used by a group of employees in the study of the effects of coronary circulation disorders on the activity of internal organs and systems. After carrying out a number of experiments on the same animal, in the future, it was enough just to place the animal in the machine and touch the skin in the place where the loop was usually controlled to cause changes typical of a violation of the coronary circulation.

Thus, the setting of experiments in which disturbances in the coronary circulation were systematically reproduced becomes a conditioned signal that causes disturbances without tightening the loop.

Conditioned reflex disorders of the coronary circulation can also occur in humans. Let's give some examples. Once, during the performance of a symphony, the conductor suddenly felt a sharp attack of pain behind the sternum and had to leave the stage. The vasodilators relieved the pain. And he continued to work. Then the conductor had to perform the same piece again. As he approached the musical phrase, during which the first attack had earlier occurred, he again had sharp pains behind the sternum. The conductor refused to perform this symphony, and the attacks stopped.

In another case, sharp pains behind the sternum arose in an employee who was in a hurry to work. The attack was eliminated by vasodilators. But the next day, when he reached the same intersection, the attack of pain was repeated. The man had to change the way he went to work, and the attacks stopped. In both cases, apparently, we are talking about patients with latent manifestations of coronary insufficiency, which were activated under the action of typical conditioned signals by the mechanism of a conditioned reflex.

The results of an 8-month follow-up of a young patient are described, in whom the tense expectation of an unpleasant procedure (an injection, intravenous injection, etc.) caused an increase in blood pressure and electrocardiogram shifts characteristic of coronary circulation disorders. It was noted that in patients with myocardial infarction, talking about the situation and difficulties that preceded the onset of a heart attack can cause pain behind the sternum and changes in the electrocardiogram, indicating a violation of the coronary circulation.

Changes in the electrocardiogram, characteristic of the state of acute coronary insufficiency, were observed in people during hypnosis, when they were inspired by a feeling of fear and anger. In experiments conducted in the laboratory of P. V. Simonov, actors and researchers mentally reproduced unpleasant events. With imaginary fear, they experienced an increase in heart rate and shifts in the electrocardiogram, which are characteristic of coronary blood flow disorders.

With continuous recording of electrocardiograms in a working environment, train drivers found that an unforeseen emergency situation causes sharp shifts in the electrical activity of the heart, characteristic of oxygen starvation of the heart muscle.

Changes in electrocardiograms typical of coronary insufficiency are described in individuals who are in a state of fear or anxiety. Emotional stress (expectation of a surgical operation, sports competitions and professional nervous tension) can cause changes in the electrocardiogram, indicating a violation of the coronary circulation.

It is known that acute disorders of the coronary circulation can develop at night during sleep against the background of mental and physical rest. Some researchers tend to see this as evidence of the coronary action of the vagus nerve, believing that night is the "kingdom of the vagus" (i.e., the state when the tone of the parasympathetic nervous system predominates). In reality, however, the situation is much more complicated. It has now been proven that sleep is not only rest, peace, and inhibition. During sleep, periods of rest are accompanied by the emergence of states of a kind of vigorous activity of the brain, disconnected for a while from the influences of the external environment. These are periods of "paradoxical sleep", during which there is, as it were, a repeated reproduction and experience of daytime impressions, which is necessary to systematize them and fix them in memory. Thus, paradoxical sleep is an active process that often proceeds with phenomena of shifts in the activity of internal organs, characteristic of strong emotional stress.

It has been suggested that disturbances of the coronary circulation that sometimes occur during sleep do not appear against the background of rest, but during paradoxical sleep and the enhanced brain activity that occurs during it, during which daytime impressions and emotions are often reproduced and experienced again. This assumption was confirmed in a number of subsequent observations.

All of the above makes it clear that even in practically healthy individuals, an overstrain of the nervous system and negative emotions can cause coronary insufficiency, i.e. oxygen starvation of the heart muscle. This can lead to a number of complications: changes in the heart rhythm, interruptions (appearance of extraordinary contractions), sometimes to the occurrence of heart muscle flutter. Acute oxygen starvation of the heart muscle causes an attack of pain, typical electrocardiogram shifts and other disorders. If the disturbed circulation is not restored, a myocardial infarction may occur.

The reserve capacity of the coronary circulation, which is so necessary for the body in emergency situations, is sharply reduced in atherosclerosis (which often leads to a direct disruption of the blood supply to the muscles of the heart and other organs).

In violation of the coronary circulation, many diseases can develop that must be treated in a timely manner. For example, VVD treatment should be started after the first signs of appearance and preferably in specialized clinics.