Angina pectoris I, II, III, IV functional classes: description, symptoms, treatment

On average, 7-10% of Russians have chronic heart failure (CHF), 4.5% suffer from clinical symptoms of heart failure that reduce quality of life and ability to work, and among people over 65 years of age, half of patients with cardiovascular diseases have symptoms of CHF, and These numbers are increasing every year.

Heart failure is a syndrome caused by abnormal structure and decreased function of the heart. It can be the outcome of diseases such as arterial hypertension, coronary heart disease, heart defects, arrhythmias, kidney and thyroid diseases, cardiomyopathies, hereditary or as a result of infections, intoxications, metabolic and other disorders.

Description of the disease

Angina pectoris, or angina pectoris, a chronic disease of the cardiovascular system, is characterized by chest pain during physical or gastronomic stress, in stressful conditions, and sudden hypothermia. This differs from another form - angina at rest. Pressing, squeezing or burning pain occurs due to the fact that the heart muscle cells are in a state of severe oxygen deficiency (ischemia).

Pain in angina pectoris quickly decreases and disappears almost immediately after a person puts a Nitroglycerin tablet under the tongue or stops doing any physical work. This is the main difference between “angina” pain and others.

Angina pectoris is considered the most common type of coronary heart disease and is classified under ICD code I20.8.

According to the World Health Organization (WHO), approximately 300,000,000 people worldwide suffer from angina. The average age of onset of the disease is 45-50 years. The male to female ratio is 2.5:1. However, this only applies to premenopausal women. After menopause, this figure is compared with men. There is a very specific explanation for this fact.

The main cause of angina pectoris is the deterioration of blood flow through the vessels that supply the heart muscle (coronary arteries) due to atherosclerosis. It occurs due to the fact that cholesterol, namely the so-called “bad” variety (low and very low density lipoproteins), is deposited in the walls of blood vessels. Female sex hormones (estrogens) have the ability to reduce the level of this fraction, which reduces the degree of formation of atherosclerotic plaque. And with the onset of menopause, the content of protective hormones in a woman’s blood sharply decreases, which increases cholesterol levels and, accordingly, the rate of development of pathology.

If angina pectoris is not recognized and treated in time, it can lead to myocardial infarction, the number one killer of all diseases.

Degree of disease development

Depending on the speed of development, the disease can be of two types:

Acute
- develops over several hours or even minutes. In acute left ventricular failure, as a rule, cardiac asthma occurs, which is quickly complicated by pulmonary edema. It is also possible to develop cardiogenic shock, which is characterized by failure of not only the left ventricle, but also the left atrium. Acute right ventricular failure is characterized by stagnation of blood in the systemic circulation. Often occurs against the background of decompensated chronic heart failure.
Chronic
– develops over a longer period of time (up to several years). The severity of the clinical picture largely depends on the underlying disease that affected the cardiac dysfunction.

It is important to classify heart failure according to the form of the disease:

Myocardial
– with this type, the myocardium is affected, causing the heart muscle to lose the ability to contract normally. The disease is determined by a disorder of both systolic and diastolic function of the heart.
Overload
- as a result of increased load on the organ, the heart muscle gradually weakens. This form of heart failure develops with heart defects that cause a disorder in the normal flow of blood.
Combined
- heart failure develops against the background of increased load on the myocardium and its damage under the influence of various factors.

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Symptoms and signs

The main symptoms that determine exertional angina are attacks of heaviness in the chest, as well as burning or squeezing pain. These sensations can occur when a person is running, working out in the gym, or even just walking up the stairs.

The pain goes away if the load stops or the person takes Nitroglycerin in the form of a tablet/spray. This point is very important, it distinguishes more dangerous conditions - heart attack and unstable form of angina from this disease, since in them the pain is not relieved by Nitroglycerin.

Angina pain is characterized by specific irradiation - return to other parts of the body. This is mainly the lower jaw, neck, left arm and shoulder blade, and upper abdomen. Moreover, the place where the pain is applied is often felt much more strongly, and discomfort in the heart may go unnoticed. I often met patients who for a long time mistook attacks of angina for toothache and unsuccessfully underwent treatment for “pulpitis” or “periodontitis” at the dentist.

In addition to physical work, pain can “overtake” a person under other circumstances. Depending on the factor provoking a painful attack, the following clinical forms of angina pectoris are distinguished:

Early morning - exacerbation appears at approximately 5-6 o'clock in the morning. Associated with increased blood viscosity and an increase in the amount of cortisol and adrenaline. They cause increased heart rate and hypertension.
Angina after eating - a large meal redistributes blood flow in favor of the digestive organs. As a result, the oxygen supply to the heart deteriorates.

Supine angina - when a person lies down, the volume load on his heart increases, which provokes increased work of the organ and, as a result, an increase in its need for oxygenation.
Cold - at low ambient temperatures, the superficial blood vessels of the skin narrow, which forces the heart to work harder.
Tobacco – components of cigarette smoke, including nicotine, increase heart rate, constrict blood vessels and thicken the blood.
Angina after stress – stress stimulates the release of adrenaline and cortisol into the blood.
Static – when a person bends over to, for example, put on shoes, pressure increases inside the chest. This, in turn, increases the volume load on the heart in the same way as supine angina occurs.

In some groups of patients, the clinical course of angina has its own characteristics. These include:

elderly people - approximately 50% of people over 65 years of age experience not pain, but sudden difficulty breathing (shortness of breath);
women - in females, due to the predominance of the emotional component during an attack, in addition to the pain associated with angina pectoris, neurotic pain develops as a result of vasospasm. I often have to accept female patients in whom it is difficult to determine the severity of angina pectoris only by symptoms and to distinguish it from other forms of ischemia;
diabetics – due to the long course of diabetes mellitus, nerve endings are damaged, including those that conduct pain impulses. Therefore, I often meet such patients with hidden or asymptomatic angina.

Prices for consultation and appointment with a cardiologist

Name	Price
Blood pressure measurement	60,00
Consultation after MRI/MSCT	540,00
Initial consultation with a pulmonologist	1800,00
Initial appointment with a cardiologist (consultation)	1800,00
Initial appointment with a rheumatologist	1800,00
Repeated consultation with a pulmonologist	960,00
Repeated appointment with a cardiologist	960,00
Repeated appointment with a rheumatologist	960,00
Preoperative examination by a cardiologist (doctor’s appointment, ECG, interpretation)	2460,00
ECG interpretation	600,00
Taking an ECG	360,00
24-hour blood pressure monitoring	2400,00
24-hour Holter ECG monitoring	3000,00
ECG with stress	1950,00

Diagnostics

In order to make a differential diagnosis, i.e. To distinguish ischemic pain from non-ischemic pain based on symptoms, I use specially developed criteria, including 3 main signs:

classic attacks of angina pectoris,
their appearance during physical work,
weakening and disappearance after taking Nitroglycerin tablet/spray or stopping the load.

The presence of all three criteria is typical for typical angina, and two for atypical angina. If the patient has only one criterion, then the diagnosis is doubtful.

I also conduct a general examination of the patient, during which symptoms of heart failure can be identified:

swelling of the legs,
thickening of the fingertips,
bluish lip color,
swollen veins in the neck,
enlarged and painful liver.

I especially often notice such signs in the elderly. In patients with heart defects, various sounds can be heard on auscultation. It is mandatory to measure blood pressure, since the vast majority of people with angina have hypertension.

To confirm or refute the diagnosis, I prescribe an additional examination, which includes:

Blood analysis. Almost all people with coronary heart disease have elevated cholesterol levels. Therefore, I always prescribe a lipid profile (cholesterol fraction) determination. Also, following the protocol, you need to check the glucose concentration and do a general blood and urine test.
Electrocardiography (ECG) is the main diagnostic method for suspected angina. The main symptom of the disease is a decrease (depression) in the ST segment. Sometimes a negative T wave is recorded. However, often these changes cannot be detected at rest, i.e. when there is no pain. Therefore, I prescribe additional ECG studies for my patients.
Electrocardiography with stress. Of all such tests, I prefer bicycle ergometry (riding an exercise bike) and treadmill test (walking or running on a treadmill). If, after a certain time, symptoms of angina appear and the ECG shows typical signs (ST segment depression greater than 1 mm and a negative T wave), the test is considered positive. It is worth noting that such studies are not suitable for everyone. For example, I do not perform them on patients over 85 years of age and people with severe heart failure (III-IV functional class).
Daily ECG monitoring. In cases where physical tests are not possible or the results obtained are questionable, it is advisable to conduct a Holter study. It is also a very good way to detect silent myocardial ischemia. Most often, I prescribe Holter ECG to patients with diabetes.
Echocardiography (Echo-CG, ultrasound of the heart). The method allows you to check the ability of an organ to pump blood, assess the condition of the valves, the degree of wall thickening, and the presence of intracardiac blood clots.
Transesophageal electrical stimulation of the heart (TEC) - the procedure is as follows. A flexible probe with an electrode is inserted through the patient's nose and installed in the esophagus in the projection closest to the heart. Then weak signals are sent, causing an attack of angina. At the same time, an ECG film is removed to record specific changes. I also perform this method on patients for whom physical tests are contraindicated.
Myocardial scintigraphy - with this method I study the intensity of blood supply to the myocardium. For this, a radioactive drug is used (I mainly use thallium-201 and technetium-99-m), which is administered intravenously to the patient. Then he begins to perform moderate physical activity, after which an image is displayed on a special device. The degree of intensity of the glow is used to judge the blood circulation of different parts of the heart. I resort to myocardial scintigraphy if the patient has serious arrhythmias (bundle branch blocks, repeated ventricular extrasystoles), in which it is impossible to see specific changes on the cardiogram. This method is of little information for women, since breast tissue accumulates a significant part of the pharmaceutical drug.
Coronary angiography is the gold standard for diagnosing coronary heart disease, allowing a reliable diagnosis. It can also be used to determine whether surgery is necessary.

Clinical forms

Congestive left ventricular failure is characteristic of mitral disease and severe forms of coronary artery disease - especially in patients with arterial hypertension. Increased pressure in the pulmonary veins helps fill the left ventricle and maintain sufficient cardiac output. At the same time, congestive changes in the lungs disrupt the function of external respiration and are the main factor aggravating the patient’s condition with this form of heart failure. Manifestations: shortness of breath, orthopnea, auscultatory signs of pulmonary congestion (dry rales below the level of the shoulder blades, migrating moist rales) and radiological, cardiac asthma and pulmonary edema, secondary pulmonary hypertension, tachycardia.
Left ventricular failure is characteristic of aortic disease (see), coronary artery disease, and arterial hypertension. Manifestations: cerebrovascular insufficiency (dizziness, darkening of the eyes, fainting), coronary insufficiency, sphygmographic and echocardiographic signs of low output. In severe cases, Cheyne-Stokes breathing, alternating pulse (rarely), presystolic gallop rhythm (pathological IV tone), and clinical manifestations of congestive left ventricular failure are possible. In the terminal stage, right ventricular failure may occur.
Congestive right ventricular failure is characteristic of mitral and tricuspid disease, constrictive pericarditis. Usually associated with congestive left ventricular failure. Manifestations: swelling of the neck veins, high venous pressure, acrocyanosis, enlarged liver, subicterus, edema - cavitary and peripheral.
Right ventricular ejection failure is characteristic of pulmonary artery stenosis and pulmonary hypertension. It is diagnosed mainly radiographically (depleted peripheral pulmonary vascular pattern). Other signs of this form may be detected: shortness of breath at a strictly defined threshold level of physical activity, right ventricular hypertrophy - palpation, then ECG signs of the “pressure load” type (high I wave and decreased T wave in the right precordial leads). In especially severe cases, gray coloration of the skin.
Dystrophic form. As a rule, end-stage right ventricular failure. Options: a) cachectic; b) edematous-dystrophic with dystrophic changes in the skin (thinning, shine, smoothness of the pattern, flabbiness), edema - widespread or limited mobile, hypoalbuminemia, in the most severe cases - anasarca; c) uncorrectable salt depletion.

In some cases, changes in the heart itself (cardiomegaly, atriomegaly, atrial fibrillation) come to the fore, which allows us to speak of a “central” form of heart failure. As special forms with specific mechanisms of circulatory disorders and manifestations, HF is considered in “blue” congenital defects with insufficient blood flow in the pulmonary circle and unreduced or excessive in the large circle, with cor pulmonale, thyrotoxicosis, anemia, arteriovenous anastomosis, cirrhosis of the liver, as well as arrhythmogenic SN.

Patients may develop “passive adaptation” from childhood (low body weight and height, poor physical development, sharply reduced physical activity, infantilism). The listed forms of CH occur in various combinations; often it is possible to isolate only the leading form.

Canadian classification

To determine the severity of symptoms of angina pectoris, the Canadian Society of Cardiology has developed a special classification in the form of a table, which includes the following functional classes of angina pectoris:

Functional class 1

When performing normal physical activity for a person, he feels good. Pain only appears during intense and prolonged work, such as weightlifting or long-distance running.

Functional class 2

Pain occurs even during normal walking, when a person walks more than 200 meters. Also, angina pectoris develops if the patient climbs stairs above the 2nd floor, goes outside in very cold weather, or overeats.

Functional class 3

The attack begins when walking from 100 to 200 meters, or when climbing to the 2nd floor.

Functional class 4

Doing any physical work causes pain. An attack can develop even in a completely calm state.

Functional classification of pulmonary hypertension

Class I	There is no restriction on physical activity. Ordinary physical activity does not cause shortness of breath, weakness, chest pain, or dizziness
Class II	some decrease in physical activity. Ordinary physical activity is accompanied by shortness of breath, weakness, chest pain, dizziness
Class III	severe limitation of physical activity. Little physical activity causes shortness of breath, weakness, chest pain, dizziness
Class IV	inability to perform any physical activity without the above clinical symptoms. Shortness of breath or weakness may be present even at rest, discomfort increases with minimal exertion

Treatment

Before starting treatment, I need to assess the risk, i.e. the likelihood of the patient developing complications in the future (myocardial infarction and death). This is necessary to choose treatment tactics.

To do this, I pay attention to the following parameters:

Results of tests with physical activity (the time of performing the exercise, after which the patient has an attack);
echocardiography indicators, namely the adequacy of the pumping function of the heart;
glow intensity on myocardial scintigraphy;
the prevalence of atherosclerosis of the coronary arteries and the degree of narrowing of their lumen.

If the patient is at low or medium risk, then I limit myself to drug therapy. And if he is at high risk, then he needs more aggressive treatment of angina pectoris in the form of surgery.

The Braunwald Guide for the treatment of cardiac diseases, the most authoritative publication, recommends the use of the following medications for angina pectoris:

Beta-blockers (Bisoprolol, Metoprolol) - reduce the pulse rate and slow down the conduction of nerve impulses, thereby reducing the myocardial need for oxygen. In addition, due to an increase in the period of relaxation (diastole) of the heart muscle, its blood circulation improves.
Slow calcium channel antagonists (Diltiazem, Verapamil) have a similar mechanism of action. I use them in case of intolerance to beta-blockers or if there are contraindications to them.
Antiplatelet drugs are necessary to prevent the formation of blood clots in the arteries, which lead to a heart attack. First, I prescribe Acetylsalicylic acid, and if the patient has a stomach or duodenal ulcer, then Clopidogrel.
Statins (Atorvastatin, Rosuvastatin) - reduce the concentration of cholesterol in the blood, thereby slowing down the process of formation of atherosclerotic plaque.
ACE inhibitors (Perindopril, Lisinopril) - these medications are needed by patients who, in addition to angina, suffer from chronic heart failure or diabetes.
Blockers of If-channels of sinus node cells (Ivabradine) are so-called pulse-lowering drugs. I use them when the patient has a very fast pulse (more than 100).

This scheme allows me to achieve clinical improvement in the form of cessation of pain in some patients. If attacks persist with the selected therapy, then I add nitrates (Nitroglycerin). These drugs relax the smooth muscle walls of the coronary arteries, which leads to their expansion and increased blood flow to the myocardium.

However, these drugs must be handled very carefully, since if they are not taken correctly, tolerance (addiction) quickly develops, and their therapeutic effect is reduced several times. Therefore, I always recommend that my patients take nitrates only when an attack begins, or no more than 2 times a day, and so that the interval between doses is at least 12 hours.

If drug treatment is unsuccessful, or if the patient has a high cardiovascular risk, surgery is performed.

There are 2 main types of operations:

Stenting, or percutaneous coronary intervention (PCI);
coronary artery bypass grafting (CABG)

The essence of PCI is the introduction of a special metal stent into the vessel, which improves its patency. The operation is performed under local anesthesia. Access is through the femoral artery. PCI is performed when stenosis in one vessel is more severe than 50%.

When performing CABG, a connection is created between the aorta and the coronary artery to bypass the narrowed vessels. CABG is an open abdominal operation with general anesthesia (anesthesia) and opening of the chest. This method is justified if several arteries are affected or stenting is not possible.

Lifestyle requirements

In order for drug and surgical treatment to have maximum effect, I recommend that my patients adhere to a certain lifestyle, which includes several aspects:

bad habits – it is advisable to limit alcoholic drinks (to about 300 ml of wine per week). Smoking is strictly prohibited;
diet - reducing the consumption of foods rich in saturated fats (meat, milk, butter) and increasing foods with a predominant content of omega-3.6 fatty acids (vegetables, fish, vegetable oil). The diet must include fruits, nuts, and cereals;
regular moderate physical activity or exercise therapy - aerobic exercises are preferable, such as swimming, running, cycling;
body weight control is achieved by strict adherence to the previous 2 points.

Chronic heart failure

The data on chronic heart failure (CHF) that have accumulated in recent years have led to the need for a unified approach to the diagnosis and treatment of this pathology, which in turn has contributed to the emergence of a number of advisory documents. Over the past 5 years alone, authoritative cardiological associations have already published several revisions of their recommendations for the diagnosis and treatment of CHF: American College of Cardiology / American Heart Association (2001, 2005), European Heart Association (2001, 2005), VNOK (1993, draft, 2006 ).

Ideas about CHF have been constantly changing over the past decades. Moreover, not only the issues of pathogenesis, diagnosis and treatment, but also approaches to determining

CHF.

Thus, in the European recommendations of 2001

CHF is presented as “
a pathophysiological syndrome
in which, as a result of a particular disease of the cardiovascular system, a decrease in pumping function occurs, which leads to an imbalance between the hemodynamic need of the body and the capabilities of the heart.”
According to the domestic recommendations of the All-Russian Scientific and Cultural Organization (2003),
CHF is also “
a syndrome
that occurs when a person has systolic and/or diastolic dysfunction, accompanied by chronic hyperactivation of neurohormonal systems and clinically manifested by shortness of breath, weakness, palpitations, limitation of physical activity, pathological fluid retention in the body "
At the same time, the modern neurohormonal theory of the pathogenesis of heart failure has convincingly shown that, regardless of the initial causes, its development occurs on a single pathophysiological basis. These provisions allowed GFCI experts to put forward a proposal that CHF is a separate nosological unit, and in the draft national recommendations of GFCI and OSCH of 2006
.
CHF is proposed to be understood as “ a disease with a complex of characteristic symptoms (shortness of breath, fatigue and decreased physical activity, edema, etc.), which are associated with inadequate perfusion of organs and tissues at rest or during exercise and often with fluid retention in the body.”
Active studies of any individual component of the pathogenesis of CHF in different years have led to the emergence of different pathophysiological definitions and, accordingly, models of its development (Table 1).

Most common etiological factors

CHF remains coronary heart disease (CHD), in particular myocardial infarction (MI), angina pectoris and ischemic cardiomyopathy, which is primarily associated with a decrease in global systolic function of the left ventricle (LV). The second and third positions are occupied by dilated cardiomyopathy and rheumatic heart defects, respectively. At the same time, in people over 70 years of age, hypertension and associated disturbances in myocardial diastolic relaxation play a leading role in the development of CHF, along with ischemic heart disease.

Diagnostics

CHF is built on three main pillars: 1) clinical manifestations, among which the most common are shortness of breath, fatigue and decreased performance, peripheral edema; 2) objective signs of heart damage, that is, evidence of the connection of clinical signs specifically with cardiac and not other pathology; 3) ex juvantibus effect. In this case, the presence of the first two criteria is mandatory.

However, diagnosing CHF is quite a difficult task, since clinical signs, like objective data, are very nonspecific and can occur in a wide variety of diseases. At the same time, they should be constantly remembered, since it is they who, already at the first communication between the doctor and the patient, allow one to suspect the presence of CHF. The most common symptoms and objective data characteristic of CHF are presented in table. 2.

It should be remembered that such characteristic clinical symptoms

CHF, such as peripheral edema, wheezing in the lungs, orthopnea and cough, are not as common - from 28 to 73%, according to the IMPROVEMENT study (2000). But the most common complaints are shortness of breath (98.4%), fatigue (94.3%) and palpitations (80.4%).

The second important “pillar” on which the diagnosis of CHF is based is the results of instrumental and laboratory tests,

making it possible to associate the occurrence of very nonspecific clinical symptoms with the pathology of the cardiovascular system, and not any other system.
The simplest and most accessible method, electrocardiography
, is almost never normal (negative predictive value >90%).
Most often, the ECG records signs of myocardial hypertrophy, focal changes of a cicatricial nature, and various disturbances of heart rhythm and conduction. Chest X-ray
allows you to verify cardiomegaly and venous congestion.
The dynamics of the last sign can be used as a criterion for the effectiveness of therapy. Extremely important and most complete information about the structural and functional state of the heart can be obtained from echocardiography.
The method allows not only to identify the very fact of a decrease in myocardial contractile function, but also to assess its degree and dynamics during the treatment process.
The most common indicator associated with the systolic function of the left ventricle is the ejection fraction, although shortening fraction, myocardial contractility index, sphericity index, etc. are also used to assess the latter. Low EF values are a predictor of an unfavorable prognosis in patients with CHF. It should be remembered that a normal ejection fraction does not exclude the presence of CHF. Individuals with normal or slightly reduced EF (≥50%) and clinical symptoms of CHF are most likely to have diastolic heart failure. In addition to the first two conditions, to verify diastolic HF, the presence of signs of impaired LV relaxation and/or its distensibility (the ratio of the peak velocity of early and late ventricular filling E/A, the time of LV isovolumic relaxation, the time of blood flow deceleration, etc.) is required. In addition to the functional characteristics, Echo-CG allows one to assess the size and volume of the chambers of the heart, as well as their dynamics during treatment, the condition of the heart valve apparatus, pressure in the cavities and large vessels, etc. When transthoracic access is limited, there is a suspicion of complicated valvular heart disease, valvular dysfunction can be performed on the prosthesis .
Routine laboratory tests

blood (clinical analysis, creatinine, urea, electrolytes, “liver” enzymes, thyroid hormones) and
urine
(general analysis, functional tests) primarily serve to exclude extracardiac (renal, thyroid, etc.) causes of clinical symptoms characteristic of CHF. However, the presence of anemia is currently recognized as an unfavorable prognostic factor in patients with CHF. A close relationship is clearly shown between the severity of CHF and the content of natriuretic peptides in plasma, which makes an increase in the latter a kind of “laboratory” criterion for CHF. Moreover, their definition should be used not so much to confirm, but rather to exclude the diagnosis of CHF (negative predictive value >90%).

Classification of CHF

provides for an assessment of the patient’s condition in two main positions: a) stage of the disease (an irreversible process that can be slowed down and even stopped for a while, but stage II will never turn into stage I) and b) the functional capacity of the cardiovascular system (functional class of CHF – a dynamic parameter that can change during treatment). With regard to the first point, the Vasilenko-Strazhesko classification was recognized as the most successful (Table 3), with regard to the second – the NYHA classification (Table 4).

Determining the functional class of CHF according to this classification is based on a certain degree of subjectivity, therefore, in practical clinical activities, a 6-minute walk test is used to objectify this process. Depending on the distance that a particular patient can walk in 6 minutes, one or another class of CHF is verified (Table 5).

The severity of heart failure, assessed by functional class, has prognostic significance. Thus, the annual mortality rate of patients with FC I CHF is about 10%, FC II - 20, FC - 40, FC IV - more than 60%. Despite the introduction of new treatment methods, the mortality rate of patients with CHF remains virtually unchanged.

Treatment of CHF

- a very complex and expensive task.
The following main goals of therapy
:

elimination or minimization of clinical symptoms;
slowing down the progression of the disease by protecting target organs (vessels, heart, kidneys, brain);
improving quality of life;
increase in life expectancy;
reduction in the number of hospitalizations.

There are six ways to achieve your goals when treating decompensation:

diet
physical activity regimen;
psychological rehabilitation, organization of medical supervision, schools for patients with CHF;
drug therapy;
electrophysiological methods of therapy;
surgical, mechanical methods of treatment.

Diet.

The main principle is to limit salt consumption, and the more, the greater the FC of CHF. In FC I, it is recommended not to eat salty foods (up to 3 g NaCl); at FC II, do not add salt to food (up to 1.5 g NaCl); at III FC plus products with reduced salt content and preparation without salt (<1.0 g NaCl). Recommendations for fluid restriction are relevant only for decompensated CHF, when parenteral administration of diuretics is required. Patients should strictly monitor their weight; an increase of 2 kg or more over several days most often indicates fluid retention and a high risk of decompensation.

Physical activity

indicated for all patients with CHF, regardless of severity. However, its nature and volume depend on the functional class (Fig. 1). During the training process, you should constantly evaluate the effectiveness of the activities carried out, determine the functional class based on the 6-minute walk test and, depending on this, move from one level to another. Moreover, the transition process should be quite long and take from 5-6 to 10-12 weeks.

Rice. 1. The volume of physical activity in patients with CHF.

Drug therapy for CHF

From the standpoint of evidence-based medicine, all drugs that are used to treat CHF are divided into three groups: main

(their effectiveness has been proven and is beyond doubt),
additional
(their effectiveness and safety have been studied, but require clarification),
auxiliary
(their effect on the prognosis has not been proven, but they improve the clinical picture).

Main

This group of drugs fully meets the criteria of evidence-based medicine and is recommended for use. These are ACE inhibitors (ACEIs), beta-blockers (BABs), aldosterone antagonists (AAs), diuretics (D), cardiac glycosides (CGs) and angiotensin receptor antagonists (AARs, currently only candesartan).

It is possible to assign additional

group of drugs, which currently consists of statins and anticoagulants.

Auxiliary

The drugs are peripheral vasodilators, antiarrhythmics, calcium channel blockers, antiplatelet agents, non-glycoside inotropic agents.

It is worth dwelling on a brief description of the drugs of the main group.

ACE inhibitors.

To date, ACEIs firmly occupy a leading position in the list of drugs for the treatment of CHF. Back in 1995, a meta-analysis that included more than 7,100 patients demonstrated the ability of ACE inhibitors to reduce the risk of death in patients with CHF by 23%, and this effect was even more pronounced in the first 90 days of treatment (44% risk reduction). These results have been repeatedly confirmed in many studies and analyzes showing that the positive effects of ACE inhibitors do not depend on age and persist in most clinical situations and with any severity of CHF.

The main provisions for the use of ACE inhibitors are as follows:

ACE inhibitors should be prescribed to all patients with CHF, regardless of the etiology and stage of the process. However, the effectiveness of ACE inhibitors for ischemic etiology of CHF and in women is somewhat lower. Concomitant use of non-steroidal anti-inflammatory drugs may also weaken the effect of ACE inhibitors.
ACE inhibitors can improve clinical symptoms, quality of life (QoL), slow the progression of the disease, reduce morbidity and improve the prognosis of patients with CHF.
The effectiveness of ACE inhibitors is manifested in all stages of CHF - from the very beginning, including asymptomatic LV dysfunction, to the most advanced stages of decompensation.
In individuals with preserved systolic cardiac function, ACEIs are the most reasonable method of treating CHF.

Most common adverse reactions

when prescribing ACE inhibitors (in total, no more than 7-9% of the reasons for cancellation) are dry cough, arterial hypotension, an increase in the degree of chronic renal failure in the form of azotemia, hyperkalemia.

ACEIs are absolutely contraindicated

only in cases of known intolerance (angioedema), bilateral renal artery stenosis and pregnancy.

The initiation of ACEI therapy should be carried out with small doses with gradual (no more than once every 2-3 days, and in case of systemic hypotension - once a week) titration to optimal (average therapeutic) doses.

Table 6 presents the doses of the main representatives of the ACEI group, the most studied in terms of the treatment and prevention of CHF and registered in the Russian Federation.

Beta blockers.

To date, more than 30 studies have been completed, including more than 20 thousand patients with CHF, which have shown the ability of blockers to reduce the mortality of patients with decompensation by 29% (it should be noted that in most cases, blockers were used in addition to ACE inhibitors). Therefore, since 1999 in the USA and European countries, and a little later in Russia, beta-blockers have been recommended for use as the main means for the treatment of CHF.

However, not all beta-blockers have a positive effect in CHF. Currently, the effectiveness of beta blockers in reducing mortality and the number of hospitalizations has been proven for only three drugs: carvedilol

(BAB with alpha-blocking activity, as well as antiproliferative and antioxidant properties),
bisoprolol
(the most selective blocker for b1 receptors) and
metoprolol succinate
(a selective lipophilic beta-blocker of prolonged action).
In addition to the three recommended beta blockers, nebivolol
of age, which does not significantly reduce mortality, but reduces the morbidity of patients and the number of re-hospitalizations (SENIORS study).

The main provisions for the use of ACE inhibitors are as follows:

In their ability to reduce the risk of morbidity and death in decompensated patients, beta blockers are even superior to ACE inhibitors.
Along with ACE inhibitors, beta blockers are the main means of treating CHF. Their use can slow down the progression of the disease, reduce the number of hospitalizations and improve the prognosis of patients.
In most cases, beta blockers are prescribed in addition to ACE inhibitors for patients in a stable condition. In rare situations (the predominance of severe tachycardia at low blood pressure, when the combination of an ACE inhibitor and a beta blocker is difficult), you can start therapy with the β1-selective beta blocker bisoprolol, followed by the addition of an ACE inhibitor (CIBIS-III study).
The starting dose of any beta-blocker in the treatment of CHF is 1/8 of the average therapeutic dose: 3.125 mg twice a day for carvedilol, 1.25 mg for bisoprolol, 12.5 mg for metoprolol, 1.25 mg for nebivolol.
Doubling the dosage of beta blockers should be done no more often than once every two weeks, provided that the patient’s condition is stable and there is no bradycardia or hypotension.

Contraindications

for the prescription of beta blockers for CHF are: bronchial asthma, symptomatic bradycardia (<50 beats/min), symptomatic hypotension (<85 mm Hg), AV block of II or more degrees, severe obliterating endarteritis.

Table 7 presents the starting, therapeutic and maximum doses of beta blockers recommended for the treatment of CHF.

Aldosterone antagonists (spironolactone)

have been used in the treatment of CHF for more than 40 years. In high doses, the drug is successfully used in complex diuretic therapy of severe CHF as a potassium-sparing diuretic, potentiating the effect of loop and thiazide diuretics. Its prescription during the period of decompensation of CHF in combination with other diuretics was not in doubt. The results of some studies (primarily RALES) have expanded the list of indications for its use, especially in patients with FC III-IV. In small dosages (the average dose in this study was 27 mg), aldactone exhibits the properties of a neurohumoral modulator and, in combination with ACE inhibitors and beta blockers, can significantly reduce the risk of death by 27%, both sudden and associated with exacerbation of decompensation.

The question of using small doses of aldactone in patients with low functional class of CHF (FC I-II) remains open. Although there is already evidence that in patients who suffered a MI complicated by the development of class II CHF, the use of the new aldosterone antagonist eplerenone reduced the risk of death, nevertheless, the administration of small doses of spironolactone to patients with class II CHF cannot yet be strictly recommended.

Based on adverse reactions

spironolactone (in addition to possible hyperkalemia and an increase in creatinine levels), the development of gynecomastia should be noted (up to 10% of patients). The frequency of the latter effect when taking a new (not yet registered in the Russian Federation) drug of this group, eplerenone, does not exceed 1%.

Diuretics.

There are currently no multicenter controlled studies examining the effectiveness of diuretics in CHF. Nevertheless, the accumulated many years of positive experience in the use of diuretics in patients with clinical signs of overhydration allowed experts to place this group of drugs on the list of “essential” drugs for the treatment of CHF.

The main provisions for the use of diuretics are as follows:

The main indication for prescribing diuretics is the elimination of edema syndrome and improvement of clinical symptoms of patients with CHF. When used correctly, these drugs can reduce the number of hospitalizations, but do not affect the progression of CHF and do not improve the prognosis of patients. Their impact on the quality of life if prescribed incorrectly (loading doses every 3-4-5-7 days) can even be negative.
Diuretics are prescribed only for clinical signs of stagnation (stage IIA). Prophylactic use of diuretics is not indicated, as they do not improve the prognosis.
Therapy with diuretics should be combined with the use of neurohormonal modulators, such as ACE inhibitors and aldosterone antagonists, to prevent refractoriness to diuretics.
Preference should be given to thiazide diuretics (hypothiazide) and only if they are insufficiently effective, proceed to the prescription of powerful “loop” diuretics (furosemide, uregit, bumetanide).
Treatment should begin with small doses, subsequently selecting the dose according to the principle of quantum satis.

Recommended doses for the most commonly used diuretics:

hypothiazide: starting = 25 mg, maximum = 75-100 mg;
furosemide: starting = 20-40 mg, maximum = up to 500 mg;
uregitis: starting = 25-50 mg, maximum = up to 250 mg;
bumetanide: starting = 0.5-1.0 mg, maximum = up to 10 mg.

In 2006, the loop diuretic torasemide was registered in the Russian Federation, which, in comparison with furosemide, demonstrated a better ability to influence the prognosis of patients with CHF. The initial dosage of the drug is 5-10 mg and can subsequently be increased to 100-200 mg per day.

We should not forget about diacarb, the main mechanism of action of which is the blockade of carbonic anhydrase in the epithelium of the proximal renal tubules, which ultimately, in addition to the diuretic effect, leads to acidification of the urine. This effect is especially necessary in the case of development of resistance to loop diuretics, as well as in patients with concomitant COPD. Diacarb is prescribed 0.25 mg three times a day for 3-4 days with an interval of 2-3 weeks.

The main indication for prescribing diuretics is the clinical signs and symptoms of excessive fluid retention in the body of a patient with CHF, but one should remember their side effects

: 1) hyperactivation of neurohumoral systems (once again emphasizing the need for parallel administration of ACE inhibitors and aldactone) and 2) changes in metabolic status (carbohydrate, lipid and electrolyte metabolism, usually in high doses - for hypothiazide more than 50 mg/day).

Diuretic therapy in patients with CHF has two phases - active and maintenance. In the first active phase, a combination of diuretics is used with the mandatory inclusion of loop diuretics. The main criterion for effectiveness is the excess of excreted urine over the administered fluid by about 1 liter per day with a decrease in body weight of about 700-900 g per day. Rapid dehydration cannot be justified and only leads to hyperactivation of neurohormonal systems and rebound fluid retention in the body. At the stage of maintenance diuretic therapy, the water balance should be zero with possible fluctuations of up to 200 ml in both positive and negative directions.

Cardiac glycosides

do not affect the prognosis and progression of CHF, but are able to improve clinical symptoms, quality of life and reduce the number of hospitalizations, which allows us to classify this group of drugs as the “main” drugs for the treatment of CHF. It should be remembered that cardiac glycosides, in addition to the positive inotropic and negative chronotropic effect on the myocardium, also have a neuromodulatory effect.

Currently, the most common cardiac glycoside in Russia is digoxin. Non-glycoside drugs that have the ability to increase myocardial contractility negatively affect the prognosis and life expectancy of patients and can only be used in short courses for decompensated CHF.

The greatest effectiveness of glycosides is achieved in patients with low EF (<25%), large heart sizes (cardiothoracic index >55%) and non-ischemic etiology of CHF. Glycosides are especially indicated in patients with atrial fibrillation. Their ability to reduce heart rate by blocking AV conduction is well known, but is not always sufficient when the patient is physically active. In the latter case, the combination of digoxin with a beta blocker is optimal, which, in addition to optimal control of the rhythm frequency, helps prevent the development of life-threatening ventricular arrhythmias.

Currently, the most optimal is to prescribe small doses of glycosides (digoxin no more than 0.25 mg per day), preferably under the control of its concentration in the blood plasma (no more than 1.2 ng/ml). It must be remembered that plasma digoxin concentrations increase exponentially by the eighth day from the start of therapy, so such patients are ideally advised to perform 24-hour ECG monitoring to monitor the PQ interval and verify rhythm disturbances.

It should be remembered that treatment with glycosides in women is more often accompanied by the development of intoxication and fatal complications, even with the same dosages of the drug as in men.

Angiotensin II receptor antagonists.

Despite the theoretical prerequisites for achieving complete blockade of the renin-angiotensin system with drugs of this group, until recently it was not possible to detect even effects comparable to ACE inhibitors on solid endpoints in patients with CHF. However, the recently completed CHARM study showed that taking candesartan in people with low ejection fraction was associated with a reduction in mortality and hospitalizations. At the same time, candesartan does not have the ability to improve the prognosis of patients with preserved LV systolic function.

The ELITE-II study showed that losartan was only slightly and nonsignificantly inferior to captopril in terms of its effect on hard endpoints in patients with decompensated CHF. In addition, in individuals with diabetic nephropathy, losartan is able to prevent the development of CHF.

The combination of an ACEI and the ARA valsartan does not affect the prognosis, but can reduce the number of hospitalizations (Val-HeFT).

Summarizing the above, it should be emphasized that in patients with CHF with reduced LV systolic function, the ARA candesartan can become an alternative to the ACEI. The prescription of other ARAs (losartan, valsartan) is especially indicated for intolerance to ACE inhibitors.

Ruslan LINCHAK,

Head of the Cardiology Department of the National Medical and Surgical Center named after. N.I. Pirogova,

Candidate of Medical Sciences, Associate Professor

Doctor's advice

In addition to the generally accepted lifestyle interventions described above, I strongly encourage my patients to monitor their blood pressure and take appropriate medications regularly.

If a person suffers from diabetes, he should regularly check his blood glucose levels and periodically take a glycated hemoglobin test. This is important, since diabetes can worsen the course of angina several times and lead to complications.

Also, if you cannot eat fish often, you can take fish oil in the form of dietary supplements. They are available in any pharmacy. To argue for the benefits of fish oil, I would like to give the example of Japan, a country where heart disease rates are extremely low, and fish as a food product occupies the top positions.

Clinical case

I would like to provide an example from personal experience.
A 52-year-old man visited his local physician for an outpatient appointment with complaints of pressing pain in the heart area, which occurs when climbing the stairs to the 3rd floor and goes away a few minutes after resting. I began to notice the appearance of these pains about a month ago. Suffering from type 2 diabetes mellitus and hypertension. She takes Metformin 1000 mg 2 times a day and Lisinopril 10 mg 1 time a day. The therapist referred him to a cardiologist, who prescribed an ECG and VEM (veloergometry). At rest, when deciphering the ECG, there were no changes. When performing a VEM, an ECG revealed ST segment depression of 2 mm. The patient was sent to the cardiology hospital for further examination with a diagnosis of coronary artery disease, angina pectoris FC 2. Coronary angiography was performed, which revealed 70% stenosis of the right coronary artery. The damage to the remaining vessels was not critical, so the decision was made to install a stent. Drug therapy was also prescribed (Acetylsalicylic acid, Rosuvastatin, Bisoprolol). The patient noted a significant improvement in his condition in the form of cessation of pain attacks. Upon discharge, recommendations for lifestyle modifications were given.

In conclusion, I would like to note that angina pectoris is a serious disease that requires due attention from both the doctor and the patient. Ignoring attacks of pain can lead to an unfavorable prognosis in the form of myocardial infarction, disability and death. However, timely diagnosis and proper treatment can improve the quality and increase the life expectancy of a person.

Make an appointment with a cardiologist

The best cardiologists at the private Multidisciplinary Medical Center in Moscow invite patients with any type of cardiac dysfunction to diagnose and treat them. If signs of heart failure are detected, the patient is prescribed a comprehensive examination, after which experienced specialists will monitor the disease through medication and other effective therapy.

You can make an appointment with a cardiologist for a fee by phone or using the feedback form. Check the price of initial and repeat appointments on the clinic’s website. If the patient’s condition is acute, cardiologists will see him without an appointment at any time of arrival at our center.

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