Cardiac ischemia. Clinic and diagnostics. Heart diseases: symptoms, treatment, list of main ailments Heart disease clinic treatment

CARDIAC ISCHEMIA

What is coronary heart disease?

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

How is IHD classified?

The following nosological forms exist:

1. Angina:

- stable angina pectoris (indicating the functional class);

- unstable angina;

- vasospastic (spontaneous) angina;

- new-onset angina pectoris;

- progressive angina pectoris;

- early post-infarction or postoperative angina.

Coronary heart disease (CHD, angina, heart attack. Pathogenesis, clinical picture, diagnosis, treatment)

Cardiac ischemia

Introduction

Coronary heart disease is the main problem in the clinic of internal diseases; in WHO materials it is characterized as an epidemic of the twentieth century. The basis for this was the increasing incidence of coronary heart disease in people in various age groups, high percent loss of ability to work, 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. Studying coronary disease hearts has a history of almost two centuries. 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 acute form of coronary heart disease. Significantly less described in the literature are forms of ischemic heart disease that occur chronically - these are atherosclerotic cardiosclerosis, chronic cardiac aneurysm, angina pectoris. At the same time, atherosclerotic cardiosclerosis, as a cause of mortality among diseases of the circulatory system, including among forms of coronary heart disease, is in first place.

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

Coronary heart disease is the most important problem of modern healthcare. For a variety of reasons, it is one of the leading causes of death among the population of industrialized countries. It strikes able-bodied men (more than women) unexpectedly, in the midst of 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 myocardial blood supply remains at a certain level, but the need for it has sharply increased, or when the need remains, but the blood supply has decreased. The discrepancy is especially pronounced in cases of decreased blood supply and an increasing need for blood flow from the myocardium.

The life of society and the preservation of public health have repeatedly posed new problems for medical science. Most often these are different. that attracted the attention of not only doctors: cholera and plague, tuberculosis and rheumatism. They were usually characterized by prevalence, difficulty of diagnosis and treatment, and tragic consequences. The development of civilization and the successes of medical science have pushed these diseases into the background.

Currently, one of the most pressing problems is undoubtedly coronary heart disease. The criteria for angina pectoris were first proposed by the English physician W. Heberden in 1772. Even 90 years ago, doctors rarely encountered this pathology and usually described it as 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 explained by the fact that every year it occurs more and more often.

Coronary insufficiency occurs as a result of a lack of oxygen supply to the heart tissue. Insufficient oxygen supply to the myocardium can result from various reasons.

Until the 80s of the 19th century, the prevailing opinion was that the main and only cause of angina pectoris (angina) was sclerosis of the coronary arteries. This was explained by 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 excluded (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, a group of experts studying atherosclerosis in World Organization health care term has been proposed to denote acute or chronic disease heart disease, 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) coronary heart disease without pain:

a) asymptomatic form, b) atherosclerotic cardiosclerosis.

In March 1979, WHO adopted a new classification of coronary heart 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 the blood supply to the myocardium

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 begins from the left posterior sinus of Vilsalva, goes down to the anterior longitudinal groove, leaving the pulmonary artery to its right, and to the left - left atrium and an ear surrounded by fatty tissue that usually covers it. It is a wide but short trunk, usually no more than 10-11 mm long. The left coronary artery is divided into two, three, in rare cases, four arteries, of which the anterior descending and circumflex branches, or arteries, are of greatest importance for pathology.

The anterior descending artery is a direct continuation of the left coronary artery. Along the anterior longitudinal cardiac groove it is directed to the region of the apex of the heart, usually reaches it, sometimes bends over it and passes to back surface hearts. 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 obtuse edge; in addition, numerous septal branches depart from it, piercing the myocardium and branching in the anterior 2/3 of the interventricular septum. The lateral branches supply the anterior wall of the left ventricle and give branches to the anterior papillary muscle of the left ventricle. The superior septal artery gives off a branch to the anterior wall of the right ventricle and sometimes to the anterior papillary muscle of the right ventricle.

Throughout its entire length, the anterior descending branch lies on the myocardium, sometimes plunging into it to form muscle bridges 1-2 cm long. Throughout 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 straight line, passes in the transverse groove, reaches the obtuse edge of the heart, goes around it, passes to the posterior wall of the left ventricle, sometimes reaches posterior interventricular groove and in the form of the posterior descending artery goes to the apex. Numerous branches extend from it to the anterior and posterior papillary muscles, the anterior and posterior walls of the left ventricle. One of the arteries supplying the sinoauricular node also departs from it.

The first hepatic artery begins in the anterior sinus of Vilsalva. It is first located deep in the adipose tissue to the right of pulmonary artery, goes around the heart along the right atrioventricular groove, passes to the posterior wall, reaches the posterior longitudinal groove, 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, partially to the anterior part of the septum, both papillary muscles of the right ventricle, the posterior wall of the right ventricle and the posterior part of the interventricular septum; a second branch also departs from it to the sinoauricular node.

There are three main types of blood supply to the myocardium: middle, left and right. This division 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 sections is quite stable and is not subject to significant deviations.

With the 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 left coronary artery system. The right ventricle, including both right papillary muscles and the posterior 1/2-1/3 of the septum, receives blood from the right coronary artery. This appears to be the most common type of blood supply to the heart.

In the left type, the blood supply to the entire left ventricle and, in addition, to the entire septum and partially to 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 sulcus and ends here in the form of the posterior descending artery, giving some branches to the posterior surface of the right ventricle.

The right type is observed with 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 the origin of the posterior descending artery, usually gives several 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.

The blood supply to the myocardium is carried out directly:

a) capillaries lying between the muscle fibers, entwining them and receiving blood from the coronary artery system through the arterioles; b) a rich network of myocardial sinusoids; c) Viessant-Tebesius vessels.

Outflow occurs through veins that collect in 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 left coronary arteries, the circumflex and anterior descending arteries), and secondly, colliterals that connect the branches of the same artery and create both would be bypass paths, 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 coronary artery disease, so closure of one of the coronary arteries is not always accompanied by necrosis in the myocardium. IN normal hearts anastomoses were found only in 10-20% of cases, and of small diameter. However, their number and magnitude increase not only with coronary atherosclerosis, but also with valvular heart defects. Age and gender by themselves do not have any effect on the presence and degree of development of anastomoses.

In a healthy heart, communication between the basins of various arteries occurs mainly through small-diameter arteries - arterioles and prearterioles - and the existing network of anastomoses cannot always ensure the filling of the basin of one of the arteries when a contrast mass is introduced into another. Under pathological conditions with coronary atherosclerosis, especially stenotic atherosclerosis, or after thrombosis, the network of anastomoses increases sharply and, what 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 the myocardial oxygen demand. In turn, each of these factors depends on a number of conditions. Thus, the magnitude 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 rich in oxygen, for example due to anemia. Myocardial oxygen demand can increase sharply with a significant increase blood pressure, at physical activity.

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

During myocardial infarction, some part of the myocardium becomes necrotic, the localization and size of which are largely determined by local factors.

Most common cause, which determines the development of coronary heart disease is atherosclerosis of the coronary vessels. Atherosclerosis acts as the main cause of the development of coronary heart disease and 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 concepts, develops both due to local changes in the intima of blood vessels and due to an increased tendency to thrombus formation in general, which is observed in atherosclerosis.

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

The functional capacity of atherosclerotic changed coronary arteries is significantly reduced not only due to a mechanical factor - narrowing of their lumen. They largely lose their adaptive capabilities, in particular to adequate expansion when blood pressure decreases or arterial hypokymia.

Serious importance in the pathogenesis of IHD is attached to the functional aspect, in particular to spasm of the coronary arteries.

The etiological factor in myocardial infarction may include septic endocarditis (embolism of the coronary arteries with thrombotic masses), systemic vascular lesions involving the coronary arteries, dissecting aortic aneurysms with compression of the mouths of the coronary arteries, and some other processes. They are rare, accounting for less than 1% of cases acute heart attack myocardium.

Changes in the activity of the sympatho-adrenol system are of no small importance in the pathogenesis of coronary heart disease. Excitation of the latter leads to increased release and accumulation of catecholamines (norepinephrine and adrenaline) in the myocardium, 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 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 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 metabolic disorders in the heart muscle due to changes in the composition of electrolytes, hormones, toxic metabolic products, hypoxia, etc. These causes are closely intertwined with each other.

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

WHO statistics indicate an extreme incidence of coronary heart disease in all countries of the world. The incidence and mortality from ischemic heart disease increases with age. When studying coronary insufficiency, a predominance of males was found, especially at the age of 55-59 years.

On March 13, 1979, WHO adopted a classification that distinguishes the following five classes, or forms, of IHD:

2. Angina pectoris

2.1. Angina pectoris

2.1.1. Newly emerging

2.1.2. Stable

2.1.3. Progressive

2.2. Angina at rest (synonym: spontaneous angina)

2.2.1. A special form of angina

3. Myocardial infarction

3.1. Acute myocardial infarction

3.1.1. Definite

3.1.2. Possible

3.2. Previous myocardial infarction

4. Heart failure

5. Arrhythmias.

WHO expert definitions provide clarifications for each of the named classes of IHD.

1. Primary circulatory arrest

Primary circulatory arrest is a sudden loss of cardiac arrest thought to be due to electrical instability of the myocardium if there are no signs to suggest another diagnosis. Most often, sudden death is associated with the development of ventricular fibrillation. Deaths occurring in the early phase of verified myocardial infarction are not included in this class and should be considered as deaths from myocardial infarction.

If resuscitation measures were not carried out or were not effective, then primary circulatory arrest is classified as sudden death, which serves as the 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 have occurred from other causes.

2. Angina pectoris

Angina is divided into exertional and spontaneous angina.

2.1. Angina pectoris

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

2.1.1. Effortful angina pectoris, which occurs for the first time, lasts less than a month.

New-onset angina is not homogeneous. It may be a harbinger or the first manifestation of acute myocardial infarction, may develop into stable angina or disappear (regressive angina). The prognosis is uncertain. Many authors identify the term with the concept. which we cannot agree with.

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

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

Angina is considered stable if it is observed in the 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 angina pectoris is a sudden increase in the frequency, severity and duration of attacks of chest pain in response to stress, which previously caused pain of a familiar nature.

In patients with progressive angina, the usual pattern of pain changes. Angina attacks begin to occur in response to less stress, and the pain itself becomes more frequent, more intense and longer lasting. The addition of attacks of resting angina to attacks of exertional angina often indicates a progressive course of the disease. The prognosis is worse in those patients in whom changes during 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 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, as can be seen in images showing the vessels of the heart.

Human heart

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

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

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

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

This is the main mechanism for the occurrence of lack of blood circulation in the heart. In most cases, the reason for the increase muscle mass Heart disease (hypertrophy) is a strain on the heart, which mainly occurs due to hypertension.

With age, due to the pathocomplex process, the coronary vessels become clogged, so a contradiction arises, and over time increases, between the 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 view official medicine, coronary heart disease was also no exception. According to the most naive theory put forward in this area, overuse salt, sugar, meat foods, and fats cause narrowing and blockage of the coronary vessels. Others believe that this disease is genetic, i.e. transmitted by hereditary factors. Some attribute this disease to human physical inactivity.

Today, the theory about the involvement of cholesterol and triglycerides in the occurrence of cardiovascular pathologies, in particular coronary heart disease and arrhythmia, occupies a leading place among all proposed theories.

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

Human coronary vessels

In the 50s, with the development of medical technology, it became possible to carry out laboratory research to identify some human blood factors. 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 the time, with primitivism of thinking, scientists came to the conclusion about the involvement of the noted substances in the occurrence of human cardiovascular pathologies, as well as heart attacks and strokes arising 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, eliminating etiological factor pathology occurs, the disease itself must 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 have to expect the complete elimination of this problem from human society. We have to observe a completely opposite picture: these problems have not disappeared, but on the contrary, they are confidently moving forward and are observed in people younger and younger in age. If in the 30s of the twentieth century only residents of a limited part of Europe suffered from cardiovascular problems, then today there is no country on the globe where 30–40% of the total and 80% of the average age population do not suffer from some kind of 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.

Coronary heart disease has only one origin: a pathocomplex process.

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

This pathology is caused by a decrease or cessation of blood supply to the myocardium as a result of occlusive damage to the coronary arteries of the heart. In the vast majority of cases, the cause is stenosing atherosclerosis of the coronary arteries - a particular form of general atherosclerosis. Much less often, ischemic heart disease is caused by heart injuries, metabolic disorders, and coronary thromboembolism. As a rule, atherosclerosis affects the proximal parts of large, subepicardially located coronary arteries. In this case, the lesion is segmental in nature and distal to the site of occlusion the vascular bed retains satisfactory or good patency. A decrease in coronary perfusion leads to tissue acidosis in the myocardium and causes anginal syndrome. As ischemic cardiosclerosis develops, myocardial contractility decreases and the oxygen demand of the heart muscle increases sharply. Physical exercise tolerance decreases. Failure of the Na+ - K+ pump leads to increased Ca2+ activity, distortion of repolarization, electrical heterogeneity of the myocardium and, consequently, to various forms of rhythm disturbances. With complete occlusion of the coronary artery with insufficient collateral circulation, acute myocardial infarction (AMI) is formed, as a result of which part of the heart muscle is turned off from the pumping function. Extensive transmural infarctions cause cardiogenic shock, cardiac muscle ruptures, ventricular fibrillation and, as a consequence, rapid sudden death. In some cases, stable angina passes into AMI through the stage of pre-infarction or so-called unstable angina.

Clinic for Coronary Heart Disease

Main clinical symptom disease is angina pectoris. In other cases, shortness of breath prevails. Anginal pain occurs in the form of attacks and is localized behind the sternum, less often in the epigastric region. The pain is provoked by physical activity, lasts 3-5 minutes and goes away with rest. Characterized by rapid pain relief by taking nitroglycerin. Typical irradiation of pain in upper limbs, left shoulder blade, neck. The occurrence of chest pain at rest indicates a worsening of the course of coronary artery disease, since this can be a consequence of myocardial oxygen deficiency only as a result of a slight slowdown in the speed of blood flow. In uncomplicated ischemic heart disease, the physical picture is poor. Against the background of stable angina, a more severe form of coronary heart disease may develop - unstable angina. It is manifested by a sharp exacerbation of habitual angina, prolongation of anginal attacks and their greater resistance to nitroglycerin. This form of angina in its outcome can lead to AMI. Clinical manifestations AMI depends on the volume of myocardial damage. However, the most typical are acute, prolonged chest pain that is not relieved by nitroglycerin, arrhythmias, a drop in hemodynamics and symptoms of heart failure (cardiogenic shock). The appearance of a pathological III tone, rough systolic murmur indicates dysfunction of the papillary muscle or separation of the chordae from the mitral valve leaflet. In rare cases, the cause of the murmur may be a rupture of the interventricular septum.

Diagnosis of coronary heart disease

The earliest sign of ischemic heart disease is prolongation of the diastolic relaxation phase of the myocardium on echocardiography. With stable angina, the ECG may show various disorders rhythm and conductivity. Many patients have an unremarkable ECG at rest. Therefore, the picture of IHD is revealed only with daily electrocardiographic monitoring. Under load conditions (bicycle ergometry, increasing transesophageal electrical stimulation of the left atrium), a decrease in coronary reserve is noted: an increase S-T interval in standard leads by at least 1 mm, in chest leads by more than 2 mm. On the ECG in patients with unstable angina, similar changes are detected at rest. However, they are expressed much more roughly (focal ischemia). In the case of transmural AMI, a deep Q wave is detected in the leads corresponding to the infarction zone. Transmural AMI is also accompanied by a significant decrease in the R wave until its complete disappearance (QT complex).

The most typical method of topical diagnosis of coronary occlusions is selective coronary angiography. It identifies the affected arteries, the degree of their narrowing, the nature collateral circulation. All this allows us to predict the further course of the pathology and, accordingly, select patients for surgical treatment.
There are 4 degrees of coronary artery stenosis:
I - moderate narrowing of the lumen of the vessel (up to 50%);
II - pronounced narrowing (from 50 to 75%);
III - sharp narrowing (from 75 to 90%);
IV - complete occlusion of the vessel.
Left ventriculography reveals areas of myocardial hypokinesia and is necessary for a comprehensive assessment when establishing indications for surgery. Radionuclide diagnostics based on 201T1, which accumulates in the functioning myocardium, makes it possible to determine the localization and extent of scarred myocardium. In case of AMI, it is rational to use “tTs, which accumulates in necrotic areas of the myocardium, creating here a focus of increased radioactivity (“hot spot”) in the first 24-28 hours after the development of the disease. In AMI, indicators of increased enzymatic activity (AST, ALT, CPK) have diagnostic value , cardiac LDH), an increase in leukocytosis in the blood.Vectorcardiography has a fairly high information content.

This disease is characterized by a change in heart rate - acceleration or slowness. Most manifestations of arrhythmia are harmless and one-time in nature. However, in some cases, symptoms can threaten a person's life.

  • Pathological condition body, preventing a stable heartbeat. One of these conditions is myocardial conduction disorder, appears when there is a failure in the transmission of impulses from the brain to the heart to signal contractions.
  • One of the forms of arrhythmia in which the heart does not work stably with normal frequency, and throws out blood with a very high frequency sometimes reaching 300 beats per minute - fibrillation. If left untreated for a long time, fibrillation can be caused by changes in the ventricles of the heart and their pathological condition.
  • When the heart is prematurely excited and a strong impulse occurs due to an erroneous impulse from the brain, extrasystole. Single extrasystoles occur in 75% of people and are felt as a strong heartbeat followed by a delay before the next impulse.
  • Inflammatory heart diseases

    1. The inner surface of the lining of the heart can become inflamed, this disease is called - endocarditis. The disease is often accompanied by inflammatory processes valves and adjacent vessels.
    2. When toxins and infections appear in the body, inflammation in the heart muscle can develop - myocarditis. The disease can be independent or exist against the background of other diseases.
    3. Pericarditis characterized by the accumulation of fluid in the pericardium, which leads to dysfunction of the heart muscle. Concomitant disease manifestations are inflammatory processes in the visceral and parietal layers of the pericardium.

    Arterial hypertension and hypotension

    1. – a disease in which high blood pressure is constantly present in the body. It occurs when blood flow is obstructed due to poor patency in the vessels. The heart requires more effort to push blood, which results in pathologies. Or the disease is also called persistent high blood pressure. Often a common heart disease that has no cure. Hypertension can only be controlled. Left untreated increases the risk of developing a host of heart diseases.
    2. - a decrease in blood pressure by more than 20% from the initial/usual values ​​of mean arterial pressure. Low blood pressure can be acute or chronic.

    Ischemic lesions

    1. Stopping the supply of blood to any part of the heart within 15 minutes leads to the death of a section of this vital organ. Myocardial infarction– the result of this incident and, concurrently, an acute form of coronary heart disease.
    2. Cardiac ischemiaoxygen starvation in the coronary arteries. A disease resulting from advanced atherosclerosis and causing a risk of myocardial infarction.
    3. The combination of coronary heart disease and atherosclerosis, which complicates blood flow, leads to a disease such as angina pectoris. Characteristic plaques appear on the walls of blood vessels, causing poor blood flow and painful sensations in heart.

    Damage to the blood vessels of the heart

    1. Cardiosclerosis– pathology of replacement of cardiac tissue with scar tissue. As a result, the load on the myocardium increases, which leads to its increase and changes in the remaining parts of the heart.
    2. Coronary disease hearts– a set of diseases that have a negative impact on the patency of blood in the coronary vessels. Such diseases appear due to blood vessels, on the walls of which plaques consisting of fat, salty deposits, etc., form.
    3. Atherosclerosis, as a rule, concerns older people and is characterized by the accumulation of plaques on the vessels, leading to difficulty in blood flow and loss of elasticity in the vessels.

    Pathological changes

    Valve defects

    1. Mitral valve narrowing - mitral stenosis, leading to fusion of the walls of the opening in the left atrial ventricle. Most often, this disease develops after suffering from rheumatism, less often - after heart disease.
    2. Mitral insufficiency valve disease - a disease in which the blood ejected by the left ventricle partially returns back, increasing the pressure and volume of the contents of the ventricle. The disease leads to stagnation of blood in the heart.
    3. Mitral valve prolapse It is common in young people and affects about 15% of the population. Prolapse is expressed as swelling of the mitral valve leaflet. The disease is congenital or hereditary.
    4. Among acquired heart defects, the most common is aortic stenosis. Every 10 people of retirement age are susceptible to this disease. Appears as a result of pathologies of the leaflets in the aortic valve.
    5. Aortic valve insufficiency– loss of the valve’s ability to effectively close the left ventricle from the reverse flow of blood from the aorta. The disease is associated with difficult diagnosis, since at the beginning of the disease there is no pain and the patient comes to the hospital late with complaints.
    6. Heart disease– a deformed structure of the parts of the heart that appears over the course of life or at birth. Leads to incorrect operation of all circulatory systems in general and interferes with the normal functioning of the heart in different variations, depending on the nature and position of the deformation.

    Hypotension (hypotension) is a significant decrease in blood (or arterial) pressure.

    This condition rarely leads to the development of any serious illnesses, but because of it a person may experience discomfort.

    What are the causes of hypotension, and how to deal with it?

    Symptoms

    Many people have experienced low blood pressure. This condition has a name - hypotension, with A/D values ​​reduced by more than 20% of normal (120/70).

    In life modern man There are always factors that negatively affect the condition of cardio-vascular system.

    Lack of exercise, stress, bad habits, overeating - all this leads to increased blood pressure, and in chronic form - To arterial hypertension(AG). This disease causes a noticeable deterioration in well-being and a decrease in quality of life, and subsequently often becomes the cause of a heart attack or stroke.

    Therefore, it is important to recognize the disease at the earliest stages, when the process is still reversible. Better yet, try to avoid it.

    A disease in which a person has high blood pressure , in medical circles is called hypertension.

    Blood pressure is stable, starting from 160/95.

    Must be recorded at least three times within 15 days.

    The disease is dangerous, since if hypertension, this disease, has gone far, it can give complications in the form of a fatal heart attack, loss of consciousness and stroke.

    One of the common pathologies of the heart is impaired myocardial conduction. You can also find this pathology under the name “heart block”.

    This is a relatively common phenomenon that can be caused by a whole range of abnormalities and diseases, so it needs to be considered in detail.

    What it is

    To be more precise, myocardial conduction disturbance is not a disease/pathology, but a whole group of diseases/pathologies.

    Left atrial hypertrophy is a disease in which the left ventricle of the heart thickens, causing the surface to lose its elasticity.

    If the compaction of the heart septum occurs unevenly, disturbances in the functioning of the aortic and mitral valves of the heart may additionally occur.

    Today, the criterion for hypertrophy is myocardial thickening of 1.5 cm or more. This disease is currently the main cause of early death among young athletes.

    Why is the disease dangerous?

    A person suffering from arrhythmia is at risk for stroke and myocardial infarction. This is due to the fact that during arrhythmia the heart contracts incorrectly, resulting in the formation of blood clots.

    With the flow of blood, these clots are carried throughout the body and where the clot gets stuck, blockage will occur and the person will get sick.


    Coronary heart disease (CHD)- this is a myocardial pathology caused by a relative deficiency of oxygen in the coronary bloodstream. This deficiency 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 the myocardial oxygen demand, for example, with heavy physical activity, extreme anxiety, with an increase in the intensity of tissue metabolism due to thyrotoxicosis, etc. d. However, as a result of all these reasons, hypoxic changes develop in the myocardium, first reversible, then organic (irreversible). IHD includes diseases such as angina pectoris, myocardial infarction and their intermediate forms.

    Atherosclerosis ranks first among the causes of mortality and disability in the developed countries of the world. More than 95% of all people over the age of 60 have vascular atherosclerosis. More than a million people suffer from myocardial infarction every year in the United States.

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

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

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

    It has been established that cholesterol and fatty acids have a direct damaging effect on the vessel wall (atherogenic effect), which “pushes” the atherosclerotic process. Overeating before bed is especially harmful. In some individuals, hypercholesterolemia is hereditary, and in them complicated ischemic heart disease (for example, myocardial infarction) occurs already in young years, which is explained by increased synthesis of cholesterol and atherogenic low-density lipoproteins, and decreased synthesis of protective high-density lipoproteins.

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

    The next serious risk factor for coronary heart disease is obesity. Body weight exceeding the norm by 30% or more already limits physical activity humans, creates an increased load on the cardiovascular system, promotes hypoventilation of the lungs (due to limited excursion of the diaphragm). All this provokes ischemic heart disease. It has been proven that overeating is harmful even in childhood.

    TO the most important factors risk of coronary heart disease) include diabetes mellitus and high blood pressure. In diabetes, tissue acidosis occurs and microcirculation deteriorates. It has been found that in Akita Prefecture (Japan), where residents consume about 25 g of salt per day, there is a sharp increase in hypertonic disease complicating ischemic heart disease.

    Note that in old age, the listed risk factors are usually summed up, which sharply intensifies the atherosclerotic process. IHD is observed much more often (2-3.6 times) in men; In women, estrogens have a certain protective effect.

    A combination of risk factors (eg, hypercholesterolemia, arterial hypertension and smoking) greatly increase the risk of myocardial infarction.
    Most researchers 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, and often with alcoholism there is a deficiency of dietary proteins.

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

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

    IHD is most common in Scandinavia, the USA, and Western Europe; it is very rare in developing and semi-colonial countries of Africa, Latin America, and Southeast Asia. It mainly affects people who do mental work.

    The clinical manifestation of fairly deep, but short-term (and therefore reversible) myocardial ischemia is angina. Main symptom angina pectoris - pain in the heart area.

    By clinical course distinguish between angina pectoris and angina at rest. Pain during exertional angina is provoked by physical activity, most often localized behind the sternum, sometimes slightly to the left, it has a pressing or squeezing nature of varying intensity, most often the pain begins gradually, then intensifies. At the time of an attack, patients try to maintain a motionless position, are afraid to take a deep breath, and in some cases they experience pallor skin due to spasm of blood vessels, skin, increased sweating. Sometimes there are burning pains, they resemble heartburn, accompanied by tightness in the chest, stiffness in the throat, neck, and a feeling of suffocation. Irradiation of pain into the arms is typical, most often to the left along its inner surface to the little finger. Very often the pain radiates to the left shoulder blade, neck, and lower jaw.

    At the beginning of an attack of angina, there may be a feeling of numbness in the left arm, a feeling that goosebumps are crawling throughout the body. The pain can be “shooting” or squeezing. Some patients experience the urge to urinate and defecate. Sometimes nausea, vomiting, dizziness, and trembling throughout 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 speeds up, and blood pressure usually rises. The boundaries of the heart remain unchanged by percussion, heart sounds are often muffled. In some cases, extrasystoles may appear during an attack, and very rarely an alternating pulse.
    In most cases, the attack is stopped quickly, 1-2 minutes after taking validol or nitroglycerin, which is also a differential diagnostic test.

    After an attack, patients feel weak and tired for some time, and the pallor of the skin gives way to hyperemia.
    Cooling increases the flow of adrenaline from the adrenal glands into the blood. In cold weather, patients often have to stop. Usually the attack begins while walking, passes when you stop, and then resumes again.

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

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

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

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

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

    Chest pain in the pre-infarction state has the same properties as with angina pectoris, however, painful 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, new irradiation zones. Very characteristic feature- poor effect of nitroglycerin; sometimes it is possible to relieve pain only after taking 20-30 tablets of nitroglycerin or sustacamite. Therefore, diagnosis of a pre-infarction condition is based on careful questioning of the patient, analysis of complaints and anamnesis.

    There are also atypical variants of the pre-infarction state: asthenic (the patient has weakness, dizziness, insomnia, and pain syndrome not expressed), asthmatic (shortness of breath 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 notice that these options correspond to the options of acute myocardial infarction, which often ends (without treatment) in a pre-infarction state.

    Among the reasons that cause the transition from angina to a pre-infarction state are nervous and mental overload, conflicts in the family and at work, drinking alcohol, smoking, etc. The ECG is characterized by a decrease in the height of the T waves in the chest leads (up to negative), moderate pronounced horizontal or arcuate displacements 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).

    No laboratory changes (blood changes, biochemical and enzymatic reactions) are observed in the pre-infarction state.

    Myocardial infarction is the most dangerous manifestation of IHD. In 20-25% of all cases, acute myocardial infarction leads to death, and in 60-70% of cases - in the first 2 hours of the disease. Let us recall that in 20% of all cases of myocardial infarction, thromboembolic complications, persistent blockades and arrhythmias, and cardiac aneurysm are observed.

    A 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 chest pain, as with angina pectoris, only more severe (“morphine”), sometimes tearing in nature, it does not disappear with rest and is not relieved by nitroglycerin.

    A thorough analysis of the properties of pain will, in most cases, allow the paramedic to recognize myocardial infarction in the anginal variant, even before taking an electrocardiogram. It has been proven that the irradiation of pain itself does not have much informative value, although the favorite zone of irradiation of anginal pain is left hand(sometimes only the hand), left shoulder blade, less often - neck, teeth, 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 “searing” pain in the epigastric region. Somewhat more often, this option 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 or stool disorders.

    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 splanchnic and sympathetic nerves and the release of biogenic amines - histamine, serotonin, bradykinin, etc.

    Acute ulcers of the stomach and intestines, often with bleeding, during myocardial infarction are caused by arterial hypotenia and shock. Patients may also experience reflex paresis of the gastrointestinal tract.

    In the asthmatic version 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.

    Listening to the heart during myocardial infarction reveals dullness of sounds, sometimes systolic murmur, various arrhythmias, and sometimes pericardial friction murmur. On percussion, the boundaries of the heart are often expanded. Sometimes a patient with myocardial infarction experiences a sudden decrease in heart rate to 60-40 per minute, which usually indicates complete atrioventricular block or bigeminy; this symptom should alert you.

    Due to the fact that the clinical symptoms of myocardial infarction are not always convincing, the electrocardiographic method of research becomes crucial in diagnosis.

    The earliest electrocardiographic symptom - a convex elevation of the ST segment in the area 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 (“dip”) in the areas corresponding to the infarction. Posterobasal 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 “mirror” changes are noted in leads V1, V2 ECG changes- increased R and T waves.

    We emphasize the mandatory registration of an ECG in cases of suspected myocardial infarction. Statistics convince us that 25% of all cases of acute myocardial infarction are not diagnosed on time, because either the ECG is not recorded or it is assessed incorrectly.

    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 (scar) 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 7-10th day, neutrophilic leukocytosis is observed in the blood (up to 9000-12,000 per μl), a moderate acceleration of ESR from the 2nd to the 20-25th day, and various changes in the biochemical spectrum of the 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 due to its complications, the most typical being cardiogenic shock and cardiac arrhythmias. It has been established that shock during myocardial infarction is caused by both excruciating pain and overirritation of the cells of the central nervous system, and a decrease in myocardial contractility due to the presence of an area of ​​necrosis and edema of neighboring zones. The main feature of cardiogenic shock is deterioration of microcirculation in vital organs: brain, heart, kidneys, liver.

    Based on an analysis of hundreds of cases of acute myocardial infarction, it was established that systolic hypotension below 100 mm Hg. Art. for more than 4 hours sharply worsens the prognosis of the disease. A serious complication of myocardial infarction is pulmonary edema due to left ventricular weakness. Early symptoms pulmonary edema - increasing pallor, cyanosis, wheezing in the lungs, and then bubbling breathing, 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 cardiac conduction system, as well as disruption of the extracardiac nervous and humoral regulation, (“symptomatic storm”). Extrasystole is usually observed, there may be attacks of atrial fibrillation or flutter; various conduction disorders. The most dangerous 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 observed, in 8-10% - ventricular fibrillation. In 12-20% of all cases, thromboembolic complications are observed - infarctions of the lungs, kidneys, and brain.

    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 the complex multi-stage, but extremely fragile structure is susceptible to a number of external aggressive factors. Even having the opportunity to see any doctor, but not having specific knowledge in this specialty, it may become a problem for the patient to find specialists or cardiology centers in Moscow and other cities of the Russian Federation.

    Cardiac care options for the patient

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

    There may be several options for cardiac services.

    The person visiting the clinic is a healthy person who has no complaints about the functioning of the cardiovascular system.. For example, medical examination is necessary. In this case, the scope of services will be as follows: electrocardiogram with interpretation, consultation with a therapist or cardiologist. Almost any multidisciplinary medical center on a paid basis or public clinic can provide such a spectrum.

    Visiting the clinic - a person with new symptoms(feeling of interruptions in the heart, changes in pressure and pulse, chest pain). These conditions may be emergencies!

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

    If such symptoms occur, you cannot postpone a visit to a specialist: if you experience chest pain, an unusual increase/decrease in blood pressure, arrhythmia, you should call an ambulance, which will take you to the nearest cardiology hospital. Will be performed in the hospital following procedures: electrocardiogram with interpretation, blood test for specific markers that increase during a heart attack, ECHO-CG ( ultrasonography heart), consultations with specialists.

    If necessary, will be carried out healing procedures and the patient can even be redirected to another (specialized) clinic for instrumental diagnostics and surgical treatment (coronary angiography, stenting procedure). Not all hospitals in Moscow carry out such manipulations, but only multidisciplinary ones that have cardiac surgery 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 – the basis effective treatment

    There are also separate, exclusively cardiology clinics that provide the full range of advisory, minimally invasive and cardiac surgical care. Such centers include those known throughout Russia and the world - the Scientific Center for Cardiovascular Surgery named after Academician A.N. Bakuleva (NCSSH) (“House of the Heart” on Rublevskoye Shosse and on the territory of City Clinical Hospital No. 1, Oktyabrskaya metro station of the circle line). The Bakulev Institute, headed for many years by an outstanding cardiac surgeon (L.A. Bockeria), is a huge complex providing cardiac 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 is the Institute of Clinical Cardiology named after. A.L. Myasnikova.

    A person visiting the clinic is a person who has been suffering from a disease of the cardiovascular system for a long time.. Depending on the specific nosology, such a patient should contact 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 each state clinic Moscow. In the case of pathology of myocardial vessels, neck vessels, coronary disease with severe vascular stenosis, when the need is obvious surgical treatment- it is carried out as planned, after proper preparation. The clinic (polyclinic, department) in which the patient was previously observed prepares all the necessary documents for applying to large cardiac centers (N.A. Bakulev National Agricultural Hospital, A.L. Myasnikov Institute, specialized departments of large Moscow City Clinical Hospitals, private clinics 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, hospitalization procedures, list necessary documents and research. It is also possible to contact via the Internet or by e-mail to receive complete information support for the patient.


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

    Choosing specialized treatment and medical center

    Thus, cardiac 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 obtain qualified and free help if necessary; the first step in solving a cardiac problem will always be the outpatient clinic (polyclinic at the place of residence, private center with consulting cardiologist and general practitioner, 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 by working in complex, outpatient and inpatient services medical care allow you to quickly refer the patient to the necessary studies and manipulations.