Ischemia Clinic. Cardiac ischemia. Clinic and diagnostics. Chronic heart failure

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, the high percentage of disability, and 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<Международную статистическую классификацию болезней, травм и причин смерти>. The study of coronary heart disease 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 coronary 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<болезни века>, which 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 a classic description of the clinical picture of 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. This concept continues to this day.

In 1957, a group of experts on the study of atherosclerosis at the World Health Organization proposed the term<ишемическая болезнь сердца>to denote an acute or chronic heart disease that occurs as a result of 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 BLOOD SUPPLY TO THE MYOCARDIAL

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 the right, and to the left the left atrium and the appendage surrounded by fatty tissue, which 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 the posterior 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 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. First, it is located deep in the adipose tissue to the right of the pulmonary artery, bends 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 branches of the left coronary artery, 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 are 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 in blood pressure during 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 of development of large-focal myocardial infarction - coronary artery thrombosis, which, according to modern concepts, develops both due to local changes in the intima of blood vessels, and in connection with an increased tendency to thrombus formation in general, which is observed with 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 of acute myocardial infarction.

Of no small importance in the pathogenesis of coronary heart disease is the change in the activity of the sympatho-adrenol system. 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.

Excess catecholamines cause disorders such as 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 reasons are closely intertwined with each other.

Social issues are also of great importance in the pathogenesis of coronary heart disease.

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

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 failure presumed to be associated with electrical instability of the myocardium if there are no signs to make another diagnosis. More often sudden death 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. Angina pectoris, which occurs for the first time - duration of existence is 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. Term<нестабильная стенокардия>many authors identify with the concept<предынфарктное состояние>, with which we cannot agree.

2.1.2. Stable exertional angina - 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.

2.2. Spontaneous angina

Spontaneous angina is characterized by attacks of chest pain that occur without any apparent connection with factors leading to an increase in myocardial oxygen demand. The pain in these cases is usually longer and more intense than with angina pectoris. The pain is worse than the action of nitroglycerin. Enzyme activity does not increase. The ECG often shows slight transient ST segment depression or changes in T wave configuration.

Attacks of spontaneous angina can occur as a result of a primary decrease in blood flow in a certain area of ​​the coronary bed, that is, vasospasm.

Spontaneous angina can exist as an isolated syndrome or be combined with exertional angina. The frequency, duration and intensity of pain may vary from patient to patient. Sometimes attacks of chest pain may resemble myocardial infarction in duration, but the characteristic changes in ECG and enzyme activity are absent.

2.2.1. In some cases of spontaneous angina, a transient elevation of the segment is observed during attacks. This form is known as a special form of angina, which is also known as Prinzmetal's angina.

3. Myocardial infarction

3.1. Acute myocardial infarction

The clinical diagnosis of acute myocardial infarction is usually based on history, ECG changes, and serum enzyme activity tests.

A typical history is considered to be the presence of a severe and prolonged attack of chest pain. Sometimes the history is atypical, and arrhythmias and heart failure often come to the fore.

ECG changes during myocardial infarction include the formation of a pathological, persistent Q or QS wave, as well as electrocardiographic signs of damage that have characteristic dynamics over the course of one day. In these cases, the diagnosis of acute myocardial infarction can be made without additional data.

The characteristic dynamics of changes in the activity of serum enzymes or an initial increase in activity followed by a subsequent decrease should be considered pathognomonic for myocardial infarction. Increased activity of cardiac-specific isoenzymes is also a pathognomonic sign of myocardial infarction. If there is an initial increase in enzyme activity without a subsequent decline or the dynamics of enzyme activity is not established, then the enzymatic picture is not pathognomonic for myocardial infarction.

3.1.1. Definite myocardial infarction. The diagnosis of definite myocardial infarction is made in the presence of pathognomonic ECG changes and pathognomonic changes in enzyme activity. However, the analysis may be atypical. In the presence of pathognomonic ECG changes, a definite myocardial infarction can be designated as transmural. If, in the absence of the Q wave or QS complexes, changes in the ST segment, E wave and typical changes in enzyme activity develop dynamically, the infarction is designated as non-transmural, or subendocardial.

3.1.2. Possible myocardial infarction. A diagnosis of possible myocardial infarction is made if non-pathognomonic changes in the ECG dynamics persist for more than a day, and enzyme changes are not of a typical nature or are completely absent; the medical history may be typical or atypical. These signs fit into the clinical picture of acute focal myocardial dystrophy, a diagnosis that is accepted in most domestic clinics.

Sometimes, during the period of recovery from acute myocardial infarction, patients complain of chest pain, which is combined with ECG changes, but enzyme activity does not increase. In such a case, Dressler's syndrome can be diagnosed, and in some patients - a relapse or expansion of the myocardial infarction zone. Additional research methods help clarify the diagnosis.

3.2. Previous myocardial infarction

Post-myocardial infarction is usually diagnosed on the basis of pathognomonic ECG changes in the absence of a typical history or enzymatic changes characteristic of acute myocardial infarction.

This diagnosis is completely equivalent to the diagnosis of post-infarction (focal) cardiosclerosis accepted in Russia. In patients who have previously suffered a myocardial infarction, signs of chronic cardiac aneurysm are periodically detected. If the ECG shows no signs of a previous myocardial infarction, the diagnosis of post-infarction cardiosclerosis can be made based on typical ECG changes and enzymatic changes in the past. The absence of electrocardiographic signs of a scar at the time of the study is not sufficient reason to reject the diagnosis of post-infarction cardiosclerosis.

4. HEART FAILURE IN IHD

This term to designate a separate form of IHD is not accepted in Russia, since heart failure in IHD can be based on various causes: acute myocardial infarction, post-infarction cardiosclerosis, cardiac aneurysm, as well as severe rhythm disturbances in atherosclerotic cardiosclerosis. If patients do not have clinical or electrocardiographic signs of CAD (subject to exclusion of all other causes of heart failure), the diagnosis of CAD remains doubtful.

5. ARRHYTHMIAS

We can talk about the arrhythmic variant of IHD only in cases where arrhythmias are the only symptom of ischemic heart disease. In such cases, the diagnosis of coronary artery disease remains presumptive until selective coronary angiography is performed, which reveals obstructive lesions of the coronary bed.

In most patients, arrhythmias are combined with other clinical manifestations of coronary artery disease, which makes the diagnosis easier. Arrhythmias in coronary artery disease are often a symptom of atherosclerotic cardiosclerosis, especially in the presence of angina or heart failure. However, isolated rhythm and conduction disturbances are not pathognomonic signs of cardiosclerosis. The diagnosis of atherosclerotic cardiosclerosis in the absence of both arrhythmias and heart failure remains questionable.

CLINICAL PICTURE OF ANGINA IN IHD

Angina may be the only manifestation of coronary artery disease - cardiosclerosis (diffuse atherosclerotic or focal post-infarction), chronic cardiac aneurysm.

Many patients who first consulted a doctor about angina pectoris, without knowing it, had previously suffered a myocardial infarction (according to ECG data), and in some patients arrhythmia or heart failure is detected as a manifestation of coronary artery disease.

More often, patients are diagnosed with exertional angina, which occurs in response to physical or emotional stress and can be provoked by other conditions accompanied by tachycardia and increased blood pressure.

Resting angina, which occurs in the absence of obvious provoking factors, but upon closer examination turns out to be heterogeneous in origin, deserves special consideration.

Angina pectoris

Recognizing angina pectoris is a reliable way to diagnose coronary artery disease, and assessing the frequency and severity of angina attacks and their dependence on the level of physical activity allows us to assess the functional state of the coronary circulation and myocardium. Already at the outpatient stage of examining the patient, relying only on a detailed questioning about the patient’s complaints and anamnesis, without resorting to complex and expensive research methods, 60% of patients can be correctly diagnosed with IHD.

An attack of angina pectoris can manifest itself in various forms, but when analyzing the patient’s complaints and questioning, it is important to be able to identify the features that are fundamental to the diagnosis. Those features of an angina attack that are not obligatory components of the anginal syndrome, but their presence can confirm the diagnosis, may also have important diagnostic significance. And finally, features of pain sensations that are not characteristic of myocardial ischemia and help exclude the diagnosis of angina can be identified.

The nature of pain deserves special consideration. Patients describe an attack of angina as a cutting, pressing pain, as if burning the heart, squeezing the throat. However, often an anginal attack is perceived by patients not as obvious pain, but as an inexpressible discomfort, which can be characterized as heaviness, compression, tightness, compression or dull pain. If the doctor limits himself in such cases to asking whether the patient is experiencing chest pain, this important symptom may go unnoticed. Sometimes a patient with obvious angina may deny the presence of pain, which leads to a diagnostic error.

The retrosternal localization of pain with irradiation to the left shoulder and arm is the most typical. In most cases, the pain begins inside the chest behind the sternum and from there spreads in all directions. The pain often begins behind the upper part of the sternum rather than the lower part. Less commonly, it begins on the left near the sternum, in the epigastrium, in the area of ​​the left scapula or left shoulder.

The irradiation of anginal pain to the shoulder blade, neck, face, jaw, teeth, as well as to the right shoulder and right shoulder blade is well known. Rare cases of pain radiating to the left half of the lower back and the left side of the abdomen, and to the lower extremities have been described. The more severe the angina attack, the wider the area of ​​pain irradiation may be.

Although radiating pain is an important sign of angina, its presence is not necessary to make a diagnosis.

The patient's gesture is important, which can sometimes tell the doctor more than a verbal description of pain in the chest.

A reliable sign of an anginal attack is the symptom<сжатого кулака>when the patient places his fist or palm, or two palms, on his sternum to describe his sensations. If the patient is not inclined to gesture, the doctor may ask the patient to indicate the location of the pain with a gesture.

The intensity and duration of anginal pain varies markedly in different patients. They are not strictly dependent on the number of affected arteries of the heart and the degree of their damage. However, in the same patient with a stable course of the disease, angina attacks are quite comparable to each other.

The duration of an anginal attack during angina is almost always more than one minute and usually less than 15 minutes. More often an attack of angina lasts 2-5 minutes and less often lasts up to 10 minutes. The attack will be shorter and less intense if the patient immediately stops the exercise and takes nitroglycerin. Thus, if an attack of angina is caused by physical stress, its duration and intensity depend to a certain extent on the patient’s behavior. If an angina attack occurs in response to emotional stress, when the patient is unable to control the situation, the attack may be protracted and more intense than in response to physical activity.

If the patient does not take nitroglycerin, the painful attack may be prolonged. A painful attack lasting more than 15 minutes requires medical intervention. In some cases, a prolonged attack of angina may immediately precede the occurrence of acute myocardial infarction.

Pain during angina pectoris increases gradually in the form of successive, increasingly intensifying attacks of burning and compression. Having reached its climax, which is always approximately the same in intensity for a given patient, the pain quickly disappears. The duration of the period of increase in pain always significantly exceeds the duration of the period of its disappearance.

Pain that lasts in seconds (less than one minute) is usually of non-cardiac origin. In most cases, prolonged attacks of pain that last many hours, if myocardial infarction has not developed, are not associated with damage to the large coronary arteries and have a different origin.

The most important sign of angina is the appearance of retrosternal discomfort during physical activity and the cessation of pain 1-2 minutes after the load is reduced.

In the classic description of the anginal syndrome, very short and expressive, made by Theberden more than 200 years ago, attention is drawn to the clear connection between the appearance of anginal pain and physical stress (walking uphill, especially after eating) and their disappearance when the load is stopped.

If the load (fast walking, climbing stairs) does not cause retrosternal discomfort, then it can most likely be assumed that the patient does not have significant damage to the large coronary arteries of the heart.

Thus, the connection between the occurrence of pain and physical activity is one of the most important signs of classic angina pectoris. If pain does not occur at the height of the load, but some time after its completion, this is not typical for angina pectoris. Pain that regularly appears after exercise or after a hard day marked by physical and emotional stress is almost never associated with cardiac ischemia. An anginal attack is typically provoked in the cold or in a cold wind, which is especially often observed in the morning when leaving the house. Cooling the face stimulates vasoregulatory reflexes aimed at maintaining body temperature. These reflexes cause vasoconstriction and systemic arterial hypertension, thereby increasing oxygen consumption by the myocardium, which provokes an attack of angina.

In patients with changes in the psychoemotional state, angina attacks may occur with a lesser degree of damage to the coronary arteries. The frequency of angina attacks largely depends on how often the circumstances that provoke the pain are repeated. If the patient avoids exposure to factors that provoke anginal pain, then angina attacks occur less frequently. Of course, not everything is determined by the patient’s behavior. The more pronounced the pathology of the coronary arteries, the lower the threshold for pain in response to provoking factors.

An attack of angina is usually relieved by nitroglycerin. Under its influence, sensations of chest discomfort disappear completely or partially. This is an important, but not mandatory sign for diagnosis.

Another important sign of anginal syndrome is that the attack is stopped more quickly when the patient is sitting or standing. During a typical attack of angina, patients avoid lying down. In the supine position, the volume of the left ventricle and the tension of the myocardial wall increase, which leads to an increase in intraventricular pressure and an increase in oxygen consumption by the myocardium. In a sitting or standing position, the myocardial oxygen demand decreases. Autonomic symptoms can sometimes accompany an attack of angina. In these cases, there is increased breathing, pale skin, dry mouth, increased blood pressure, extrasystole, tachycardia, and the urge to urinate.

Expressiveness autonomic symptoms cannot serve as a criterion for the severity of anginal syndrome, since the vegetative coloring of an attack is also characteristic of cardialgia of various origins. Some authors even believe that the more severe the degree of coronary insufficiency, the more stingy the patient is with external manifestations during an attack of angina.

ANGINA AT REST

The occurrence of attacks of resting angina in a patient who previously suffered only from exertional angina marks a transition to a more severe phase of the disease. In patients with angina at rest, who usually have severe stenosing coronary atherosclerosis, compensatory mechanisms for maintaining coronary blood supply are disrupted. As the disease progresses, a period comes when minimal stress is required for an angina attack to occur (low-tension angina) and, finally, attacks begin to occur in conditions of physical rest (in bed, in sleep, etc.). Angina at rest, joining exertional angina, is usually combined with it. During the day, such a patient experiences attacks of angina pectoris associated with walking or other physical activity, and at night attacks of angina pectoris at rest may occur.

In some patients, attacks of resting angina may occur as a result of a primary decrease in blood flow through a large coronary artery, as a consequence of an increase in its vasomotor tone (i.e., as a result of vasospasm). In a number of patients in this group, attacks of angina at rest can be combined with a relatively high tolerance to physical activity, and sometimes they can be isolated, that is, observed in the absence of attacks of angina pectoris.

The factors that provoke attacks of angina at rest are diverse. In most cases, the onset of an attack is preceded by conditions that increase the myocardial oxygen demand. The cause of an attack of angina at rest may be a transistor increase in blood pressure or an attack of paroxysmal tachycardia.

Attacks of angina at rest often occur at night during sleep. The patient wakes up from the feeling that someone is preventing him from breathing, or due to pain in the heart area. Sometimes the patient reports that in the dream he had to perform heavy physical activity (lifting weights, running fast).

The intensity and duration of pain with angina at rest is much greater than with angina on exertion. Attacks may be accompanied by fear of death and pronounced vegetative reactions. These attacks force patients to wake up, sit up in bed, and take nitroglycerin. An attack of angina occurs during the so-called rapid phase of sleep. More often, angina attacks of this origin occur in the early morning hours. The administration of beta-blockers to such patients appears to be effective.

In a number of patients, angina at rest occurs due to left ventricular failure, which intensifies in the horizontal position of the patient. In the supine position of the patient, the volume of the left ventricle increases, which leads to an increase in myocardial tension. This increases the myocardium's need for oxygen. This type of angina usually occurs in patients with a marked decrease in myocardial function.

In the pathogenesis of nocturnal angina attacks in these patients, water-electrolyte balance disorders are of particular importance.

The administration of diuretics and cardiac glycosides can have a good therapeutic effect in this type of angina, helping to prevent attacks. The attack itself can be stopped by the patient moving to a sitting position, as well as by taking nitroglycerin, which, being a powerful, fast-acting vasodilator, promotes blood redistribution and unloading of the pulmonary circulation.

SPECIAL FORM OF ANGINA

A number of patients may have a special form of angina (variant angina, Prinzmetal type angina). Named after the clinician who was one of the first to describe it as an independent form of angina in 1959.

A special form of angina (Prinzmetal type) is characterized by attacks of anginal pain that occur at rest, which are accompanied by transient electrocardiographic signs of damage to the subepicardial parts of the myocardium.

In the pathogenesis of Prinzmetal's angina, the periodically occurring spasm of the coronary arteries of the heart is of decisive importance. Angiospasm can occur in patients with both unchanged and slightly changed coronary arteries, and with a widespread stenotic process in the coronary arteries.

The anatomical state of the coronary bed largely determines the nature of clinical manifestations in a particular form of angina. Three groups of patients with a special form of angina (Prinzmetal type) can be distinguished in which spasm occurs:

1) in a normal or slightly changed coronary artery;

2) in a single coronary artery affected by atherosclerosis;

3) against the background of widespread atherosclerosis of the coronary arteries.

The nature and location of chest pain differs little from the pain associated with ordinary angina. An attack usually occurs at rest or during the patient’s normal physical activity. In approximately half of patients, Prinzmetal's angina develops without warning. One of the signs of a special form of angina is the cyclical nature of pain.

A special form of angina pectoris often occurs in the form of series consisting of 2-5 painful attacks, which follow one after another at intervals of 2-3 to 10-15 minutes. In some patients, attacks may have a shorter or longer duration. The maximum duration of an attack can reach 45 minutes. A prolonged attack of a special form of angina is usually regarded by doctors as a threatening myocardial infarction and serves as a basis for hospitalization. The period of pain increase in a special form of angina is approximately equal to the period of its disappearance, whereas in ordinary angina the first period is noticeably longer than the second.

The most important diagnostic sign of Prinzmetal's angina is the elevation of the ST segment of the ECG at the time of a painful attack, which indicates ischemia of not only the subendocardial, but also the subepicardial layer of the myocardium. The severity of ECG changes varies from a slight upward shift of the ST segment by 2 mm to a sharp rise of 20-30 mm, as a result of which the ECG curve becomes monophasic. ST segment elevation is recorded more often within 10-20 minutes, after which it reaches the isoelectric level.

A special form of angina does not include prolonged elevations of the ST segment, which are one of the phases in the evolution of the electrocardiographic picture of acute myocardial infarction.

Depending on the location of the spasm in the coronary artery, in some patients a sign of a special form of angina may be transient depression of the ST segment, which requires special evidence in each individual case. At the time of the attack, other less specific ECG changes of a transient nature are also possible, in particular - an increase in the voltage of the waves and the widening of the R wave, the transient appearance of the Q wave and a short-term sharpening of the T wave. In approximately half of patients with a special form of angina, various transient disturbances of heart rhythm are recorded: extrasystole , paroxysmal tachycardia.

Cases of clinical death caused by ventricular fibrillation have been described. ECG changes more often correspond to the anterior localization of myocardial damage, less often lesions of the posteroinferior or lateral are detected.

In most patients, the localization of ECG changes corresponds to the localization of the coronary arteries supplying blood to this area of ​​the myocardium. This pattern is especially clear when one coronary artery is affected. Between attacks, the ECG may be normal or altered.

The resting ECG outside an attack is normal, as a rule, in patients with unchanged or slightly changed coronary arteries. ECG abnormalities in the interictal period are detected more often, the greater the prevalence of coronary arteriosclerosis. With stenosis of several branches of the coronary arteries, resting ECG changes are found in 90% of patients.

A patient suffering from a special form of angina can tolerate physical activity well and feel healthy throughout the day. The results of an electrocardiographic exercise test may be negative. Good tolerance to physical activity and a negative bicycle ergometer test do not provide grounds to exclude the diagnosis of a special form of angina, but suggest that the patient’s coronary arteries are either unchanged or have a single local stenosis.

In the diagnosis of a special form of angina, urgent registration of an ECG immediately at the time of an attack of resting angina is of great importance. Identification of specific ECG changes provides important prerequisites for the diagnosis of angina pectoris of this form. In patients with typical attacks of Prinzmetal's angina, accompanied by characteristic ECG changes, transient elevations of the ST segment may be observed, not accompanied by pain.

Not every attack of chest pain with a special form of angina is a manifestation of the underlying disease. Registration of a daily ECG in these cases has differential diagnostic value. In patients with multiple spontaneous attacks of Prinzmetal's angina during the day, most attacks may not be accompanied by pain, but are manifested only by transient ischemic ECG changes. Diagnosis of a special form of angina is of great practical importance, as it allows the application of pathogenetic treatment and determination of the prognosis. The appearance of attacks of a special form of angina pectoris against the background of angina pectoris has an unfavorable prognostic value.

Prinzmetal's angina, which develops against the background of severe damage to the coronary arteries, often leads to the development of myocardial infarction or death associated with severe cardiac arrhythmias, in particular, paroxysmal ventricular tachycardia.

Patients with a special form of angina require inpatient monitoring and treatment. Relapses of a particular form of angina have an unfavorable prognostic value.