Heart clinic. Clinic and diagnosis of coronary heart disease Heart disease clinic treatment

CORONARY ARTERY DISEASE

What is ischemic heart disease?

Coronary artery disease (CHD) is a collective term that includes a group of diseases characterized by an imbalance between the demand of the myocardium (heart muscle) for oxygen and its actual delivery. The cause of coronary artery disease is usually atherosclerosis of the coronary arteries.

How is CAD classified?

There are the following nosological forms:

1. Angina:

- stable angina pectoris (indicating the functional class);

- unstable angina;

- vasospastic (spontaneous) angina pectoris;

- first-time angina pectoris;

- progressive angina;

- early postinfarction or postoperative angina pectoris.

Ischemic heart disease (CHD, angina pectoris, heart attack. Pathogenesis, clinic, diagnosis, treatment)

Coronary artery disease

Introduction

Ischemic heart disease is the main problem in the clinic of internal diseases, in the materials of WHO it is characterized as an epidemic of the twentieth century. The reason for this was the increasing incidence of coronary heart disease in people in various age groups, a high percentage of disability, as well as the fact that it is one of the leading causes of mortality.

Currently, coronary heart disease in all countries of the world is regarded as an independent disease and is included in. The study of coronary heart disease has almost two hundred years of history. To date, a huge amount of factual material has been accumulated, indicating its polymorphism. This made it possible to distinguish several forms of coronary heart disease and several variants of its course. The main attention is drawn to myocardial infarction, the most severe and common form of acute coronary heart disease. Significantly less described in the literature are forms of coronary heart disease that occur chronically - these are atherosclerotic cardiosclerosis, chronic heart aneurysm, angina pectoris. At the same time, atherosclerotic cardiosclerosis, as a cause of death among diseases of the circulatory system, including forms of coronary heart disease, is in the first place.

Coronary heart disease has become notorious, almost epidemic in modern society.

Ischemic heart disease is the most important problem of modern health care. For a variety of reasons, it is one of the leading causes of death among the industrial population. developed countries. It strikes able-bodied men (to a greater extent than women) unexpectedly, in the midst of the most vigorous activity. Those who do not die often become disabled.

Coronary heart disease is understood as a pathological condition that develops when there is a violation of the correspondence between the need for blood supply to the heart and its actual implementation. This discrepancy can occur when the blood supply to the myocardium remains at a certain level, but the need for it has sharply increased, with the need remaining, but the blood supply has fallen. The discrepancy is especially pronounced in cases of a decrease in the level of blood supply and an increasing need for the myocardium in blood flow.

The life of society, the preservation of the health of the population has repeatedly posed new problems for medical science. Most of the time they are different. attracted the attention of not only doctors: cholera and plague, tuberculosis and rheumatism. Usually they were characterized by prevalence, difficulty in diagnosis and treatment, and tragic consequences. The development of civilization, the success of medical science pushed these diseases into the background.

Currently, one of the most acute problems, of course, is coronary heart disease. For the first time, the criteria for angina pectoris were proposed by the English physician W. Heberden in 1772. Even 90 years ago, doctors rarely encountered this pathology and usually described it as a casuistry. Only in 1910 V.P. Obraztsov and N.D. Strazhesko in Russia, and in 1911 Herrik in the United States of America gave classic description clinical picture myocardial infarction. Now myocardial infarction is known not only to doctors, but also to the general population. This is due to the fact that every year it occurs more and more often.

Coronary insufficiency occurs as a result of a deficiency in the supply of oxygen to the tissues of the heart. Insufficient supply of myocardium with oxygen can be the result of various reasons.

Until the 80s of the nineteenth century, the opinion prevailed that the main and only cause of angina pectoris (angina pectoris) was sclerosis of the coronary arteries. This was due to the one-sided study of this issue and its main morphological direction.

By the beginning of the twentieth century, thanks to the accumulated factual material, domestic clinicians pointed to the neurogenic nature of angina pectoris (angina pectoris), although the frequent combination of spasms of the coronary arteries with their sclerosis was not ruled out (E.M. Tareev, 1958; F.I. Karamyshev, 1962 ; A.L. Myasnikov, 1963; I.K. Shvatsoboya, 1970, etc.). This concept continues to this day.

In 1957, the World Health Organization's atherosclerosis panel proposed a term for acute or chronic disease heart resulting from a decrease or cessation of blood supply to the myocardium, due to a pathological process in the coronary artery system. This term was adopted by WHO in 1962 and included the following forms:

1) angina pectoris;

2) myocardial infarction (old or fresh);

3) intermediate forms;

4) ischemic heart disease without pain syndrome:

a) asymptomatic form, b) atherosclerotic cardiosclerosis.

In March 1979, WHO adopted a new classification of coronary artery disease, which distinguishes five forms of coronary heart disease:

1) primary circulatory arrest;

2) angina pectoris;

3) myocardial infarction;

4) heart failure;

5) arrhythmias.

Anatomical and physiological features of myocardial blood supply

The blood supply to the heart is carried out through two main vessels - the right and left coronary arteries, starting from the aorta immediately above the semilunar valves. The left coronary artery starts from the left posterior sinus of Vilsalva, goes down to the anterior longitudinal groove, leaving the pulmonary artery to the right of itself, and the left atrium and the ear surrounded by adipose tissue, which usually covers it, to the left. It is a wide, but short trunk, usually no more than 10-11 mm long. The left coronary artery divides into two, three, in rare cases four arteries, of which highest value for pathology, they have an anterior descending and circumflex branches, or arteries.

The anterior descending artery is a direct continuation of the left coronary artery. Along the anterior longitudinal cardiac sulcus, it goes to the region of the apex of the heart, usually reaches it, sometimes bends over it and passes to the back surface of the heart. Several smaller lateral branches depart from the descending artery at an acute angle, which are directed along the anterior surface of the left ventricle and can reach the blunt edge; in addition, numerous septal branches depart from it, perforating the myocardium and branching in the anterior 2/3 of the interventricular septum. Lateral branches feed the anterior wall of the left ventricle and give branches to the anterior papillary muscle of the left ventricle. The superior septal artery gives a branch to the anterior wall of the right ventricle and sometimes to the anterior papillary muscle of the right ventricle.

Throughout the entire length of the anterior descending branch lies on the myocardium, sometimes plunging into it with the formation of muscle bridges 1-2 cm long. For the rest of its length, its anterior surface is covered with fatty tissue of the epicardium.

The circumflex branch of the left coronary artery usually departs from the latter at the very beginning (the first 0.5-2 cm) at an angle close to a right one, passes in the transverse groove, reaches the blunt edge of the heart, goes around it, passes to the posterior wall of the left ventricle, sometimes reaches the posterior interventricular sulcus and in the form of the posterior descending artery goes to the apex. Numerous branches depart from it to the anterior and posterior papillary muscles, the anterior and posterior walls of the left ventricle. One of the arteries that feed the sinoauricular node also departs from it.

The first hepatic artery originates in the anterior sinus of Vilsalva. First, it is located deep in the adipose tissue to the right of the pulmonary artery, goes around the heart along the right atrioventricular sulcus, passes to the posterior wall, reaches the posterior longitudinal sulcus, and then, in the form of a posterior descending branch, descends to the apex of the heart.

The artery gives 1-2 branches to the anterior wall of the right ventricle, partly to the anterior septum, both papillary muscles of the right ventricle, the posterior wall of the right ventricle and the posterior interventricular septum; the second branch also departs from it to the sinoauricular node.

There are three main types of myocardial blood supply: middle, left and right. This subdivision is based mainly on variations in the blood supply to the posterior or diaphragmatic surface of the heart, since the blood supply to the anterior and lateral regions is fairly stable and not subject to significant deviations.

With an average type, all three main coronary arteries are well developed and fairly evenly developed. The blood supply to the entire left ventricle, including both papillary muscles, and the anterior 1/2 and 2/3 of the interventricular septum is carried out through the system of the left coronary artery. The right ventricle, including both right papillary muscles and the posterior 1/2-1/3 septum, receives blood from the right coronary artery. This appears to be the most common type of blood supply to the heart.

With the left type, the blood supply to the entire left ventricle and, in addition, the entire septum and partly the posterior wall of the right ventricle is carried out due to the developed circumflex branch of the left coronary artery, which reaches the posterior longitudinal groove and ends here in the form of the posterior descending artery, giving part of the branches to the posterior surface of the right ventricle.

The right type is observed with a weak development of the circumflex branch, which either ends before reaching the obtuse margin, or passes into the coronary artery of the obtuse margin, without extending to the posterior surface of the left ventricle. In such cases, the right coronary artery, after leaving the posterior descending artery, usually gives a few more branches to the posterior wall of the left ventricle. In this case, the entire right ventricle, the posterior wall of the left ventricle, the posterior left papillary muscle and partly the apex of the heart receive blood from the right coronary arteriole.

Myocardial blood supply is carried out directly:

a) capillaries lying between the muscle fibers, braiding them and receiving blood from the system of coronary arteries through the aterioles; b) a rich network of myocardial sinusoids; c) Viessant-Tebesia vessels.

Outflow occurs through the veins, going to the coronary sinus.

Intercoronary anastomoses play an important role in coronary circulation, especially in pathological conditions. There are, firstly, anastomoses between different arteries (intercoronary or intercoronary, for example, between the right and branches of the left coronary artery, circumflex and anterior descending artery), and secondly, colliterals connecting the branches of the same artery and creating both there would be workarounds, for example, between the branches of the anterior descending branch, extending from it at different levels.

There are more anastomoses in the hearts of people suffering from ischemic disease, so the closure of one of the coronary arteries is not always accompanied by necrosis in the myocardium. In normal hearts, anastomoses are found only in 10-20% of cases, and they are of small diameter. However, their number and magnitude increase not only in coronary atherosclerosis, but also in valvular heart disease. Age and gender by themselves have no effect on the presence and degree of development of anastomoses.

In a healthy heart, the communication of pools of various arteries occurs mainly through arteries of small diameter - arterioles and prearterioles - and the existing network of anastomoses cannot always ensure the filling of the pool of one of the arteries when a contrast mass is injected into another. Under conditions of pathology in coronary atherosclerosis, especially stenosing, or after thrombosis, the network of anastomoses increases sharply and, which is especially important, their caliber becomes much larger. They are found between branches of the 4th-5th order.

Etiology and pathogenesis of IHD

The adequacy of the coronary blood supply to the metabolic demands of the myocardium is determined by three main factors: the amount of coronary blood flow, the composition of arterial blood (primarily the degree of its oxygenation), and myocardial oxygen demand. In turn, each of these factors depends on a number of conditions. Thus, the value of coronary blood flow is determined by the level of blood pressure in the aorta and the resistance of the coronary vessels.

The blood may be less oxygenated, such as in anemia. Myocardial oxygen demand can increase sharply with a significant increase in blood pressure during exercise.

An imbalance between myocardial oxygen demand and its delivery leads to myocardial ischemia, and in more severe cases, to its ischemic necrosis.

In myocardial infarction, some part of the myocardium is necrotized, the localization and size of which are largely determined by local factors.

most common cause that determines the development of coronary heart disease is atherosclerosis of the coronary vessels. Atherosclerosis is the main cause of the development of coronary heart disease, myocardial infarction, for example, with occlusion of the coronary artery. It also plays a leading role in the most common mechanism for the development of large-focal myocardial infarction - thrombosis of the coronary arteries, which, according to modern ideas, develops both due to local changes in the intima of the vessels, and in connection with an increase in the tendency to thrombosis in general, which is observed in atherosclerosis.

Against the background of partial occlusion of the coronary artery, any reasons leading to an increase in myocardial oxygen demand can be a provoking, resolving factor. Such reasons can be, for example, physical and psycho-emotional stress, hypertensive crisis.

The functional capacity of atherosclerotically altered coronary arteries is significantly reduced not only because of the mechanical factor - the narrowing of their lumen. They largely lose their adaptive capabilities, in particular, to adequate expansion with a decrease in blood pressure or arterial hypokemia.

Serious importance in the pathogenesis of coronary artery disease is attached to the functional moment, in particular, spasm of the coronary arteries.

As an etiological factor in myocardial infarction, septic endocarditis (embolism of the coronary arteries with thrombotic masses), systemic vascular lesions with involvement of the coronary arteries, exfoliating aortic aneurysms with compression of the orifices of the coronary arteries, and some other processes can act. They are rare, accounting for less than 1% of cases of acute myocardial infarction.

Changes in the activity of the sympathetic-adrenal system are of no small importance in the pathogenesis of coronary heart disease. Excitation of the latter leads to increased release and accumulation in the myocardium of catecholamines (norepinephrine and adrenaline), which, by changing the metabolism in the heart muscle, increase the heart's need for oxygen and contribute to the occurrence of acute myocardial hypoxia up to its necrosis.

In coronary vessels not affected by atherosclerosis, only an excessive accumulation of catecholamines can lead to myocardial hypoxia. In the case of sclerosis of the coronary arteries, when their ability to expand is limited, hypoxia can also occur with a slight excess of catecholamines.

An excess of catecholamines causes disturbances in both metabolic processes and electrolyte balance, which contributes to the development of necrotic and degenerative changes in the myocardium. Myocardial infarction is considered as a result of a metabolic disorder in the heart muscle due to a change in the composition of electrolytes, hormones, toxic metabolic products, hypoxia, etc. These reasons are closely intertwined with each other.

In the pathogenesis of coronary heart disease, social issues are also of great importance.

WHO statistics indicate an extraordinary frequency of coronary heart disease in all countries of the world. Morbidity and mortality from coronary artery disease increases with age. When studying coronary insufficiency, a predominance of males was established, especially at the age of 55-59 years.

On March 13, 1979, the WHO adopted a classification in which the following five classes, or forms, of IHD are distinguished:

2. Angina

2.1. angina pectoris

2.1.1. emerging for the first time

2.1.2. stable

2.1.3. progressive

2.2. Angina at rest (synonymous with spontaneous angina)

2.2.1. A special form of angina pectoris

3. Myocardial infarction

3.1. Acute myocardial infarction

3.1.1. Definite

3.1.2. Possible

3.2. Past myocardial infarction

4. Heart failure

5. Arrhythmias.

In the definitions of WHO experts, clarifications are given for each of the named classes of IHD.

1. Primary circulatory arrest

Primary circulatory arrest is a sudden non-existence, presumably associated with electrical instability of the myocardium, if there are no signs allowing another diagnosis. Most often, sudden death is associated with the development of ventricular fibrillation. Death occurring in the early phase of a verified myocardial infarction is not included in this class and should be treated as death from myocardial infarction.

If resuscitation was not carried out or was not effective, then the primary circulatory arrest is classified as sudden death, which serves as an acute final manifestation of coronary artery disease. The diagnosis of primary circulatory arrest as a manifestation of coronary artery disease is greatly facilitated if there is a history of indications of angina pectoris or myocardial infarction. If death occurs without witnesses, the diagnosis of primary circulatory arrest remains presumptive, since death could also have occurred from other causes.

2. Angina

Angina pectoris is subdivided into exertional angina and spontaneous angina.

2.1. angina pectoris

Angina pectoris is characterized by transient attacks of pain caused by exercise or other factors leading to an increase in myocardial oxygen demand. As a rule, pain quickly disappears at rest or when taking nitroglycerin under the tongue. Angina pectoris is divided into three forms:

2.1.1. Angina pectoris, for the first time arising - the duration of existence is less than a month.

First-time angina pectoris is not homogeneous. It may be a precursor or the first manifestation of acute myocardial infarction, it may turn into stable angina pectoris or disappear (regressive angina pectoris). The prognosis is uncertain. The term is identified by many authors with the concept. with which one cannot agree.

2.1.2. Stable exertional angina - existing for more than one month.

Stable (resistant) angina is characterized by a patient's stereotypical reaction to the same load.

Angina pectoris is considered stable if it has been observed in a patient for at least one month. In most patients, angina pectoris can be stable for many years. The prognosis is more favorable than with unstable angina.

2.1.3. Progressive exertional angina is a sudden increase in the frequency, severity, and duration of attacks of retrosternal pain in response to exercise that previously caused pain of a habitual nature.

In patients with progressive angina pectoris, the usual stereotype of pain changes. Attacks of angina pectoris begin to occur in response to smaller loads, and the pains themselves become more frequent, more intense and longer. Accession of attacks of angina pectoris to attacks of angina pectoris often indicates a progressive course of the disease. The prognosis is worse in those patients in whom changes in the course of the disease are accompanied by changes in the final part of the ventricular ECG complex, which may indicate a pre-infarction state.

Complete elimination of coronary heart disease

Every organ needs a blood supply to perform its function. The heart, as the most sensitive and most active organ of the human body, is not excluded from these rules.

The heart is supplied with blood by two, right and left, coronary arteries. Both arteries originate from the ascending aorta and completely cover the heart with their branches.

These arteries are called coronary arteries because they encircle the heart like a crown, which can be seen in images depicting the vessels of the heart.

human heart

The ratio between the functioning and nutrition of the tissue of any organ can be disturbed for three reasons:

1. The volume of the tissue of this organ increases with its fixed blood circulation;

2. The blood supply to the tissue of this organ decreases due to vasoconstriction at a fixed volume;

3. Both options arise, i.e. the volume of the tissue of this organ increases and at the same time its blood circulation decreases.

This is the main mechanism for the occurrence of a lack of blood circulation in the heart. In most cases, the cause of an increase in the muscle mass of the heart (hypertrophy) is the load on the heart, which is mainly due to hypertension.

With age, due to the pathocomplex process, the coronary vessels become clogged, therefore, a contradiction arises and increases over time between a large volume of the heart and its insufficient blood circulation, therefore, the muscles of the heart cannot receive sufficient blood circulation.

There are many different opinions about the causes of coronary heart disease. However, like many other incurable diseases according to the current official medicine, coronary heart disease is no exception. According to the most naive theory put forward in this area, excessive consumption of salt, sugar, meat, and fat causes constriction and blockage of the coronary vessels. Others believe that this disease is genetic, i.e. transmitted by a hereditary factor. Some attribute this disease to human hypodynamia.

To date, the theory of the involvement of cholesterol and triglycerides in the occurrence of cardiovascular pathologies, in particular coronary heart disease and arrhythmias, occupies a leading position among all the proposed theories.

Since the 30s of the twentieth century, humanity, especially the medical world, suddenly faces the pathology of the cardiovascular system, accompanied by heart attacks, strokes. Doctors began an intensive search for a way out of this situation.

human coronary vessels

In the 50s, with the development of medical technology, it became possible to conduct laboratory studies to identify certain factors in human blood. It was these tests that indicated an increase in the level of cholesterol and triglycerides in the blood of people suffering from cardiovascular pathologies. Hastily, as required by the need of time, by primitivism of thinking, scientists concluded that the substances noted were involved in the occurrence of human cardiovascular pathologies, as well as heart attacks and strokes emanating from them.

This theory arose about 50 years ago, and drugs against cholesterol and triglycerides, about 30 years ago. According to the rules of logic and science, having eliminated the etiological factor in the occurrence of pathology, the disease itself should disappear forever. No one anywhere in the World can show at least one patient suffering from cardiovascular pathologies who would be cured of these diseases by using drugs against cholesterol and triglycerides. Although, based on the proposed theory, one would expect the complete elimination of this problem from human society. We have to observe a completely opposite picture: these problems have not disappeared anywhere, but on the contrary, they are confidently stepping forward and are observed in people younger and younger. If in the 30s of the twentieth century only residents of a limited part of Europe suffered from cardiovascular problems, today there is no country on globe, where 30–40% of the general and 80% of the average age of the population do not suffer from any disease of the cardiovascular system.

This theory has long been rejected in scientific circles, and the preservation and maintenance of this theory continues only for commercial purposes.

Ischemic heart disease has only one origin: the pathocomplex process.

Eliminating the pathocomplex process, it is possible to completely cure coronary heart disease in an individual, as we have proven in practice for thousands of patients.

The pathology of the cardiovascular system, according to official WHO data, has been a leading cause of death for many years, and this is understandable, because a complex multi-stage, but extremely fragile structure is subject to a number of external aggressive factors. Even having the opportunity to go to any doctor, but not having certain knowledge in this specialty, it can become a problem for the patient to find specialists or cardiological centers in Moscow and other cities of the Russian Federation.

Patient Cardiac Care Options

Before choosing a specific center where cardiac services are provided, it is important to decide what kind of help is needed in your particular situation?

There may be several options for cardiac services.

Applicant to the clinic - a healthy person who has no complaints about the work of the cardiovascular system. For example, a dispensary is needed. In this case, the scope of services will be as follows: an electrocardiogram with a transcript, a consultation with a therapist or a cardiologist. Almost any diversified medical center on a paid basis or a state polyclinic is able to provide such a spectrum.

Clinical visitor - a person with new symptoms(feeling of interruptions in the heart, pressure and pulse drops, retrosternal pain). These conditions can be emergency!

Pain behind the sternum or in the region of the heart is a serious reason to consult a cardiologist

If such symptoms occur, a visit to a specialist should not be postponed: if chest pain, non-standard increase / decrease in blood pressure, arrhythmia appear, you should call an ambulance, which will take you to the nearest cardiological hospital. The following procedures will be performed in the hospital: an electrocardiogram with interpretation, a blood test for specific markers that increase during a heart attack, ECHO-KG (ultrasound examination of the heart), consultations of specialists.

If necessary, medical procedures will be carried out and the patient can even be redirected to another (profile) clinic for instrumental diagnostics and surgical treatment (coronary angiography, stenting procedure). Not all hospitals in Moscow are engaged in such manipulations, but only multidisciplinary ones with cardiosurgical departments and departments in which cardiovascular procedures are performed. Such multidisciplinary hospitals include, for example, City Clinical Hospital No. 15 in the Veshnyakovsky district of Moscow.

Qualitative diagnostics in cardiology is the basis effective treatment

There are also separate, exclusively cardiological clinics that provide the full range of consultative, minimally invasive and cardiac surgery care. Such centers include well-known throughout Russia and the world - the Scientific Center for Cardiovascular Surgery named after Academician A.N. Bakuleva (NTSSSH) ("House of the Heart" on Rublevsky Highway and on the territory of City Clinical Hospital No. 1, Oktyabrskaya Ring Line metro station). The Bakulev Institute, headed for many years by an outstanding cardiac surgeon (L.A. Bokeria), is a huge complex that provides cardiological treatment for adults and children from all over the country. No less famous for the experience of its specialists and the complexity of the procedures performed - the Institute of Clinical Cardiology named after. A.L. Myasnikova.

Applicant to the clinic - a person suffering from a disease of the cardiovascular system for a long time. Depending on the specific nosology, such a patient should be referred to clinics of different profiles. Thus, with long-term arterial hypertension, hospitalization in a therapeutic hospital is necessary, where the optimal treatment regimen will be carried out.

There are therapeutic departments in every state clinic in Moscow. In the case of pathology of myocardial vessels, neck vessels, coronary disease with severe vascular stenosis, when the need for surgical treatment is obvious, it is carried out according to plan, after proper preparation. The clinic (polyclinic, department) in which the patient was seen earlier prepares all the necessary documents for contacting large cardiocenters (NSSH named after A.N. and many others).

Many of the listed centers have a permanent line of communication, through which you can clarify information on quotas for free treatment, the procedure for hospitalization, the list required documents and research. There is also the possibility of accessing via the Internet, e-mail to receive full information support for the patient.

You need to choose a doctor carefully, since the health of the patient depends on his professionalism.

Choice of specialized treatment and medical center

Thus, cardiological care today is a complex of complex, highly professional manipulations that require specialized equipment and competent personnel.

Despite the apparent complexity, it is not difficult to get qualified and free help if necessary, the first step in solving a cardiological problem will always be an outpatient link (a polyclinic at the place of residence, a private center with a consulting cardiologist and a general practitioner, a hospital outpatient department).

The receiving specialist will be able to assess the current state of the cardiovascular system and suggest further options for medical, surgical treatment and rehabilitation. It is precisely by working in a complex that the outpatient and inpatient links of medical care allow the patient to be directed to the necessary examinations and manipulations as quickly as possible.

Ischemic heart disease (CHD)- this pathology of the myocardium, due to the relative oxygen deficiency in the coronary blood flow. This deficit can be associated both with an absolute decrease in the efficiency of blood flow (for example, with atherosclerotic narrowing of the coronary arteries), and with a relative increase in myocardial oxygen demand, for example, with great physical exertion, extreme excitement, with an increase in the intensity of tissue metabolism due to thyrotoxicosis, etc. However, as a result of all these reasons, hypoxic changes in the myocardium develop, initially reversible, then organic (irreversible). IHD combines diseases such as angina pectoris, myocardial infarction and their intermediate forms.

Atherosclerosis ranks first among the causes of death and disability in the developed countries of the world. More than 95% of all persons over the age of 60 have vascular atherosclerosis. Every year in the United States, more than a million people develop a myocardial infarction.

Etiology. One of the main causes of coronary artery disease is atherosclerosis, i.e., excessive lipid deposition in the inner lining (intima) of the coronary arteries. It has been established that the atherosclerotic process begins already at the age of 20-30 (the stage of lipid stripes and spots), and then continues at different rates depending on the so-called risk factors. Risk factors are not the causes of coronary artery disease, but its necessary prerequisites.

Pathological anatomical data show that 20% of people aged 26-30 already have atherosclerosis of the coronary arteries.

The most important risk factor is a high level of cholesterol in the blood, which “triggers” the atherosclerotic process. With hypercholesterolemia above 260 mg% (due to the abuse of fatty foods or hereditary predisposition), coronary artery disease is steadily progressing.

It has been found that cholesterol and fatty acid have a direct damaging effect on the vessel wall (atherogenic effect), which "pushes" the atherosclerotic process. It is especially harmful to overeat before going to bed. In some individuals, hypercholesterolemia is hereditary, and they have complicated coronary heart disease (for example, myocardial infarction) occurs already in their youth, which is explained by increased synthesis of cholesterol and atherogenic low-density lipoproteins, and a decrease in the synthesis of protective high-density lipoproteins.

Hypercholesterolemia is supported by insufficient physical activity (physical inactivity), so typical for modern urban residents, as well as chronic nervous tension, overwork. It has been established that in physically inactive people the frequency of myocardial infarction increases by 3 times.

The next major risk factor for CHD is obesity. Body weight, exceeding the norm by 30% or more, in itself already limits physical activity of a person, creates an increased load on the cardiovascular system, contributes to hypoventilation of the lungs (due to the limitation of the excursion of the diaphragm). All this provokes IBS. It has been proven that overeating is harmful already in childhood.

The most important risk factors for coronary artery disease) include diabetes mellitus and increased blood pressure. With diabetes, tissue acidosis occurs, microcirculation worsens. It has been established that in Akita Prefecture (Japan), where residents consume about 25 g of salt per day, hypertension is sharply increasing, complicating coronary artery disease.

Note that in old age, the listed risk factors are usually summed up, which sharply enhances the atherosclerotic process. Significantly more often (2-3.6 times) ischemic heart disease observed in men; in women, estrogens have a certain protective effect.

A combination of risk factors (eg, hypercholesterolemia, hypertension, and smoking) greatly increases the risk of myocardial infarction.
Most researchers also include smoking (more than 10 cigarettes per day), alcohol abuse, and excessive consumption of tea and coffee as risk factors. It has been established that alcohol has a direct toxic effect on the myocardium, increases blood clotting, blood pressure, cholesterol and adrenaline levels, causes tissue acidosis and hyperglycemia, often with alcoholism there is a deficiency of food proteins.

With a high degree of atherosclerosis, there is a sharp thickening of the wall of the coronary arteries, parietal thrombosis in the area of ​​atheromatous plaques, deposition of calcium salts; sometimes the plaque covers the coronary artery in a circular manner, reducing its lumen to the thickness of a hair. Of course, these changes make it difficult for the arteries to expand; which is necessary during physical or emotional stress, and therefore oxygen starvation (ischemia) of the myocardium occurs.

The reserves of the coronary circulation are large, therefore, atherosclerotic vasoconstriction, even by 50%, is not yet clinically manifested, neither the patient nor the doctor yet suspect that the process of coronary artery disease has already gone far, and only when the coronary lumen is narrowed by 75%, symptoms of angina pectoris appear, changes in ECG data .

The most common ischemic heart disease in the Scandinavian countries, the USA, Western Europe, it is very rare in the developing and semi-colonial countries of Africa, Latin America, and Southeast Asia. Mostly persons engaged in mental work are ill.

The clinical manifestation of a sufficiently deep, but short-term (and therefore reversible) myocardial ischemia is angina pectoris. The main symptom of angina pectoris is pain in the region of the heart.

According to the clinical course, angina pectoris of exertion and rest are distinguished. Pain in angina pectoris is provoked by physical activity, most often localized behind the sternum, sometimes somewhat to the left, it is pressing or compressive in nature of varying intensity, most often the pain begins gradually, then intensifies. At the time of the attack, patients try to maintain a stationary position, they are afraid to take a deep breath, in some cases, there is pallor of the skin due to spasm of blood vessels, skin, increased sweating. Sometimes there are burning pains, they resemble heartburn, chest tightness, stiffness in the throat, neck, and a feeling of suffocation join. Typical irradiation of pain in the hands, often in the left on its inner surface to the little finger. Very often the pain radiates to the left shoulder blade, neck, lower jaw.

At the beginning of an attack of angina pectoris, there may be a feeling of numbness in the left arm, a feeling that goosebumps are crawling through the body. Pain can be in the nature of "shooting" or squeezing. Some patients have an urge to urinate and defecate. Sometimes nausea, vomiting, dizziness, trembling all over the body begin. Usually the attack lasts 5-10 minutes, less often - up to 30 minutes. All these are very important differential diagnostic symptoms.

During an attack, the pulse slows down or accelerates, blood pressure, as a rule, rises. The borders of the heart percussion remain unchanged, heart sounds are often muffled. In some cases, during an attack, extrasystoles may appear, very rarely an alternating pulse.
The attack in most cases stops quickly, 1-2 minutes after taking validol or nitroglycerin, which is also a differential diagnostic test.

After an attack, patients feel weakness, weakness for some time, and the pallor of the skin is replaced by hyperemia.
Cooling increases the flow of adrenaline from the adrenal glands into the blood. Patients in cold weather often have to stop. Usually the attack begins while walking, passes at the moment of stopping, then resumes again.

The main electrocardiographic signs of angina pectoris are ST segment displacement, T wave changes - its flattening, negativity or increase ("giant" T wave). It is characteristic that in all these cases the T wave is isosceles. If ST-segment depression and T-wave inversion persist after an attack, then chronic coronary insufficiency can be assumed.

It has been established that the most valuable for the early diagnosis of coronary insufficiency is an electrocardiographic test with dosed physical activity, less valuable is coronary angiography - a method of probing the aortic orifice with the introduction of a radiopaque substance into the coronary arteries. The picture of peripheral blood and biochemical tests do not change.

In elderly and senile people, a painless form of angina pectoris very often develops, manifested by shortness of breath or a significant circulatory disorder; sometimes a painful attack occurs against the background of paroxysmal tachycardia or atrial fibrillation.

Resting angina is manifested by paroxysmal anginal pain that occurs with minimal physical exertion (for example, turning in bed), with the slightest excitement, sometimes at night.

Very close to rest angina is such a form of IBO as a pre-infarction state. It is characterized by deep insufficiency of the coronary circulation and, as a rule, ends with myocardial infarction if the patient does not have time to prescribe adequate treatment.

Chest pain in a pre-infarction state has the same properties as in angina pectoris, however, pain attacks become constantly progressive, they become more frequent (up to 20-30 times a day), occur at night, their duration increases to 20-30 minutes, appear new radiation zones. A very characteristic symptom is the poor effect of nitroglycerin; sometimes it is possible to relieve pain only after taking 20-30 tablets of nitroglycerin or sustacamite. Therefore, the diagnosis of a pre-infarction state is based on a careful questioning of the patient, analysis of complaints and anamnesis.

There are also atypical variants of the pre-infarction state: asthenic (the patient is dominated by weakness, dizziness, insomnia, and the pain syndrome is not expressed), asthmatic (dyspnea increases), abdominal (pain is localized in the epigastric zone), arrhythmic, when the leading symptom is extrasystole, an attack of tachycardia , heart block, etc. It is easy to see that these options correspond to options for acute myocardial infarction, which often ends (without treatment) in a pre-infarction state.

Among the reasons causing the transition from angina pectoris to a pre-infarction state, there are nervous and mental overloads, conflicts in the family and at work, alcohol intake, smoking, etc. The ECG is characterized by a decrease in the height of the T waves in the chest leads (up to negative), moderately pronounced horizontal or arcuate displacement of the ST segment in the same leads. Unlike myocardial infarction, these changes are unstable, they normalize within 1-2 weeks (with adequate treatment of the patient).

There are no laboratory changes (blood changes, biochemical and enzymatic reactions) in the preinfarction state.

Myocardial infarction is the most formidable manifestation of coronary artery disease. In 20-25% of all cases, acute myocardial infarction is fatal, and in 60-70% of cases - in the first 2 hours of illness. Recall that in 20% of all cases of myocardial infarction, thromboembolic complications, persistent blockades and arrhythmias, and heart aneurysm are noted.

The classic description of the symptoms of acute myocardial infarction was given in 1909 by Russian doctors V.P. Obraztsov and N.D. Strazhesko. They identified 3 main clinical variants of the disease: anginal, asthmatic and gastralgic.

For the anginal variant, the leading symptom is retrosternal pain, as in angina pectoris it is only stronger (“morphine”), sometimes tearing, it does not disappear at rest and is not stopped by nitroglycerin.

A thorough analysis of the properties of pain will in most cases allow the paramedic to recognize myocardial infarction in the anginal version, even before taking the electrocardiogram. It has been proven that the irradiation of pain itself is not of great informative value, although the favorite zone of irradiation of anginal pain is the left arm (sometimes only the hand), the left shoulder blade, less often the neck, teeth, and tongue. However, every 4th case of myocardial infarction is atypical or asymptomatic.

The gastralgic (abdominal) variant of myocardial infarction is characterized by dyspeptic disorders: heartburn, nausea, vomiting, dysphagia, and "baking" pain in the epigastric region. Somewhat more often, this variant is observed with damage to the posterior diaphragmatic zone of the left ventricle. It is characteristic that the abdomen is usually soft, there is no irritation of the peritoneum and disorders of the stool.

Dyspeptic disorders are also observed in the anginal variant of myocardial infarction: pain in the epigastric region, flatulence, hiccups, they are explained by irritation of the celiac and sympathetic nerves and the release of biogenic amines - histamine, serotonin, bradykinin, etc.

Acute ulcers of the stomach and intestines, often with bleeding, in myocardial infarction are caused by arterial hypotension, shock. In patients, reflex paresis of the gastrointestinal tract is also possible.

In the asthmatic variant of myocardial infarction, the leading symptom is acute circulatory failure, manifested by cyanosis, cold sweat, severe shortness of breath, and a drop in blood pressure.

Auscultation of the heart during myocardial infarction reveals deafness of tones, sometimes systolic murmur, various arrhythmias, sometimes pericardial friction noise. Percussion borders of the heart are often expanded. Sometimes a patient with myocardial infarction has a sudden decrease in heart rate to 60-40 per minute, which usually indicates a complete atrioventricular blockade or bigeminia, this symptom should alert.

Due to the fact that clinical symptoms myocardial infarction is not always convincing, the electrocardiographic method of research is of decisive importance in the diagnosis.

The earliest electrocardiographic symptom - a convex rise of the ST segment in the zone corresponding to myocardial damage - is recorded already in the first hour of a heart attack. Somewhat later, a deep and wide Q wave is formed, reflecting necrosis of the heart muscle.

There is also a decrease in the amplitude of the R waves ("failure") in the zones corresponding to the infarction. Posterior basal myocardial infarction is not easy to recognize even with the help of electrocardiography - there are no “direct” infarct changes in any of the generally accepted leads, only in leads V1, V2 there are “mirror” ECG changes - an increase in R and T waves.

We emphasize the obligation to register an ECG in case of suspected myocardial infarction. Statistics show that 25% of all cases of acute myocardial infarction are not diagnosed on time, because either the ECG is not recorded or it is incorrectly assessed.

According to the electrocardiographic picture, an acute stage of myocardial infarction is distinguished, which lasts 5-7 days, a subacute stage (5-7 weeks) and a chronic (cicatricial) stage, which practically lasts a lifetime.

Quite typical for myocardial infarction is a moderate increase in body temperature (up to 37.5 ° C) from the 2nd to the 5-8th day. From the 1st to the 7th-10th day, neutrophilic leukocytosis (up to 9000-12000 per μl) is noted in the blood, a moderate acceleration of ESR from the 2nd to the 20-25th day, diverse shifts in the biochemical spectrum of blood. In cardiology clinics, the diagnosis of myocardial infarction can also be confirmed by assessing the level of creatine phosphokinase, lactate dehydrogenase and its isoenzymes.

Myocardial infarction is dangerous for its complications, the most typical are cardiogenic shock and cardiac arrhythmias. It has been established that shock in myocardial infarction is caused both by excruciating pain and re-irritation of the cells of the central nervous system, and by a drop in myocardial contractility due to the presence of an area of ​​necrosis and swelling of neighboring zones. Main feature cardiogenic shock - deterioration of microcirculation in vital organs: brain, heart, kidneys, liver.

Based on the analysis of hundreds of cases of acute myocardial infarction, it was found that systolic hypotension is below 100 mm Hg. Art. for more than 4 hours dramatically worsens the prognosis of the disease. A terrible complication of myocardial infarction is pulmonary edema due to left ventricular weakness. Early symptoms of pulmonary edema - increasing pallor, cyanosis, wheezing in the lungs, and then bubbling breath, the release of foamy fluid from the mouth.

Severe cardiac arrhythmias occur in 40% or more of all cases of myocardial infarction, they are caused by necrosis or edema of the conduction system of the heart, as well as a breakdown of extracardiac nervous and humoral regulation (“symptomatic storm”). Extrasystole is usually noted, there may be attacks of atrial fibrillation or flutter; various conduction disorders. The most formidable symptoms are group and early ventricular extrasystoles. Detailed diagnosis of arrhythmias is possible only with the help of electrocardiography. In 20% of all cases of myocardial infarction, cardiac arrest (asystole) is noted, in 8-10% - ventricular fibrillation. In 12-20% of all cases, thromboembolic complications are observed - heart attacks of the lungs, kidneys, and brain.

Ischemic heart disease is an acute or chronic myocardial injury that occurs as a result of a decrease or cessation of the supply of arterial blood to the heart muscle, which is based on pathological processes in the coronary artery system.

IHD is a widespread disease. One of the main causes of death, temporary and permanent disability worldwide. In the structure of mortality, cardiovascular diseases are in the first place, of which about 40% are accounted for by coronary artery disease.

Forms of ischemic disease

IHD classification (ICD-10; 1992)

1. angina pectoris
   • - Stable exertional angina
   • - Unstable angina
2. Primary myocardial infarction
3. Recurrent myocardial infarction
4. Old (earlier) myocardial infarction (postinfarction cardiosclerosis)
5. Sudden cardiac (arrhythmic) death
6. Heart failure (myocardial damage due to coronary artery disease)

The main reason for the disruption of myocardial oxygen supply is the mismatch between coronary blood flow and the metabolic needs of the heart muscle. This may be due to:

• - Atherosclerosis of the coronary arteries with a narrowing of their lumen by more than 70%.
• - Spasm of unchanged (little changed) coronary arteries.
• - Violations of microcirculation in the myocardium.
• - Increased activity of the blood coagulation system (or decreased activity of the anticoagulant system).

The main etiological factor in the development of coronary heart disease is atherosclerosis of the coronary arteries. Atherosclerosis develops consistently, undulating and steadily. As a result of the accumulation of cholesterol in the wall of the artery, an atherosclerotic plaque is formed. Excess cholesterol leads to an increase in plaque in size, there are obstructions to blood flow. In the future, under the influence of systemic adverse factors, the plaque is transformed from stable to unstable (cracks and ruptures occur). The mechanism of platelet activation and formation of blood clots on the surface of an unstable plaque is triggered. Symptoms aggravate with the growth of atherosclerotic plaque, gradually narrowing the lumen of the artery. A decrease in the arterial lumen area by more than 90-95% is critical, causing a decrease in coronary blood flow and deterioration of well-being even at rest.

Risk factors for coronary heart disease:

1. Gender (male)
2. Age >40-50 years
3. Heredity
4. Smoking (10 or more cigarettes per day for the last 5 years)
5. Hyperlipidemia (plasma total cholesterol > 240 mg/dL; LDL cholesterol > 160 mg/dL)
6. arterial hypertension
7. Diabetes
8. Obesity
9. Hypodynamia

Symptoms

Clinical picture of coronary artery disease

The first description of angina pectoris was offered by the English physician William Heberden in 1772: “... chest pain that occurs while walking and makes the patient stop, especially while walking shortly after eating. It seems that this pain, if it continues or intensifies, is capable of depriving a person of life; at the moment of stopping, all unpleasant sensations disappear. After the pain continues to occur for several months, it stops immediately when stopped; and in the future it will continue to arise not only when a person walks, but also when he lies ... " Symptoms usually first appear after the age of 50. In the beginning, they occur only during physical exertion.

The classic manifestations of coronary heart disease are:

• - Pain behind the sternum, often radiating to the lower jaw, neck, left shoulder, forearm, hand, back.
• - The pain is pressing, squeezing, burning, suffocating. The intensity is different.
• - Provoked by physical or emotional factors. At rest, they stop on their own.
• - Lasts from 30 seconds to 5-15 minutes.
• - Rapid effect of nitroglycerin.

Treatment of coronary heart disease

Treatment is aimed at restoring normal blood supply to the myocardium and improving the quality of life of patients. Unfortunately, purely therapeutic methods of treatment are not always effective. There are many surgical methods of correction, such as coronary artery bypass grafting, transmyocardial laser myocardial revascularization and percutaneous coronary interventions (balloon angioplasty, coronary artery stenting).

The "gold standard" in the diagnosis of obstructive lesions of the coronary arteries of the heart is considered selective coronary angiography. It is used to find out whether the narrowing of the vessel is significant, which arteries and how many of them are affected, in what place and for how long. In recent years, multislice computed tomography (MSCT) with intravenous bolus contrast has become increasingly popular. In contrast to selective coronary angiography, which is essentially an X-ray surgical intervention on the arterial bed, and is performed only in a hospital setting, MSCT of the coronary arteries is usually performed on an outpatient basis using intravenous administration of a contrast agent. Another fundamental difference may be that selective coronary angiography shows the lumen of the vessel, and MSCT and the lumen of the vessel, and, in fact, the vessel wall, in which the pathological process is localized.

Depending on the changes in the coronary vessels detected during coronary angiography, various methods of treatment can be offered:

Coronary artery bypass grafting is an operation that has been practiced for many years, in which the patient's own vessel is taken and sutured to the coronary artery. This creates a bypass route for the affected area of ​​the artery. Blood in a normal volume enters the myocardium, which leads to the elimination of ischemia and the disappearance of angina attacks. CABG is the method of choice for a number of pathological conditions, such as diabetes mellitus, stem disease, multivessel disease, etc. The operation can be performed with cardiopulmonary bypass and cardioplegia, on a beating heart without cardiopulmonary bypass, and on a beating heart with cardiopulmonary bypass. Both veins and arteries of the patient can be used as shunts. The final decision on the choice of one or another type of operation depends on the specific situation and the equipment of the clinic.

Popular at the time, balloon angioplasty has lost its relevance. The main problem is the short-term effect of the performed X-ray surgery.

A more reliable and, at the same time, minimally invasive method of restoring and maintaining a normal vessel lumen is stenting. The method is essentially the same as balloon angioplasty, but a stent (a small transformable metal mesh frame) is mounted on the balloon. When introduced into the narrowing site, the balloon with the stent is inflated to the normal diameter of the vessel, the stent is pressed against the walls and retains its shape permanently, leaving the lumen open. After the stent is installed, the patient is prescribed long-term antiplatelet therapy. During the first two years, control coronary angiography is performed annually.

In severe cases of obliterating atherosclerosis of the coronary arteries, when there are no conditions for CABG and X-ray surgical interventions, the patient may be offered transmyocardial laser myocardial revascularization. In this case, the improvement of myocardial circulation occurs due to the flow of blood directly from the cavity of the left ventricle. The surgeon places a laser on the affected area of ​​the myocardium, creating many channels with a diameter of less than 1 millimeter. The channels promote the growth of new blood vessels through which blood enters the ischemic myocardium, providing it with oxygen. This operation can be performed both independently and in combination with coronary artery bypass grafting.

After the elimination of aortocoronary stenosis, the quality of life is noticeably improved, working capacity is restored, the risk of myocardial infarction and sudden cardiac death is significantly reduced, and life expectancy increases.

Currently, the diagnosis of coronary artery disease is not a sentence, but a reason for active action to choose the best treatment tactics that will save lives for many years.

A healthy heart is a strong and round-the-clock muscular pump, only slightly larger than an adult's fist.

The heart consists of four chambers. The top two are the atria, the bottom two are the ventricles. Blood goes from the atria to the ventricles, after which it enters the main arteries through the heart valves (there are four of them). The valves allow blood to pass only in one direction, working like pool "skimmers" - opening and closing.

Heart defects are such changes in the structures of the heart (partitions, walls, valves, outgoing vessels, etc.), in which blood circulation is disturbed in the systemic and pulmonary circulation, or inside the heart itself. Defects are congenital and acquired.

Causes of the occurrence and development of heart defects

Between five and eight newborns out of a thousand have congenital heart defects. These occur in the fetus even in the womb, and quite early - between the second and eighth weeks of pregnancy. Doctors still cannot unequivocally diagnose the causes of most cases of congenital heart defects. However, something medicine is still known. In particular, the fact that the risk of having a child with a heart disease is higher if the family already has a child with the same diagnosis. True, the probability of having a defect is still not very large - 1-5%.

The risk group also includes future babies whose mothers abuse drugs or drugs, smoke or drink a lot, and have also been exposed to radiation. Potentially dangerous for the fetus are also infections that affect the body of the expectant mother in the first trimester of pregnancy (for example, diseases such as hepatitis, rubella and influenza).

Recent medical studies have also found that the risk of having a child with a congenital heart disease increases by 36 percent if the expectant mother is overweight. However, it is still not clear what is the connection between the development of heart disease in a baby and the obesity of his mother.

Acquired heart disease most often occurs due to rheumatism and infective endocarditis. Less commonly, syphilis, atherosclerosis and various injuries become the causes of the development of defects.

Classification of heart defects

Specialists divide the most severe and common heart defects into two groups. The former are caused by the fact that there are shunts (workarounds) in the human body. They carry oxygen-rich blood (from the lungs) back to the lungs. At the same time, the load that falls on the right ventricle and the vessels through which blood enters the lungs increases. These are the vices:

atrial septal defect. It is diagnosed if by the time of birth of a person, a hole has been preserved between the two atria

occlusion of the ductus arteriosus. The fact is that the lungs do not immediately begin to work in the fetus

ductus arteriosus is a vessel through which blood flows around the lungs

a ventricular septal defect, which is a "gap" between the ventricles

There are also vices associated with the fact that the blood encounters obstacles in its path, due to which the heart has a much greater load. These are problems such as narrowing of the aorta (coarctation of the aorta), as well as stenosis (narrowing) of the aortic or pulmonary valves of the heart.

Valvular insufficiency also belongs to heart defects. This is the name of the expansion of the valve opening, due to which the valve leaflets in the closed state are not completely closed, as a result of which part of the blood flows back. In adults, this heart disease can be based on the gradual degeneration of the valves in two types of congenital disorders:

The arterial valve consists of two leaflets (should consist of three). According to statistics, this pathology occurs in one person out of a hundred.

Mitral valve prolapse. This disease rarely causes significant valve insufficiency. It affects five to twenty people out of a hundred.

Not only are all the described vices completely self-sufficient, they are often found in different combinations.

The combination in which the defect of the interventricular septum, hypertrophy (enlargement) of the right ventricle, aortic displacement and narrowing of the exit from the right ventricle are simultaneously expressed is called Fallot's tetrad. This same tetrad often causes cyanosis ("cyanosis") of the child.

Acquired heart defects are formed in humans as failure of one of the heart valves or stenosis. In most cases, the mitral valve suffers - this is the one that is located between the left atrium and the left ventricle. Less common is the aortic valve, located between the left ventricle and the aorta. Even safer are the pulmonic valve (the one that separates the right ventricle and, you guessed it, the pulmonary artery) and the tricuspid valve that separates the right atrium and ventricle.

There are cases when both insufficiency and stenosis occur in one valve. Combined valvular defects are also not uncommon, when not one, but several valves are simultaneously affected.

About manifestations of heart defects

In the first years of life in children, congenital heart disease may not manifest itself at all. However, imaginary health lasts no longer than three years, and then the disease nevertheless floats to the surface. It begins to manifest as shortness of breath with physical activity, pallor and cyanosis of the skin. In addition, the child begins to lag behind peers in physical development.

The so-called "blue vices" are often accompanied by sudden attacks. The child begins to behave uneasily, is overly excited, shortness of breath appears and cyanosis of the skin (“cyanosis”) increases. Some children even lose consciousness. This is how seizures go in children under the age of two years. In addition, children of the "risk group" like to relax while squatting.

Another group of vices was characterized as "pale". They manifest themselves in the form of a child lagging behind their peers in terms of the development of the lower half of the body. In addition, starting from the age of 8-12, the child complains of shortness of breath, dizziness and headache, and also often experiences pain in the abdomen, legs and heart itself.

1. The concept of dysfunction of the heart muscle

Heart dysfunction. Many heart diseases, including primary damage to the heart muscle, eventually lead to myocardial, or congestive heart failure. Most effective ways its prevention consists in the treatment of arterial hypertension, the timely replacement of affected heart valves and the treatment of coronary heart disease. Even when congestive heart failure has developed, it is often possible to help the patient by using digitalis preparations, diuretics (diuretics), and vasodilators that reduce the workload on the heart.

Abnormal heart rhythms (arrhythmias) are common and may be accompanied by symptoms such as interruptions or dizziness. The most common rhythm disturbances detected by electrocardiography include premature contractions of the ventricles (extrasystoles) and a sudden short-term increase in atrial contractions (atrial tachycardia); these violations are functional, i.e. may occur in the absence of any underlying heart disease. They are sometimes not felt at all, but can also cause considerable anxiety; in any case, such arrhythmias are rarely serious. More severe rhythm disturbances, including rapid erratic atrial contractions (atrial fibrillation), excessive acceleration of these contractions (atrial flutter), and an increase in ventricular contractions (ventricular tachycardia), require the use of digitalis or antiarrhythmic drugs. To identify and evaluate arrhythmias in cardiac patients and select the most effective medicinal products Currently, continuous ECG recording is carried out throughout the day using a portable device, and sometimes through sensors implanted in the heart.

Its blockade leads to severe dysfunction of the heart, i.e. the delay of an electrical impulse on its way from one part of the heart to another. With complete heart block, the ventricular rate can drop to 30 beats per minute or less (the normal rate in an adult at rest is 60-80 beats per minute). If the interval between contractions reaches several seconds, loss of consciousness is possible (the so-called Adams-Stokes attack) and even death due to a cessation of blood supply to the brain.

2. Etiology of the disease.

The specific causes of congenital heart defects are unknown. They are often associated with chromosomal abnormalities detected by karyotyping in more than 1/3 of patients with congenital heart defects. Most often, trisomy is detected on chromosomes 21, 18 and 13. In addition to Down's disease, there are about twenty hereditary syndromes, often accompanied by congenital heart defects. In total, syndromal pathology is found in 6-36% of patients. The monogenic nature of congenital heart defects has been proven in 8% of cases; about 90% are inherited multifactorially, i.e. is the result of a combination of genetic predisposition and exposure to environmental factors. The latter act as provoking, revealing a hereditary predisposition when the "threshold" of their joint action is exceeded.

Defects in the genetic code and violations of embryogenesis can also be acquired when the fetus and mother's body are exposed to certain adverse factors [radiation, alcoholism, drug addiction, endocrine diseases of the mother (diabetes mellitus, thyrotoxicosis), viral and other infections suffered by a woman in the first trimester of pregnancy (rubella , influenza, hepatitis B), taking some pregnant women medicines(lithium preparations, warfarin, thalidamide, antimetabolites, anticonvulsants)]. Of great importance in the occurrence of pathology of the heart and blood vessels are mixed viral-viral and enterovirus infections transferred by the fetus in utero.

The main reason for the formation of acquired heart defects is known to be transferred endocarditis.

Endocarditis (endocarditis) - inflammation of the inner lining of the heart. The first description of inflammation of the endocardium belongs to J. Buyo (1835). He also suggested calling this pathological process endocarditis, for the first time he revealed the etiological connection of the latter with rheumatism; he also proved that acquired heart defects develop as a result of endocarditis. In 1838 G.M. Sokolsky in his monograph "The Doctrine of Chest Diseases" emphasized the close relationship between rheumatism and acquired heart defects, which often arise from "oversight" and improper treatment of rheumatism.

With endocarditis, the inflammatory process is most often localized in the region of the valves. This endocarditis is called valvular. The valves of the left heart (mitral, somewhat less often aortic), less often tricuspid and very rarely the pulmonary valve are affected most often.

The inflammatory process can be localized in the area of ​​chords (chordal endocarditis), papillary muscles, endocardium lining the inner surface of the atria and ventricles (parietal endocarditis); the latter localization is quite rare.

The defeat of the endocardium mainly occurs as a result of exposure to microbes or their toxins (streptococci, staphylococci, etc.) - Important role in the development of endocarditis belongs to the sensitization of the body. In 70-80% of children, endocarditis is a manifestation of rheumatism (A.B. Volovik, 1948), septic endocarditis can be ranked second in frequency.

According to the etiological principle, all endocarditis can be divided into 3 large groups:

I. Rheumatic endocarditis.

II. Septic endocarditis (bacterial).

III. Endocarditis of various etiologies:

1. Traumatic (postoperative).

2. Tuberculous.

3. Non-bacterial endocarditis (endocarditis with uremia, diabetic coma).

4. Endocarditis with collagenoses.

5. Endocarditis in myocardial infarction.

6. Endocarditis of other etiology.

According to the severity of the disease and the severity of the prognosis, endocarditis is usually divided into benign and malignant.

Pathologically, endocarditis is divided into warty, diffuse (rheumatic valvulitis), ulcerative, fibrinous.

According to the course, endocarditis is divided into acute, subacute, chronic, continuously recurrent, as well as primary and recurrent.

3. Pathogenesis of the disease. The main link of pathogenesis.

The factors listed above, affecting the fetus at critical moments of development, disrupt the formation of heart structures, cause dysplastic changes in its frame. Incomplete, incorrect or untimely closure of the partitions between the atria and ventricles, defective formation of valves, insufficient rotation of the primary heart tube with the formation of aplastic ventricles and an incorrect location of the main vessels occur, the openings characteristic of the fetal circulation are preserved. Fetal hemodynamics usually do not suffer, and the child is born well developed. Compensation may persist for some time after birth. In this case, congenital heart defects appear only after a few weeks or months, and sometimes even in the second or third year of life.

Depending on the characteristics of blood circulation in the large and small circle, congenital heart defects are divided into three groups.

Table 1. Classification of congenital heart defects

Malformations with overflow of the pulmonary circulation account for up to 80% of all congenital heart defects. They are united by the presence of a pathological communication between the large and small circles of blood circulation and (initially) the discharge of blood from the arterial bed into the venous. The overflow of the right parts of the heart leads to their gradual hypertrophy, as a result of which the direction of the discharge can change to the opposite. As a result, total heart failure and circulatory failure develop. The overflow of the small circle contributes to the occurrence of acute, and then chronic pathology respiratory organs.

The basis of defects with depletion of the pulmonary circulation is most often the narrowing of the pulmonary artery. Insufficient saturation of venous blood with oxygen leads to constant hypoxemia and cyanosis, developmental delay, and the formation of fingers in the form of "drumsticks".

With defects with depletion of the systemic circulation, hypertension develops above the site of narrowing, spreading to the vessels of the head, shoulder girdle, and upper limbs. The vessels of the lower half of the body receive little blood. Chronic left ventricular failure develops, often with cerebrovascular accidents or coronary insufficiency.

4. Clinic of the disease.

It depends on the size and location of the septal defect, the degree of vasoconstriction, the direction of blood flow and changes in this direction, the degree of pressure drop in the pulmonary artery system, etc. Small defects (eg, in the atrial septum, muscular ventricular septum, mild pulmonary stenosis) may be asymptomatic.

Congenital heart defects should be suspected when a child is lagging behind in physical development, shortness of breath occurs during movements, pallor (aortic defects) or cyanotic coloration of the skin, severe acrocyanosis (pulmonary artery stenosis, tetralogy of Fallot). When examining the chest, a "heart hump" can be detected, with palpation of the heart area - systolic (with high VSD) or systolic-diastolic (with open ductus arteriosus) trembling. Percussion reveals an increase in size and / or a change in the configuration of the heart. During auscultation, attention is paid to the splitting of tones, the accent of the II tone on the aorta or pulmonary artery. With most defects, you can hear a systolic rough, sometimes scraping noise. It is often carried out on the back and usually does not change with a change in body position and load.

The features of the "blue" defects, combined with narrowing of the pulmonary artery (primarily tetralogy of Fallot), in addition to total cyanosis, include a favorite squatting position and shortness of breath-cyanotic (hypoxemic) attacks associated with spastic narrowing of the outflow tract of the right ventricle and acute brain hypoxia. A hypoxemic attack occurs suddenly: anxiety, agitation appear, shortness of breath and cyanosis increase, loss of consciousness is possible (fainting, convulsions, apnea). Attacks last from several minutes to 10-12 hours, and they are more often observed in young children (up to 2 years) with iron deficiency anemia and perinatal encephalopathy.

Narrowing of the aorta at any level leads to systolic and diastolic overload of the left ventricle and changes in blood pressure: with stenosis in the aortic valve, blood pressure is lowered, with coarctation of the aorta, it is increased in the arms and lowered in the legs. Aortic malformations are characterized by a lag in the development of the lower half of the body and the appearance (at 8-12 years) of complaints that are not characteristic of children and associated with circulatory disorders in a large circle (headache, weakness, shortness of breath, dizziness, pain in the heart, abdomen and legs) .

The course of congenital heart defects has a certain periodicity, which makes it possible to distinguish three phases.

Phase of primary adaptation. After birth, the child's body adapts to hemodynamic disturbances caused by congenital heart disease. Insufficient compensation opportunities, unstable condition of the child in early age sometimes lead to severe malformation and even death.

The phase of relative compensation begins in the 2nd or 3rd year of life and may last for several years. The condition of the child and his development are improved due to hypertrophy and hyperfunction of the myocardium of different parts of the heart.

The terminal (irreversible) phase is associated with gradually developing myocardial dystrophy, cardiosclerosis, and a decrease in coronary blood flow.

Complications. Congenital heart disease can be complicated by cerebral hemorrhages, myocardial infarction, as well as the addition of infective endocarditis.

Laboratory and instrumental research

In blood tests with "blue" defects, a decrease in pa02 and an increase in PaCO2, an increase in the content of erythrocytes, hematocrit and hemoglobin concentration are detected. The ECG reveals signs of hypertrophy and overload of individual chambers of the heart: the right sections - with "blue" defects, the left - with "pale". On PCG, systolic and diastolic murmurs are recorded, typical for each defect in form, amplitude, frequency, location and duration. Echocardiography allows visualization of septal defects, caliber of large vessels, distribution of blood flows.

X-ray reveals cardiomegaly, defiguration of the heart shadow [mitral, with a smoothed "waist of the heart", with an open arterial duct, aortic ("slipper") with tetrade Fallo], narrowing of the vascular bundle in the frontal plane and its expansion in the sagittal (with transposition of the main vessels) . With defects accompanied by overflow of the small circle (pulmonary hypertension), the vascular pattern of the lungs increases.

Diagnosis and differential diagnosis

The diagnosis of congenital heart disease is based on the early (from the moment of birth or during the first 2-3 years of life) the appearance of fatigue, shortness of breath, cyanosis, "heart hump", trembling over the region of the heart, cardiomegaly, constant intense noise, conducted on the back. Measure blood pressure in the arms and legs. The diagnosis is confirmed by the detection of ECG signs of hypertrophy and overload of the heart chambers, fixation of typical murmurs on FCG, visualization of the defect on EchoCG, and detection of arterial blood gas disorders. A change in the configuration of the heart is detected on a chest x-ray.

Differential diagnosis in the neonatal period and in early childhood is carried out with congenital early and late carditis. After 3 years, congenital heart defects are differentiated from non-rheumatic carditis, rheumatism, bacterial endocarditis, cardiomyopathies, and functional disorders of the cardiovascular system. The latter are often based on dysplasia of the connective tissue structures of the heart and its congenital minor anomalies (additional chords, PMC, structural features of the septa, papillary muscles, etc.). It is also necessary to differentiate congenital heart defects among themselves.