Historically, there has been an idea that absolute or relative insufficiency of coronary blood flow underlies ischemia (bleeding) of the myocardium and leads to coronary artery disease. In turn, IHD: a) a very common pathology; b) often severe course with loss of ability to work and disability; c) often fatal.

Coronary insufficiency is a condition in which the coronary vessels do not provide the myocardium with sufficient blood, oxygen and nutrients.

Coronary insufficiency is absolute - due to a decrease in the lumen of the coronary vessels and a decrease in the volume of coronary blood flow.

Relative coronary insufficiency - due to an increase in myocardial oxygen demand with an unnamed lumen of the coronary vessels.

Classification of nosological forms of IHD (WHO, 1979):

• Sudden coronary death.
• Angina pectoris of various functional classes.
• coronary cardiosclerosis.
• Heart failure.
• Arrhythmias.
• The main factor in the pathogenesis of coronary artery disease: a mismatch between myocardial oxygen demand and oxygen delivery to the myocardium.
• Features of coronary blood flow are normal.

Normally, the myocardium uses 75% of the oxygen supplied to the coronary bed. Myocardial metabolism is aerobic in nature. Normally, with an increase in myocardial oxygen demand, oxygen delivery increases only due to increased coronary blood flow.

Blood supply to the subendocardial layer of the myocardium of the left ventricle occurs only during diastole. The blood flow in other parts of the left ventricle and in all parts of the right ventricle is continuous. But! The subendocardial layer of the left ventricle receives blood only in diastole. In systole, the arterioles of the subendocardial layer are almost completely compressed under the influence of an increase in blood pressure in the left ventricle. Only 15% of the blood from the norm washes the subendocardial layer in systole.

On the other hand: normally, the cardiomyocytes of the subendocardial layer contract with the greatest intensity compared to other parts of the heart. Hence, the highest oxygen demand among all cardiomyocytes is combined with natural flaws in the delivery of blood and oxygen.

In other words, there is no reserve in the subendocardial layer for oxygen delivery under increased stress.

Conclusion: The subendocardial layer of the left ventricle is primarily affected by ischemia due to;

a) the highest O2 requirement;

b) intermittent nature of blood flow;

c) lack of reserves for the delivery of O2 at increased load.

ETIOLOGICAL FACTORS OF MYCARDIUM ISCHEMISE.

Not all ischemia gives coronary artery disease. All factors leading to ischemia are divided into 3 (three) types:

• A. Coronary.
• B. Cardiac.
• B. Extracardiac.

A. Coronary ischemia factors - those that, as a result of any mechanisms, give a narrowing coronary arteries and drastically reduce blood flow to the myocardium. These include:

1) narrowing of the arteries from the outside (adhesions, scars, tumors, etc.);

2) blockage of the arteries from the inside (thrombosis and embolism of various origins);

3) pathological changes vascular wall- lead to

Deformations of the vascular wall (AT, obliterating endarteritis);

Narrowing of the lumen due to edema or proliferation of connective tissue (inflammation, infection, allergy: periarteritis nodosa, rheumatic vasculitis, infectious aortitis);

4) spasm of the vascular wall - active narrowing of the lumen of the vessels due to contraction of the smooth muscles of the vessel against the background of an increase in the tone of the vascular wall. The etiology and pathogenesis of spasm are diverse. Here:

Pathological reflexes;

Perverted reaction to catecholamines;

Other factors.

B. Cardiac ischemic factors - do not affect the coronary vessels, but affect other parts of the heart and lead to ischemia. All coronary vessels are absolutely passable. The main cardiac factors:

1) heart failure (HF);

2) tachycardia.

B.1. Heart failure HF as a cardiac factor in myocardial ischemia

The pathogenesis of ischemia against the background of HF:

HF of any origin (especially left-sided)

Decreased SV + Decreased IOC

Decrease in diastolic pressure in the aorta

Decreased blood flow to the coronary arteries

Myocardial ischemia

Decreased myocardial contractility

Worsening of heart failure

Thus, heart failure HF and myocardial ischemia mutually aggravate each other, are links of the same vicious circle. HF can occur against the background of various diseases. In this case, myocardial ischemia develops:

a) at the expense of CH, as such;

b) due to the underlying disease, which has its own specific mechanisms of ischemia.

Example 1 - aortic stenosis: with aortic stenosis, myocardial ischemia necessarily occurs due to:

Specific mechanisms of ischemia in aortic stenosis:

The aortic opening is narrowed, i.e. there is an obstruction to the flow of blood into the aorta;

In the left ventricle, blood pressure increases, the myocardium works with an overload, such an overload is called "pressure overload";

Blood is completely pushed out into the aorta due to the lengthening of the phase of expulsion of blood from the left ventricle and systole as a whole;

The lengthening of the systole occurs due to the shortening of the diastole;

The blood filling of the coronary vessels decreases (= ischemia).

Example 2 - aortic insufficiency: in aortic insufficiency, myocardial ischemia necessarily occurs due to:

b) specific mechanisms inherent only to this disease.

Specific mechanisms of ischemia in aortic insufficiency:

The aortic opening is dilated, the valves do not close completely;

In systole, blood is pushed into the aorta, but then part of it returns to the left ventricle - "volume overload";

The volume and pressure of blood in the aorta decreases;

The blood filling of the coronary vessels decreases;

aggravation of CH.

Due to these specific mechanisms, aortic malformations are less well tolerated than mitral ones.

B.2. Tachycardia as a cardiac factor of myocardial ischemia

The pathogenesis of ischemia against the background of tachycardia of any genesis:

Tachycardia of any origin;

Change in the ratio of systole and diastole in favor of systole;

The proportion of systole increases and the proportion of diastole decreases;

The total time of blood filling of the coronary vessels decreases;

Myocardial ischemia and weakening of the strength of heart contractions;

An aggravating factor: with tachycardia of any origin, the energy costs of the heart for rapid heart contractions increase sharply.

IN. Extracardiac ischemia factors - with generalized hemodynamic disorders not associated with cardiac dysfunction. These include:

1) anemia;

2) vascular insufficiency;

3) thickening of the blood.

So, there are many factors of myocardial ischemia, but among them are the leading ones, most often leading to myocardial ischemia and coronary artery disease. These leading factors are:

1) spasm of the coronary arteries;

2) stenosis of the coronary arteries, which may be the result of compression from the outside, blockage from the inside and pathological changes in the vascular wall.

SPASM OF THE CORONARY ARTERIES AS A LEADING FACTOR OF MYOCARDIAL ISCHEMIZATION

Spasm of the coronary arteries is an active narrowing of the lumen of the coronary vessels due to contraction of the smooth muscles of the vessel against the background of an increased tone of the vascular wall.

Causes of violation of the tone of the coronary vessels:

1) violation of sympathetic regulation;

2) violations of parasympathetic regulation;

3) simultaneous excitation n. vagus and sympathetic nervous system;

4) perverted reactions of the coronary vessels to catecholamines;

5) pathological reflexes.

1. Violation of sympathetic regulation. The sympathetic nervous system influences the tone of the coronary vessels through catecholamines. Catecholamines are mediators for adrenergic receptors. There are 2 (two) types of adrenoreceptors in the walls of the coronary vessels: α (alpha) and β (beta).

With emotional and physical stress on the body, the concentration of catecholamines in the blood increases, which irritate the α- and β-adrenergic receptors of the coronary vessels.

In response to the action of catecholamines, the coronary vessels give a two-phase reaction:

1) short-term narrowing of the coronary vessels;

2) persistent expansion due to the action of metabolites on the synapses.

Ultimately, there is a persistent increase in blood flow through the coronary arteries.

But this is not the only reaction of the myocardium to the presence of catecholamines in the blood. At the same time, the following phenomena are observed:

1) an increase in the frequency and strength of heart contractions;

2) histotoxic hypoxia - i.e. the action of catecholamines on myocardial enzymes.

Thus, with an increased need for O2 oxygen, the SAS is activated, catecholamines are released, and the following phenomena are observed from the myocardium:

1. Increased blood flow through the coronary arteries - this increases the delivery of oxygen O2.

2. Increase in the frequency and strength of heart contractions. This, on the one hand, is aimed at increasing the supply of oxygen O2, on the other hand, it in itself requires energy expenditure, shortens the diastole and worsens the blood supply to the myocardium.

3. Histotoxic hypoxia - a direct effect of catecholamines on myocardial enzymes. Leads to increased myocardial oxygen demand O2.

So, catecholamines not only dilate coronary vessels and increase coronary blood flow. They also have negative effects:

Absorption of oxygen O2 by the heart increases sharply, much more than it is necessary for mechanical work;

The need of the heart for oxygen O2 sharply increases.

Conclusion: even in normal conditions, with SAS irritation, the heart hardly covers the increased myocardial oxygen demand, despite the expansion of coronary vessels and an increase in myocardial blood supply. But normally, this emergency situation is justified by the fact that in the 1st (adrenal) phase of stress, this allows you to dramatically increase the work performed.

In pathology, this mechanism becomes a mechanism of damage.

Example: atherosclerosis. SAS stimulation increases myocardial oxygen demand O2, but this does not lead to simultaneous expansion of the coronary arteries and the volume of coronary blood flow does not increase. The reason is that the vessels affected by atherosclerosis cannot adequately expand. There are so-called "scissors" in the need and delivery of oxygen O2.

2. Influence of the parasympathetic nervous system. Irritation n. vagus results in coronary vasodilatation and an increase in O2 oxygen delivery with a simultaneous decrease in myocardial oxygen demand for O2. This reaction is small in magnitude, but constant.

3. Simultaneous excitation n. vagus and CAC. This is thought to underlie rest angina.

4. Perverted reactions of coronary vessels to catecholamines. This is a prolongation of the action of catecholamines on α-adrenergic receptors. The spasm phase lengthens, and the expected expansion does not occur at all. Situations: a) hypernatremia; b) inflammation of the vascular wall.

5. Pathological reflexes. There are: a) unconditional;

b) conditional.

Unconditioned reflexes - viscero-visceral and viscero-cutaneous. Example: cholecysto-cardiac, tonsillo-cardiac, gastro-cardiac reflexes.

Conditioned reflexes are a repeated combination of an external factor with irritation of a cortical area and internal pathological changes. Example: bad news on the phone → an attack of angina pectoris → the sound of a phone call provokes a pain attack.



Normally, the cardiovascular system optimally provides the current needs of organs and tissues for blood supply. dysfunction of the heart, 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 vascular 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, ischemic 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 "coloring", 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 biologically impaired outflow from the myocardium. active substances, metabolites and ions.

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 with normal level 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, more and more scientists now believe that real life CI is a consequence 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 for 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 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 mitochondria. The loss of potassium by cardiomyocytes is accompanied by an increase in its content in the interstitial fluid and blood. Due to this 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. On initial stage 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- this is a discrepancy between the coronary circulation and the energy needs of the myocardium, manifested by myocardial ischemia.

The main causes of coronary insufficiency:

• 1) a decrease in blood flow in the vessels with unchanged metabolic demands of the myocardium;
• 2) strengthening of the work of the heart with an increase in metabolic needs with the inability of the coronary vessels to increase blood flow;
• 3) a combination of vascular and metabolic factors.

Forms of coronary insufficiency

Distinguish between acute and chronic forms of insufficiency.

• Acute coronary insufficiency characterized by an acute discrepancy between blood flow and the metabolic demands of the myocardium, more often with altered than with unchanged coronary arteries of the heart.

This is manifested by attacks of angina pectoris, often severe disorders heart rate and conduction, ECG changes. Acute coronary insufficiency can lead to the development of myocardial infarction.

• Chronic coronary insufficiency characterized by a constant discrepancy between the blood supply and the metabolic needs of the heart muscle. A prerequisite for its development are structural changes in the coronary arteries (narrowing of the coronary bed).

Causes of coronary insufficiency, etiology and pathogenesis

Coronary insufficiency occurs in a variety of pathological processes: atherosclerosis of the coronary arteries (the most common cause), vasculitis (coronitis), infiltration of the coronary vessels by tumor cells, vascular injury, acquired and congenital heart defects and main vessels (aortic defects, pulmonary stenosis, anomalies of the coronary vessels), septic endocarditis, cardiomyopathies, some forms of myocarditis (for example, the Abramov-Fiedler type), syphilitic aortitis, dissecting aortic aneurysm, shock and collaptoid conditions, anemia and other heart diseases.

The development of acute coronary insufficiency is associated with a sudden violation of the patency of the coronary arteries due to their spasm, thrombosis or embolism. At the same time, the metabolic demands of non-ischemic areas of the heart muscle increase, which is accompanied by an increase in blood flow in the unchanged adjacent coronary vessels. In this case, redistribution of blood in favor of non-ischemic areas and increased ischemia in the area of ​​the affected artery (the “steal phenomenon”) is possible.

In the origin of non-coronary insufficiency may play a role pathological processes accompanied by a decrease in cardiac output and perfusion pressure in the system of coronary arteries (pronounced arterial hypotension, significant bradycardia, hypovolemia), as well as anemia, arterial hypoxia and impaired oxyhemoglobin dissociation in respiratory failure, carbon monoxide poisoning, benzene nitro compounds, etc. Even the maximum vasodilation of perfectly normal coronary arteries cannot satisfy the metabolic needs of the myocardium under these conditions. Depending on the time and intensity of the action of one or another factor, acute or chronic coronary insufficiency develops.

In origin Ph.D. metabolic (non-coronary or more often mixed) genesis, increased release of catecholamines during arousal matters sympathetic department autonomic nervous system (acute and chronic stressful situations, accompanied by psycho-emotional stress) or their excessive production by the adrenal glands. Under the influence of catecholamines, the need of the heart muscle for oxygen for their oxidation increases significantly. Coronary vessels altered by the atherosclerotic process (and even unchanged), often with inadequate spasms, are unable to provide sufficient blood supply, which leads to ischemia and even necrosis of certain sections of the heart muscle (the theory of the origin of coronary insufficiency, angina pectoris and myocardial infarction - W. Raab , 1963).

Pathogenetic significance in the occurrence of coronary insufficiency is also tachycardia, especially in combination with arrhythmias (paroxysmal tachycardia, tachyarrhythmia, frequent group extrasystoles). In these cases, the coronary circulation is impaired due to a decrease in coronary perfusion (shortening of diastole and a decrease in cardiac output) and an increase in the metabolic needs of the myocardium. If this happens against the background even moderately severe atherosclerosis coronary arteries, pathogenetic factors are summarized.

Chronic coronary insufficiency develops when the coronary arteries are damaged, narrowed or reduced in their ability to expand. In most cases, it is due to atherosclerosis of the coronary arteries, but may be associated with inflammatory changes, cicatricial deformity, infiltration (rheumatism, systemic diseases connective tissue, syphilitic arteritis, etc.). There are known cases of development of acute and chronic coronary insufficiency after a non-penetrating injury to the organs of the chest cavity (with impact, compression, blast wave, falling from a height). With injuries, embolism of the coronary arteries from the pulmonary veins, rupture of the coronary vessels, hemorrhage, the formation of a cardiac aneurysm, blood vessels are possible.

There is no direct and strict relationship between the degree of vasoconstriction and manifestations of chronic coronary insufficiency. This is due to the development of collateral circulation, in some cases functionally and organically complete, in others - defective.

Against the background of chronic coronary insufficiency, acute coronary insufficiency occurs more easily. At the same time, such a significant increase in the work of the heart or an increase in metabolic demands is not required.

The degree of chronic coronary insufficiency increases in the presence of heart failure, anemia, hypoxemia, thyrotoxicosis, arterial hypertension, heart defects that violate intracardiac hemodynamics.

Uneconomical work of the heart as one of the most important reasons chronic coronary insufficiency occurs with acquired and congenital heart defects, hypertrophy and dilatation of the heart (primarily with hypertension in the systemic and pulmonary circulation), violation of synchrony in the contraction of the left ventricle or changes in the configuration of its cavity (mainly with chronic aneurysm), hyperthyroidism and chronic anemia.

It is quite clear that the issues of etiology and pathogenesis of coronary insufficiency cannot be considered in isolation from those various diseases and pathological conditions that invoke it.

The pathoanatomical picture depends on the underlying disease, which leads to the development of coronary insufficiency and, above all, atherosclerosis. Not so rarely, morphological changes in the coronary arteries are not detected, especially in cases where non-coronary and non-cardiac factors play a role in the origin of coronary insufficiency.

Classification of coronary insufficiency

As already mentioned, coronary insufficiency can be acute, which is most often identified with angina pectoris, and chronic. In practical cardiology and currently used clinical classification chronic coronary insufficiency as one of the forms of coronary heart disease according to L. I. Fogelson (1955) with 3 degrees.

• I degree (mild form).

Attacks of pain (angina pectoris) occur rarely and only under the influence of pronounced physical stress or severe experiences. There are no clear indications of the presence of atherosclerotic changes in the arterial system, in particular the coronary arteries, in these patients. The appearance of a pain attack is associated with spasm of the coronary arteries with minor atherosclerotic changes in them, which are difficult to diagnose with modern methods.

• II degree (moderate form).

Attacks of pain in the region of the heart often occur under the influence of various external influences, mainly after physical exertion (fast walking, climbing stairs, etc.). Examination reveals atherosclerotic changes in the arterial system, primarily in the aorta. Most patients have ECG waveform changes. These changes are an expression of developing cardiosclerosis or a consequence of myocardial infarction. During an angina attack, there may be ECG changes and violation of the heart rhythm, which disappear with the end of the pain attack. In some cases, persistent changes in heart rate and conduction are found (extrasystoles, atrial fibrillation and various types of blockades). Under the influence of physical stress, attacks of pain and ECG changes appear, which disappear with the cessation of physical stress.

• III degree (severe form).

Frequent attacks of pain in the heart, occurring under the influence of minor physical effort or neuropsychic stress. Often there are attacks of angina pectoris at complete rest or in the middle of sleep, which are often accompanied by attacks of cardiac asthma. During the examination, significant atherosclerotic changes in the vascular system and cardiosclerosis are established, signs of a violation of the general circulation are often noted. The electrocardiographic picture corresponds to severe cardiosclerosis.

In more modern classification L. A. Myasnikova and V. I. Metelitsa (1969, 1972, 1973) took into account the data not only of clinical and electrocardiographic examination of patients, but also of bicycle ergometric and coronary angiography. According to this classification, 3 groups of patients are also distinguished, which to a certain extent corresponds to 3 degrees of chronic coronary insufficiency according to Fogelson.

• 1st group.

Coronary-metabolic disadaptation of a functional order. This includes patients with initial symptoms of atherosclerosis of the coronary arteries with a functionally underdeveloped collateral network. The disease is based on functional changes in the coronary circulation (spasm) and metabolic disorders. During a clinical examination, they have angina pectoris that occurs with pronounced physical effort or, especially, with neuropsychic overload. Angina pectoris can sometimes be conditioned reflex in nature. Such patients are often young, some of them have a history of myocardial infarction. At rest, changes in the electrocardiogram are mostly absent. They can be identified during functional tests. Tolerance to physical activity during a bicycle ergometric test is usually not changed. With coronary angiography, severe stenosis or occlusion in the coronary system is not detected.

• 2nd group.

Significant atherosclerosis with local coronary stenosis in some branches and underdeveloped collateral network in the affected area. These are predominantly middle-aged and elderly patients with frequent attacks angina pectoris, less often - angina pectoris and rest. A history of myocardial infarction is possible. Tolerance to physical activity (veloergometric test) in them, in contrast to patients of the first group, is often reduced. On the electrocardiogram there are changes (periodic or constant) characteristic of coronary insufficiency (changes S - T And T). With the help of selective coronary angiography, occlusion or severe stenosis (more than 75%) of at least one large coronary artery is detected.

• 3rd group.

Widespread stenosing atherosclerosis of all major branches of the coronary arteries with the most developed collaterals. In the metabolism of the myocardium, not only aerobic, but also anaerobic processes are of certain importance. Attacks of angina pectoris are associated with very limited physical activity, often occur at rest. Patients have a sharply reduced tolerance to physical activity. In the anamnesis - frequent repeated small- or large-focal myocardial infarctions in various parts of the myocardium. On the electrocardiogram, significant changes are usually detected, and with selective coronary angiography, a common stenosing process is detected.

Clinic and symptoms of coronary insufficiency

Coronary insufficiency is manifested by attacks of angina pectoris or its equivalents (for example, paroxysmal dyspnea), myocardial infarction, heart failure with the development of ischemic myocardial dystrophy and cardiosclerosis. Possibly atypical and clinically asymptomatic course coronary insufficiency up to the appearance of signs of heart failure or the onset of sudden death. In the presence of angina attacks, it is possible to clinically assess the severity of the course of chronic coronary insufficiency according to the above Fogelson classification.

Diagnostics

Among the auxiliary diagnostic methods highest value has electrocardiography under conditions of dosed physical activity. Segment depression is a reliable electrocardiographic criterion for coronary insufficiency. S - T, occurring during maximum (submaximal) physical activity or some time later (2 - 5 minutes). Cardiac arrhythmia and conduction disturbances that occur during exercise stress tests, are also considered as indirect sign coronary insufficiency.

The most widespread bicycle ergometric test. On a special device such as a bicycle, sitting or lying down, an ever-increasing physical activity is given (constantly every 3 or 5 minutes or intermittently with rest intervals) until either pain syndrome or changes in the electrocardiogram appear. Normally, signs of coronary insufficiency appear at a load of 150-160 W, with chronic coronary insufficiency - at a lower load. At the same time, the lower the tolerance to physical activity, the more pronounced coronary insufficiency.

A test with a dosed physical activity can also be carried out on a treadmill (a tape moving at a variable speed along which the patient walks).

In the absence of a bicycle ergometer or treadmill, you can carry out Master's test on a two-step ladder (height and width of each step 22.5 cm, ladder height 45 cm and length 65 cm). The subject during a certain time goes up and down the stairs. The number of ascents is determined according to a special table (taking into account the sex, age and weight of the patient). An electrocardiogram is recorded before, immediately after the test, after 2 and 6 minutes.

The test is performed within 1.5 minutes. With absence ischemic changes myocardium, a double test of the Master is performed (up and down the stairs for 3 minutes). For the diagnosis of chronic coronary insufficiency, a double Master's test is mainly used.

Other methods, including the method of rapid electrical stimulation of the atria, have not yet received wide distribution.

Positive stress tests indicate the presence of coronary insufficiency, make it possible to determine the severity of its clinical manifestations, but do not give a morphological characteristic of the lesion of the coronary arteries of the heart. Negative results These tests do not exclude the presence of coronary insufficiency. Coronarography is used to directly assess the state of the myocardial arterial system and identify the localization, extent and severity of stenotic or occlusive lesions of the coronary vessels of the heart, as well as the compensatory possibilities of collateral circulation.

Coronary angiography- X-ray method of intravital study of the coronary arteries of the heart by contrasting them. Selective coronary angiography is usually used, when a contrast agent is injected directly into each (left and right) coronary artery. Coronary angiography is indicated for chronic coronary insufficiency (chronic coronary heart disease), especially without typical electrocardiographic changes, post-infarction heart aneurysm in case of its intended surgical treatment, congenital anomalies coronary arteries.

In case of previously diagnosed chronic coronary insufficiency (with the obligatory use of samples with dosed physical activity), coronary angiography is performed in cases of proposed surgical treatment (imposition of aortocoronary anastomosis) to clarify the nature, degree and localization of coronary circulation lesions.

The results of tests with dosed physical activity (mainly veloergometric tests) in patients with chronic coronary insufficiency in 80-85% of cases coincide with the data of coronary angiography, although there is no complete correspondence between ECG changes during dosed physical activity and data from coronary angiography or scintigraphy. With the functional nature of acute myocardial ischemia, pathological changes on coronary angiograms are often absent or very slightly expressed.

Treatment

In addition to targeted treatment of the underlying disease, it is also necessary to stop anginal attacks and prevent angina attacks in the interictal period. The latter includes the complex use of a number of antianginal agents, i.e., is aimed at the treatment of chronic coronary insufficiency.

Complex treatment of coronary insufficiency

Complex therapy insufficiency of the coronary circulation includes:

• 1) general events
- fight against risk factors for coronary heart disease (correct alternation of work, rest and sleep, increased physical activity, exercise therapy, exclusion of overeating, smoking and alcohol, diet, normalization of body weight, spa treatment, treatment of hypertension and diabetes mellitus and etc.);
• 2) special treatment:
the use of antianginal (prevention and relief of angina attacks) and antiarrhythmic (prevention and treatment of rhythm and conduction disturbances) agents;
• 3) other types of therapy:
anticoagulants, lipid-lowering agents, treatment of heart failure, etc.

Chronic coronary insufficiency is usually treated with drugs:

• 1) vasodilators
- a group of nitrates (nitroglycerin for the relief of seizures, sustak, nitrong, nitromak retard, erinite, nitrosorbitol for prevention), carbocromen (intecordin, intensain), dipyridamole (curantil), diphril (corontin), lidoflazin, verapamil, purine and isoquinoline derivatives, chloracizine and etc.;
• 2) drugs that affect the adrenergic innervation of the heart
- monoamine oxidase inhibitors (iprazid, nialamide), beta-blockers (anaprilin and its analogues inderal and obzidan, trazikor, visken, aptin, etc.), beta- and a-blockers (amiodarone), beta-adrenergic receptor stimulants (oxyphedrine, nonahlazine) ;
• 3) anti-bradykinin agents
- parmidin (prodectin, anginin);
• 4) anabolic agents
- methandrostenolone (dianabol, nerobol), phenobolin (nerobolil), retabolil, potassium orotate, inosine (inosie-F);
• 5) other means
- pyridinol-glyoxylate (glio-6), methyluracil, mercazolil.

Among vasodilators, coronary insufficiency is most often treated with nitrates (for the relief and prevention of angina attacks), carbocromen, dipyridamole and verapamil are used. The latter has not only antianginal, but also antiarrhythmic effect; among antiadrenergic drugs - beta-blockers, amiodarone (cordarone), oxyphedrine and nonahlazine. Among the last two (3rd and 4th) groups, it is difficult to give preference to any drug: they mainly serve as a background when prescribing drugs from the first two groups.

Complex application drugs of the above groups has a coronary dilating effect, increases the volume of coronary perfusion, reduces the metabolic demand of the myocardium, protects the myocardium from hypoxia and reduces the work of the heart, improves hemodynamics and facilitates cardiohemodynamics by reducing coronary inflow and reducing cardiac output resistance, improves microcirculation. Ultimately, it reduces or eliminates the discrepancy existing in coronary insufficiency between the energy demands of the myocardium and its blood supply.

Chronic coronary insufficiency should be differentiated depending on which degree (1st, 2nd or 3rd according to Fogelson) or which clinical group (1st, 2nd or 3rd according to Myasnikov and Metelitsa ) can be attributed to patients (see classification) and, depending on this, therapy is carried out.

Below are the main drugs recommended for patients in each of the clinical groups. Patients of the first group are prescribed sedatives, tranquilizers and any vasodilators; patients of the second group - the same drugs and additionally beta-blockers, antiadrenergic drugs such as amiodarone and anti-bradykinin drugs (prodectin); patients of the third group, in addition to sedatives, tranquilizers and vasodilators, are recommended adrenoblockers, anti-thyroid drugs (mercasolil), drugs that increase myocardial tolerance to hypoxia (glio-6), as well as anabolic hormones

In addition to these drugs, heparin has recently been recommended for the treatment of coronary insufficiency. In coronary heart disease, heparin has an anticoagulant, analgesic and anti-catecholamine effect, improves coronary circulation and microcirculation, has antihypoxic, antidystrophic, antiallergic, antihistamine and hypolipidemic effects, improves the energy supply of the heart, regenerative processes and increases myocardial contractility, stabilizes the permeability of connective tissue structures and cell membranes .

Heparin is prescribed intravenously, intramuscularly, and more recently subcutaneously (deeply under the skin in the epigastric region) 1-2-3 times a day, 5000-10,000 IU for 10-15 days or more, or, as in myocardial infarction, i.e. in higher parenteral doses (10,000-20,000 IU every 4 hours, total 60,000-120,000 IU per day under the control of blood coagulation) for 3-5 days, followed by a transition to lower doses of heparin, or for anticoagulants indirect action. The tactics of using heparin depends on the severity and degree of coronary insufficiency, as well as the severity of the pre-thrombotic state.

With the ineffectiveness of conservative treatment, the question of coronary artery bypass surgery is raised. The prognosis for coronary insufficiency is always unfavorable, especially if myocardial infarction develops. Prevention depends on the etiology of the underlying disease.

Spicy coronary syndrome: causes, risk factors, treatment, chronic form insufficiency

Definition acute coronary syndrome (OKS) combines the signs characteristic of a sharp exacerbation stable form. In fact OKS can not be called a diagnosis, it's just a set of manifestations (symptoms), characteristic of both the pattern of development and the unstable one.

Doctors use the term acute coronary syndrome for an approximate assessment of the patient's condition and the provision of adequate assistance even before the final diagnosis is established.

Anatomy of the myocardial blood supply system

Blood enriched with oxygen goes to myocardium(cardiac muscle) through the arteries located in the form of a crown on its surface, and the venous, with a high content of carbon dioxide and metabolic products, is discharged through the veins. It is due to the resemblance to the royal attribute that the coronary vessels of the heart were called "coronary" in the Russian version, and in the Latin accepted in medicine - precisely "coronary" (from "corona" - a crown). The great Leonardo da Vinci made the first anatomical sketches human organs, he came up with some, so poetic, names.

From lyrics, let's move on to utilitarian comparisons, so that complex things become simpler and clearer. So any wall arteries has a peculiar standard of construction, similar to the well-known braided water hose. Outside - a dense layer of connective tissue, then - the muscular part, it is able to contract and relax, creating a pulse wave and helping blood flow. Then - the inner shell, the thinnest and perfectly smooth intima, or endothelium improves blood flow by reducing friction. It is with her that the problems of most "heart" patients are associated. coronary heart disease, in the anatomical sense, begins with damage to the inner shell coronary arteries.

For metabolic disorders lipids, at the border of the muscle layer and intima cholesterol can accumulate and form conglomerates - soft. The endothelium above them rises and becomes thinner, as a result, a thin layer of cells breaks through and an elevation is formed inside the artery.

The blood flow gives local eddies and slows down, creating conditions for new deposits and precipitation of insoluble calcium salts - them. Such “grown up” plaques, with uneven and hard calcifications, are already very dangerous: they can ulcerate, damaging the muscular layer of the arteries; thrombotic masses are deposited on them, reducing the lumen until it is completely blocked. Eventually - ischemia, angina pectoris, heart attack, it is in this sequence that events unfold.

Reasons for the development of ACS

Development mechanisms ( pathogenesis) are the same for all ischemic, that is, associated with a lack of oxygen, heart diseases, including for acute coronary syndrome. There are only two reasons that disrupt the normal movement of blood through the arteries: change in arterial tone And reduction of their lumen.

1. Spasm of the vascular wall may result from increased emission adrenaline such as in a stressful situation. The expression "heart clenched in the chest" accurately describes the condition of a person with a brief attack of ischemia. A brief lack of oxygen is easy compensated: heart rate (HR) increases, blood flow increases, oxygen supply increases, well-being and mood become even better.

People who are keen on extreme sports and recreation constantly get short adrenaline "attacks" on the heart and the pleasant sensations associated with them - joyful excitement, an influx of energy. The physiological bonus of any, even small, loads is a decrease in the sensitivity of coronary vessels to spasm, and hence ischemia prevention.

If the stressful situation drags on (the time varies depending on the “training” of the heart), then decompensation phase. Muscle cells consume an emergency supply of energy, the heart begins to beat slower and weaker, carbon dioxide accumulates and reduces the tone of the arteries, the blood flow in the coronary arteries slows down. Accordingly, the exchange in the heart muscle is disturbed, part of it may become dead ( necrosis). Foci of necrosis of the muscular wall of the heart are called myocardial infarction.

2. Decrease in the lumen of the coronary arteries is associated either with violations of the normal state of their inner membrane, or with the blocking of the blood flow by a thrombus ( blood clot, atherosclerotic plaque). The frequency of the problem depends on risk factors, with prolonged exposure leading to metabolic disorders and education.

Main external factors:

• Smoking - general intoxication, violation of the cells of the inner layer of the arteries, increased risk thrombus formation;
• Unbalanced diet -; inadequate intake of proteins to the needs of the body; change in the balance of vitamins and trace elements; metabolic imbalance;
• Malaya physical activity- "untrained" heart, decrease in the force of contractions of the heart, deterioration in the supply of oxygen to the tissues, accumulation of carbon dioxide in them;
• Stress - constantly increased adrenaline background, prolonged arterial spasm.

Agree, the name "external" is not accidental, their level can be lowered or increased by the person himself, just by changing the way of life, habits and emotional attitude to what is happening.

As time passes, the quantitative effect of risks accumulates, there is a transformation into qualitative changes - diseases that are already internal factors risk acute coronary insufficiency:

1. Heredity- features of the structure of blood vessels, metabolic processes are also transmitted from parents, but as relative risk factors. That is, they can be both aggravated and significantly reduced, avoiding external factors.
2. WITH persistent increase in blood lipids and- deposits in the arteries in the form of atherosclerotic plaques with narrowing of the lumen, myocardial ischemia.
3. ABOUT obesity- an increase in the total length of the vessels, an increased load on the heart, thickening of the muscle wall ().
4. - consistently high blood pressure figures, changes in the walls of the arteries (sclerosis) with a decrease in their elasticity, congestive manifestations - edema
5. - blood viscosity and the risk of blood clots increase, changes in arterioles (the smallest arterial vessels) lead to ischemia of organs, including myocardium.

Combination several factors increases the likelihood of blood clots that completely block the heart's own arteries. The consequence of the development of events according to this scenario will be sudden coronary death , the second most common (after myocardial infarction) outcome of acute coronary syndrome.

Clinical forms of ACS and the degree of risk for the patient

There are two main forms of ACS:

• Unstable angina- retrosternal pain, characteristic of a heart attack, which appeared for the first time or already repeatedly, immediately after physical or emotional stress, or in a calm position.
• myocardial infarction- necrosis (necrosis) of the muscular wall of the heart. Depending on the area of ​​the lesion, small-focal () and extensive are distinguished, according to localization - according to the accepted names of the walls of the heart - anterior, lateral, posterior diaphragmatic and interventricular septum. The main life-threatening complications are fatal and.

Classification is important both for assessing the severity of the condition and for analyzing the level of risk of sudden coronary death(comes no more than 6 hours after the onset of the attack).

high risk

presence of at least one of the following:

1. An attack of angina pectoris for more than 20 minutes and to the present;
2. Pulmonary edema (difficulty breathing, wheezing, pinkish frothy sputum, forced sitting position);
3. On the ECG: a decrease or rise in the ST segment of more than 1 mm above the isoline;
4. Angina pectoris with a decrease in pressure in the arteries;
5. Laboratory: turn of the level of markers of myocardial necrosis.

Medium Risk

Discrepancy with high-risk items, or the presence of one of the mentioned signs:

1. An attack of angina less than 20 minutes, which stopped when taking nitroglycerin;
2. Angina at rest less than 20 minutes, which stopped after taking nitroglycerin;
3. Night attacks of retrosternal pain;
4. Severe angina, first appeared within the last 14 days;
5. Age over 65 years;
6. On the ECG: dynamic changes in the T wave to normal, Q waves more than 3 mm, a decrease in the ST segment at rest (in several leads).

low risk

in case of discrepancy with the criteria of high and medium risk:

1. More frequent and more severe than usual seizures;
2. Lower level of physical stress that causes an attack;
3. Angina appeared for the first time, from 14 days to 2 months;
4. On the ECG: a normal curve in accordance with age, or no new changes compared to previously obtained data.

How does acute coronary syndrome manifest?

Main symptoms acute coronary insufficiency are few and characteristic for each form of ACS.

• First and the most important feature- severe, constant pain behind the sternum, compressing, burning or squeezing in nature. The duration of an attack can vary from half an hour to several hours, but there are cases when patients suffered pain that lasted more than a day. Many complain of irradiation (conduction of pain impulses through local nerve endings) in the left upper part of the body - the shoulder blade, arm and hand (little finger area), neck and lower jaw. With myocardial infarction with localization in the posterior diaphragmatic wall of the heart, pain can focus only in the region of the costal angle, at the junction of the ribs with the sternum.
• The pain begins either immediately after physical exertion, or against the background of complete rest - at night or in the early morning, when the person is still in bed.
• The reaction of the nervous system to extreme stress: a state of excitement and extremely restless. Characterized by a feeling that only intensifies compared to the onset of the attack. Self-control is minimal, consciousness is confused.
• The skin is pale, a cold sweat appears on the forehead. The patient feels a constant lack of air, tries to take a more comfortable position for inhalation (orthopnea), asks for a pillow higher or tries to sit down.

What treatment can help before the arrival of the doctor?

Further treatment tactics are determined by the doctor, it depends on the final diagnosis made on the basis of electrocardiogram data and biochemical research blood. Patients with acute coronary insufficiency must hospitalized.

Diagnostic tests for ACS

Electrocardiogram and its meanings in various forms of ACS

Coronary angiography (coronography)

Introduction to the arteries x-ray contrast medium, which allows you to visualize the coronary pattern, assess the degree occlusion(overlapping) of vessels. The method has a leading place in the diagnosis ischemic lesions hearts. The risk of complications of the procedure is no more than 1%, there are no absolute contraindications, relative ones are acute renal failure, shock conditions.

Disadvantages: exposure to 6.5 mSv

Execution is possible only after making an appropriate entry in the medical history (separate protocol) about the indications, and after the consent of the patient or his next of kin.

Computed tomography (CT)

Allows you to identify stenosis of the coronary arteries, atherosclerotic plaques of various sizes and densities. Disadvantage: The patient is asked to hold their breath for a few seconds to obtain high-quality images.

electron beam CT: high temporal resolution, the required breath holding is only 1-2 seconds, scanning in layers of 1.5 - 3 mm, the entire heart is examined in 1-2 respiratory pauses.

Multilayer CT: The x-ray tube rotates rapidly around the patient, only one breath-hold is needed to obtain a complete image of the heart.

Disadvantages of the CT method: irradiation (from 1 mSievert to 3.5 mSv), intravenous administration of an iodine-containing contrast agent - contraindications for allergic reactions for iodine.

MRI of the heart(Magnetic resonance imaging)

Allows you to take layered shots with wide view, in any plane. Measurements of arterial blood flow and filling of the atria and ventricles are possible, the blood supply to the myocardium and the characteristics of heart contractions are assessed. The patient is not exposed to ionizing radiation (radiation) at all.

Treatment in a hospital

Endovascular(intravascular) and surgical methods to restore blood flow in the coronary arteries:

• And. Through the artery of the thigh, the catheter is inserted into the coronary artery, at its end the balloon is inflated, expanding the lumen of the artery. Then a prosthesis is installed, resembling a metal spring - a stent, which strengthens the wall of the coronary vessel.
• . Using a heart-lung machine (with cardiac arrest), or in conditions of a working heart, bypass routes (shunts) are formed around the affected area of ​​the coronary arteries. According to them, normal blood flow in the heart muscle is recreated.
• Direct coronary atherectomy. For this, a cylindrical device with a side "window" is used, located at the end of the catheter. It is fed under the plaque, cuts it off with a rotary knife and removes it.
• Rotational ablation. The tool is a special micro-drill ( rotablator), designed to remove calcified plaques. Rotation speed 180,000 rpm, equipped with an elliptical tip. Introduced into the artery, it grinds the plaque into microscopic fragments, freeing the way for blood flow. In the future, it is desirable to stenting. The method is not shown thromboses.

Video: acute coronary syndrome and resuscitation

Chronic coronary insufficiency

The concept of " coronary insufficiency" means a state of reduced blood flow through the coronary vessels. Unlike the acute form, chronic coronary insufficiency develops gradually, as consequence atherosclerosis, hypertension or diseases leading to "thickening" of the blood ( diabetes). All chronic forms of insufficiency of the coronary circulation are united under the name "ischemic heart disease" or " coronary disease hearts."

The most common cause of coronary insufficiency is atherosclerosis, and the severity of the pathology often depends on the degree of vascular neglect.

The main symptoms of chronic coronary insufficiency similar at various forms and functional stages of the disease:

1. Shortness of breath, dry cough - signs of stagnation in a small circle blood circulation, edema of intercellular spaces lung tissue (interstitial edema) and pneumosclerosis (replacement of active tissue with connective tissue);
2. Compressive, dull pains of the type of angina that occur after exercise (walking long distances or up stairs; after a heavy meal or nervous tension);
3. Digestive system disorders: nausea, flatulence (bloating);
4. Increased frequency of urination.

Diagnostics

An approximate diagnosis is made after listening to complaints and examining the patient. For the final diagnosis, laboratory and instrumental studies are needed.

Standard Methods:

• Complete blood count: detailed formula, ESR;
• Biochemical: lipoproteins, transferases, markers of inflammation;
• Blood clotting: the degree of tendency to form blood clots;
• Coronary angiography: the level of overlap of the lumen of the coronary arteries;
• : the degree of myocardial ischemia, its conductive and contractile ability are determined;
• Chest x-ray, ultrasound: assessment of the presence of other diseases, study of the cause of cardiac ischemia.

Treatment of chronic coronary insufficiency (principles)

1. Stabilize the course of the underlying disease that caused myocardial ischemia (atherosclerosis, hypertonic disease, diabetes);
2. Reduce the impact of external risk factors (smoking, physical inactivity, obesity, stress, inflammation);
3. Prevention of angina attacks (, soothing, reducing blood viscosity means);
4. If necessary, the use of surgical methods (angioplasty, bypass surgery).

Target complex treatment - provide the heart muscle with a normal supply of oxygen. Surgical methods are indicated only in those cases when they are recognized as the most effective for this patient.

Chronic form of coronary insufficiency never not completely cured Therefore, doctors give the following recommendations to people with such a diagnosis:

• Maintain an optimal metabolic rate for your age: normalization of body weight, balanced diet with restriction of fats, intake of vitamin-mineral complexes and Omega-3 (polyunsaturated fatty acids).
• Adequate daily physical activity: exercise, swimming, exercise on a stationary bike, walking (at least an hour a day) in the fresh air.
• Hardening: strengthening immunity and preventing colds.
• Periodic visits to the attending physician, tests and ECG - twice a year.

1. It has been proven that pets prolong a person's life. Just by petting the cat, you can normalize arterial pressure, and walking with a dog will put the nervous system in order. So consider getting a four-legged companion.

Most often, coronary blood flow is disturbed due to atherosclerosis or thrombosis of any branch of the coronary artery. However, the lumen reserve of these arteries is such that in the case of stenosis, a significant deterioration in blood supply is observed: at rest - only with a decrease in diameter by 80%, and under conditions of muscle load - by 50%. At the same time, the severity of hemodynamic disturbances depends on a number of additional factors. These include: the degree of development of collateral circulation, the tone of the coronary vessels, blood pressure (especially diastolic), hematocrit, the degree of dissociation of oxyhemoglobin.

Atherosclerosis of the coronary arteries. Main cause (about 99%) ischemic heart disease (CHD) is atherosclerosis of the coronary arteries. In turn, about 65% of all diseases of cardio-vascular system belongs to IBS. Atherosclerosis of the coronary arteries mainly affects large arteries located directly behind the coronary sinuses. As a rule, sclerotic plaques do not occur in deep arteries passing through the thickness of the myocardium.

thrombosis of the coronary artery. Sclerotic plaque or other damage to the endothelium can cause the formation blood clot. But with platelet aggregation and their interaction with the vascular endothelium, there is also an increased release of prostacyclin in the latter. The most active of them is thromboxane A 2, which is one of the most powerful vasoconstrictors. The mechanism of development of atherosclerosis is discussed in more detail below.

Spasm of the coronary arteries It is also a fairly common cause of impaired blood supply to the myocardium. But in a "pure" form, coronary spasm is rare. Most patients with spasm of the coronary arteries show signs of coronary atherosclerosis. Spasm of the coronary arteries causes significant ECG changes. Of these, the most typical are transient ST-segment elevation and Q-wave appearance. The genesis of vasospasm is discussed in more detail below.

Myocardial ischemia

Myocardial ischemia- a state of relative deficiency of oxygen supply with the blood in relation to the global or local needs of the heart for oxygen. Ischemia occurs when blood flow through the coronary vessels or with excessive hypertrophy of any part of the heart. The consequences of ischemia according to the time of their development are:

• violation of the process of electromechanical pairing, leading to a decrease or total loss contractile activity,
• development of abnormal electrical activity, which can lead to the occurrence of various kinds of arrhythmias,
• gradual damage to the structure of cells up to their irreversible death ( myocardial infarction).

In addition, changes in adrenergic innervation occur during ischemia. On the one hand, the density of a- and b-adrenergic receptors increases on the membrane of cardiomyocytes, and on the other hand, the release of the norepinephrine mediator increases. Moreover, the effect of an increased amount of catecholamines on the altered receptor population plays a role in vasospasm and the development of ischemic damage.

total ischemia. The complete cessation of coronary blood flow is accompanied by a relatively rapid depletion of macroergs. The depletion of oxygen reserves leads to the transition of the myocardium to the anaerobic pathway of ATP resynthesis. This is accompanied by:

a) the development of acidosis,

b) redistribution of ions and fluid between intracellular and extracellular spaces,

c) violation of contractility with subsequent changes in structures,

d) complete cell necrosis.

Moreover, irreversible changes in the cardiomyocytes of the left ventricle develop faster than in the right and conduction system.

Three phases of the development of the process in total myocardial ischemia can be distinguished.

• I - latent period,
• II - period of survival,
• III - the period of the possibility of restoring the functions of the heart.

In the latent period, the functions do not change yet, while oxygen comes from the "repositories": blood oxyhemoglobin, oxymyoglobin, physically dissolved. For example, in the muscle of the left ventricle there is about 2 ml / 100 g of such oxygen. But this oxygen is enough for no more than a few seconds (1-20 s) of a beating heart.

Usually, oxygen bound to myoglobin in the myocardium provides oxidative processes in those areas in which the blood supply is reduced for a short time or stops completely, as, for example, during left ventricular systole. Myoglobin begins to release oxygen when the O 2 tension in muscle cells drops below 10-15 mmHg.

As soon as the level of RO 2 drops below 5 mm Hg. the myocardium switches to the anaerobic pathway. But with glycolysis, a far insufficient amount of macroergs is produced to provide all the processes of a functioning heart. As a result, the level of creatine phosphate (CP) is the first to decrease. When the content of CF is below 3 µmol/g of the tissue of the left ventricle, there is a violation of contractility up to a complete stop. This happens due to the fact that hypoxia, intracellular acidosis on the membrane of cardiomyocytes blocks slow Ca 2+ channels, thereby inhibiting contractile activity.

Cardiac arrest occurs with some amount of ATP still remaining. Since the most energy-intensive function, contractility, is turned off, this energy is spent on maintaining the integrity of cardiomyocyte structures and maintaining ionic gradients. This manifests the effect of self-protection of the heart, since ATP "unspent" on contraction ensures the preservation of the viability of cardiomyocytes. And, if hypoxia is eliminated, then the remaining cardiomyocytes are again included in the performance of their pumping function. Due to this given period and called survival period. This period lasts no more than 5 minutes, and then under conditions of hypothermia at 25 ° C.

The deepening of the situation already leads to a decrease in the content of ATP. AND, if the ATP level falls below 2 µmol/g(for the left ventricle), That full recovery heart function does not occur. The duration of the phase from the onset of ischemia to the limit of reversibility of damage during anoxia is no more than 40 minutes.

Occurs with a heart attack pain syndrome causes emotional stress response. In this case, a complex of corresponding hormones appears in the blood, which, as a rule, have a vasoconstrictor effect. As a result, necrosis of the heart muscle deepens, which expands the zone of infarction.

Myocardial hypoxia and impaired ion permeability. Under conditions of ischemia or another kind of hypoxia, various disturbances in the state of plasma membranes occur, leading to a change in their ion permeability. First of all, the function of the sodium-potassium pump is disrupted. An increase in cell permeability leads to the accumulation of sodium and chloride ions inside them, and potassium ions outside. On the one hand, this contributes to the swelling of cardiomyocytes due to the attraction of water. On the other hand, a change in ionic permeability significantly disrupts the normal course of excitation processes.

Leakage of potassium ions from the cell leads to a decrease in the level of membrane potential. The loss of potassium during hypoxia is due to:

• an increase in the concentration of free calcium in the cell,
• a decrease in the activity of the sodium-potassium pump,
• the influence of the increased extracellular potassium itself, which in itself further increases the permeability of the membrane for this ion.

An increase in potassium permeability leads to a decrease in the duration of the action potential due to a shortening of the plateau phase. In addition, an increase in the extracellular concentration of potassium ions may be one of the reasons for the depolarization of the cardiomyocytes of the conducting system. As a result, the frequency of their spontaneous activity increases. This is seen in acute ischemia. When saving it this situation gradually disappears.

The most common changes during ischemia calcium transmembrane transport. As a result, cells are overloaded with free calcium. It is noteworthy that this occurs both during hypoxia and after its removal during reperfusion (see below). A decrease in the level of ATP and CF during hypoxia leads to a decrease in the activity of the calcium pump both on the sarcolemma of cardiomyocytes and in their sarcoplasmic reticulum. As a result, the excretion of this ion from the cytosol sharply decreases. The simultaneous decrease in the activity of the sodium-potassium pump contributes to the increase in the level of intracellular calcium, since this also leads to a decrease in the activity of the sodium-calcium conjugation.

It is very significant that, in this case, calcium ions in in large numbers accumulate in mitochondria. As a result, the activity of ATP synthesis in them decreases. Therefore, the less the heart tissue has managed to accumulate calcium ions in mitochondria during ischemia, the better will be the subsequent restoration of its function.

Usually in ischemic cells increasing refractory period. The period of absolute refractoriness can take up the whole time of the development of the action potential and even extend to diastole, and relative refractoriness can capture most of the diastole. Moreover, an abnormal relationship is often observed: the greater the heart rate, the longer the refractoriness period.

With prolonged ischemia, the nature of ion permeability in different parts of the focus can vary greatly. Along with the shortening of the repolarization process, there may also be its lengthening. One of the reasons for the changes that occur in cells on late stages ischemia, may be the influence of ischemic products. An increase in the content of lactate, lysophosphoglycerides, CO 2, acidosis slows down the repolarization of cardiomyocytes.

Myocardial infarction and tension in the heart wall. Naturally, with the increase in tension in the heart muscle itself during systole, one has to reckon with a number of pathological conditions. So, in a heart attack, when myocardial cells are destroyed or replaced by less durable connective tissue, in this place the wall of the heart begins to protrude. And during systole, especially of the left ventricle, the wall can burst.

Rice. 60. Swelling of the wall of a non-functioning area of ​​the myocardium.