Heart failure coronary heart disease. What is ischemic heart disease and treatment

Ischemic disease heart disease is an extremely common pathological condition that develops as a result of chronic coronary insufficiency and impaired saturation of myocardial tissues with nutrients. IHD is considered the most common cause of premature disability. In addition, this condition often leads to the death of people suffering from coronary artery disease. When coronary heart disease develops, what it is and the reasons for its appearance, to a person who does not have medical education, is very difficult to understand. But at the same time, it is very important for the patient to fully understand the danger of ischemia and follow the doctor's recommendations.

Most often similar violation observed in men, which is the reason for their premature death. In women, signs of coronary heart disease, as a rule, are clearly manifested over the age of 50, since until this time the body is reliably protected. hormonal background. In case of any deviations in the work of cardio-vascular system do not self-medicate, as only a timely visit to the doctor and early start therapy avoids the most negative consequences.

Causes of coronary heart disease

For modern medicine the etiology of this condition is no longer a mystery. Approximately in 70% of cases, ischemic changes in the tissues of the heart develop against the background of atherosclerosis of the coronary arteries. Even a slight narrowing of the lumen of the blood channels that feed the myocardium, due to the formation cholesterol plaque may lead to the appearance of such a pathological condition. As a rule, with 75% coronary stenosis, patients develop severe angina pectoris. The etiology of CAD includes other endogenous and exogenous factors, including:

• sedentary lifestyle;
• obesity;
• irrational nutrition;
• psycho-emotional overstrain;
• a long course of taking hormonal contraceptives;
• smoking;
• alcohol abuse;
• hypertension;
• atrial fibrillation;
• elevated blood cholesterol levels;
• violation of water and electrolyte balance;
• thyroid dysfunction;
• diabetes;
• cholelithiasis.

In addition, there is a high risk development of coronary artery disease those with a genetic predisposition. Significantly increases the chance of this pathological condition in the elderly, which in most cases is associated with hormonal disruptions. As practice shows, the higher the slew rate ischemic injury myocardial tissue is observed in the presence of a combination adverse factors. In some cases, the prerequisites for the appearance of this pathological condition are laid when intrauterine development. Especially dangerous are heart defects that have not been identified and treated.

Classification of coronary disease

Modern cardiology takes into account a lot of parameters that characterize the development of this condition. Depending on the characteristics of the existing manifestations, there are the following types ischemic heart disease:

• sudden coronary death;
• angina pectoris;
• painless form of myocardial ischemia;
• heart attack;
• postinfarction cardiosclerosis;
• conduction and rhythm disturbances;
• heart failure.

Each of these forms has its own characteristics of development and course. For example, sudden coronary death, as a rule, is the result of an abrupt cessation of myocardial oxygen supply as a result of coronary artery thrombosis. In addition, a similar pathological condition, accompanied by sudden stop heart, may develop due to electrical instability of the myocardium. In most cases, with such a rapid aggravation of the degree of tissue ischemia, the death of the patient is observed in a matter of minutes. Sometimes from the onset of an attack to lethal outcome may take up to 6 hours.

Myocardial infarction can be both large-focal and small-focal. In this case, acute ischemic heart disease is observed, which can manifest itself characteristic symptoms. In the presence of given state some parts of the heart begin to suffer from a lack of oxygen, so myocardial cells die. May develop cor pulmonale. With timely provision medical care the chances of avoiding death are quite high.

After a heart attack and in the presence of chronic atherosclerosis, first cardiac ischemia is observed, which then leads to the replacement of dead myocytes. fibrous tissue. This process leads to the formation of heart failure. Painless ischemia of the posterior wall of the myocardium is characteristic of people suffering from diabetes mellitus, as well as those who have a high pain threshold. In this case, atrial fibrillation, that is, spontaneous atrial fibrillation, can cause the death of a person who previously complained of heart problems. Such sharp deterioration conditions are often the first symptom of coronary artery disease.

A common form of ischemic disease is angina pectoris. It can be stable, unstable and spontaneous. A similar form of coronary heart disease in most cases long time does not appear severe symptoms. Usually this pathological condition ends with myocardial infarction. In some cases, atrial fibrillation or severe arrhythmia may occur.

It is worth noting: when coronary heart disease occurs, the clinic largely depends on its form of flow and the severity of damage to the heart tissues. In cardiology, the term acute coronary syndrome is now increasingly used, under which various types of this pathological condition are hidden, including:

• myocardial infarction;
• unstable angina;
• atrial fibrillation;
• and sudden coronary death resulting from tissue death.

Symptomatic manifestations of ischemic disease

Usually this pathological condition is characterized by an undulating course, characterized by periods of relapses and remissions. However, in about 1/3 of patients, developing cardiac ischemia, which often causes premature death, does not lead to any deterioration in well-being and the appearance of pain.

In most cases, the disease develops over decades without manifesting severe symptoms. However, after changes in the myocardium reach a critical point, they can be detected as common signs pathology, and specific symptoms, inherent separate form course of IBS. TO characteristic manifestations cardiac ischemia include:

• chest pain radiating to arms lower jaw or back;
• deterioration in physical or emotional overstrain;
• clouding of consciousness;
• fainting;
• general weakness;
• dyspnea;
• bouts of dizziness;
• excessive sweating;
• swelling of the lower extremities.

As a rule, all these symptoms of coronary heart disease do not appear simultaneously. In most patients, against the background of a decrease in the nutrition of brain tissues, various neurological disorders, including causeless feelings of anxiety, apathy, panic attacks and Bad mood. The most acute ischemic heart disease manifests itself in the form of sudden coronary death. In this case, respiratory arrest is observed, and the pulse ceases to be detected. In addition, there is a loss of consciousness, pupils dilate, heart sounds are not audible, skin take on a pale gray tint.

In most cases of cardiac ischemia with such an acute onset, the death of the patient is observed within a few minutes, less often it can take from 2 to 6 hours. Only in rare cases with timely medical care, doctors manage to save the patient's life, although this does not guarantee the absence of the consequences of this condition. For example, a patient often has persistently increased pressure, arrhythmia and other abnormalities appear. Thus, it is very important to understand why ischemia is dangerous and to undergo scheduled examinations at regular intervals.

Complications of coronary heart disease

Hemodynamic disturbances in the heart muscle and increasing ischemic damage tissues provoke numerous morphological changes, which determine the form of the course and the prognosis of coronary artery disease. Due to the development of this condition, the appearance of insufficiency of the energy metabolism of myocardial cells is observed. In most patients, due to damage to the tissues of the heart, there is a violation contractile function left ventricle, which carries transitory nature. Due to such processes, a rapid decrease in the number of cardiomyocytes can be detected. They are replaced connective tissue that is unable to fulfill their function.

Among other things, there is a violation of diastolic and systolic function. Due to damage to the tissues of the heart, there is a disorder of conduction, excitability and contractility myocardium. All these changes, as a rule, are irreversible and lead to persistent heart failure. Among other things, against the background of IHD, acute conditions appear, including heart attacks and strokes.

Methods for diagnosing coronary heart disease

Since IHD is manifested by a wide variety of symptoms, it is necessary to entrust the definition of the problem to the doctor. If you suspect the presence of this pathological condition, you must definitely consult a cardiologist and undergo comprehensive examination. First of all, the doctor needs the most complete history to find out the conditions under which certain symptoms appear, the duration pain attacks and the nature of the symptoms present. In addition, an important diagnostic criterion is the evaluation of the effectiveness of the use of nitroglycerin preparations.

Next, auscultation is carried out, which allows you to obtain certain data regarding the available pathological changes and make a preliminary diagnosis. To clarify it, electrocardiography and ECG are usually prescribed first of all. This is the main research method for IHD, which allows you to identify characteristic changes even in cases where the expressed manifestation of the disease is absent. In addition, there are lab tests blood, which allow to determine the presence of enzymes and substances resulting from the destruction of cardiomyocytes. Among other things, a study of the level of cholesterol and glucose, ALT and AST is required. Deciphering the data received by the doctor allows him to determine how this condition will develop further.

An echocardiogram may be done to determine the size of the heart. This research method allows you to evaluate the contractile capabilities of the myocardium, determine the condition of the valves and cavities of the heart and identify acoustic noise. In cases of dispute and when there are suspicions about the presence of other pathological conditions stress echocardiography may be indicated, which allows to detect the presence of myocardial ischemia during dosed physical activity. Transesophageal electrocardiography is often performed to assess conduction. This research method is not used in all cases. During this diagnostic test, a special catheter is inserted into the esophagus, through which it is possible to register all indicators of the work of the heart without the interference that is usually created by the skin and adipose tissue. Given that such an examination for coronary heart disease is not very pleasant for the patient, it is far from always carried out.

Often, coronary angiography is prescribed to determine the patency of the vessels that feed the myocardium. Usually this study allows you to determine the degree of need for surgery on the coronary arteries. Similar Method diagnosis is not 100% safe, as it is quite possible allergic reactions including anaphylactic shock.

Comprehensive treatment of coronary heart disease

The approach to therapy depends largely on the available symptomatic manifestations with IHD, as well as the general condition of the patient's body. Ischemic heart disease can be treated with conservative methods And surgical interventions various types. Methods of therapy are selected by the attending physician, depending on the severity of the existing symptomatic manifestations.

If this disease is detected at an early stage and is not accompanied by pronounced signs hemodynamic disturbances, it will be enough non-drug treatment. Usually the doctor recommends the rejection of all bad habits. Among other things, the patient needs to completely change his lifestyle. Strenuous exercise, long walks fresh air, as well as a sparing diet low in substances that contribute to the formation of atherosclerotic plaques, can eliminate areas of damage to the heart muscle and improve general state of cardio-vascular system.

A necessary measure is to reduce the level of salt consumed. In the presence of excess weight prescribed a low-fat diet. Patients are advised to reduce daily dose consumed water to reduce the risk of edema and other manifestations of this pathological condition. In such mild cases, when the patient does not have chest pain, and complaints are limited to periodic discomfort, it can help restore the functioning of the organ and prevent further development of heart wall damage. Spa treatment. Often, patients themselves neglect the recommendations of doctors, considering them optional, which usually has extremely adverse consequences.

If the stage at which the development of coronary heart disease was detected is advanced, in addition to the methods of conservative therapy, targeted treatment with drugs is required. The scheme for taking such drugs is prescribed by the doctor individually, depending on the characteristics of the existing symptomatic manifestations. In most cases, beta-blockers, antiplatelet agents and hypocholesterolemic agents are prescribed. When the patient has no contraindications, antiarrhythmic drugs, diuretics, nitrates and other drugs may be additionally prescribed.

In the presence of a severe form of ischemia of the heart, when conservative therapy does not allow to achieve a pronounced effect, the patient is assigned a consultation with a cardiac surgeon to determine whether surgical intervention. Often surgical therapy used when there is a risk of developing a heart attack. To restore blood circulation in the affected tissue area, it is often performed coronary artery bypass grafting. This surgical intervention involves the imposition of an autovenous anastomosis. This allows blood to bypass the affected areas of the blood vessels, which contributes to the nutrition of tissues damaged by ischemia. Such an intervention can be carried out both using an artificial education apparatus and on a working organ. In some cases, a minimally invasive operation called transmissible coronary angioplasty can be performed. This technique involves the introduction of a catheter with a balloon into the damaged areas of the arteries, which allows you to expand the narrowed blood vessels.

Currently, combined methods of treatment are actively used, including both prompt elimination existing sections of blood vessels that prevent the nutrition of myocardial tissues, and conservative methods impact. In most cases, this therapy, combined with lifestyle changes, restores the health of the heart tissues. The prognosis for coronary artery disease depends on many factors, including the stage of neglect of the process, the complexity of therapy and the person's willingness to follow the doctor's recommendations.

Prevention of coronary disease

Currently the only way prevent the formation severe pathologies cardiovascular system is to maintain the maximum healthy lifestyle life. very important with young age avoid bad habits, including smoking and drinking alcohol. Toxic Substances contained in this tobacco smoke, and the decomposition products of alcohol, lead to damage to the tissues of the heart and the walls of blood vessels. In addition, it is very important to support normal weight body. You should start eating right, including a large number of vegetables and fruits in the diet.

Physical inactivity provokes ischemic changes, so it is necessary to perform physical exercises in order to create a sufficient load on the cardiovascular system. Among other things, people who are predisposed to the appearance of coronary heart disease should try to avoid serious emotional upheavals. Compliance with the regime of work and rest is necessary measure to reduce the risk of developing this pathological condition.

Section 1. Definition of the concept of CHF, causes of development, pathogenesis, classification and goals of therapy

1.1 Definition of the concept and causes of CHF development

CHF is a syndrome that develops as a result of various diseases cardiovascular system, leading to a decrease in the pumping function of the heart (although not always), chronic hyperactivation of neurohormonal systems, and manifested by shortness of breath, palpitations, increased fatigue, limitation of physical activity and excessive delay fluids in the body.

It should be remembered that the severity of CHF symptoms can be completely different - from minimal manifestations that occur only when performing significant loads, to severe shortness of breath that does not leave the patient even at rest. As discussed in section 1.2, the number of patients with early manifestations CHF is several times greater than severe patients requiring hospital treatment. For patients with decreased LV pumping [defined as ejection fraction (EF) less than 40%], without overt symptoms of CHF, apply special definition- asymptomatic LV dysfunction.

On the other hand, CHF is a progressive syndrome, and those patients who today have only latent CHF can move into the group of the most severe patients who are difficult to treat within 1-5 years. That's why early diagnosis CHF and LV dysfunction, and, consequently, early treatment of such patients is the key to success in the treatment of heart failure. Unfortunately, in Russia, diagnoses of the initial stages of CHF are extremely rare, which indicates an underestimation by practitioners of the severity of this syndrome.

CHF syndrome can complicate the course of almost all diseases of the cardiovascular system. But the main causes of CHF, accounting for more than half of all cases, are ischemic (coronary) heart disease (CHD) and arterial hypertension, or a combination of these diseases.

With coronary artery disease, development acute infarction myocardium(AMI) with subsequent focal decrease in myocardial contractility and dilatation of the LV cavity (remodeling) is the most common cause of CHF. With long-term chronic coronary insufficiency without myocardial infarction, loss of myocardial viability, a diffuse decrease in contractility ("sleeping" or hibernating myocardium), dilatation of the heart chambers and the development of symptoms of CHF can progress. This situation is interpreted in the world as ischemic cardiomyopathy.

In arterial hypertension, changes in the LV myocardium, called hypertensive heart, may also be a cause of CHF. Moreover, in many of these patients, myocardial contractility and LV EF remain normal for a long time, and the cause of decompensation may be disturbances in diastolic filling of the heart with blood.

Due to the insufficient prevalence of surgical correction, acquired (most often rheumatic) valvular heart disease is the third leading cause of CHF in Russia. This testifies to the insufficient radicalism of practicing therapists, who often do not refer such patients for surgical treatment. From a modern standpoint, the presence valvular disease heart disease in the vast majority requires mandatory surgical treatment, and the presence of valvular stenosis is a direct indication for surgery.

The next common cause of CHF is non-ischemic cardiomyopathies, including both idiopathic dilated cardiomyopathy (DCM) and specific ones, of which most widespread have cardiomyopathy as an outcome of myocarditis and alcoholic cardiomyopathy.

Other diseases of the cardiovascular system rarely lead to the development of CHF, although, as mentioned earlier, cardiac decompensation can be the final of any disease of the heart and blood vessels.

1.2 Pathogenesis and characterization different forms CHF

The fundamental "novelty" of modern ideas about the pathogenesis of CHF is associated with the fact that not all patients have symptoms of decompensation as a result of a decrease in the pumping (propulsive) capacity of the heart. Modern scheme The pathogenesis of CHF shows that the three key events in the development and progression of CHF are:

• disease of the cardiovascular system;
• decrease in cardiac output (in most patients);
• sodium retention and excess fluid in organism.

After a disease of the cardiovascular system, a sufficiently long period of time may pass (for example, with arterial hypertension, chronic form coronary artery disease, DCM, after myocarditis or the formation of heart disease) to a decrease in cardiac output (CO). Although in acute macrofocal myocardial infarction, the time between the onset of the disease, the decrease in output and the onset of symptoms of acute heart failure can be calculated in hours and even minutes. But in any case, already at a very early stage, compensatory mechanisms are activated to maintain normal cardiac output. From point of view modern theory, the main role in the activation of compensatory mechanisms (tachycardia, Frank-Starling mechanism, constriction peripheral vessels) plays hyperactivation of local or tissue neurohormones. This is mainly the sympathetic-adrenal system (SAS) and its effectors - norepinephrine (NA) and adrenaline and the renin-angiotensin-aldosterone system (RAAS) and its effectors - angiotensin II (A II) and aldosterone (ALD), as well as the natriuretic system. factors. The problem is that the "running" mechanism of hyperactivation of neurohormones is irreversible. physiological process. Over time, short-term compensatory activation of tissue neurohormonal systems turns into its opposite - chronic hyperactivation. Chronic hyperactivation of tissue neurohormones is accompanied by the development and progression of systolic and diastolic LV dysfunction (remodeling). The CO gradually decreases, but the classic manifestations of CHF during this period of time, as a rule, cannot be identified. Patients have symptoms of the earliest stages of CHF. which are revealed only when applying special load tests. These facts were identified and described in detail by N.M. Mukharlyamov, L. Olbinskaya et al.

In the future, the development of CHF symptoms (sodium retention and excess fluid) occurs along the classical path. After a decrease in the pumping function of the heart, involvement in pathological process other organs and systems, primarily the kidneys, which is supported by the activation of circulating neurohormones (mainly HA, A-11, ADD). Chronic hyperactivation of circulating neurohormonal systems is accompanied by the development of clinical symptoms of CHF in one or both circulations.

In addition, it is clear that in some patients only the development of severe diastolic dysfunction leads to the progression of disorders. neurohumoral regulation with the involvement of circulating hormones in the process and the appearance of fluid retention and obvious signs of decompensation with preserved CO. As a rule, the largest part of this group is made up of patients with arterial hypertension. These patients have long-term high blood pressure accompanied by the development of LV myocardial hypertrophy, thickening of its walls. At the same time, LV myocardial rigidity increases and its filling with blood in diastole is disturbed, which may be accompanied by the appearance of signs of CHF in normal CO.

Thus, not all patients with symptoms of CHF have the same mechanism for the development of the syndrome. There are three main types of patients. Only half of patients with CHF have obvious symptoms decompensation of cardiac activity, while the rest, despite the decrease in the pumping function of the heart, clear signs there are no decompensations. Among patients with obvious manifestations of decompensation, only half have a reduced CO, and the other half are diagnosed with LV diastolic dysfunction. This scheme is called the "rule of halves". It shows that patients with a detailed picture of decompensation, congestion - this is only the visible part of the iceberg, constituting no more than a quarter of all patients with CHF.

1.3 Classification of CHF

The most convenient and practical classification is the functional classification of the New York Heart Association, which involves the allocation of four functional classes according to the ability of patients to endure physical activity. This classification is recommended for use by WHO.

As is well known, any classification is conditional to a certain extent and is created in order to distinguish either the causes of the disease, or the course of the disease, or the manifestations of the disease in terms of severity, treatment options, etc. The meaning of the classification is to give doctors the keys to better diagnosis and treatment of any disease. The most brilliant idea of ​​creating a perfect classification is doomed to failure if it is not needed or too complicated and confusing. And vice versa, if the classification is easily perceived, then it lives, despite the fact that the principles underlying it are not ideal, and some provisions may cause controversy. best example of this type is the domestic classification of CHF (circulatory failure), created by V.Kh. Vasilenko and ND. Strazhesko with the participation of G.F. Lan-ga. This classification was adopted at the XII All-Union Congress of Therapists in 1935. We can safely say that this was the achievement of the Russian medical school, since the classification was the first in which an attempt was made to systematize the nature of the changes, the staging of the process and the manifestations of CHF. We deliberately do not draw a line between CHF (as this syndrome is designated by the entire medical world) and circulatory failure, as was customary in the USSR, and now in Russia, taking them as synonyms.

1.3.1 Functional classification of CHF

Why in last years so many discussions around the well-tested and so beloved by doctors classification of CHF, which, despite all the shortcomings, is quite applicable and, with additions, outlines almost all stages of CHF, from the mildest to the most severe? There are 2 answers to this.

Fully functional classifications are obviously simpler and more convenient in terms of controlling the dynamics of the process and physical abilities patient. This proved the successful application of the functional classification of coronary artery disease, which also hardly made its way into the minds and hearts of Russian doctors.

"One soldier cannot keep up, but the whole platoon cannot," i.e. one cannot ignore the fact that all countries of the world, with the exception of Russia, use the functional classification of the New York Heart Association, which is recommended for use by the International and European Societies of Cardiology.

New York Heart Association Functional Classification of CHF was adopted in 1964. It has been revised, supplemented and criticized many times, but nevertheless it is successfully used all over the world. Its fate is similar to the fate of the classification of V.Kh. Vasilenko and ND. Strazhesko. "Only lazy" among self-respecting cardiologists does not criticize it, but all practical doctors continue to use it with success.

The principle underlying it is simple - an assessment of the patient's physical (functional) capabilities, which can be identified by a doctor with a targeted, thorough and accurate history taking, without the use of complex diagnostic techniques. Four functional classes (FC) were identified.

/ FC. The patient does not experience restrictions in physical activity. Ordinary exercise does not cause weakness (lightheadedness), palpitations, shortness of breath, or anginal pain.

P FC Moderate limitation of physical activity. The ballroom is comfortable at rest, but doing normal physical activity causes weakness (lightheadedness), palpitations, shortness of breath, or anginal pain.

III FC. Severe limitation of physical activity. The patient feels comfortable only at rest, but less than usual physical activity leads to the development of weakness (lightheadedness), palpitations, shortness of breath or anginal pain.

IV FC Inability to perform any load without discomfort. Symptoms of heart failure or angina syndrome may occur at rest. When performing a minimum load, discomfort increases.

As you can see, everything is very simple and clear, although there are some difficulties here. How to draw a line between, for example, moderate and severe restriction physical activity? This assessment becomes subjective and largely depends on the patient's perception of his well-being and the real interpretation of these perceptions of the patient by the doctor, who must eventually set only the Roman numeral from I to IV.

However, the results of numerous studies have shown that there are quite noticeable differences between FCs. The easiest way to determine the FC in patients is by the distance of a 6-minute walk. This method has been widely used in the last 4-5 years in the USA, including in clinical trials. Patient condition capable of 6 min. overcome from 426 to 550 m, corresponds to mild CHF; from 150 to 425 m - medium, and those who are not able to overcome even 150 m - severe decompensation. That is, the trend of the mid and late 90s is the use of the simplest methods to determine functionality patients with CHF.

Thus, the functional classification of CHF reflects the ability of patients to perform physical activity and outlines the degree of changes in the functional reserves of the body. This is especially significant in assessing the dynamics of the patients' condition. Just what domestic classification looks faulty, belongs to the most strengths functional classification.

1.3.2. Methods for assessing the severity of CHF

Assessment of the severity of the patient's condition and especially the effectiveness of the treatment is an urgent task for every practitioner. From this point of view, a single universal criterion for the condition of a patient with CHF is needed.

It is the dynamics of FC during treatment that allows us to objectively decide whether our therapeutic measures are correct and successful. The conducted studies have also proved the fact that the definition of FC to a certain extent predetermines and possible forecast diseases.

The use of a simple and affordable 6-minute corridor walk test makes it possible to quantitatively measure the severity and dynamics of the state of a patient with CHF during treatment and his tolerance to physical activity.

In addition to the dynamics of FC and exercise tolerance, the following are used to monitor the condition of patients with CHF:

• grade clinical condition patient (severity of dyspnea, diuresis, changes in body weight, degree congestion and so on.);
• dynamics of LV EF (in most cases according to the results of echocardiography);
• assessment of the quality of life of the patient, measured in points using special questionnaires, the most famous of which is the questionnaire of the University of Minnesota, designed specifically for patients with CHF.

The annual mortality of patients with CHF, despite the introduction of new methods of treatment, remains high. With FC I, it is 10%, with P, about 20%, with W, about 40%, and with IV, it reaches 66%.

1.4 Goals in the treatment of CHF

main idea modern tactics treatment of a patient with CHF is an attempt to start therapy as early as possible, at the most initial stages disease in order to achieve the greatest possible success and prevent the progression of the process. The ideal outcome of therapy is to return the patient to normal life ensuring its high quality.

Based on the foregoing, the goals in the treatment of CHF are;

1. Elimination of the symptoms of the disease - shortness of breath, palpitations, increased fatigue and fluid retention in the body.
2. Protection of target organs (heart, kidneys, brain, blood vessels, muscles) from damage.
3. Improving the "quality of life".
4. Reducing the number of hospitalizations.
5. Improved prognosis (life extension).

Unfortunately, in practice, only the first of these principles is often implemented, which leads to a rapid return of decompensation, requiring repeated hospitalization. One of the main objectives of this publication is to give practitioners the keys to the successful implementation of all five basic principles of the treatment of CHF. Separately, I would like to define the concept of "quality of life". This is the ability of the patient to live the same full life as his healthy peers who are in similar economic, climatic, political and national conditions. In other words, the doctor must remember the desire of his patient with CHF, who is already doomed to take drugs, often quite unpleasant, to live full life. This concept includes physical, creative, social, emotional, sexual, political activity. It must be remembered that changes in "quality of life" do not always parallel clinical improvement. For example, the prescription of diuretics is usually accompanied by clinical improvement, but the need to be "tied" to the toilet, numerous adverse reactions, characteristic of this group of drugs, definitely worsen the "quality of life". Therefore, when prescribing maintenance therapy, it is advisable to keep in mind not only the clinical improvement, but also the "quality of life" and, of course, the prognosis of patients.

V.Yu.Mareev
Research Institute of Cardiology. A.L. Myasnikova RKNPK Ministry of Health of the Russian Federation

What is heart failure?

Heart failure is a condition in which the function of the heart as a pump that circulates blood and delivers oxygen is insufficient to meet the needs of the body. Heart failure can be caused by:

The heart has two atria (right and left) - these are the upper chambers of the heart and two ventricles (right and left). The ventricles are muscular chambers that push blood out of the heart when the muscles contract (ventricular contraction is called systole). Many diseases can weaken the pumping action of the ventricles. For example, the muscles of the ventricles can be weakened due to a heart attack or myocarditis. Decreased pumping ability of the ventricles due to muscle weakness is called systolic dysfunction. After each contraction of the ventricles (systole), the muscles need to rest in order for blood from the atria to fill the ventricles. This relaxation of the ventricles is called diastole. A disease such as hemochromatosis can cause stiffening of the heart muscle and impair the ability of the ventricles to rest and fill. This is called diastolic dysfunction. In addition, in some patients, although the pumping function and filling potential of the heart may be normal, but abnormally high oxygen demands of body tissues (for example, in patients with hyperthyroidism) can make it difficult for the heart to supply enough blood (so-called high rates of heart failure).

Heart failure can affect many organs in the body. For example, weakened heart muscles cannot supply enough blood to the kidneys, which then begin to lose their normal ability to excrete salt (sodium) and water. Impaired renal function may lead to retention more fluids in organs. For example, fluid may accumulate in the lungs ( pulmonary edema). Fluid can also accumulate in the liver, resulting in a decrease in its ability to rid the body of toxins and produce essential proteins. The absorption of nutrients and drugs may be reduced in the intestines.

Chronic coronary insufficiency

Definitions of the concepts "Coronary insufficiency" and "Ischemic heart disease":

coronary insufficiency is a clinical and pathophysiological concept denoting a reduced ability to provide blood flow through the coronary (coronary) arteries of the heart to the myocardium in accordance with its oxygen needs and nutrients.

Chronic coronary insufficiency due to atherosclerosis coronary vessels and manifested clinically by angina pectoris, is the most frequent form ischemic heart disease (CHD).

According to modern ideas, coronary heart disease can be defined as follows:

Cardiac ischemia is a syndrome that is characterized by a mismatch between myocardial oxygen demand and its supply through the coronary bed due to atherosclerosis of the coronary vessels or spasm, the possibility of a combination of both mechanisms is also recognized.

Classification of chronic coronary insufficiency:

In respect of clinical diagnostics, therapeutic tactics and expert assessment, especially in outpatient settings, the most acceptable classification of chronic coronary insufficiency, proposed by L. I. Fogelson back in 1951

There are three degrees of chronic coronary insufficiency.

I degree of chronic coronary insufficiency - initial: angina attacks are rare and are caused by significant psycho-emotional or physical stress. There are no pronounced atherosclerotic changes in the arteries; a bicycle ergometric test may also be negative.

II degree of chronic coronary insufficiency - stable (pronounced): angina attacks often occur under the influence of moderate, normal physical exertion. The atherosclerotic process narrows the lumen of 1–2 branches of the coronary system by more than 50%.

III degree chronic coronary insufficiency - severe: characterized by angina attacks that occur at low loads and at rest, as well as symptoms of heart failure and heart rhythm disturbances.

stands out clinical variant with a sudden increase in rest angina attacks as unstable angina (a condition threatened by a heart attack).

Treatment of coronary insufficiency:

The therapy of coronary insufficiency is built taking into account the variants of systemic circulatory disorders.

In the hyperkinetic type, a large cardiac output, tachycardia, arterial hypertension. Excitation of the sympathetic-adrenal system is observed.

In the hypokinetic type, cardiac output is reduced, there is a tendency to bradycardia and hypotension.

Affects medical tactics and the presence of circulatory failure.

In complex medical measures chronic coronary insufficiency provides for measures to prevent the progression and treatment of atherosclerosis, as well as agents that improve oxygen balance or increase coronary blood flow. A number of medicines have a complex effect.

In the treatment of each individual patient, his condition, the degree of coronary insufficiency, the presence and severity of heart failure, as well as the mechanism of action of the drugs are taken into account.

Drugs used to treat coronary insufficiency:

Used in an attack of angina pectoris fast acting remedies. Usually it is nitroglycerin (Nitroglycerinum). Assign 0.25 mg under the tongue or 2-3 drops of 1% nitroglycerin solution per sugar cube also under the tongue. herbal medicines there is no such action.

Antianginal drugs are represented by the following groups (classes):

I class. Coronary dilators:

– A. Coronary dilators that reduce venous return of blood to the heart:

1) nitroglycerin, prolonged deponitroglycerins (trinitrolong, sustak, nitrong, etc.);

2) other organic nitrates: nitropentone (erinite), nitrosorbide.

If nitroglycerin is a means of stopping an angina attack, then long-acting drugs are used to prevent angina attacks in patients with coronary insufficiency II-III degree. They are prescribed for several weeks, breaks are necessary, as addiction develops to the drugs.

– B. Coronary dilators that do not significantly increase myocardial oxygen demand:

This group includes intensain, chimes, lidoflazin, ditrimin, papaverine, no-shpa, difril. These drugs are mainly used in early stages coronary heart disease (I-II degree of chronic coronary insufficiency) only with an exacerbation of the disease. Intensain, chimes and lidoflazin also have the property (when taken for at least 2-3 months) to improve collateral circulation.

– B. Coronary dilators that increase myocardial oxygen demand:

Purine derivatives (eufillin, etc.), preparations of β-stimulating action (oxyphedrine, myofedrin, nonahlazine). They are used mainly in the early stages of coronary insufficiency in patients with hypokinetic syndrome (hypotension, bradycardia). Oxyphedrine (ildamen) is also prescribed for conduction disorders, weakness of the sinus node.

– D. Coronary dilating drugs that reduce myocardial oxygen demand (CA ++ -antagonistic action):

Phenigidine, Isoptin, Corinfar. Indicated in the treatment of coronary heart disease of moderate severity. At the same time, isoptin also has antiarrhythmic properties, Corinfar can be used in the combination of coronary heart disease with arterial hypertension.

II class. Means that reduce myocardial oxygen demand:

– A. Anti-adrenergics:

1. Blockers of β-adrenergic receptors: anaprilin, trazikor, visken, aptin, cordanum, benzodixin, etc.

Beta-blockers reduce the work of the heart, myocardial oxygen demand. This property underlies their use in coronary heart disease. They are indicated in patients with II-III degree of chronic coronary insufficiency, including the most severe angina. In these cases, a combination with nitrates may also be useful. In heart failure, it is necessary to combine β-blockers with cardiac glycosides. In such cases, visken, aptin, trazikor are more indicated, which, unlike anaprilin, have some positive inotropic effect. With concomitant bronchial asthma only cordanum is shown, which, unlike other β-blockers, does not have a bronchospastic property.

2. Cordarone reduces the work of the heart and myocardial oxygen demand, and also has an antiarrhythmic effect. It is indicated in the treatment of patients with coronary heart disease with exertional angina pectoris, as well as rest angina pectoris.

– B. Antithyroid drugs(Mercasolil, etc.) also reduce the work of the heart.

They are currently used as an exception in the absence of the effect of other means.

III class. Means that increase myocardial tolerance to hypoxia (antihypoxants):

cytochrome C, pyridoxinyl-glyoxylate (gliosus), etc.

Shown mainly in severe patients in combination with other antianginal drugs.

IV class. Means that improve metabolic processes in the myocardium (anabolic action):

retabolil, nerobol, potassium orotate, riboxin, etc.

Shown in cases where it is required to improve the performance of the myocardium (III degree of chronic coronary insufficiency).

It is used in combination with the main antianginal agents.

V class. Means of anti-bradykinin action:

anginin (prodectin, parmidin). Indicated for patients with severe microcirculation disorders, including patients with coronary heart disease with atherosclerosis of the lower extremities.

VI class. Means of antiplatelet action:

have antiaggregatory properties acetylsalicylic acid, mikristin, chimes, anginin, intensain, papaverine, etc.

All of these drugs can be used to prevent thrombosis, especially when Not stable angina. However, they should in no way replace other antianginal agents, as well as anticoagulants.

Thus, there is currently a large group of antianginal drugs. To the most effective drugs should include depot nitroglycerins and β-blockers. However, in different stages illness is necessary rational use certain drugs or their combination from the indicated groups.

The normalization of lifestyle, the fight against risk factors is important.

Phytotherapy for coronary insufficiency:

Preparations plant origin used in long-term treatment chronic coronary insufficiency or during an exacerbation, belong to the group of coronary dilators that do not significantly increase myocardial oxygen demand. They are used only in the early stages of the disease.

Kellin (Khellinum) is obtained from the seeds of the plant ammi tooth (Ammi visnaga L.). Kellin has a moderate coronary dilating effect. It is used at a dose of 0.02 g 3-4 times a day. The course of treatment is 2-3 weeks. Therapeutic effect observed on the 5-7th day of treatment. Kellin is part of the Kellathrin tablets, which are taken 1/2 or 1 tablet 3 times a day. It is necessary to monitor the dynamics of blood pressure.

To prevent angina attacks in systemic neuroses accompanied by coronary spasm, pastinacin (Pastinacinum) from the seeds of parsnip (Pastinaca sativa L.) is recommended. The drug is prescribed at a dose of 0.02 g 2-3 times a day before meals. The therapeutic result is usually noted 2-5 days after the start of the drug. The course of treatment is 2-4 weeks.

Preparations from flowers and fruits of hawthorn (Flor. Crataegi), as well as from white mistletoe grass (Herbae Visci albi) are widely used. A decoction of hawthorn flowers is taken 1/2 cup 2 times a day. The course of treatment is 3-4 weeks.

In mild forms of angina, to prevent spasms of the coronary vessels, orangelin (Orangelinum) is used, obtained from the roots of the mountain mustard (Peucedanum oreogelinum). Assign inside 0.1-0.4 g 2-4 times a day 30 minutes before meals. The course of treatment is 2-3 months.

Dimidin preparation (Dimidinum) was obtained from the roots of Siberian bloater (Phlojodicarpus sibiricus). Assign inside with mild forms of chronic coronary insufficiency 1-2 tablets (0.025 g per tablet) 2-3 times a day after meals. The course of treatment is 2-4 weeks. If necessary, spend 2-3 courses.

From methylxanthines in case of insufficiency of coronary vessels, theobromine and theophylline are used, as well as their synthetic derivatives - aminophylline, aminophylline, diprophylline. They expand the peripheral arterial vessels, especially coronary vessels (see class I coronary dilators). This series of herbal preparations in the treatment of coronary insufficiency also includes the isoquinoline alkaloid papaverine (Papaverinum). Assign papaverine at a dose of 0.04-0.06 g 3-4 times a day alone or as a component of mixed preparations (for example: Papaverini hydrochloridi 0.04; Phenobarbitali 0.02; Salsolini hydrochloridi 0.03. Powder 3 times a day day).

In chronic coronary insufficiency, anti-sclerotic preparations are also used (see treatment of atherosclerosis).

Cardiac ischemia.

The device for bioresonance therapy according to F. Morell and E. Rashe "Akutest-BRT" is a device of a new generation. The device is programmable. i.e. it allows for basic bioresonance therapy in automatic mode, by advance given by the doctor program. Having two independent channels, the device allows you to bring into the therapeutic circuit homeopathic preparations, without losing them, as well as allowing independent adjustment of the parameters of the working channels. The device is equipped not only with all the electrodes necessary for operation, but also with a small basic set test ampoules.

This variety of manifestations of the disease determines the wide range of therapeutic and preventive measures used in his treatment. In the period of remission of the disease, sanatorium treatment is indicated; V climatic conditions middle lane Russia - throughout the year, in the conditions of southern resorts - in cool months.

The prognosis and working capacity of patients depend on the frequency of exacerbations of the disease, as well as on the nature and persistence of dysfunctions of the heart (and other organs) resulting from complications of the disease.

Angina pectoris (angina pectoris).

Attacks of sudden chest pain due to an acute lack of blood supply to the heart muscle are clinical form coronary heart disease called angina pectoris.

In most cases, angina pectoris, like other forms of coronary artery disease, is caused by atherosclerosis of the arteries of the heart. Atherosclerotic plaques at the same time narrow the lumen of the arteries and prevent their reflex expansion. Which, in turn, causes a shortage of cardiac blood supply, especially acute with physical and (and) emotional overstrain.

With angina pectoris, pain is always characterized by the following symptoms:

1. has the character of an attack, that is, it has a clear expressed time occurrence and cessation, remission;
2. occurs under certain conditions, circumstances;
3. begins to subside or completely stops under the influence of taking nitroglycerin.

The conditions for the onset of an angina attack are most often walking (pain when accelerating, when climbing a mountain, with a sharp headwind, when walking after eating or with a heavy burden), but also other physical effort, or (and) significant emotional stress. The conditionality of pain by physical effort is manifested in the fact that with its continuation or increase, the intensity of pain will certainly increase, and when the effort is stopped, the pain subsides or disappears within a few minutes. These three features of pain are sufficient for setting clinical diagnosis an attack of angina pectoris and to delimit it from various pain in the region of the heart and in general in the chest, which are not angina pectoris.

It is often possible to recognize angina pectoris at the first visit of the patient, while to reject this diagnosis, monitoring of the course of the disease and analysis of the data of repeated questioning and examination of the patient are necessary. The following signs complement clinical characteristics angina, but their absence does not exclude this diagnosis:

1. localization of pain behind the sternum (the most typical!), it can give to the neck, to the lower jaw, and teeth, to the arm, usually the left, to the shoulder girdle and shoulder blade (often to the left);
2. the nature of the pain - pressing, squeezing, less often - burning (like heartburn) or sensation foreign body in the chest (sometimes the patient may experience not pain, but a painful sensation behind the sternum, and then he denies the presence of the actual pain);
3. simultaneous with an attack of angina pectoris, an increase in blood pressure, pallor of the integument, perspiration, fluctuations in the pulse rate, the appearance of a sensation of interruptions in the region of the heart. All of the above characterizes the so-called angina pectoris, that is, a variant of angina pectoris that occurs during exercise.

The thoroughness of medical questioning determines the timeliness and correctness of the diagnosis of the disease. It should be borne in mind that often the patient, experiencing sensations typical of angina pectoris, does not report them to the doctor as "not related to the heart", or, on the contrary, fixes attention on diagnostically secondary sensations "in the region of the heart".

Angina at rest, unlike angina pectoris, occurs out of touch with physical effort, more often at night, but otherwise retains all the features of a severe attack of angina pectoris and is often accompanied by a feeling of lack of air, suffocation.

It should be borne in mind that an attack of angina pectoris may be the beginning of the development of such a formidable form of coronary artery disease as myocardial infarction . Therefore, an attack that lasts for 20-30 minutes, as well as an increase or increase in seizures, requires an electrocardiographic examination in the next few hours (day), as well as, medical supervision for the further development of the process. To ensure all this, an indispensable hospitalization of the patient is necessary.

Help with an attack of angina pectoris.

The first thing a person should do during an angina attack is to take a calm, preferably sitting position. The second no less important is taking nitroglycerin under the tongue (1 tablet or 1 - 2 drops of a 1% solution on a piece of sugar, on a validol tablet), re-taking the drug if there is no effect after 2 - 3 minutes. In order to calm the patient, Corvalol (valocardin) is indicated - 30 - 40 drops inside. An increase in blood pressure during an attack does not require emergency measures, since its decrease occurs spontaneously in most patients when the attack stops.

The general principles of the behavior of a patient suffering from angina attacks are the need to: avoid stress (both physical and emotional) leading to an attack, use nitroglycerin without fear, take it "prophylactically" in anticipation of tension fraught with an attack. Treatment is also important concomitant diseases, especially the digestive organs, measures to prevent atherosclerosis, maintaining and gradually expanding the limits of physical activity.

In addition to taking nitroglycerin itself, which acts for a short time, it is important to constantly take drugs long-acting, the so-called, prolonged nitrates (nitromazine, nitrosorbide, trinitrolong, etc.). They should be used systematically, and after the cessation of seizures (stabilization of the course) - only before loads (a trip around the city, emotional stress and so on.).

Myocardial infarction.

As mentioned above, with a prolonged attack of angina pectoris, the latter can move into the next phase of the disease - myocardial infarction . This form ischemic heart disease due to acute insufficiency blood supply to the heart muscle, with the occurrence of a focus of necrosis (tissue necrosis) in the latter.

The mechanism of occurrence of this formidable disease, as a rule, is as follows: there is an acute blockage of the lumen of the artery by a thrombus or a narrowing of its lumen by a swollen atherosclerotic plaque. In the first variant of development, the lumen of the artery is blocked more completely, which usually leads to large-focal necrosis of the heart muscle, in the second case, to the so-called small-focal myocardial infarctions. The last category of infarcts is by no means "small" in terms of its clinical significance, in terms of the frequency of complications and the consequences for the patient, the mortality in them is not lower than in large-focal ones.

The onset of myocardial infarction is considered to be the onset of an attack of intense and prolonged (more than 30 minutes, often many hours) retrosternal pain, which is not stopped by repeated nitroglycerin administration. Less commonly, the picture of an attack is dominated by suffocation or pain is concentrated in the epigastric region, such variants of the development of the disease are classified as atypical.

IN acute period arterial hypertension (often significant) is observed, which disappears after the pain subsides and does not require application antihypertensive drugs, increased heart rate (not always), increased body temperature (from 2-3 days).

Such a serious condition as myocardial infarction requires unconditional and emergency hospitalization, help with home remedies in this case can lead to loss of time, therefore, if an attack of angina pectoris does not stop within 20-30 minutes, it is urgent to call " ambulance". While waiting for the brigade, however, you should not give up trying to help the patient in all the ways described in the section "Help for an angina attack."

The timing of the transfer of the patient to the outpatient regimen or sanatorium rehabilitation, as well as return to work and employment, after discharge from the hospital are determined individually.

Postinfarction cardiosclerosis.

Post-infarction cardiosclerosis is another form of coronary artery disease, it is a direct consequence of a previous myocardial infarction, one can even say that this is its logical conclusion, since the dead areas of the heart muscle are not restored, they are replaced by scar tissue. Therefore, postinfarction cardiosclerosis is a lesion of the heart muscle, and often the valves of the heart, due to the development of scar tissue in the form of areas of various sizes and prevalence, replacing the myocardium.

Cardiosclerosis, however, may be a consequence of other heart diseases, however clinical significance cardiosclerosis of another origin (atherosclerotic cardiosclerosis, the existence of which is disputed by some clinicians, cardiosclerosis as an outcome of myocardial dystrophy and hypertrophy, heart injury, and other diseases) is small.

Direct consequences of cardiosclerosis of any origin can be conditions such as heart failure, or circulatory failure and heart rhythm disturbances or arrhythmias.

Arrhythmias.

Arrhythmias are violations of the frequency, rhythm and sequence of heart contractions. The resting heart rate in most healthy adults is 60-75 bpm. Often, even with pronounced structural changes in the heart muscle, arrhythmia is due in part or mainly to metabolic disorders. The severity of the arrhythmia may not correspond to the severity of the underlying heart disease. Arrhythmias are diagnosed mainly by ECG.

Treatment of arrhythmias always includes treatment of the underlying disease and proper antiarrhythmic measures. Depending on the cause and mechanism of development, arrhythmias are very different. In this article, intended not for specialists, there is no way to dwell on the classification of arrhythmias, however, it should be noted that the conditions that occur with heart rhythm disturbances can be very serious. In some cases, the use of drugs may be absolutely necessary, in others it is not mandatory, only a doctor can decide this issue. Here we will focus on summary major antiarrhythmic drugs, leaving for the specialists both the decision of the question of the need for their appointment, and the selection of a specific drug and its dosage. So, the most commonly used drugs of this series are: verapamil, quinidine, novocainamide, difenin, ethmozine, disopyramide. The drugs listed here belong to different groups, have different mechanism actions, and, accordingly, are prescribed for certain forms of rhythm disturbance.

With the so-called tachyarrhythmias, that is, arrhythmias with heart palpitations caused by heart failure, prescribe drugs from the group cardiac glycosides, we will talk about them in the Heart Failure section.

Heart failure.

Heart failure is a pathological condition caused by the failure of the heart as a pump that provides adequate blood circulation. It is a manifestation and consequence of pathological conditions that affect the heart muscle and (and) impede the work of the heart: coronary heart disease, heart defects, arterial hypertension, diffuse diseases lungs, myocarditis, myocardial dystrophy, including thyrotoxic, sports and others. Heart failure caused by disorders of the heart, due to the formation of scar tissue that replaces the heart muscle after a heart attack, is a direct continuation of the pathological process that makes up the chain: angina pectoris - heart attack - post-infarction cardiosclerosis (that is, a scar), and as a result, heart failure.

Symptoms of heart failure are symptoms such as edema, mainly on lower limbs, shortness of breath, especially aggravated by horizontal position the patient, which causes a desire to be even in bed in a semi-sitting position, dizziness, darkening of the eyes and other characteristic signs.

The extreme manifestation of heart failure is pulmonary edema, severe acute condition, life threatening patient requiring emergency medical care with mandatory hospitalization intensive care. Pulmonary edema occurs as a manifestation of the so-called stagnation in the small (pulmonary) circulation, when an increase in pressure in the latter leads to leakage of the liquid part of the blood (plasma) directly into the pulmonary alveoli. Ultimately, this fluid fills the lungs and disrupts them. respiratory function. A patient in this condition develops severe shortness of breath with characteristic bubbling breathing, fear of death, the desire to be in a sitting position.

Help with heart failure.

Pulmonary edema is an option acute development heart failure and correctly help the patient with such a development of the situation is extremely important. Giving to the patient sitting position, at the beginning of an attack, the first and most affordable way help him. Needless to say, it is necessary to immediately call an ambulance. In addition, even before the arrival of the team, it is possible to use under the tongue, any drug from the group of cardiac glycosides, as a rule, digoxin (the most common drug) or celanide. It makes sense to give a potent diuretic, which is most often lasix (furosemide). All further activities should be carried out by professionals.

The main means used in the chronic variant of the development of heart failure are all the same cardiac glycosides belonging to a group of drugs called cardiotonic, that is, they increase the tone of the heart muscle, and thus raise the efficiency of the heart pump. The main drug is the same digoxin, less often celanide is used. The selection of the dosage of cardiac glycosides should be carried out only by a cardiologist under the supervision of ECG research, due to their toxicity in case of overdose and the ability to accumulate in the body. Both of these features determine the intake of these drugs according to a special scheme individually developed by the doctor for each patient. The patient must strictly adhere to the doctor's prescriptions.

In addition, such a drug as coenzyme Q10, produced mainly as a dietary supplement (biologically) has a cardiotonic effect. active additive). Its use can reduce the need for cardiac glycosides, and in mild cases, completely abandon them. Therefore, when using it, the doctor must conduct mandatory monitoring and adjustment of the dose of glycosides.

Another group of drugs prescribed for almost all patients are diuretics, often having the property of excreting potassium from the body, and therefore, they must also be taken according to the prescribed scheme, either combined with each other, or with the appointment of correction with potassium preparations (panangin, asparkam) and be sure with certain pauses between courses of admission.

Folk remedies used in cardiac pathology.

Means used traditionally among the people can often real help in the cardiac pathology described at the beginning of this article, in addition, they tend to be milder and do not cause side effects(although among the same herbs there are quite potent and even poisonous, extremely dangerous in case of overdose and improper use). Using these recipes, it should be understood that: firstly, it is worth counting on the effect of their use in the case chronic development process, since the action from them develops gradually (except for methods emergency assistance, such as acupressure with an attack of angina pectoris), and secondly, their use may reduce the need for prescribed medications. Considering in particular the last fact, it is necessary to keep the attending physician informed of all the methods of treatment used by the patient, so that he, having all the information, can consciously analyze the possibilities of drug interactions and adjust their dosage in a timely manner.

Having made this introduction, let's move on to the presentation of specific recipes.

1. 1 liter of honey, squeeze 10 lemons, peel 10 heads of garlic (whole heads, not cloves) and grind the garlic into a pulp. All this is mixed together and put for a week in a closed jar. Drink every day 4 teaspoons once. Do not swallow immediately, slowly dissolving. This amount should be enough for 2 months. This recipe is used for angina pectoris and circulatory failure.
2. Take 2 tablespoons of dried hawthorn flowers in a glass of water. Boil for 10 minutes, and when cool - strain. Take one tablespoon 3-4 times a day. Hawthorn tones the heart muscle, eliminates arrhythmia and tachycardia, lowers arterial pressure. Indications are similar to the previous recipe.
3. Hawthorn tincture: 10 g of dried flowers per 100 g of vodka. Insist 21 days in a dark place. Strain, squeeze. Take 7 drops in a small amount warm water gradually dissolving in the mouth. The indications are the same.
4. St. John's wort - 1 part. Yarrow - 1 part. Valerian (root) - 1 part. Take a tablespoon of the collection in a glass of water. Insist 3 hours. Then put on fire, let it boil, boil for 5 minutes. When cool, strain. Take a glass during the day in three doses. The recipe is used for angina pectoris.
5. Take 1 - 2 teaspoons of blue cornflower and brew a glass of boiling water. Insist hour, strain. Drink 14 cups 3 times a day 10-15 minutes before meals. The infusion is used for palpitations.
6. Removal method pain syndrome with an attack of angina with the help of acupressure (acupressure).

Before proceeding to the description of pain relief with the help of acupressure of an angina attack, it is necessary to dwell on general principles and the rules that you need to know when applying this technique.

The figure shows the approximate location of the points, so when performing the technique, their localization must be clarified. Deviations in the location of points can be in various options, therefore, the dotted line in the figures indicates the possible value of this deviation. It almost always happens that the desired acupressure point responds to strong pressure with a clear pain signal, which highlights it in the area of ​​the body being examined.

At acute pain, and at primary care the use of a light circular massage of the point is shown, which in this case is carried out with the thumbs, holding the brush lightly with the index and thumbs massaging hand. Light acupressure is best in the supine position. The duration of such a massage is from one to five minutes. The movement of the finger should be horizontally rotating clockwise, or vibrating, but always non-stop.

Application this method anesthesia does not exclude, however, the implementation of all the recommendations discussed above when describing the methods of official medicine.

For citation: Ageev F.T., Skvortsov A.A., Mareev V.Yu., Belenkov Yu.N. Heart failure against the background of coronary heart disease: some issues of epidemiology, pathogenesis and treatment // BC. 2000. No. 15. S. 622

Research Institute of Cardiology. A.L. Myasnikova RKNPK of the Ministry of Health of the Russian Federation, Moscow

One of the basic postulates of medicine says that the optimal treatment of a disease is impossible without knowing its cause. However, this principle is difficult to apply when it comes to chronic heart failure (CHF). This is due to the fact that although diseases leading to the development of CHF are numerous and varied, the final result for all is the same - decompensation of cardiac activity . There is an illusion that the cause of CHF no longer matters and the treatment is the same in all cases: whether it is coronary heart disease (CHD), dilated cardiomyopathy (DCM) or hypertonic heart. However, it is not. Any disease underlying CHF has its own characteristics that leave an imprint on the course of heart failure, its therapy and prognosis. This is especially true for such a frequent and serious disease, which is currently coronary artery disease.

Epidemiology

Currently, it is considered proven that coronary artery disease is the main etiological cause of heart failure. This conclusion can be drawn on the basis of an analysis of the results of special epidemiological studies in populations, as well as an assessment of the contingent of patients included in multicenter survival studies. patients with CHF. Thus, in 10 such studies conducted in recent years, ischemic etiology of decompensation was observed in an average of 64% of patients (Table 1). The scatter in the results of these studies is explained by the difference diagnostic criteria CHD used in different centers, population differences, and may also be related to the study drug. So, in the works related to b-blockers (in the table - these are the CIBISI and USCT studies), DCM occupies a significant place among the causes of CHF along with IHD (36 and 52%, respectively); where ACE inhibitors are being investigated, the main cause of decompensation is, as a rule, coronary artery disease, and the incidence of DCM does not exceed 22%.

Epidemiological studies in populations also indicate a significant predominance of coronary artery disease among the main causes of CHF (Table 2). In a study of the prevalence of CHF in the city of Glasgow, IHD, as the cause of CHF, was observed in 95% of patients (!). From the results of these studies, it follows that arterial hypertension also occupies a significant place in the structure of the causes of CHF, although in clinical practice hypertension is most often combined with coronary artery disease. But the role of DCMP, as causes of CHF, in such epidemiological studies is small and is estimated at 0-11%.

In a retrospective study conducted at the Research Institute of Cardiology. A.L. Myasnikov, it was also revealed that coronary artery disease in recent years has become main reason development of heart failure, and the “contribution” of coronary artery disease to the overall structure of the incidence of CHF is constantly increasing (Table 3).

Pathophysiology of heart failure in coronary artery disease

There may be several mechanisms for the development and progression of heart failure in IHD. The most important of these is, of course, myocardial infarction (THEM). The sudden “loss” of a more or less extensive portion of the heart muscle leads to the development of dysfunction of the ventricle (s), and if the patient does not die (which happens in 50% of cases), dysfunction over time, as a rule, manifests itself with symptoms of heart failure. In the study TRACE in 40% of patients who underwent MI, severe LV dysfunction was noted already in the first days, and in 65% it was the first heart attack in their lives; 74% of them soon developed clinical picture heart failure. However, even those 60% of patients who manage to avoid the development of dysfunction on early stage disease, cannot consider themselves "safe". Behind massive heart attack followed by changes in the heart muscle, called "remodeling" of the heart. This phenomenon includes processes affecting the affected area and healthy areas of the myocardium, when the infarcted area “stretches”, unable to withstand the increased intraventricular pressure, and unaffected areas hypertrophy and dilate, adapting to new functioning conditions. Remodeling is a process that includes a change in the shape and function of the ventricles over time, the expansion of scar tissue, which is closely associated with changes in the neurohumoral background of the body.

However, the features of the development of CHF in patients with coronary artery disease are due not only to ventricular dysfunction, but also to the constant participation of coronary insufficiency in this process.

Frequent episodes of local ischemia lead to periods of increased local systolic dysfunction , manifested by shortness of breath (equivalent to angina pectoris). For example, in a study SOLVD 37% of CHF patients also complained of angina pain. Frequent episodes of the appearance and disappearance of ischemia contribute to the prolongation of systolic dysfunction in these areas, which is equivalent to the state of “stunned” (stunning) myocardium, described with occlusion and subsequent “opening” of the corresponding coronary artery. Persistent coronary insufficiency makes an important contribution to the development of both systolic and diastolic LV dysfunction.

Another mechanism of systolic dysfunction in patients with coronary artery disease is associated with such a phenomenon as “hibernation” of the myocardium , which is an adaptive response under conditions of constantly reduced coronary blood flow. Tissue perfusion under these conditions is sufficient to maintain the existence of cardiomyocytes (including ionic currents), but insufficient for their normal contractility. This process leads to gradual hypocontractility of the entire myocardium and progression of LV dysfunction. Recent evidence suggests that myocardial hibernation inevitably ends in necrosis unless coronary blood flow increases.

Thus, in addition to these irreversible changes, as a post-infarction scar, persistent myocardial ischemia, stunned and hibernated myocardium still join - all together contribute their own specifics to the development of CHF in patients with coronary artery disease.

Another important factor in the occurrence of myocardial dysfunction in patients with coronary artery disease is a dysfunction of the endothelium of the coronary vessels, which is characteristic of this pathology. Endothelial dysfunction refers to a violation of the ability of these cells to produce specific (vascular) relaxation factors (NO, prostacyclin, hyperpolarization factor). It has been proven that endothelial dysfunction activates the activity of neurohormones responsible for the development and progression of CHF: endothelin-1, renin-angiotensin-aldosterone and sympathetic-adrenal systems, tumor necrosis factor-a. In addition, endothelial dysfunction in patients with coronary heart disease blocks the migration of smooth muscle cells and their proliferation in the vessel wall, increases the permeability of the wall for lipids, which contributes to the further development of atherosclerosis and coronary thrombosis, which, in turn, causes persistent myocardial ischemia and LV dysfunction.

The effectiveness of drug therapy for CHF in IHD

Digoxin

In the study DIG It was shown that in patients with CHF, digoxin increases the incidence of MI by 26%, which indirectly may indicate a potential adverse influence glycosides for IHD. This may be due to an increase in O2 consumption against the background of an increase in myocardial contractility. Despite this, such important indicator, as the risk of death and / or involuntary hospitalization due to progression of CHF with the use of digoxin, nevertheless tended to decrease, although the degree of this decrease in patients with coronary artery disease was less significant (by 21%) than in patients with CHF of non-ischemic etiology (down 33%).

ACE inhibitors

Almost all clinical researches testify to expressed positive influence ACE inhibitor Not only on mortality rates , but also for the development of coronary artery disease , including in patients with CHF or systolic myocardial dysfunction. So, according to the main multicenter studies, the reduction in the risk of MI with the use of ACE inhibitors in such patients reaches 12-25% (Fig. 1).

The success of the use of ACE inhibitors in patients with CHF of ischemic origin may be associated with the unique property of drugs of this class to improve not only the hemodynamic and neurohumoral status, but also to normalize the endothelial function of the coronary arteries, the role of which in the pathogenesis of heart failure is no longer in doubt. In addition, ACE inhibitors contribute to the improvement of plasma fibrinolytic activity, which has preventive action to the development of coronary thrombosis.

Clinical confirmation of the actual “anti-ischemic” properties of ACE inhibitors can be the results of a study QUIET , in which the addition of an ACE inhibitor quinapril patients with coronary artery disease with preserved ventricular function reduced the frequency coronary complications on 10% . When IHD is combined with CHF, the average reduction in the risk of death associated with the use of drugs of this class reaches 23%, as evidenced by the results of a meta-analysis Garg&Yusuf based on the results of 32 placebo-controlled studies. Another important conclusion of this meta-analysis indicates that in a subgroup of patients with heart failure of non-ischemic etiology (not CHD), the effect of ACE was also positive, but still somewhat less than in patients with myocardial ischemia (Table 4).

Despite such favorable conditions for IHD patients, in 2 largest studies with enalapril (V-HeFT II and SOLVD prevention & treatment), the effectiveness of the treatment of heart failure of ischemic etiology was significantly lower than with decompensation of non-ischemic genesis (see Table 4).

The fact that the action of ACE inhibitors depends on the etiology of decompensation and may be less effective in CHF of ischemic origin was confirmed in a retrospective study conducted at the Research Institute of Cardiology named after. A.L. Myasnikov. 6-year use of ACE inhibitors in patients with CHF of ischemic etiology reduced the risk their deaths by an average of 26% , while similar patients with DCMP - by 60% .

b-blockers

Myocardial ischemia is one of the main indications for the use of b-blockers, however, accession to IHD insufficiency until recently, it was considered dangerous for the use of drugs with negative inotropic properties and even served as a contraindication for such therapy. However, back in the 1980s, it was known that the effectiveness of b-blockers in patients with MI complicated by CHF is even higher than in patients without heart failure (Fig. 2).

After a long period of search and hesitation, the feasibility of using b-blockers in the treatment of patients with CHF has ceased to be a subject of discussion and has become apparent only in the last 1-2 years, after the completion of three large multicenter studies with carvedilol ( USCT ), bisoprolol ( CIBIS II ) and metoprolol ( MERIT-HF ).

In all these works the use of b-blockers in addition to the main therapy (ACE inhibitors + diuretics / glycosides) reduced the risk of death by an average of 34-65% . Moreover, a positive effect of therapy was observed in subgroups of patients with both ischemic and non-ischemic genesis of cardiac decompensation.

The anti-ischemic and antianginal properties of b-blockers theoretically suggest their advantage when used in patients with CHF of ischemic etiology. However, in real clinical practice, this is only partially confirmed. As can be seen from Table. 5, in CHD, b-blockers had an unsignificant advantage in only 2 studies out of 4. Moreover, in one of the studies ( CIBIS I ) bisoprolol had practically no effect on mortality in patients with myocardial ischemia with severe positive effect in patients with DCMP.

Amiodarone

The efficacy of amiodarone in patients with coronary artery disease is associated mainly with a reduction in sudden, arrhythmic death.

So, in Canadian CAMIAT ) and European ( EMIAT ) studies in patients in the postinfarction period, amiodarone did not affect the overall mortality of patients, but significantly reduced the risk of sudden (arrhythmic) death (Table 6).

According to a meta-analysis ATMA , which included 13 major studies in patients with LV dysfunction and / or heart failure, along with a decrease in arrhythmic death (by 29%), the use of amiodarone was still accompanied by a decrease in risk and overall mortality by an average of 13%.

However, the relationship between the etiology of CHF and the effectiveness of this drug is ambiguous. So, in the study CHF-STAT a trend towards a decrease in mortality during amiodarone therapy was observed only in patients with non-ischemic decompensation (20%, p=0.07); at the same time, the effectiveness of therapy in patients with coronary artery disease approached 0. In contrast to this work, in an Argentine study GESICA the reduction in the risk of death and / or hospitalization with the use of amiodarone in patients with CHF averaged 31%, but patients with coronary artery disease had a relative “success”: their risk reduction was 38% versus 23% in patients with cardiomyopathies.

calcium antagonists

The effectiveness of the use of calcium antagonists in patients with CHF has not been studied enough. However, the data of even single works give contradictory results. Study PRAISE I with amlodipine showed that the appointment of this drug (against the background of ACE inhibitors, diuretics, glycosides) is accompanied by an unreliable decrease in fatal and non-fatal complications, as well as the frequency deaths by an average of 9%. Moreover, this “success” was achieved solely “thanks to” patients with CHF of non-ischemic etiology (DCMP, hypertensive heart, etc.), in whom the reduction in the risk of death associated with amlodipine was 46%; at the same time, this indicator practically did not change in patients with coronary artery disease (Table 7).

Directly opposite results were obtained in the study V-HeFT-III with calcium antagonist III generation felodipine: with CHF in patients with coronary artery disease, there was a decrease in mortality by an average of 18%; at the same time, in the subgroup of patients without coronary artery disease, the number of deaths on the background of this therapy even slightly exceeded those in the control group.

Conclusion

Immediate and distant trends in development cardiovascular disease indicate that the increase in the number of patients with IHD will continue and CHF, as a complication of IHD, will become one of the main causes of hospitalizations and mortality in the next century, especially in older people. age group. In this regard, the question arises: are there reliable ways to prevent and treat this syndrome?

Analysis of the main multicenter studies does not give a clear answer: The effectiveness of treatment of patients with CHF in IHD is often worse than in patients with decompensation of non-ischemic etiology. , for example, with DCMP.

The reasons for this phenomenon may be associated with the “double” pathogenesis of CHF in occlusive lesions of the coronary arteries, which requires the impact not only on the processes of heart remodeling, but also effective recovery myocardial perfusion. From this it can be assumed that without adequate revascularization of the heart muscle, it is difficult to achieve success in the prevention and treatment of circulatory failure in patients with coronary atherosclerosis . Unfortunately, there is no strong evidence for this concept yet, as patients with symptoms of heart failure are generally excluded from myocardial revascularization studies. Separate work carried out with patients without severe dysfunction myocardial infarction, show that with 3-11% operative mortality, the 5-year survival of operated patients is relatively satisfactory, but not better (and possibly worse) than in those who received adequate drug therapy. Of course, these conclusions cannot be final, since the solution to the question of effectiveness surgical methods treatment of such patients requires specially organized studies.

The need for a “vascular coronary” effect on patients with CHF of ischemic etiology was unexpectedly confirmed in the study of the effects of lipid-lowering drugs (statins) in patients with dyslipoproteinemia and coronary artery disease. So, in the study CARE pravastatin reduced the incidence of recurrent heart attacks and mortality in patients with asymptomatic LV dysfunction, and simvastatin in the 4S study generally prevented the development of heart failure. The results of these studies suggest that if ACE inhibitors can become an important tool treatment of patients with coronary artery disease, then statins are a necessary component of the treatment of patients with CHF of ischemic etiology.

Thus, heart failure in patients with coronary artery disease currently remains a serious problem, the solution of which is possible only by combining the efforts of epidemiologists and therapists, cardiologists and cardiac surgeons, aimed at both prevention and treatment. coronary disease, and to eliminate its complications - ventricular dysfunction and heart failure.

Literature

1. Cleland J.F.G., McGowan J. Heart Failure due to Ischaemic Heart Disease: Epidemiology, Pathophysiology and Progression. J Cardiovasc Pharmacol 1999; 33 (suppl. 3): S17-S29.

2. Yu.N.Belenkov, V.Yu.Mareev, F.T.Ageev. Medical routes improve the prognosis of patients with chronic heart failure. M., "Insight", 1997.

3. Kober L., Torp Pedersen., Carlsen J.E. et al. A clinical trial of the angio-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 1995; 333: 1670-6.

4. Effects of enalapril on survival in patients with reduced left ventricular ejection fraction and congestive heart failure. The SOLVD investigators. N Engl J Med. 1991; 325:293-302.

5. The Digitalis Investigation Group. The effect of Digoxin on mortality and morbidity in patients with heart failure. N Engl J Med 1997; 336:525-33.

6. Cashin-Hemphill L, Dinsmore RE, Chan RC et al. Atherosclerosis progression in subjects with and without post-angioplasty restenosis in QUIET. J am Coll Cardiol 1997; 29 (suppl. A): 418A.

7. Garg R, Yusuf S. Overview of randomized trial of angiotensin-converting enzyme inhibitors on mortality and morbidity in patients with heart failure. JAMA 1995; 1450-6.

8. MERIT-HF Study Group. Effect of metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomized Intervention Trial in Congestive Heart Failure (MERIT-HF). Lancet 1999; 353: 2001-07.

9. Julian DG, Camm AJ, Frangin G. Et al. Randomized trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT. Lancet 1997; 349:667-74.

10. Cairns JA, Connolly SJ, Roberts R. Et al. Randomized trial of outcome after myocardial infarction in patient with frequent or repetitive premature depolarisation: CAMIAT. Lancet 1997; 349:675-82.

11. Amiodaron Trials Meta-Analisis (ATMA). Lancet 1997; 350: 1417-24.

Timolol - Norwegian study with timolol;
VNAT - study with propranolol;
Gothenburg - study with metoprolol (1).

Cardiac ischemia

Cardiovascular diseases are the leading cause of death and disability worldwide. According to the researchers, in Russian Federation mortality from cardiovascular diseases is 8 times higher than in France, and is approximately 58% of overall structure mortality. Every year more than 1.2 million people die from cardiovascular diseases in our country, while in Europe a little more than 300 thousand. The leading role in the structure of mortality from cardiovascular diseases belongs to coronary heart disease (CHD) - 35%. If this continues further, then the population of Russia by 2030 will be approximately 85 million. These are frightening figures. But the situation can and should be changed if each of us is aware of it. "You know - armed" - said the ancients.
The structure and function of the heart, coronary arteries
To understand CHD, let's first look at what affects CHD - our heart.
Heart is hollow muscular organ, consisting of four chambers: 2 atria and 2 ventricles. In size, it is equal to a clenched fist and is located in the chest just behind the sternum. The mass of the heart is approximately equal to 1/175 -1/200 of body weight and ranges from 200 to 400 grams.
It is conditionally possible to divide the heart into two halves: left and right. In the left half (this is the left atrium and left ventricle) flows arterial blood, rich in oxygen, from the lungs to all organs and tissues of the body. Myocardium, i.e. the muscle of the heart, the left ventricle is very powerful and able to carry high loads. Between the left atrium and left ventricle is mitral valve consisting of 2 wings. The left ventricle opens into the aorta through the aortic (it has 3 cusps) valve. At the base aortic valve from the side of the aorta are the mouths of the coronary or coronary arteries hearts.
Right half, which also consists of the atrium and ventricle, pumps venous blood, poor in oxygen and rich in carbon dioxide from all organs and tissues of the body to the lungs. Between the right atrium and the ventricle is the tricuspid, i.e. tricuspid valve, and the ventricle pulmonary artery separates the valve of the same name, the pulmonary valve.
The heart is located in the heart bag, which performs a shock-absorbing function. The heart sac contains a fluid that lubricates the heart and prevents friction. Its volume can normally reach 50 ml.
The heart works according to the one and only law “All or nothing”. His work is done cyclically. Before the contraction begins, the heart is in a relaxed state and passively fills with blood. Then the atria contract and send an additional portion of blood into the ventricles. After this, the atria relax.
Then comes the systole phase, i.e. ventricular contractions and blood is ejected into the aorta to the organs and into the pulmonary artery to the lungs. After a powerful contraction, the ventricles relax and the diastole phase begins.
The heart beats with one unique property. It is called automatism, i.e. is the ability to create nerve impulses and shrink under their influence. There is no such feature in any organ. These impulses are generated by a special part of the heart located in the right atrium, the so-called pacemaker. From it, impulses go through a complex conducting system to the myocardium.
As we said above, the heart is supplied with blood by the coronary arteries, left and right, which are filled with blood only in the diastolic phase. The coronary arteries play a crucial role in the life of the heart muscle. The blood flowing through them brings oxygen and nutrients to all the cells of the heart. When the coronary arteries are patent, the heart works adequately and does not get tired. If the arteries are affected by atherosclerosis and are narrow because of this, then the myocardium cannot work at full capacity, it lacks oxygen, and because of this, biochemical and then tissue changes begin, and IHD develops.
What do coronary arteries look like?
The coronary arteries are made up of three layers different structure(drawing).

Two major coronary arteries branch off from the aorta. right and left. Left main coronary artery has two large branches:
- The anterior descending artery, which delivers blood to the anterior and anterolateral wall of the left ventricle (figure) and to the greater part of the wall that separates the two ventricles from the inside - the intraventricular septum? not shown in the figure);
- circumflex artery, which runs between the left atrium and ventricle and delivers blood to the lateral wall of the left ventricle. Less commonly, the circumflex artery supplies blood to the superior and back left ventricle
The right coronary artery delivers blood to the right ventricle, to the inferior and back wall left ventricle.
What are collaterals?
The main coronary arteries branch into smaller blood vessels that form a network throughout the myocardium. These small blood vessels are called collaterals. If the heart is healthy, the role collateral arteries in the supply of myocardial blood is not significant. When coronary blood flow is impaired due to an obstruction in the lumen of the coronary artery, collaterals help increase blood flow to the myocardium. It is thanks to these small "reserve" vessels that the size of myocardial damage in case of cessation of coronary blood flow in any main coronary artery is smaller than it could be.
Cardiac ischemia
Ischemic heart disease is myocardial damage caused by impaired blood flow in the coronary arteries. That is why in medical practice the term coronary heart disease is often used.
What are the symptoms of coronary heart disease?
Typically, people with coronary artery disease show symptoms after the age of 50. They only occur during exercise. Typical manifestations diseases are:
- pain in the middle chest(angina pectoris);
- feeling short of breath and difficulty in breathing;
- circulatory arrest due to too frequent contractions of the heart (300 or more per minute). This is often the first and last manifestation of the disease.
Some patients suffering from coronary heart disease do not experience any pain and feeling of lack of air even during myocardial infarction.
In order to find out the probability of developing a myocardial infarction in the next 10 years, use a special tool: "Know your risk"
How do you know if you have coronary heart disease?
Seek help from a cardiologist. Your doctor will ask you questions to help identify symptoms and risk factors for the disease. The more risk factors a person has, the more likely it is to have the disease. The influence of most risk factors can be reduced, thereby preventing the development of the disease and the occurrence of its complications. These risk factors include smoking, high level cholesterol and blood pressure, diabetes.
In addition, the doctor will examine you and prescribe special methods examinations that will help confirm or deny the presence of your disease. These methods include: registration of an electrocardiogram at rest and with a stepwise increase in physical activity (stress test), chest x-ray, biochemical analysis blood (with the determination of the level of cholesterol and blood glucose). If your doctor, based on the results of the conversation, examination, tests received and instrumental methods of examination, suspects a severe lesion of the coronary arteries requiring surgery, you will be prescribed coronary angiography. Depending on the condition of your coronary arteries and the number of affected vessels, in addition to drugs, you will be offered either angioplasty or coronary artery bypass grafting. If you turned to the doctor on time, you will be prescribed medications, helping to reduce the influence of risk factors, improve the quality of life and prevent the development of myocardial infarction and other complications:
- statins to lower cholesterol levels;
- beta-blockers and angiotensin-converting enzyme inhibitors to lower blood pressure;
- aspirin to prevent the formation of blood clots;
- nitrates to facilitate the cessation of pain during an angina attack
Remember that the success of treatment depends largely on your lifestyle:
- do not smoke. It's the most important. Do not people who smoke the risk of myocardial infarction and death is significantly lower than that of smokers;
- eat foods low in cholesterol;
- exercise regularly, every day for 30 minutes physical activity(walking at an average pace);
- Reduce your stress levels.
In the section life style are given detailed recommendations for each item.
What else needs to be done?
- See your cardiologist regularly. The doctor will monitor your risk factors, treatment, and make adjustments as needed;
- Take your prescribed medications regularly at the doses prescribed by your doctor. Do not change your treatment without consulting your doctor;
- if your doctor has prescribed you nitroglycerin to relieve the pain of angina pectoris, always carry it with you;
- tell your doctor about all episodes of chest pain if they occur again;
- change your lifestyle in accordance with these recommendations.
Coronary arteries and atherosclerosis
In people with a predisposition, cholesterol and other fats accumulate in the walls of the coronary arteries, which form an atherosclerotic plaque (figure).
Why is atherosclerosis a problem in the coronary arteries?
A healthy coronary artery is like a rubber tube. It is smooth and flexible and the blood flows through it freely. If the body needs more oxygen, for example, during exercise, the healthy coronary artery will stretch and flow to the heart. more blood. If the coronary artery is affected by atherosclerosis, it becomes like a clogged pipe. Atherosclerotic plaque narrows the artery and makes it stiff. This leads to a restriction of blood flow to the myocardium. When the heart begins to work harder, such an artery cannot relax and deliver more blood and oxygen to the myocardium. If the atherosclerotic plaque is so large that it completely blocks the lumen of the artery, or this plaque ruptures and a blood clot is formed that blocks the lumen of the artery, then blood does not flow to the myocardium and its area dies.
Ischemic heart disease in women
In women, the risk of developing coronary heart disease increases 2-3 times after menopause. During this period, cholesterol levels increase and blood pressure rises. Causes this phenomenon are not entirely clear. In women with coronary heart disease, the manifestations of the disease sometimes differ from the symptoms of the disease in men. So in addition to typical pain, women may experience shortness of breath, heartburn, nausea, or weakness. Women are more likely to develop myocardial infarction during mental stress or strong fear, during sleep, while "male" myocardial infarction often occurs during exercise.
How can a woman prevent the development of coronary heart disease?
See a cardiologist. The doctor will give you recommendations on lifestyle changes, prescribe medications. In addition, consult a gynecologist to determine the need for replacement hormone therapy after menopause.
Symptoms of coronary heart disease
IHD is the most extensive pathology of the heart and has many forms.
Let's start in order.
a. Sudden cardiac or coronary death is the most severe of all forms of CAD. It is characterized by high mortality. Death occurs almost instantly or within the next 6 hours from the onset of an attack of severe chest pain, but usually within an hour. The causes of such a cardiac catastrophe are different kind arrhythmias, complete blockage of the coronary arteries, severe electrical instability of the myocardium. The causative factor is alcohol intake. As a rule, patients do not even know that they have coronary artery disease, but they have many risk factors.
b. Myocardial infarction. Terrible and often disabling form of coronary artery disease. With myocardial infarction, there is a strong, often tearing, pain in the region of the heart or behind the sternum, radiating to left shoulder blade, arm, lower jaw. The pain lasts more than 30 minutes, when taking nitroglycerin, it does not completely disappear and only briefly decreases. There is a feeling of lack of air, may appear cold sweat, severe weakness, lowering blood pressure, nausea, vomiting, feeling of fear. Reception of nitropreparations does not help or assist. The part of the heart muscle deprived of nutrition becomes dead, loses its strength, elasticity and ability to contract. And the healthy part of the heart continues to work with maximum tension and, contracting, can break the dead area. It is no coincidence that a heart attack is colloquially referred to as a heart rupture! It is only in this state that a person has to make even the slightest physical effort, as he is on the verge of death. Thus, the meaning of the treatment is that the place of the rupture is healed and the heart is able to work normally further. This is achieved both with the help of medications and with the help of specially selected physical exercises.
c. Angina. The patient develops pain or discomfort behind the sternum, in the left half of the chest, heaviness and a feeling of pressure in the region of the heart - as if something heavy had been placed on the chest. In the old days they said that a person angina pectoris". The pain can be different in nature: pressing, squeezing, stabbing. It can give (radiate) to left hand, under the left shoulder blade, lower jaw, stomach area and be accompanied by the appearance of severe weakness, cold sweat, a sense of fear of death. Sometimes, during exercise, it is not pain that occurs, but a feeling of lack of air, passing at rest. The duration of an angina attack is usually a few minutes. Since pain in the region of the heart often occurs when moving, a person is forced to stop. In this regard, angina pectoris is figuratively called "the disease of shop window observers" - after a few minutes of rest, the pain, as a rule, disappears.
d. Violations heart rate and conductivity. Another form of IBS. It has a large number various kinds. They are based on a violation of the conduction of an impulse along the conduction system of the heart. It is manifested by sensations of interruptions in the work of the heart, a feeling of "fading", "gurgling" in the chest. Cardiac arrhythmia and conduction disturbances may occur under the influence of endocrine, metabolic disorders, with intoxication and medicinal effects. In some cases, arrhythmias can occur with structural changes in the conduction system of the heart and myocardial diseases.
e. Heart failure. Heart failure is manifested by the inability of the heart to provide sufficient blood flow to the organs by reducing contractile activity. The basis of heart failure is a violation of the contractile function of the myocardium, both due to its death during a heart attack, and in violation of the rhythm and conduction of the heart. In any case, the heart contracts inadequately and its function is unsatisfactory. Heart failure is manifested by shortness of breath, weakness during exertion and at rest, swelling of the legs, enlargement of the liver and swelling of the jugular veins. The doctor may hear wheezing in the lungs.
Factors in the development of coronary heart disease
Risk factors are features that contribute to the development, progression and manifestation of the disease.
Many risk factors play a role in the development of coronary artery disease. Some of them can be influenced, others cannot. Those factors that we can influence are called removable or modifiable, those that we cannot influence are called irremovable or non-modifiable.
1. Non-modifiable. Fatal risk factors are age, gender, race and heredity. Thus, men are more prone to developing coronary artery disease than women. This trend persists until approximately 50–55 years of age, that is, until the onset of menopause in women, when the production of female sex hormones (estrogens), which have a pronounced “protective” effect on the heart and coronary arteries, is significantly reduced. After 55 years, the incidence of coronary artery disease in men and women is approximately the same. Nothing can be done about such a clear trend as the increase and aggravation of diseases of the heart and blood vessels with age. In addition, as already noted, race affects the incidence: residents of Europe, or rather those living in the Scandinavian countries, suffer from coronary artery disease and arterial hypertension several times more often than people of the Negroid race. Early development IHD often occurs when the direct male relatives of the patient had a myocardial infarction or died of a sudden heart disease before the age of 55, and direct female relatives had a myocardial infarction or sudden cardiac death before the age of 65.
2. Modifiable. Despite the impossibility of changing either one's age or one's gender, a person is able to influence his condition in the future by eliminating avoidable risk factors. Many of the avoidable risk factors are interrelated, so eliminating or reducing one of them can eliminate the other. So, reducing the fat content in food leads not only to a decrease in blood cholesterol levels, but also to a decrease in body weight, which, in turn, leads to a decrease in blood pressure. Together, this helps to reduce the risk of coronary artery disease. And so we list them.
o Obesity is excess accumulation adipose tissue in the body. More than half of the world's people over the age of 45 are overweight. What are the reasons overweight? In the vast majority of cases, obesity is of alimentary origin. This means that the causes of overweight are overeating with overuse high-calorie, first of all fatty foods. The second leading cause of obesity is lack of physical activity.
o Smoking is one of the most important factors development of IHD. Smoking is highly likely to contribute to the development of coronary artery disease, especially if combined with an increase in the level total cholesterol. On average, smoking shortens life by 7 years. Smokers also have increased levels of carbon monoxide in the blood, which reduces the amount of oxygen that can reach the body's cells. In addition, the nicotine contained in tobacco smoke leads to spasm of the arteries, thereby leading to an increase in blood pressure.
o An important risk factor for coronary artery disease is diabetes mellitus. In the presence of diabetes, the risk of coronary artery disease increases on average by more than 2 times. Patients with diabetes often suffer from coronary disease and have a worse prognosis, especially with the development of myocardial infarction. It is believed that with a duration of overt diabetes mellitus of 10 years or more, regardless of its type, all patients have a fairly pronounced atherosclerosis. Myocardial infarction is the most common cause of death in patients with diabetes.
o Emotional stress may play a role in the development of coronary artery disease, myocardial infarction, or lead to sudden death. At chronic stress heart starts to work increased load, blood pressure rises, the delivery of oxygen and nutrients to the organs worsens. To reduce the risk of cardiovascular disease from stress, it is necessary to identify the causes of its occurrence and try to reduce its impact.
o Physical inactivity or lack of physical activity is rightly called a disease of the twentieth, and now the twenty-first, century. It is another avoidable risk factor for cardiovascular disease, so being physically active is essential to maintaining and improving your health. Nowadays, in many areas of life, the need for physical labor. It is known that coronary artery disease is 4-5 times more common in men under the age of 40-50 years who were engaged in easy labor(compared to those performing heavy physical work); Athletes remain at low risk of coronary artery disease only if they remain physically active after retirement. big sport.
- arterial hypertension well known as a risk factor for CHD. Hypertrophy (increase in size) of the left ventricle as a consequence of arterial hypertension is an independent strong predictor of mortality from coronary disease.
- Increased clotting blood. Thrombosis of the coronary artery - essential mechanism myocardial infarction and circulatory failure. It also promotes the growth of atherosclerotic plaques in the coronary arteries. disorders predisposing to advanced education blood clots are risk factors for the development of complications of coronary artery disease.
- metabolic syndrome.
- Stress.
metabolic syndrome
Metabolic syndrome is a pathological process that contributes to an increase in the incidence of diabetes mellitus and diseases based on atherosclerosis - coronary heart disease, myocardial infarction, stroke.
Mandatory feature metabolic syndrome is the presence abdominal obesity(waist circumference over 94 cm for men and over 80 cm for women) in combination with at least two of the following indicators:
- an increase in the level of blood triglycerides more than 1.7 mmol / l;
- decrease in lipoproteins high density less than 1.03 mmol/l in men and less than 1.29 mmol/l in women;
- increased blood pressure: systolic more than 130 mm Hg. or diastolic more than 85 mm Hg;
- an increase in fasting blood glucose in the venous plasma of more than 5.6 mmol / l or previously diagnosed type II diabetes mellitus.
Prevention of coronary heart disease
All prevention of coronary heart disease is reduced to simple rule"I.B.S."
I. Get rid of smoking.
B. Move more.
C. Watch your weight.
I. Getting rid of smoking
Smoking is one of the most important factors in the development of coronary artery disease, especially if it is combined with an increase in total cholesterol. On average, smoking shortens life by 7 years.
The changes are to reduce the time of blood clotting and increase its density, increase the ability of platelets to stick together and reduce their viability. Smokers increase the level of carbon monoxide in the blood, which leads to a decrease in the amount of oxygen that can enter the cells of the body. In addition, the nicotine contained in tobacco smoke leads to spasm of the arteries, thereby contributing to an increase in blood pressure.
Smokers have a 2 times higher risk of myocardial infarction and 4 times the risk of sudden death than non-smokers. When smoking a pack of cigarettes per day, mortality increases by 100%, compared with non-smokers of the same age, and mortality from coronary artery disease - by 200%.
The association of smoking with heart disease is dose dependent. more cigarettes you smoke, the higher the risk of coronary artery disease.
smoking cigarettes with low level tar and nicotine or pipe smoking does not provide a reduction in the risk of cardiovascular disease. Passive smoking (when people smoke near you) also increases the risk of death from coronary artery disease. It was found that passive smoking increases the incidence of coronary disease by 25% among individuals working in a team of smokers.
B. Move more.
Hypodynamia or lack of physical activity is rightly called the disease of the XXI century. It is another avoidable risk factor for cardiovascular disease, so being physically active is essential to maintaining and improving your health. In our time, in many areas of life, the need for physical labor has disappeared.
It is known that coronary artery disease is 4-5 times more common in men under the age of 40-50 who were engaged in light work (compared to those performing heavy physical work); in athletes, a low risk of coronary artery disease persists only if they remain physically active after leaving the big sport. It is useful to practice exercise 30-45 minutes at least three times a week. Physical activity should be increased gradually.
C. Watch your weight.
Obesity is an excess accumulation of adipose tissue in the body. More than half of the world's people over the age of 45 are overweight. In a person with normal weight, up to 50% of fat reserves lie directly under the skin. An important criterion for health is the ratio of adipose tissue and muscle mass. In muscles devoid of fat, the metabolic process proceeds 17-25 times more actively than in body fat.
The location of body fat is largely determined by the sex of a person: in women, fat is deposited mainly on the hips and buttocks, and in men - around the waist in the abdomen: such an abdomen is also called a “lump of nerves”.
Obesity is one of the risk factors for CHD. When you are overweight, your resting heart rate increases, which increases your heart's need for oxygen and nutrients. In addition, obese individuals tend to have a metabolic disorder of fats: high levels of cholesterol and other lipids. Among overweight people, arterial hypertension and diabetes mellitus are much more common, which, in turn, are also risk factors for coronary artery disease.

What are the reasons for being overweight?
1. In the vast majority of cases, obesity is of alimentary origin. This means that the causes of overweight are overeating with excessive consumption of high-calorie, primarily fatty foods.
2. The second leading cause of obesity is lack of physical activity.
The most unfavorable is the abdominal type, in which fatty tissue accumulates mainly in the abdomen. This type of obesity can be recognized by waist circumference (>94 cm in men and >80 cm in women).
What to do when discovering overweight body? Program effective reduction weight loss is based on improving nutrition and increasing physical activity. More effective and physiological are dynamic loads, such as walking. The diet should be based on foods low in fat and carbohydrates, rich in vegetable proteins, trace elements, fiber. In addition, it is necessary to reduce the amount of food consumed.
Small fluctuations in weight during the week are completely natural. For example, women during menstruation can gain up to two kilograms in weight due to the accumulation of water in the tissues.
Complications of ischemic heart disease
Complications of coronary artery disease are subject to the following mnemonic rule "I.B.S.".
I. Myocardial infarction.
B. Blockade and arrhythmia of the heart.
C. Heart failure.
myocardial infarction
So, about a heart attack. Myocardial infarction is one of the complications of coronary artery disease. Most often, a heart attack affects people suffering from a lack of motor activity on the background of psycho-emotional overload. But the "scourge of the twentieth century" can also strike people with a good physical training, even young ones.
The heart is a muscular sac that pumps blood through itself like a pump. But the heart muscle itself is supplied with oxygen through the blood vessels that come to it from the outside. And so, as a result various reasons, some part of these vessels is affected by atherosclerosis and can no longer pass enough blood. Ischemic heart disease occurs. In myocardial infarction, the blood supply to part of the heart muscle stops suddenly and completely due to a complete blockage of the coronary artery. This usually results in the development of a thrombus on atherosclerotic plaque, less often - spasm of the coronary artery. The section of the heart muscle deprived of nutrition dies. In Latin, dead tissue is a heart attack.
What are the signs of myocardial infarction?
With myocardial infarction, there is a strong, often tearing, pain in the region of the heart or behind the sternum, extending to the left shoulder blade, arm, lower jaw. The pain lasts more than 30 minutes, when taking nitroglycerin, it does not completely disappear and only briefly decreases. There is a feeling of lack of air, cold sweat, severe weakness, lowering blood pressure, nausea, vomiting, a feeling of fear may appear.
Prolonged pain in the region of the heart, which last more than 20-30 minutes and do not disappear after taking nitroglycerin, may be a sign of the development of myocardial infarction. Please refer to "03".
Myocardial infarction is a very life-threatening condition. Myocardial infarction should only be treated in a hospital. Hospitalization of the patient should be carried out only by the ambulance team.
Blockades and arrhythmias of the heart
Our heart works according to one single law: "All or nothing." It should work at a frequency of 60 to 90 beats per minute. If it is below 60, then this is bradycardia, if the heart rate exceeds 90, then they speak of tachycardia. And of course, our well-being depends on how it works. Violation of the heart is manifested in the form of blockades and arrhythmias. Their main mechanism is the electrical instability of cardiac muscle cells.
Blockades are based on the principle of disconnection, it's like a telephone line: if the wire is not damaged, then the connection will be, if there is a break, then it will not be possible to talk. But the heart is a very successful "communicator", and in the event of a break in communication, it finds workarounds for signaling thanks to a developed conduction system. And as a result, the heart muscle continues to contract even with “a break in some transmission lines,” and doctors, taking an electrocardiogram, register a blockade.
Arrhythmias are a little different. There is also a “break in the line”, but the signal is reflected from the “break point” and begins to circulate continuously. This causes chaotic contractions of the heart muscle, which affects its overall work, causing hemodynamic disturbances (blood pressure drops, dizziness and other symptoms occur). That is why arrhythmias are more dangerous than blockades.
Main symptoms:
1. Feeling of palpitations and interruptions in the chest;
2. Very fast heartbeat or slow heartbeat;
3. Sometimes chest pains;
4. Shortness of breath;
5. Dizziness;
6. Loss of consciousness or feeling close to it;
Therapy of blockades and arrhythmias includes surgical and therapeutic methods. Surgical is the installation of artificial pacemakers or pacemakers. Therapeutic: with various groups drugs called antiarrhythmics, and electrical impulse therapy. Indications and contraindications in all cases are determined only by the doctor.
Heart failure
Heart failure is a condition in which the ability of the heart to provide blood supply to organs and tissues in accordance with their needs is impaired, which, most often, is a consequence of coronary artery disease. As a result of damage, the heart muscle weakens and cannot satisfactorily perform its pumping function, resulting in a decrease in the blood supply to the body.
Heart failure is often characterized according to the severity clinical symptoms. In recent years, the New York Heart Association's classification for the severity of heart failure has gained international acceptance. Mild, moderate, severe heart failure is distinguished depending on the severity of symptoms, primarily shortness of breath:
- I functional class: only enough heavy loads provoke the occurrence of weakness, palpitations, shortness of breath;
- II functional class: moderate limitation of physical activity; performing normal physical activity causes weakness, palpitations, shortness of breath, angina attacks;
- III functional class: pronounced limitation of physical activity; comfortable only at rest; with minimal physical exertion - weakness, shortness of breath, palpitations, pain behind the sternum;
- IV functional class: inability to perform any load without the appearance of discomfort; symptoms of heart failure appear at rest.
Scientific research recent decades have shown that moderate physical training in patients with chronic heart failure reduces the severity of symptoms of heart failure, but physical activity must be dosed and carried out under the supervision and supervision of a physician.
Typical angina:
Chest pain or discomfort of characteristic quality and duration
Occurs during exercise or emotional stress
Passes at rest or after taking nitroglycerin.
Atypical angina:
Two of the above signs.
Non-cardiac pain:
One or none of the above symptoms.
Laboratory research with ischemic heart disease
Minimum list biochemical indicators if coronary heart disease and angina pectoris are suspected, it includes determining the content in the blood:
- total cholesterol;
- high-density lipoprotein cholesterol;
- low density lipoprotein cholesterol;
- triglycerides;
- hemoglobin;
- glucose;
- AST and ALT.
Diagnosis of coronary heart disease
To the main instrumental methods diagnosis of stable angina is the following studies:
- electrocardiography,
- test with physical activity (veloergometry, treadmill),
- echocardiography,
- coronary angiography.
Note. If it is impossible to conduct a test with physical activity, as well as to identify the so-called bosebolic ischemia and variant angina, daily (Holter) ECG monitoring is indicated.
Coronary angiography
coronary angiography (or coronary angiography) is a method for diagnosing the state of the coronary bed. It allows you to determine the localization and degree of narrowing of the coronary arteries.
The degree of narrowing of the vessel is determined by a decrease in the diameter of its lumen compared to the proper one and is expressed in%. Until now, visual assessment has been used with the following characteristics: normal coronary artery, altered artery contour without determining the degree of stenosis, narrowing< 50%, сужение на 51-75%, 76-95%, 95-99% (субтотальное), 100% (окклюзия). Существенным рассматривают сужение артерии >50%. Hemodynamically insignificant is the narrowing of the lumen of the vessel< 50%.
In addition to the location and extent of the lesion, coronary angiography may reveal other characteristics of an arterial lesion, such as the presence of a thrombus, tear (dissection), spasm, or myocardial bridging.
Absolute contraindications for coronary angiography currently does not exist.
The main tasks of coronary angiography:
- clarification of the diagnosis in cases of insufficient information content of the results of non-invasive examination methods (electrocardiography, daily monitoring ECG, exercise tests, etc.);
- determination of the possibility of restoring adequate blood supply (revascularization) of the myocardium and the nature of the intervention - coronary artery bypass grafting or angioplasty with stenting of the coronary vessels.
Coronary angiography is performed to resolve the issue of the possibility of myocardial revascularization in the following cases:
- severe angina pectoris III-IV functional class, which persists with optimal therapy;
- signs of severe myocardial ischemia based on the results of non-invasive methods (electrocardiography, daily ECG monitoring, bicycle ergometry, and others);
- the patient has a history of episodes of sudden cardiac death or dangerous ventricular arrhythmias;
- progression of the disease (according to the dynamics of non-invasive tests);
- doubtful results of non-invasive tests in persons with socially significant professions (drivers public transport, pilots, etc.).

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Acute and chronic heart failure

Heart failure is a complex of symptoms and clinical signs that appear against the background of a violation of the pumping function of the heart. Symptoms of heart failure can be very different and, to a certain extent, depend on the form of heart failure. In this article, we will give a simplified classification of heart failure and describe the most common symptoms this cardiac syndrome. To preserve the health and life of the patient is very important, timely detection symptoms of heart failure, and hence the disease itself. This is largely facilitated by the acquaintance of patients with the main signs of this disease.
What is heart failure?
As you know, the heart is the central organ of the human cardiovascular system. In violation of the pumping function of the heart (the ability of the heart to pump blood), a syndrome of heart failure occurs, that is, the patient develops a number of signs and symptoms that indicate a violation of the heart. The causes of heart failure can be very different (see Causes of heart failure), but the symptoms of heart failure depend less on the causes that led to the development of the syndrome, and more depend on the form of heart failure in a particular patient.
The classification of heart failure is based on the mechanisms of its occurrence and the type of heart failure observed in this case.
Depending on the rate of development of heart failure, it distinguishes between acute and chronic heart failure.
Depending on the area of ​​the heart, the damage to which caused heart failure, we distinguish between right heart (right ventricular) and left heart (left ventricular) heart failure. Left ventricular heart failure is observed more often than right ventricular, since the left ventricle is under heavy stress and, therefore, more often "fails" than the right one.
Isolated heart failure (left or right ventricular) occurs mainly in acute form, while chronic heart failure is more often mixed (biventricular, total heart failure).
Acute and chronic heart failure - what is it?
Acute and chronic heart failure are the two main forms of heart failure, differing in the rate of development of symptoms and the evolution of the disease itself.
Acute heart failure is characterized by rapid (minutes to hours) onset of symptoms. The main manifestations (signs) of acute heart failure are cardiac asthma and pulmonary edema - life-threatening conditions that require immediate medical attention.
Pulmonary edema and cardiac asthma are manifested by an attack of progressive shortness of breath with the appearance of a bluish coloration of the integument, dizziness or loss of consciousness, and moist rales in the lungs. These symptoms may develop simultaneously with myocardial infarction or with hypertensive crisis, which indicates acute decompensation of the heart.
Sometimes acute heart failure develops as a complication of chronic heart failure.
Most common causes development of acute heart failure:
myocardial infarction
Decompensation of chronic heart failure
Acute valvular insufficiency
Heart rhythm disorders
Heart injury
Cardiac tamponade
Pulmonary embolism

Chronic heart failure is characterized by a slow and relatively stable development of the symptoms of the disease. In most cases, the symptoms of chronic heart failure increase gradually over time, which indicates a slow decompensation of the heart, however, there are cases when chronic heart failure is established after an attack of acute heart failure (for example, after an attack of myocardial infarction).
The most common causes of chronic heart failure:
Chronic ischemic heart disease (angina pectoris)
Cardiosclerosis
Chronic cor pulmonale
arterial hypertension
Diseases of the valvular apparatus of the heart

The most common symptoms of chronic heart failure are: swelling, shortness of breath, chronic dry cough, weakness, palpitations.
Shortness of breath is one of the earliest and most persistent symptoms of heart failure. At first, shortness of breath appears only with severe physical exertion, but over time, shortness of breath at rest and orthopnea are established (the appearance of shortness of breath when the patient is in a supine position). In patients with chronic heart failure, shortness of breath is a kind of indicator of their functional potential. This relationship between shortness of breath and physical activity of the patient formed the basis for the classification of heart failure into functional classes (FC)
I FC - the daily activity of the patient is practically not disturbed. Shortness of breath, muscle weakness, palpitations and other symptoms appear only during intense physical exertion (walking up stairs).
II FC - daily activity is slightly limited. Shortness of breath and other symptoms of heart failure appear with moderate and ordinary physical activity (walking on a flat road). At rest, there are no symptoms of heart failure.
III FC - a pronounced limitation of the physical activity of the patient. Symptoms of heart failure (including shortness of breath) appear at the slightest effort of the patient.
IV FC - symptoms of heart failure are present at rest, and any even slight physical effort (talking, getting out of bed) significantly increases them.
The appearance of shortness of breath in heart failure is associated with a violation of blood circulation through the vessels of the lungs ( venous congestion in the pulmonary vessels) due to the inability of the heart to pump the blood coming to it. Stagnation of blood in the lungs (small circulation), in addition to shortness of breath, also causes symptoms such as:
Dry cough - very characteristic of chronic heart failure (heart cough). The occurrence of dry cough is associated with edema lung tissue. Usually, cough, like shortness of breath, occurs during physical exertion or when the patient is lying down, when it is especially difficult for the heart to cope with the task assigned to it. In some cases severe attacks heart cough and shortness of breath turn into one attack of suffocation (cardiac asthma), which is a sign of the development of acute heart failure.
Because most patients with chronic heart failure are on antihypertensive treatment, which often uses ACE inhibitor drugs (eg, captopril), which can cause a dry cough ( side effect), patients are advised to observe the cough and report its characteristics to the doctor. If your cough is not related to exercise, position, or shortness of breath, and you are taking an ACE inhibitor, it may be possible to change your treatment to help get rid of the cough.
Edema in chronic heart failure is most often located on the legs. At the beginning of the disease, edema appears in the ankles. They grow in the evening and completely disappear by the morning. At further development edema diseases capture the area of ​​​​the lower leg and thigh, as well as other parts of the body, and intensify in the evening. Often, in addition to edema in patients with chronic heart failure, one can also note trophic changes skin and its appendages (skin pigmentation, ulceration, hair loss, nail deformity, etc.).
Muscle weakness is another sign of chronic heart failure. The appearance of this symptom is associated with a decrease in blood supply to the muscles. Patients usually complain about fatigue and strong muscle weakness during physical exertion.
Pain in the right hypochondrium is less persistent symptom chronic heart failure. The presence of such pains (dull, aching pain) indicates blood stasis in big circle circulation (particularly in the liver). Usually, in this case, the patient also has other symptoms of congestive chronic heart failure: swelling in the legs, ascites, hydrothorax, swelling of the jugular veins, etc.
These and other less common symptoms of chronic heart failure may be present at the same time as symptoms of underlying heart disease (eg, pain during angina attacks).
If you experience any of the symptoms described above, you should immediately contact your doctor.

Let's remember:
Acute heart failure is characterized by a sharp disruption of the heart.
The main signs of acute heart failure: severe shortness of breath, turning into suffocation, a sudden onset of dry cough, loss of consciousness;
Chronic heart failure is characterized by slow decompensation of the heart against the background of one of chronic diseases cardiovascular system (hypertension, cardiosclerosis, angina pectoris).
The main symptoms of chronic heart failure are: shortness of breath, dry cough (cardiac cough), aggravated by lying down, swelling in the legs, muscle weakness.
A patient with heart failure needs the help of qualified specialists.