ICD 10 IHD code refers to the classification of symptoms associated with coronary heart disease. The abbreviation ICD stands for “International Classification of Diseases” and represents the entire list of currently recognized diseases and pathologies of human development.

The number 10 indicates the number of revisions of the list - ICD 10 is the result of the tenth worldwide revision. Codes are assistants in searching for the necessary symptoms and disorders of the body.

IHD, or “coronary disease” is a disease associated with insufficient oxygen enrichment of the muscle tissue of the heart - the myocardium. The most common cause of the development of IHD is atherosclerosis, a dysfunction characterized by the deposition of plaques on the walls of the arteries.

There are a number of complications and accompanying syndromes of coronary heart disease. They are described in the ICD code from I20 to I25 number.

MBK codes

Number I20 is angina pectoris. The classification of diseases divides it into: unstable and other types of angina. Unstable angina is an intermediate period in the development of coronary artery disease, between the stable course of dysfunction and complication. During this period, the likelihood of an infarction of the middle muscular layer of the heart is especially high.

Number I21 is acute myocardial infarction, which may not be caused by stable angina. Myocardial infarction is acute form ischemic disease, and occurs when blood supply to an organ is stopped.

If normal blood flow does not return, the area of ​​the heart deprived of blood dies without the ability to resume its functions.

Code I22 indicates recurrent myocardial infarction. It is divided into infarction of the anterior and inferior myocardial wall, other specified localization and unspecified localization. A recurrent heart attack carries a risk of death for the patient.

The second time the disease may appear with the same symptoms as the first time - severe pain in the sternum, extending into the arm, the space between the shoulder blades, into the neck and jaw. The syndrome can last from 15 minutes to several hours. Complications may occur - pulmonary edema, loss of creation, suffocation, immediate drop in pressure.

But a variant of an almost undetected heart attack is also possible, when the patient notes only a general weakness of the condition.

Complaints of rapid heartbeat are typical for the arrhythmic form; the abdominal type may be accompanied by abdominal pain, and the asthmatic type may be accompanied by shortness of breath.

It is impossible to determine exactly which patients will have a second heart attack - sometimes this is not related to lifestyle and habits.

Number I23 lists some current complications of acute myocardial infarction. Among them: hemopericardium, atrial and interventricular septal defect, damage to the heart wall without hemopericardium, chordae tendineus and papillary muscle, thrombosis of the atrium, atrial appendage and ventricle of the organ, as well as other possible complications.

Code I24 offers options for other forms of acute coronary heart disease.

Among them: coronary thrombosis, which does not lead to myocardial infarction, post-infarction syndrome - an autoimmune complication of a heart attack, coronary insufficiency and inferiority, unspecified acute coronary heart disease. The list concludes with a list of codes number I25, with chronic coronary heart disease.

It includes atherosclerotic disease - a syndrome in which blood vessels are clogged with atherosclerotic deposits, myocardial infarction suffered and cured, which does not show its symptoms at this time, aneurysm of the heart and coronary artery, cardiomyopathy, myocardial ischemia, and other listed forms of the disease, including and unspecified.

Diseases cardiovascular systems They are recognized as the leading causes of death worldwide.

One of the most dangerous pathologies that cannot be cured is post-infarction cardiosclerosis - an inevitable consequence of myocardial infarction. Without the necessary treatment, the disease leads to complete cessation of cardiac activity.

– acute stage caused by insufficient blood flow. If blood is not delivered to any part of the organ for more than 15 minutes, it dies, forming a necrotic area.

Gradually, dead tissue is replaced by connective tissue - this is the process of sclerotization, which determines what post-infarction cardiosclerosis is. It is diagnosed after a heart attack in 100% of patients.

Connective fibers cannot contract and conduct electrical impulses. Loss of functionality of areas of the myocardium causes a decrease in the percentage of blood ejection, disrupts the conductivity of the organ and the rhythm of the heartbeat.

The diagnosis of “cardiosclerosis” is made on average three months after a heart attack. By this time, the scarring process is completed, which makes it possible to determine the severity of the disease and the area of ​​sclerotization. By this parameter the disease is divided into two types:

1. Large-focal post-infarction cardiosclerosis is the most dangerous. In this case, significant areas of the myocardium are subject to scarring, and one of the walls may become completely sclerotized.
2. The small-focal form consists of small inclusions of connective fibers, in the form of thin whitish stripes. They can be single or evenly distributed in the myocardium. This type of cardiosclerosis occurs due to hypoxia (oxygen starvation) of cells.

After a heart attack, a small focal form of cardiosclerosis occurs very rarely. More often, large areas of heart tissue are affected, or an initially small amount of scar tissue grows as a result of untimely treatment. It is possible to stop sclerosis only with the help of competent diagnosis and therapy.

ICD 10 code

ICD 10 does not provide for such a diagnosis as “post-infarction cardiosclerosis”, since in the full sense it cannot be called a disease. Instead, codes for other diseases are used that manifest themselves against the background of myocardial sclerotization: post-infarction syndrome, disorders heart rate And so on.

Could it be the cause of death?

The risk of sudden clinical death for people with this diagnosis is quite high. The forecast is made based on information about the degree of neglect of the pathology and the location of its foci. A life-threatening condition occurs when the blood flow is less than 80% of normal, and the left ventricle is susceptible to sclerotization.

When the disease reaches this stage, a heart transplant is required. Without surgery, even with supportive drug therapy, the survival prognosis does not exceed five years.

In addition, with post-infarction cardiosclerosis, the causes of death are:

• uncoordination of ventricular contractions ();
• cardiogenic shock;
• aneurysm rupture;
• cessation of bioelectrical conduction of the heart (asystole).

To avoid irreversible consequences, the patient after a heart attack needs to carefully monitor the body’s reactions. At the first sign of exacerbation, immediately visit a cardiologist.

Signs

While small areas of the myocardium are exposed to sclerotic processes, the disease does not manifest itself in any way, since at the initial stage of the disease the heart walls remain elastic and the muscle does not weaken. As the area of ​​sclerosis increases, the pathology becomes more noticeable. If the left ventricle undergoes changes to a greater extent, the patient experiences:

• increased fatigue;
• increased heart rate;
• cough, often dry, but foamy sputum may be produced;

Left ventricular post-infarction cardiosclerosis is characterized by the formation of so-called cardiac asthma - severe shortness of breath at night, causing attacks of suffocation. She forces the patient to sit down. In a vertical position, breathing returns to normal after an average of 10-15 minutes; when returning to a horizontal position, the attack may recur.

If the right ventricle becomes scarred, symptoms such as:

• cyanosis of lips and limbs;
• swelling and pulsation of the veins in the neck;
• , worse in the evening; start from the feet, gradually rise, reaching the groin;
• soreness in the right side caused by an enlarged liver;
• accumulation of water in the peritoneum (edema in the systemic circulation).

Arrhythmias are characteristic of scarring of any localization, even when small parts of the myocardium are affected.

Attention: severe cardiosclerosis causes dizziness and fainting. These symptoms indicate cerebral hypoxia.

The earlier the pathology is detected, the more favorable the treatment prognosis. The specialist will be able to see initial stage post-infarction cardiosclerosis on ECG.

Symptoms of post-infarction cardiosclerosis

On ECG

Electrocardiography data have great diagnostic value in the analysis of cardiovascular diseases.

Signs of post-infarction cardiosclerosis on the ECG are:

• myocardial changes;
• the presence of Q waves (normally their values ​​are negative) almost always indicates a violation of the functionality of the heart vessels, especially when on the graph the Q wave reaches a quarter of the height of the R peak;
• the T wave is weakly expressed or has negative indicators;
• bundle branch block;
• enlarged left ventricle;
• heartbeat disturbances.

When ECG results in a static position do not go beyond the normative limits, and symptoms appear periodically, suggesting a sclerotic process, tests with physical activity or Holter monitoring (24-hour study of heart function over time).

The decoding of the cardiogram should be carried out by a qualified specialist who, based on the graphic picture, will determine clinical picture diseases, localization of pathological foci. To clarify the diagnosis, other laboratory diagnostic methods can be used.

Diagnostic procedures

In addition to collecting anamnesis and ECG, the diagnosis of post-infarction cardiosclerosis includes the following laboratory tests:

• echocardiography is performed to detect (or exclude) chronic aneurysm, assess the size and condition of the chambers, as well as the heart wall, and help identify contraction disorders;
• ventriculography analyzes the work mitral valve, percentage of ejection, degree of scarring;
• Ultrasound of the heart;
• X-ray shows an increase in the shadow of the heart (usually on the left);
• scintigraphy using radioactive isotopes (when the composition is introduced, these elements do not penetrate pathological cells) allows you to separate damaged areas of the organ from healthy ones;
• PET reveals stable areas with weak blood microcirculation;
• Coronary angiography allows assessment of coronary blood supply.

The volume and number of diagnostic procedures is determined by a cardiologist. Based on the analysis of the data obtained, adequate treatment is prescribed.

There is no single method (or set of tools) for restoring damaged myocardium. For post-infarction cardiosclerosis clinical guidelines are aimed at:

• slowing the development of heart failure;
• pulse stabilization;
• stopping scarring;
• minimizing the likelihood of a recurrent heart attack.

The tasks set can be solved only with an integrated approach. The patient needs:

• maintain a daily routine;
• limit loads;
• quit smoking;
• avoid stress;
• stop drinking alcoholic beverages.

Diet therapy plays an important role in the treatment of post-infarction cardiosclerosis. It is recommended to eat six meals a day in small portions. Preference should be given to “light” foods high in magnesium, potassium, vitamins and microelements.

It is necessary to minimize the consumption of foods that provoke stimulation of the nervous and cardiovascular systems, as well as increase gas formation. This:

• coffee;
• legumes;
• cocoa;
• radish;
• strong tea;
• garlic;
• cabbage.

Daily consumption of table salt should not exceed 3 g.

To avoid the formation of new cholesterol plaques that worsen the patency of blood vessels, you will have to completely avoid fried foods, smoked foods, spices, and sugar. Limit fatty foods.

Conservative treatment

Since damaged tissue cannot be restored, treatment of post-infarction cardiosclerosis is aimed at blocking symptoms and preventing complications.

IN conservative therapy drugs from the following pharmaceutical groups are used:

• ACE inhibitors (,), slow down scarring, lower blood pressure, reduce the load on the heart;
• anticoagulants reduce the risk of thrombosis; this group includes: Aspirin, Cardiomagnyl, etc.;
• diuretics prevent fluid retention in body cavities; the most common are: Furosemide, Indapamide, Hydrochlorothiazide, etc. (with prolonged use, laboratory monitoring of the electrolyte balance in the blood is required);
• nitrates (Nitrosorbide, Monolong, Isosorbide mononitrate) reduce the load on vascular system pulmonary circulation;
• metabolic drugs (Inosine, potassium drugs);
• beta-blockers (Atenolol, Metoprolol) prevent the formation of arrhythmias, reduce the pulse, and increase the percentage of blood ejected into the aorta;
• statins are recommended for correcting cholesterol levels in the body;
• antioxidants (Riboxin, Creatine phosphate) help saturate heart tissue with oxygen and improve metabolic processes.

Attention: drug names are given for informational purposes. It is unacceptable to take any pharmaceuticals without a doctor's prescription!

If drug treatment does not produce results, the patient is indicated for surgical intervention.

Revascularization operations (CABG, etc.)

When a large area of ​​the myocardium is affected, only a heart transplant can significantly help. This drastic measure is resorted to when all other methods have not brought a positive result. In other situations, manipulations related to palliative surgery are performed.

One of the most common interventions is coronary artery bypass grafting. The surgeon dilates the blood vessels of the myocardium, which improves blood flow and stops the spread of sclerotized areas.

If necessary, CABG surgery for post-infarction cardiosclerosis is performed simultaneously with resection of the aneurysm and strengthening of weakened areas of the heart wall.

When the patient has a history of complex forms of arrhythmias, installation of a pacemaker is indicated. These devices, due to a stronger impulse, suppress the discharges of the sinus node, thereby reducing the likelihood of cardiac arrest.

Surgery is not a panacea; after it, further compliance with all medical recommendations is required.

The need and limits of exercise therapy

Exercise therapy for post-infarction cardiosclerosis is prescribed with great caution. In especially severe cases, the patient is prescribed strict bed rest. If physical activity is acceptable, physiotherapy will help stabilize the condition, avoiding myocardial overload.

Attention: playing sports if you have cardiosclerosis is prohibited!

Cardiologists are inclined to believe that it is necessary to gradually introduce a weak load as early as possible. After a heart attack, the patient is initially hospitalized. During this period, it is necessary to restore motor functions. Slow walks are usually practiced. You need to walk no more than a kilometer at a time, gradually increasing the number of approaches to three.

If the body can withstand training, light gymnastic exercises are added to restore habitual skills, prevent hypokinetic disorders, and form “bypass” pathways in the myocardium.

After switching to outpatient treatment, for the first time you need to attend exercise therapy classes in a medical institution, where they take place under the close supervision of a specialist. Later, you need to continue classes on your own. Slow walks are suitable as a daily exercise. Weight lifting exercises should be avoided.

Physiotherapy

It is good to do the following set of exercises in the morning:

1. Stand up straight, put your hands on your lower back. As you inhale, move them apart, and as you exhale, return to the starting position.
2. Without changing your posture, bend to the sides.
3. Train your hands using an expander.
4. From a standing position, while inhaling, raise your arms up, and while exhaling, bend forward.
5. Sitting on a chair, bend your knees, then stretch them forward.
6. Clasp your hands above your head in a “lock” and perform torso rotations.
7. Walk around the room (you can stand still) for 30 seconds, then take a break and walk some more.

Perform all exercises 3-5 times, maintaining even breathing. Gymnastics should not take more than 20 minutes. The pulse should be monitored - its maximum increase after exercise should not exceed 10% compared to the initial value.

Contraindications to physical therapy:

• acute heart failure;
• the likelihood of another heart attack;
• pleural edema;
• complex forms of arrhythmias.

A physiotherapist should select a set of exercises and assess the possibility of performing them.

Consequences

A patient with the diagnosis in question needs lifelong medical supervision. Knowing what post-infarction cardiosclerosis is, one cannot ignore the situation, as this leads to inevitable complications in the form of the following consequences:

• pericardial tamponade;
• thromboembolism;
• blockades;
• pulmonary edema;
• decreased automaticity of the sinoatrial node.

These processes negatively affect a person’s quality of life. The patient loses tolerance to physical activity, loses the opportunity to work and lead a normal life. Advanced cardiosclerosis provokes the appearance of an aneurysm, the rupture of which leads to death in 90% of non-operated patients.

Useful video

Useful information about post-infarction cardiosclerosis can be found in the following video:

conclusions

1. Cardiosclerosis is one of the most serious heart pathologies.
2. A complete cure is impossible, but supportive therapy will help prolong life for many years.
3. The complex of rehabilitation measures after myocardial infarction includes: medication, sanatorium treatment, control diagnostic procedures, physical therapy, diet therapy.
4. You should not try to treat yourself! Reception of any medicines or folk remedies Without diagnosis and professional assessment of your health, it can result in serious complications and death.

RCHR ( Republican Center healthcare development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols Ministry of Health of the Republic of Kazakhstan - 2013

Other forms of angina (I20.8)

Cardiology

general information

Short description

Approved by the Protocol
Expert Commission on Health Development Issues
dated June 28, 2013

IHD is an acute or chronic lesion of the heart caused by a decrease or cessation of blood supply to the myocardium due to a disease process in the coronary vessels (WHO definition 1959).

Angina pectoris is a clinical syndrome manifested by a feeling of discomfort or pain in the chest of a compressive, pressing nature, which is most often localized behind the sternum and can radiate to left hand, neck, lower jaw, epigastric region. Pain is provoked by physical activity, going out into the cold, eating a lot of food, and emotional stress; goes away with rest or is eliminated by taking sublingual nitroglycerin within a few seconds or minutes.

I. INTRODUCTORY PART

Name: IHD stable angina pectoris
Protocol code:

MKB-10 codes:
I20.8 - Other forms of angina

Abbreviations used in the protocol:
AG - arterial hypertension
AA - antianginal (therapy)
BP - blood pressure
CABG - coronary artery bypass grafting
ALT - alanine aminotransferase
AO - abdominal obesity
ACT - aspartate aminotransferase
BKK - blockers calcium channels
GPs - general practitioners
VPN - upper limit norm
VPU - Wolff-Parkinson-White syndrome
HCM - hypertrophic cardiomyopathy
LVH - left ventricular hypertrophy
DBP - diastolic blood pressure
DLP - dyslipidemia
PVC - ventricular extrasystole
IHD - coronary heart disease
BMI - body mass index
ICD - short-acting insulin
CAG - coronary angiography
CA - coronary arteries
CPK - creatine phosphokinase
MS - metabolic syndrome
IGT - impaired glucose tolerance
NVII - continuous intravenous insulin therapy
THC - total cholesterol
ACS BPST - acute coronary syndrome without ST segment elevation
ACS SPST - acute coronary syndrome with ST segment elevation
OT - waist size
SBP - systolic blood pressure
SD - diabetes
GFR - speed glomerular filtration
ABPM - daily monitoring blood pressure
TG - triglycerides
TIM - thickness of the intima-media complex
TSH - glucose tolerance test
U3DG - ultrasound Dopplerography
PA - physical activity
FC - functional class
FN - physical activity
RF - risk factors
COPD - chronic obstructive pulmonary disease
CHF - chronic heart failure
HDL cholesterol - high density lipoprotein cholesterol
LDL cholesterol - low density lipoprotein cholesterol
4KB - percutaneous coronary intervention
HR - heart rate
ECG - electrocardiography
EX - pacemaker
EchoCG - echocardiography
VE - minute volume of respiration
VCO2 - the amount of carbon dioxide released per unit of time;
RER (respiratory quotient) - VCO2/VO2 ratio;
BR - respiratory reserve.
BMS - non-drug eluting stent
DES - drug eluting stent

Date of development of the protocol: year 2013.
Patient category: adult patients undergoing hospital treatment with a diagnosis of coronary artery disease and stable angina pectoris.
Protocol users: general practitioners, cardiologists, interventional cardiologists, cardiac surgeons.

Classification

Clinical classification

Table 1. Classification of the severity of stable angina pectoris according to the Canadian Heart Association classification (Campeau L, 1976)

FC	Signs
I	Normal daily physical activity (walking or climbing stairs) does not cause angina. Pain occurs only when performing very intense, and very fast, or prolonged physical activity.
II	Slight limitation of usual physical activity, which means the occurrence of angina when walking quickly or climbing stairs, in cold or windy weather, after eating, during emotional stress, or in the first few hours after waking up; while walking > 200 m (two blocks) on level ground or while climbing more than one flight of stairs in normal
III	Significant limitation of usual physical activity - angina occurs as a result of calm walking for a distance of one to two blocks (100-200 m) on level ground or when climbing one flight of stairs in normal
IV	The inability to perform any physical activity without the appearance of unpleasant sensations, or angina pectoris can occur at rest, with minor physical exertion, walking on level ground for a distance of less than

Diagnostics

II. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

Lab tests:
1. OAC
2. OAM
3. Blood sugar
4. Blood creatinine
5. Total protein
6. ALT
7. Blood electrolytes
8. Blood lipid spectrum
9. Coagulogram
10. HIV ELISA (before CAG)
11. ELISA for markers of viral hepatitis (before CAG)
12. Ball on i/g
13. Blood for microreaction.

Instrumental examinations:
1. ECG
2. EchoCG
3. FG/radiography of the OGK
4. EGD (according to indications)
5. ECG with stress (VEM, treadmill test)
6. Stress EchoCG (according to indications)
7. Daily Holter ECG monitoring (according to indications)
8. Coronary angiography

Diagnostic criteria

Complaints and anamnesis
The main symptom of stable angina is a feeling of discomfort or pain in the chest of a squeezing, pressing nature, which is most often localized behind the sternum and can radiate to the left arm, neck, lower jaw, and epigastric region.
The main factors that provoke chest pain: physical activity - brisk walking, climbing a mountain or stairs, carrying heavy objects; increased blood pressure; cold; large meals; emotional stress. Usually the pain goes away with rest after 3-5 minutes. or within seconds or minutes after taking sublingual nitroglycerin tablets or spray.

table 2 - Symptom complex of angina pectoris

Signs	Characteristic
Localization of pain/discomfort	the most typical is behind the sternum, often in the upper part, the “clenched fist” symptom.
Irradiation	in the neck, shoulders, arms, lower jaw, most often on the left, epigastrium and back, sometimes there may be only radiating pain, without substernal pain.
Character	unpleasant sensations, a feeling of compression, tightness, burning, suffocation, heaviness.
Duration (duration)	more often 3-5 minutes
Seizures	has a beginning and an end, increases gradually, stops quickly, leaving no unpleasant sensations.
Intensity (severity)	from moderate to unbearable.
Conditions for attack/pain	physical activity, emotional stress, in the cold, with heavy food or smoking.
Conditions (circumstances) causing the cessation of pain	stopping or reducing the load by taking nitroglycerin.
Uniformity (stereotypicity)	Each patient has his own pain stereotype
Associated symptoms and patient behavior	the patient's position is frozen or excited, shortness of breath, weakness, fatigue, dizziness, nausea, sweating, anxiety, etc. confusion.
Duration and nature of the disease, dynamics of symptoms	determine the course of the disease in each patient.

Table 3 - Clinical classification of chest pain

When collecting anamnesis, it is necessary to note the risk factors for IHD: male gender, elderly age, dyslipidemia, hypertension, smoking, diabetes mellitus, increased heart rate, low physical activity, excess body weight, alcohol abuse.

Conditions that provoke myocardial ischemia or aggravate its course are analyzed:
increasing oxygen consumption:
- non-cardiac: hypertension, hyperthermia, hyperthyroidism, intoxication with sympathomimetics (cocaine, etc.), agitation, arteriovenous fistula;
- cardiac: HCM, aortic heart defects, tachycardia.
reducing oxygen supply:
- non-cardiac: hypoxia, anemia, hypoxemia, pneumonia, bronchial asthma, COPD, pulmonary hypertension, sleep apnea syndrome, hypercoagulation, polycythemia, leukemia, thrombocytosis;
- cardiac: congenital and acquired heart defects, systolic and/or diastolic dysfunction of the left ventricle.

Physical examination
When examining a patient:
- it is necessary to assess body mass index (BMI) and waist circumference, determine heart rate, pulse parameters, blood pressure in both arms;
- you can detect signs of lipid metabolism disorders: xanthomas, xanthelasmas, marginal opacification of the cornea of ​​the eye (“senile arch”) and stenosing lesions of the main arteries (carotid, subclavian peripheral arteries lower limbs and etc.);
- during physical activity, sometimes at rest, the 3rd or 4th heart sounds may be heard during auscultation, as well as systolic murmur at the apex of the heart, as a sign of ischemic dysfunction of the papillary muscles and mitral regurgitation;
- pathological pulsation in the precordial region indicates the presence of a cardiac aneurysm or expansion of the borders of the heart due to pronounced hypertrophy or dilatation of the myocardium.

Instrumental studies

Electrocardiography in 12 leads is a mandatory method for diagnosing myocardial ischemia in stable angina. Even in patients with severe angina, changes in the ECG at rest are often absent, which does not exclude the diagnosis of myocardial ischemia. However, the ECG may reveal signs of coronary heart disease, for example, a previous myocardial infarction or repolarization disorders. An ECG may be more informative if it is recorded during an attack of pain. In this case, it is possible to detect ST segment displacement due to myocardial ischemia or signs of pericardial damage. Registration of an ECG during stool and pain is especially indicated if the presence of vasospasm is suspected. Other changes that may be detected on the ECG include left ventricular hypertrophy (LVH), bundle branch block, ventricular preexcitation syndrome, arrhythmias, or conduction disturbances.

Echocardiography: 2D and resting Doppler echocardiography can rule out other heart diseases, such as valvular disease or hypertrophic cardiomyopathy, and examine ventricular function.

Recommendations for performing echocardiography in patients with stable angina
Class I:
1. Auscultatory changes indicating the presence of valvular heart disease or hypertrophic cardiomyopathy (B)
2. Signs of heart failure (B)
3. Previous myocardial infarction (B)
4. Left bundle branch block, Q waves or other significant pathological changes on the ECG (C)

Daily ECG monitoring is indicated:
- for the diagnosis of silent myocardial ischemia;
- to determine the severity and duration of ischemic changes;
- to detect vasospastic angina or Prinzmetal angina.
- for diagnosing rhythm disturbances;
- to assess heart rate variability.

The criterion for myocardial ischemia during 24-hour ECG monitoring (CM) is ST segment depression > 2 mm with a duration of at least 1 min. The duration of ischemic changes according to SM ECG data is important. If the total duration of ST segment depression reaches 60 minutes, then this can be regarded as a manifestation of severe CAD and is one of the indications for myocardial revascularization.

ECG with stress: Exercise testing is a more sensitive and specific method for diagnosing myocardial ischemia than resting ECG.
Recommendations for performing exercise testing in patients with stable angina
Class I:
1. The test should be performed in the presence of symptoms of angina pectoris and a moderate/high probability of coronary heart disease (taking into account age, gender and clinical manifestations) unless the test cannot be performed due to exercise intolerance or changes in the resting ECG (B).
Class IIb:
1. Presence of ST segment depression at rest ≥1 mm or treatment with digoxin (B).
2. Low probability of having coronary heart disease (less than 10%), taking into account age, gender and the nature of clinical manifestations (B).

Reasons for stopping the load test:
1. The onset of symptoms, such as chest pain, fatigue, shortness of breath, or claudication.
2. The combination of symptoms (for example, pain) with pronounced changes in the ST segment.
3. Patient safety:
a) severe ST segment depression (>2 mm; if ST segment depression is 4 mm or more, then this is absolute indication to stop the test);
b) ST segment elevation ≥2 mm;
c) the appearance of a threatening rhythm disturbance;
d) persistent decrease in systolic blood pressure by more than 10 mm Hg. Art.;
e) high arterial hypertension (systolic blood pressure more than 250 mm Hg or diastolic blood pressure more than 115 mm Hg).
4. Achieving the maximum heart rate can also serve as a basis for stopping the test in patients with excellent exercise tolerance who do not show signs of fatigue (the decision is made by the doctor at his own discretion).
5. Refusal of the patient from further research.

Table 5 - Characteristics of the FC of patients with coronary artery disease with stable angina according to the results of the FN test (Aronov D.M., Lupanov V.P. et al. 1980, 1982).

Indicators	FC
	I	II	III	IV
Number of metabolic units (treadmill)	>7,0	4,0-6,9	2,0-3,9	<2,0
“Double product” (HR. SAD. 10-2)	>278	218-277	15l-217	<150
Power of the last load stage, W (VEM)	>125	75-100	50	25

Stress echocardiography superior to stress ECG in prognostic value, has greater sensitivity (80-85%) and specificity (84-86%) in the diagnosis of coronary artery disease.

Myocardial perfusion scintigraphy with load. The method is based on the Sapirstein fractional principle, according to which the radionuclide during the first circulation is distributed in the myocardium in quantities proportional to the coronary fraction of cardiac output and reflects the regional distribution of perfusion. The FN test is a more physiological and preferable method for reproducing myocardial ischemia, but pharmacological tests can be used.

Recommendations for performing stress echocardiography and myocardial scintigraphy in patients with stable angina pectoris
Class I:
1. The presence of changes in the resting ECG, left bundle branch block, ST segment depression of more than 1 mm, pacemaker, or Wolff-Parkinson-White syndrome that does not allow interpretation of the results of the exercise ECG (B).
2. Ambiguous results of an exercise ECG with acceptable tolerance in a patient with a low probability of coronary heart disease, if the diagnosis is in doubt (B)
Class IIa:
1. Determination of the localization of myocardial ischemia before myocardial revascularization (percutaneous intervention on the coronary arteries or coronary artery bypass grafting) (B).
2. An alternative to exercise ECG if appropriate equipment, personnel and facilities are available (B).
3. An alternative to stress ECG when the likelihood of coronary heart disease is low, for example, in women with atypical chest pain (B).
4. Assessment of the functional significance of moderate coronary artery stenosis detected by angiography (C).
5. Determination of the localization of myocardial ischemia when choosing a revascularization method in patients who underwent angiography (B).

Recommendations for the use of echocardiography or myocardial scintigraphy with a pharmacological test in patients with stable angina
Class I, IIa and IIb:
1. The indications listed above, if the patient cannot perform adequate exercise.

Multispiral CT scan heart and coronary vessels:
- prescribed for the examination of men aged 45-65 years and women aged 55-75 years without established CVD for the purpose of early detection of initial signs of coronary atherosclerosis;
- as an initial diagnostic test in outpatient settings in elderly patients< 65 лет с атипичными болями в грудной клетке при отсутствии установленного диагноза ИБС;
- as an additional diagnostic test in elderly patients< 65 лет с сомнительными результатами нагрузочных тестов или наличием традиционных коронарных ФР при отсутствии установленного диагноза ИБС;
- for differential diagnosis between CHF of ischemic and non-ischemic origin (cardiopathy, myocarditis).

Magnetic resonance imaging of the heart and blood vessels
Stress MRI can be used to detect dobutamine-induced LV wall asynergy or adenosine-induced perfusion abnormalities. The technique is new and therefore less studied than other non-invasive imaging techniques. The sensitivity and specificity of LV contractility abnormalities detected by MRI are 83% and 86%, respectively, and perfusion abnormalities are 91% and 81%. Stress perfusion MRI has similar high sensitivity but reduced specificity.

Magnetic resonance coronary angiography
MRI is characterized by a lower success rate and less accuracy in diagnosing coronary artery disease than MSCT.

Coronary angiography (CAT)- the main method for diagnosing the condition of the coronary bed. CAG allows you to choose the optimal treatment method: medication or myocardial revascularization.
Indications for prescribing CAG for a patient with stable angina when deciding whether to perform PCI or CABG:
- severe angina pectoris III-IV FC, persisting with optimal antianginal therapy;
- signs of severe myocardial ischemia according to the results of non-invasive methods;
- the patient has a history of episodes of VS or dangerous ventricular arrhythmias;
- progression of the disease according to the dynamics of non-invasive tests;
- early development of severe angina (FC III) after MI and myocardial revascularization (up to 1 month);
- questionable results non-invasive tests for people with socially significant professions (public transport drivers, pilots, etc.).

There are currently no absolute contraindications for prescribing CAG.
Relative contraindications to CAG:
- Spicy renal failure
- Chronic renal failure (blood creatinine level 160-180 mmol/l)
- Allergic reactions for contrast agent and iodine intolerance
- Active gastrointestinal bleeding, exacerbation peptic ulcer
- Severe coagulopathies
- Severe anemia
- Acute cerebrovascular accident
- Severe disturbance of the patient’s mental state
- Serious concomitant diseases that significantly shorten the patient’s life or sharply increase the risk of subsequent medical interventions
- Refusal of the patient from possible further treatment after the study (endovascular intervention, CABG)
- Severe peripheral arterial disease limiting arterial access
- Decompensated HF or acute pulmonary edema
- Malignant hypertension, difficult to treat drug treatment
- Intoxication with cardiac glycosides
- Severe disturbance of electrolyte metabolism
- Fever of unknown etiology and acute infectious diseases
- Infective endocarditis
- Exacerbation of severe non-cardiological chronic disease

X-ray recommendations chest in patients with stable angina
Class I:
1. Chest X-ray is indicated if symptoms of heart failure are present (C).
2. Chest X-ray is warranted if there are signs of pulmonary involvement (B).

Fibrogastroduodenoscopy (FGDS) (according to indications), study for Helicobtrecter Pylori (according to indications).

Indications for consultation with specialists
Endocrinologist- diagnosis and treatment of disorders of glycemic status, treatment of obesity, etc., teaching the patient the principles of dietary nutrition, transferring to treatment with short-acting insulin before planned surgical revascularization;
Neurologist- presence of symptoms of brain damage (acute cerebrovascular accidents, transient cerebrovascular accidents, chronic forms vascular pathology of the brain, etc.);
Oculist- presence of symptoms of retinopathy (according to indications);
Angiosurgeon- diagnosis and treatment recommendations for atherosclerotic lesions of peripheral arteries.

Laboratory diagnostics

Class I (all patients)
1. Fasting lipid levels, including total cholesterol, LDL, HDL and triglycerides (B)
2. Fasting glycemia (B)
3. General analysis blood, including determination of hemoglobin and leukocyte formula(IN)
4. Creatinine level (C), calculation of creatinine clearance
5. Function indicators thyroid gland(according to indications) (C)

Class IIa
Oral glucose load test (B)

Class IIb
1. Highly sensitive C-reactive protein(IN)
2. Lipoprotein (a), ApoA and ApoB (B)
3. Homocysteine ​​(B)
4. HbAlc(B)
5.NT-BNP

Table 4 - Assessment of lipid spectrum indicators

Lipids	Normal level (mmol/l)	Target level for ischemic heart disease and diabetes (mmol/l)
General HS	<5,0	<14,0
LDL cholesterol	<3,0	<:1.8
HDL cholesterol	≥1.0 in men, ≥1.2 in women
Triglycerides	<1,7

List of basic and additional diagnostic measures

Basic Research
1. General blood test
2. Determination of glucose
3. Determination of creatinine
4. Determination of creatinine clearance
5. Determination of ALT
6. Definition of PTI
7. Determination of fibrinogen
8. Determination of MHO
9. Determination of total cholesterol
10. Determination of LDL
11.Determination of HDL
12.Determination of triglycerides
13. Determination of potassium/sodium
14.Determination of calcium
15.General urine test
16.ECG
17.3XOK
18.ECG test with physical activity (VEM/treadmill)
19. Stress EchoCG

Additional Research
1. Glycemic profile
2. Chest X-ray
3. EGDS
4. Glycated hemoglobin
5.. Oral glucose load test
6.NT-proBNP
7. Determination of hs-CRP
8. Definition of ABC
9. Determination of APTT
10. Determination of magnesium
11. Determination of total bilirubin
12. CM BP
13. SM ECG according to Holter
14. Coronary angiography
15. Myocardial perfusion scintigraphy / SPECT
16. Multislice computed tomography
17. Magnetic resonance imaging
18. PET

Differential diagnosis

Differential diagnosis

Table 6 - Differential diagnosis of chest pain

Cardiovascular causes

Ischemic

Coronary artery stenosis restricting blood flow

Coronary vasospasm

Microvascular dysfunction

Non-ischemic

Stretching of the wall of the coronary artery

Uncoordinated contraction of myocardial fibers

Aortic dissection

Pericarditis

Pulmonary embolism or hypertension

Non-cardiac causes

Gastrointestinal

Esophageal spasm

Gastroesophageal reflux

Gastritis/duodenitis

Peptic ulcer

Cholecystitis

Respiratory

Pleurisy

Mediastinitis

Pneumothorax

Neuromuscular/skeletal

Chest pain syndrome

Neuritis/radiculitis

Shingles

Tietze syndrome

Psychogenic

Anxiety

Depression

Coronary syndrome X

The clinical picture suggests the presence of three signs:
- typical angina that occurs during exercise (less commonly, angina or shortness of breath at rest);
- positive result of ECG with physical function or other stress tests (ST segment depression on ECG, myocardial perfusion defects on scintigrams);
- normal coronary arteries on CAG.

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Treatment

Treatment goals:
1. Improve the prognosis and prevent the occurrence of myocardial infarction and sudden death and, accordingly, increase life expectancy.
2. Reduce the frequency and intensity of angina attacks and, thus, improve the patient’s quality of life.

Treatment tactics

Non-drug treatment:
1. Patient information and education.

2. Stop smoking.

3. Individual recommendations for acceptable physical activity depending on the FC of angina and the state of LV function. It is recommended to do physical exercises because... they lead to an increase in FTN, a decrease in symptoms and have a beneficial effect on BW, lipid levels, blood pressure, glucose tolerance and insulin sensitivity. Moderate exercise for 30-60 minutes ≥5 days a week, depending on the FC of angina (walking, light jogging, swimming, cycling, skiing).

4. Recommended diet: eating a wide range of foods; control of food calories to avoid obesity; increasing the consumption of fruits and vegetables, as well as whole grain cereals and breads, fish (especially fatty varieties), lean meats and low-fat dairy products; replace saturated fats and trans fats with monounsaturated and polyunsaturated fats from vegetable and marine sources, and reduce total fat (of which less than one-third should be saturated) to less than 30% of total calories consumed, and reduce salt intake , with an increase in blood pressure. A body mass index (BMI) of less than 25 kg/m2 is considered normal and weight loss is recommended for a BMI of 30 kg/m2 or more, as well as for a waist circumference of more than 102 cm in men or more than 88 cm in women, since weight loss may improve many obesity-related risk factors.

5. Alcohol abuse is unacceptable.

6. Treatment of concomitant diseases: for hypertension - achieving the target blood pressure level<130 и 80 мм.рт.ст., при СД - достижение количественных критериев компенсации, лечение гипо- и гипертиреоза, анемии.

7. Recommendations for sexual activity - sexual intercourse can provoke the development of angina, so you can take nitroglycerin before it. Phosphodiesterase inhibitors: sildenafil (Viagra), tadafil and vardenafil, used to treat sexual dysfunction, should not be used in combination with long-acting nitrates.

Drug treatment
Medicines that improve the prognosis in patients with angina pectoris:
1. Antiplatelet drugs:
- acetylsalicylic acid (dose 75-100 mg/day - long-term).
- in patients with aspirin intolerance, the use of clopidogrel 75 mg per day is indicated as an alternative to aspirin
- dual antiplatelet therapy with aspirin and oral use of ADP receptor antagonists (clopidogrel, ticagrelor) should be used for up to 12 months after 4KB, with a strict minimum for patients with BMS - 1 month, patients with DES - 6 months.
- Gastric protection using proton pump inhibitors should be performed during dual antiplatelet therapy in patients at high risk of bleeding.
- in patients with clear indications for the use of oral anticoagulants (atrial fibrillation on the CHA2DS2-VASc scale ≥2 or the presence of mechanical valve prostheses), they should be used in addition to antiplatelet therapy.

2. Lipid-lowering drugs that reduce LDL cholesterol levels:
- Statins. The most studied statins for ischemic heart disease are atorvastatin 10-40 mg and rosuvastatin 5-40 mg. The dose of any statin should be increased at an interval of 2-3 weeks, since during this period the optimal effect of the drug is achieved. The target level is determined by LDL cholesterol - less than 1.8 mmol/l. Monitoring indicators during treatment with statins:
- it is necessary to initially take a blood test for lipid profile, AST, ALT, CPK.
- after 4-6 weeks of treatment, the tolerability and safety of treatment should be assessed (patient complaints, repeated blood tests for lipids, AST, ALT, CPK).
- when titrating doses, they are primarily focused on the tolerability and safety of treatment, and secondly, on achieving target lipid levels.
- if the activity of liver transaminases increases by more than 3 VPN, it is necessary to repeat the blood test again. It is necessary to exclude other causes of hyperfermentemia: drinking alcohol the day before, cholelithiasis, exacerbation of chronic hepatitis or other primary and secondary liver diseases. The cause of increased CPK activity may be damage to skeletal muscles: intense physical activity the day before, intramuscular injections, polymyositis, muscular dystrophy, trauma, surgery, myocardial damage (MI, myocarditis), hypothyroidism, CHF.
- if AST, ALT >3 VPN, CPK > 5 VPN, statins are canceled.
- An inhibitor of intestinal cholesterol absorption - ezetimibe 5-10 mg 1 time per day - inhibits the absorption of dietary and biliary cholesterol in the villous epithelium of the small intestine.

Indications for the use of ezetimibe:
- as monotherapy for the treatment of patients with the heterozygous form of FH who cannot tolerate statins;
- in combination with statins in patients with a heterozygous form of FH, if the LDL-C level remains high (more than 2.5 mmol/l) against the background of the highest doses of statins (simvastatin 80 mg/day, atorvastatin 80 mg/day) or poor tolerance of high doses of statins. The fixed combination is the drug Ineji, which contains ezetimibe 10 mg and simvastatin 20 mg in one tablet.

3. β-blockers
The positive effects of using this group of drugs are based on reducing the myocardial oxygen demand. BL-selective blockers include: atenolol, metoprolol, bisoprolol, nebivolol, non-selective - propranolol, nadolol, carvedilol.
β - blockers should be preferred in patients with coronary artery disease with: 1) the presence of heart failure or left ventricular dysfunction; 2) concomitant arterial hypertension; 3) supraventricular or ventricular arrhythmia; 4) previous myocardial infarction; 5) there is a clear connection between physical activity and the development of an attack of angina pectoris
The effect of these drugs in stable angina can only be counted on if, when prescribed, a clear blockade of β-adrenergic receptors is achieved. To do this, you need to maintain your resting heart rate within 55-60 beats/min. In patients with more severe angina, the heart rate can be reduced to 50 beats/min, provided that such bradycardia does not cause discomfort and AV block does not develop.
Metoprolol succinate 12.5 mg twice a day, if necessary increasing the dose to 100-200 mg per day with twice a day.
Bisoprolol - starting with a dose of 2.5 mg (with existing decompensation of CHF - from 1.25 mg) and, if necessary, increasing to 10 mg for a single dose.
Carvedilol - starting dose 6.25 mg (for hypotension and symptoms of CHF 3.125 mg) in the morning and evening with a gradual increase to 25 mg twice.
Nebivolol - starting with a dose of 2.5 mg (with existing decompensation of CHF - from 1.25 mg) and, if necessary, increasing to 10 mg, once a day.

Absolute contraindications to the prescription of beta blockers for coronary artery disease - severe bradycardia (heart rate less than 48-50 per minute), atrioventricular block of 2-3 degrees, sick sinus syndrome.

Relative contraindications- bronchial asthma, COPD, acute heart failure, severe depressive states, peripheral vascular diseases.

4. ACE inhibitors or ARA II
ACE inhibitors are prescribed to patients with coronary artery disease if there are signs of heart failure, arterial hypertension, diabetes mellitus and there are no absolute contraindications to their use. Drugs with a proven effect on long-term prognosis are used (ramipril 2.5-10 mg once daily, perindopril 5-10 mg once daily, fosinopril 10-20 mg daily, zofenopril 5-10 mg, etc.). If ACEIs are intolerant, angiotensin II receptor antagonists with a proven positive effect on long-term prognosis for coronary artery disease (valsartan 80-160 mg) can be prescribed.

5. Calcium antagonists (calcium channel blockers).
They are not the main means in the treatment of coronary artery disease. May relieve symptoms of angina pectoris. The effect on survival and complication rates in contrast to beta blockers has not been proven. Prescribed when there are contraindications to the use of b-blockers or their insufficient effectiveness in combination with them (with dihydropyridines, except short-acting nifedipine). Another indication is vasospastic angina.
Currently, long-acting CCBs (amlodipine) are mainly recommended for the treatment of stable angina; they are used as second-line drugs if symptoms are not eliminated by b-blockers and nitrates. CCBs should be preferred in case of concomitant: 1) obstructive pulmonary diseases; 2) sinus bradycardia and severe atrioventricular conduction disturbances; 3) variant angina (Prinzmetal).

6. Combination therapy (fixed combinations) patients with stable angina pectoris class II-IV is performed for the following indications: impossibility of selecting effective monotherapy; the need to enhance the effect of monotherapy (for example, during periods of increased physical activity of the patient); correction of unfavorable hemodynamic changes (for example, tachycardia caused by CCBs of the dihydropyridine group or nitrates); when angina is combined with hypertension or heart rhythm disturbances that are not compensated for in cases of monotherapy; in case of intolerance to the patient of standard doses of AA drugs during monotherapy (in order to achieve the required AA effect, small doses of drugs can be combined; in addition to the main AA drugs, other drugs are sometimes prescribed (potassium channel activators, ACE inhibitors, antiplatelet agents).
When carrying out AA therapy, one should strive for the almost complete elimination of anginal pain and the return of the patient to normal activity. However, therapeutic tactics do not produce the desired effect in all patients. In some patients, during exacerbation of coronary artery disease, there is sometimes an aggravation of the severity of the condition. In these cases, consultation with cardiac surgeons is necessary in order to be able to provide cardiac surgery to the patient.

Relief and prevention of anginal pain:
Anganginal therapy solves symptomatic problems in restoring the balance between the need and delivery of oxygen to the myocardium.

Nitrates and nitrate-like. If an angina attack develops, the patient should stop physical activity. The drug of choice is nitroglycerin (NTG and its inhaled forms) or short-acting isosorbide dinitrate, taken sublingually. Prevention of angina is achieved with various forms of nitrates, including oral isosorbide di- or mononitrate tablets or (less commonly) a once-daily nitroglycerin transdermal patch. Long-term therapy with nitrates is limited by the development of tolerance to them (i.e., a decrease in the effectiveness of the drug with prolonged, frequent use), which appears in some patients, and withdrawal syndrome - with an abrupt cessation of taking the drugs (symptoms of exacerbation of coronary artery disease).
The undesirable effect of developing tolerance can be prevented by providing a nitrate-free interval of several hours, usually while the patient is asleep. This is achieved by intermittent administration of short-acting nitrates or special forms of retard mononitrates.

If channel inhibitors.
Inhibitors of If channels of sinus node cells - Ivabradine, which selectively reduce sinus rhythm, have a pronounced antianginal effect, comparable to the effect of b-blockers. Recommended for patients with contraindications to b-blockers or if it is impossible to take b-blockers due to side effects.

Recommendations for pharmacotherapy that improves prognosis in patients with stable angina
Class I:
1. Acetylsalicylic acid 75 mg/day. in all patients in the absence of contraindications (active gastrointestinal bleeding, allergy to aspirin or intolerance to it) (A).
2. Statins in all patients with coronary heart disease (A).
3. ACEI in the presence of arterial hypertension, heart failure, left ventricular dysfunction, previous myocardial infarction with left ventricular dysfunction or diabetes mellitus (A).
4. β-AB orally to patients after a history of myocardial infarction or with heart failure (A).
Class IIa:
1. ACEI in all patients with angina pectoris and a confirmed diagnosis of coronary heart disease (B).
2. Clopidogrel as an alternative to aspirin in patients with stable angina who cannot take aspirin, for example, due to allergies (B).
3. High-dose statins in the presence of high risk (cardiovascular mortality > 2% per year) in patients with proven coronary heart disease (B).
Class IIb:
1. Fibrates for low levels of high-density lipoproteins or high triglycerides in patients with diabetes mellitus or metabolic syndrome (B).

Recommendations for antianginal and/or anti-ischemic therapy in patients with stable angina.
Class I:
1. Short-acting nitroglycerin for angina relief and situational prophylaxis (patients should receive adequate instructions for the use of nitroglycerin) (B).
2. Assess the effectiveness of β,-AB and titrate its dose to the maximum therapeutic dose; assess the feasibility of using a long-acting drug (A).
3. In case of poor tolerability or low effectiveness of β-AB, prescribe monotherapy with AK (A), long-acting nitrate (C).
4. If β-AB monotherapy is not effective enough, add dihydropyridine AK (B).
Class IIa:
1. If β-AB is poorly tolerated, prescribe an inhibitor of the I channels of the sinus node - ivabradine (B).
2. If AA monotherapy or combination therapy of AA and β-AB is ineffective, replace AA with long-acting nitrate. Avoid developing nitrate tolerance (C).
Class IIb:
1. Metabolic-type drugs (trimetazidine MB) can be prescribed to enhance the antianginal effectiveness of standard drugs or as an alternative to them in case of intolerance or contraindications for use (B).

Essential drugs
Nitrates
- Nitroglycerin table. 0.5 mg
- Isosorbide mononitrate cape. 40 mg
- Isosorbide mononitrate cape. 10-40 mg
Beta blockers
- Metoprolol succinate 25 mg
- Bisoprolol 5 mg, 10 mg
AIF inhibitors
- Ramipril tab. 5 mg, 10 mg
- Zofenopril 7.5 mg (preferably prescribed for CKD - ​​GFR less than 30 ml/min)
Antiplatelet agents
- Acetylsalicylic acid tab. coated 75, 100 mg
Lipid-lowering drugs
- Rosuvastatin tablet. 10 mg

Additional medications
Nitrates
- Isosorbide dinitrate tab. 20 mg
- Isosorbide dinitrate aeros dose
Beta blockers
- Carvedilol 6.25 mg, 25 mg
Calcium antagonists
- Amlodipine tablet. 2.5 mg
- Diltiazem cape. 90 mg, 180 mg
- Verapamil tablet. 40 mg
- Nifedipine tab. 20 mg
AIF inhibitors
- Perindopril tablet. 5 mg, 10 mg
- Captopril tablet. 25 mg
Angiotensin II receptor antagonists
- Valsartan tab. 80 mg, 160 mg
- Candesartan tab. 8 mg, 16 mg
Antiplatelet agents
- Clopidogrel tablet. 75 mg
Lipid-lowering drugs
- Atorvastatin tablet. 40 mg
- Fenofibrate tab. 145 mg
- Tofisopam tab. 50mg
- Diazepam tablet. 5mg
- Diazepam amp 2ml
- Spironolactone tab. 25 mg, 50 mg
- Ivabradin tablet. 5 mg
- Trimetazidine tablet. 35 mg
- Esomeprazole lyophilisate amp. 40 mg
- Esomeprazole tab. 40 mg
- Pantoprazole tab. 40 mg
- Sodium chloride 0.9% solution 200 ml, 400 ml
- Dextrose 5% solution 200 ml, 400 ml
- Dobutamine* (stress tests) 250 mg/50 ml
Note:* Medicines not registered in the Republic of Kazakhstan, imported under a one-time import permit (Order of the Ministry of Health of the Republic of Kazakhstan dated December 27, 2012 No. 903 “On approval of maximum prices for medicines purchased within the framework of the guaranteed volume of free medical care for 2013”).

Surgical intervention
Invasive treatment of stable angina is indicated primarily for patients with a high risk of complications, because revascularization and medical treatment do not differ in the incidence of myocardial infarction and mortality. The effectiveness of PCI (stenting) and medical therapy has been compared in several meta-analyses and a large RCT. Most meta-analyses found no reduction in mortality, an increased risk of nonfatal periprocedural MI, and a decreased need for repeat revascularization after PCI.
Balloon angioplasty combined with stent placement to prevent restenosis. Stents coated with cytostatics (paclitaxel, sirolimus, everolimus and others) reduce the rate of restenosis and repeated revascularization.
It is recommended to use stents that meet the following specifications:
Drug-eluting coronary stent
1. Everolimus drug-eluting balloon-expandable stent on a quick-change delivery system, 143 cm long. Made of cobalt-chromium alloy L-605, wall thickness 0.0032". Balloon material - Pebax. Passage profile 0.041". Proximal shaft 0.031", distal - 034". Nominal pressure 8 atm for 2.25-2.75 mm, 10 atm for 3.0-4.0 mm. Burst pressure - 18 atm. Lengths 8, 12, 15, 18, 23, 28, 33, 38 mm. Diameters 2.25, 2.5, 2.75, 3.0, 3.5, 4.0 mm. Dimensions upon request.
2. Stent material is cobalt-chromium alloy L-605. Cylinder material - Fulcrum. Coated with a mixture of the drug zotarolimus and BioLinx polymer. Cell thickness 0.091 mm (0.0036"). Delivery system 140 cm long. Proximal catheter shaft size 0.69 mm, distal shaft 0.91 mm. Nominal pressure: 9 atm. Burst pressure 16 atm. for diameters 2.25- 3.5 mm, 15 atm. for a diameter of 4.0 mm. Sizes: diameter 2.25, 2.50, 2.75, 3.00, 3.50, 4.00 and stent length (mm) -8, 9, 12, 14, 15, 18, 22, 26, 30, 34, 38.
3. Stent material - platinum-chromium alloy. The share of platinum in the alloy is at least 33%. The share of nickel in the alloy is no more than 9%. The thickness of the stent walls is 0.0032". The drug coating of the stent consists of two polymers and a drug. The thickness of the polymer coating is 0.007 mm. The profile of the stent on the delivery system is no more than 0.042" (for a stent with a diameter of 3 mm). The maximum diameter of the expanded stent cell is not less than 5.77 mm (for a stent with a diameter of 3.00 mm). Stent diameters - 2.25 mm; 2.50 mm; 2.75 mm; 3.00 mm; 3.50 mm, 4.00 mm. Available stent lengths are 8 mm, 12 mm, 16 mm, 20 mm, 24 mm, 28 mm, 32 mm, 38 mm. Nominal pressure - not less than 12 atm. Maximum pressure - not less than 18 atm. The profile of the tip of the balloon of the delivery system of the stent is no more than 0.017". The working length of the balloon catheter on which the stent is mounted is not less than 144 cm. The length of the tip of the balloon of the delivery system is 1.75 mm. 5-leaf balloon placement technology. X-ray contrast markers made of platinum -iridium alloy. Length of radiopaque markers - 0.94 mm.
4. Stent material: cobalt-chromium alloy, L-605. Passive coating: amorphous silicone carbide, active coating: biodegradable polylactide (L-PLA, Poly-L-Lactic Acid, PLLA) including Sirolimus. The thickness of the stent frame with a nominal diameter of 2.0-3.0 mm is not more than 60 microns (0.0024"). Crossing profile of the stent - 0.039" (0.994 mm). Stent length: 9, 13, 15, 18, 22, 26, 30 mm. Nominal diameter of stents: 2.25/2.5/2.75/3.0/3.5/4.0 mm. Diameter of the distal end part (entry profile) - 0.017" (0.4318 mm). The working length of the catheter is 140 cm. The nominal pressure is 8 atm. The calculated burst pressure of the cylinder is 16 atm. Stent diameter 2.25 mm at a pressure of 8 atmospheres: 2.0 mm. Stent diameter 2.25 mm at a pressure of 14 atmospheres: 2.43 mm.

Coronary stent without drug coating
1. Balloon-expandable stent on a 143 cm rapid delivery system. Stent material: non-magnetic cobalt-chromium alloy L-605. Cylinder material - Pebax. Wall thickness: 0.0032" (0.0813 mm). Diameters: 2.0, 2.25, 2.5, 2.75, 3.0, 3.5, 4.0 mm. Lengths: 8, 12, 15, 18, 23, 28 mm. Stent profile on 0.040" balloon (stent 3.0x18mm). The length of the working surface of the balloon beyond the edges of the stent (balloon overhang) is no more than 0.69 mm. Compliance: nominal pressure (NP) 9 atm., design burst pressure (RBP) 16 atm.
2. Stent material is cobalt-chromium alloy L-605. Cell thickness 0.091 mm (0.0036"). Delivery system 140 cm long. Proximal catheter shaft size 0.69 mm, distal shaft 0.91 mm. Nominal pressure: 9 atm. Burst pressure 16 atm. for diameters 2.25- 3.5 mm, 15 atm. for a diameter of 4.0 mm. Sizes: diameter 2.25, 2.50, 2.75, 3.00, 3.50, 4.00 and stent length (mm) - 8, 9, 12, 14, 15, 18, 22, 26, 30, 34, 38.
3. Stent material - 316L stainless steel on a rapid delivery system 145 cm long. The presence of M coating of the distal shaft (except for the stent). The delivery system design is a three-lobe balloon boat. Stent wall thickness: no more than 0.08 mm. The stent design is open cell. Availability of a low profile of 0.038" for a stent with a diameter of 3.0 mm. Possibility of using a guiding catheter with an internal diameter of 0.056"/1.42 mm. The nominal pressure of the cylinder is 9 atm for a diameter of 4 mm and 10 atm for diameters from 2.0 to 3.5 mm; burst pressure 14 atm. The diameter of the proximal shaft is 2.0 Fr, the distal one is 2.7 Fr, Diameters: 2.0; 2.25; 2.5; 3.0; 3.5; 4.0 Length 8; 10; 13; 15; 18; 20; 23; 25; 30 mm.
Compared with drug therapy, coronary artery dilatation does not reduce mortality and the risk of myocardial infarction in patients with stable angina, but increases exercise tolerance and reduces the incidence of angina and hospitalization. Before PCI, the patient receives a loading dose of clopidogrel (600 mg).
After implantation of non-drug-eluting stents, combination therapy with aspirin 75 mg/day is recommended for 12 weeks. and clopidogrel 75 mg/day, and then continue taking aspirin alone. If a drug-eluting stent is implanted, combination therapy continues for up to 12-24 months. If the risk of vascular thrombosis is high, then therapy with two antiplatelet agents can be continued for more than a year.
Combination therapy with antiplatelet agents in the presence of other risk factors (age >60 years, taking corticosteroids/NSAIDs, dyspepsia or heartburn) requires prophylactic administration of proton pump inhibitors (for example, rabeprazole, pantoprazole, etc.).

Contraindications to myocardial revascularization.
- Borderline stenosis (50-70%) of the coronary artery, except for the trunk of the left coronary artery, and the absence of signs of myocardial ischemia during non-invasive examination.
- Insignificant coronary stenosis (< 50%).
- Patients with stenosis of 1 or 2 coronary arteries without significant proximal narrowing of the anterior descending artery, who have mild or no symptoms of angina and have not received adequate drug therapy.
- High operative risk of complications or death (possible mortality > 10-15%) unless it is offset by the expected significant improvement in survival or QoL.

Coronary artery bypass surgery
There are two indications for CABG: improvement of prognosis and reduction of symptoms. A reduction in mortality and the risk of developing MI has not been convincingly proven.
Consultation with a cardiac surgeon is necessary to determine the indications for surgical revascularization as part of a collegial decision (cardiologist + cardiac surgeon + anesthesiologist + interventional cardiologist).

Table 7 - Indications for revascularization in patients with stable angina or occult ischemia

	Anatomical subpopulation of CAD	Grade and level of evidence
To improve the forecast	Lesion of the left artery trunk >50% s Involvement of the proximal part of the LAD >50% with Damage to 2 or 3 coronary arteries with impaired LV function Proven widespread ischemia (>10% LV) Lesion of a single patent vessel >500 Single vessel involvement without proximal LAD involvement and ischemia >10%	IA IA I.B. I.B. IС IIIA
To relieve symptoms	Any stenosis >50% accompanied by angina or angina equivalents that persist during OMT Dyspnea/chronic heart failure and ischemia >10% of the LV supplied by the stenotic artery (>50%) Absence of symptoms during OMT	I.A.

OMT = optimal medical therapy;

FFR = fractional flow reserve;
LAD = anterior descending artery;
LCA = left coronary artery;
PCI = percutaneous coronary intervention.

Recommendations for myocardial revascularization to improve the prognosis in patients with stable angina
Class I:
1. Coronary artery bypass grafting with severe stenosis of the main trunk of the left coronary artery or significant narrowing of the proximal segment of the left descending and circumflex coronary arteries (A).
2. Coronary artery bypass grafting for severe proximal stenosis of the 3 main coronary arteries, especially in patients with reduced left ventricular function or rapidly occurring or widespread reversible myocardial ischemia during functional tests (A).
3. Coronary artery bypass grafting for stenosis of one or two coronary arteries in combination with a pronounced narrowing of the proximal part of the left anterior descending artery and reversible myocardial ischemia in non-invasive studies (A).
4. Coronary artery bypass grafting with severe stenosis of the coronary arteries in combination with impaired left ventricular function and the presence of viable myocardium according to non-invasive tests (B).
Class II a:
1. Coronary artery bypass grafting for stenosis of one or two coronary arteries without significant narrowing of the left anterior descending artery in patients who have suffered sudden death or persistent ventricular tachycardia (B).
2. Coronary bypass surgery for severe stenosis of 3 coronary arteries in patients with diabetes mellitus, in whom signs of reversible myocardial ischemia are determined during functional tests (C).

Preventive actions
Key lifestyle interventions include smoking cessation and tight blood pressure control, advice on diet and weight control, and encouragement of physical activity. Although GPs will be responsible for the long-term management of this group of patients, these interventions will have a better chance of being implemented if they are initiated while patients are in hospital. In addition, the benefits and importance of lifestyle changes must be explained and suggested to the patient - who is the key player - before discharge. However, life habits are not easy to change, and implementing and following up on these changes is a long-term challenge. In this regard, close collaboration between the cardiologist and general practitioner, nurses, rehabilitation specialists, pharmacists, nutritionists, and physiotherapists is critical.

To give up smoking
Patients who quit smoking had a reduced mortality rate compared with those who continued to smoke. Smoking cessation is the most effective of all secondary preventive measures and therefore every effort should be made to achieve this. However, it is common for patients to resume smoking after discharge, and ongoing support and advice are required during the rehabilitation period. The use of nicotine substitutes, buproprion, and antidepressants may be helpful. A smoking cessation protocol should be adopted by each hospital.

Diet and weight control
Prevention guidelines currently recommend:
1. rational balanced diet;
2. control of calorie content of foods to avoid obesity;
3. increasing the consumption of fruits and vegetables, as well as whole grain cereals, fish (especially fatty varieties), lean meat and low-fat dairy products;
4. Replace saturated fats with monounsaturated and polyunsaturated fats from vegetable and marine sources, and reduce total fat (of which less than one-third should be saturated) to less than 30% of total caloric intake;
5. limiting salt intake with concomitant arterial hypertension and heart failure.

Obesity is a growing problem. Current EOC guidelines define a body mass index (BMI) of less than 25 kg/m2 as the optimal level, and recommend weight loss for a BMI of 30 kg/m2 or more, and a waist circumference of more than 102 cm in men or more than 88 cm in women, as weight loss can improve many obesity-related risk factors. However, weight loss alone has not been found to reduce mortality rates. Body mass index = weight (kg): height (m2).

Physical activity
Regular exercise brings improvement to patients with stable coronary artery disease. For patients, it can reduce anxiety associated with life-threatening illnesses and increase self-confidence. It is recommended that you do thirty minutes of moderate-intensity aerobic exercise at least five times a week. Each increment in peak exercise power results in a 8-14% reduction in all-cause mortality risk.

Blood pressure control
Pharmacotherapy (beta blockers, ACE inhibitors, or angiotensin receptor blockers) in addition to lifestyle changes (reducing salt intake, increasing physical activity, and losing weight) usually helps achieve these goals. Additional drug therapy may also be needed.

Further management:
Rehabilitation of patients with stable angina pectoris
Dosed physical activity allows you to:
- optimize the functional state of the patient’s cardiovascular system by including cardiac and extracardiac compensation mechanisms;
- increase TFN;
- slow down the progression of coronary artery disease, prevent the occurrence of exacerbations and complications;
- return the patient to professional work and increase his self-care capabilities;
- reduce the dose of antianginal drugs;
- improve the patient’s well-being and quality of life.

Contraindications to the prescription of dosed physical training are:
- unstable angina;
- heart rhythm disturbances: constant or frequently occurring paroxysmal form of atrial fibrillation or flutter, parasystole, migration of the pacemaker, frequent polytopic or group extrasystole, AV block of the II-III degree;
- uncontrolled hypertension (BP > 180/100 mmHg);
- pathology of the musculoskeletal system;
- history of thromboembolism.

Psychological rehabilitation.
Virtually every patient with stable angina needs psychological rehabilitation. On an outpatient basis, if specialists are available, the most accessible classes are rational psychotherapy, group psychotherapy (coronary club) and autogenic training. If necessary, patients can be prescribed psychotropic drugs (tranquilizers, antidepressants).

Sexual aspect of rehabilitation.
During intimate intimacy in patients with stable angina, due to an increase in heart rate and blood pressure, conditions may arise for the development of an anginal attack. Patients should be aware of this and take antianginal drugs in time to prevent angina attacks.
Patients with high class angina (III-IV) should adequately assess their capabilities in this regard and take into account the risk of developing cardiovascular complications. Patients with erectile dysfunction, after consulting a doctor, can use phosphodiesterase type 5 inhibitors: sildenafil, vardanafil, tardanafil, but taking into account contraindications: taking long-acting nitrates, low blood pressure, exercise therapy.

Work ability.
An important stage in the rehabilitation of patients with stable angina is the assessment of their ability to work and rational employment. The ability to work in patients with stable angina is determined mainly by its FC and the results of stress tests. In addition, one should take into account the state of contractility of the heart muscle, the possible presence of signs of CHF, a history of MI, as well as CAG indicators, indicating the number and degree of damage to the coronary artery.

Dispensary observation.
All patients with stable angina, regardless of age and the presence of concomitant diseases, must be registered with a dispensary. Among them, it is advisable to identify a high-risk group: a history of myocardial infarction, periods of instability in the course of coronary artery disease, frequent episodes of silent myocardial ischemia, serious cardiac arrhythmias, heart failure, severe concomitant diseases: diabetes, cerebrovascular accidents, etc. Dispensary observation involves systematic visits to a cardiologist ( therapist) once every 6 months with mandatory instrumental examination methods: ECG, Echo CG, stress tests, determination of lipid profile, as well as Holter monitoring of ECG and ABPM according to indications. An essential point is the appointment of adequate drug therapy and correction of risk factors.

Indicators of treatment effectiveness and safety of diagnostic and treatment methods described in the protocol:
Antianginal therapy is considered effective if it is possible to eliminate angina completely or transfer the patient from a higher FC to a lower FC while maintaining good quality of life.

Hospitalization

Indications for hospitalization
Maintaining a high functional class of stable angina (FC III-IV), despite full drug treatment.

Information

Sources and literature

1. Minutes of meetings of the Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan, 2013
   1. 1. ESC Guidelines on the management of stable angina pectoris. European Heart Journal. 2006; 27(11): I341-8 I. 2. BHOK. Diagnosis and treatment of stable angina. Russian recommendations (second revision). Cardiovascular. ter. and prophylaxis. 2008; Appendix 4. 3. Recommendations for myocardial revascularization. European Society of Cardiology 2010.

Information

III. ORGANIZATIONAL ASPECTS OF PROTOCOL IMPLEMENTATION

List of protocol developers:
1. Berkinbaev S.F. - Doctor of Medical Sciences, Professor, Director of the Research Institute of Cardiology and Internal Medicine.
2. Dzhunusbekova G.A. - Doctor of Medical Sciences, Deputy Director of the Research Institute of Cardiology and Internal Diseases.
3. Musagalieva A.T. - Candidate of Medical Sciences, Head of the Department of Cardiology, Research Institute of Cardiology and Internal Medicine.
4. Salikhova Z.I. - Junior Researcher, Department of Cardiology, Research Institute of Cardiology and Internal Medicine.
5. Amantaeva A.N. - Junior Researcher, Department of Cardiology, Research Institute of Cardiology and Internal Medicine.

Reviewers:
Abseitova SR. - Doctor of Medical Sciences, Chief Cardiologist of the Ministry of Health of the Republic of Kazakhstan.

Disclosure of no conflict of interest: absent.

Indication of the conditions for reviewing the protocol: The protocol is revised at least once every 5 years, or upon receipt of new data on the diagnosis and treatment of the corresponding disease, condition or syndrome.

Attached files

Attention!

• By self-medicating, you can cause irreparable harm to your health.
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Right

• This includes the right ventricle and right atrium. This part of the heart pumps venous blood, which has low oxygen content. Carbon dioxide comes here from all organs and tissues of the body.
• There is a tricuspid valve on the right side of the heart that connects the atrium to the ventricle. The latter is also connected to the pulmonary artery by the valve of the same name.

The heart is located in a special bag that performs a shock-absorbing function. It is filled with fluid that lubricates the heart. The bag volume is usually 50 ml. Thanks to it, the heart is not subject to friction with other tissues and functions normally.

The heart works cyclically. Before contracting, the organ is relaxed. In this case, passive filling with blood occurs. Both atria then contract, pushing more blood into the ventricles. The atria then return to a relaxed state.

The ventricles then contract, thereby pushing blood into the aorta and pulmonary artery. Afterwards, the ventricles relax, and the systole phase is replaced by the diastole phase.

The heart has a unique function - automaticity. This organ is capable, without the help of external factors, of aggregating nerve impulses, under the influence of which the heart muscle contracts. No other organ of the human body has such a function.

The pacemaker located in the right atrium is responsible for generating impulses. It is from there that impulses begin to flow to the myocardium through the conduction system.

Coronary arteries are one of the most important components ensuring the functioning and vital activity of the heart. They deliver the necessary oxygen and nutrients to all heart cells.

If the coronary arteries have good patency, then the organ works normally and is not overstrained. If a person has atherosclerosis, then the heart does not work at full strength, it begins to feel a serious lack of oxygen. All this provokes the appearance of biochemical and tissue changes, which subsequently lead to the development of IHD.

Self-diagnosis

It is very important to know the symptoms of IHD. They usually appear at the age of 50 years and older. The presence of IHD can be detected during physical activity.

Symptoms of this disease include:

• angina pectoris (pain in the center of the chest);
• lack of air;
• heavy breath of oxygen;
• very frequent contractions of the heart muscle (over 300 times), leading to a stop in blood flow.

In some patients, IHD is asymptomatic. They do not even suspect the presence of the disease when a myocardial infarction occurs.

To understand the likelihood of a patient developing the disease, he should use a special cardio test “Is your heart healthy?”

People who want to understand whether they have coronary artery disease go to a cardiologist. The doctor conducts a dialogue with the patient, asking questions, the answers to which help to create a complete picture about the patient. This way, the specialist identifies possible symptoms and studies risk factors for the disease. The more of these factors, the higher the likelihood of a patient having IHD.

The manifestations of most factors can be eliminated. This helps prevent the disease from developing, and the likelihood of complications also decreases.

Avoidable risk factors include:

• diabetes;
• high blood pressure;
• smoking;
• high cholesterol.

The attending physician also examines the patient. Based on the information received, he prescribes examinations. They help to arrive at a final diagnosis.

The methods used include:

• ECG with stress test;
• chest x-ray;
• biochemical blood test, including determination of cholesterol and glucose levels in the blood.

The doctor, suspecting that the patient has serious arterial damage that requires urgent surgery, prescribes another type of study - coronary angiography. Next, the type of surgical intervention is determined.

It could be:

• angioplasty;
• coronary artery bypass grafting.

In less severe cases, drug treatment is used.

It is important that the patient seeks help from a doctor in time. The specialist will do everything to ensure that the patient does not develop any complications.

To avoid the development of the disease, the patient must:

Visit a cardiologist on time	The doctor carefully monitors all existing risk factors, prescribes treatment and makes timely changes if necessary.
Take prescribed medications	It is very important to follow the dosage prescribed by your doctor. Under no circumstances should you change or refuse treatment on your own.
Carry nitroglycerin with you if prescribed by your doctor	This medication may be needed at any time. It relieves pain due to angina pectoris.
Lead a correct lifestyle	The doctor will provide details at the appointment.
Bring the attending physician up to date	Be sure to talk about chest pain and other slightest manifestations of the disease.

Preventive measures

To prevent coronary heart disease, you need to follow 3 rules:

No nicotine	Smoking is one of the risk factors for the development of coronary artery disease in a patient. Especially when it is accompanied by high cholesterol in the blood. At the same time, do not forget that due to smoking, life is shortened by about 7 years. Due to the high nicotine content in the blood, its density noticeably increases. Platelets begin to stick together, they become less adapted to life. The amount of carbon monoxide in a smoker's blood increases sharply. This automatically reduces the oxygen content, which is necessary for the normal functioning of cells and the body as a whole. Nicotine, entering the blood, promotes spasm of the arteries, which leads to a sharp increase in blood pressure. People addicted to cigarettes are 2 times more likely to die from myocardial infarction. At the same time, sudden death occurs 4 times more often than in people leading a healthy lifestyle. Thus, one pack of cigarettes smoked increases mortality by 2 times, and mortality from coronary artery disease by 3 times. The more a person smokes, the higher the risk of developing IHD. Even using cigarettes with low nicotine and tar content does not reduce the risk of developing one of the cardiovascular diseases. Passive smokers also have a 25% greater risk of death from coronary heart disease than healthy people.
An active lifestyle is required	To maintain your health, you need to exercise. It is physical activity that reduces the likelihood of developing coronary artery disease. To maintain a healthy body, you need to exercise at least 3 times a week for 30-45 minutes. Under no circumstances should you sharply increase the load; you need to know when to stop.
Keep your weight normal	One of the most important criteria for health is the ratio of muscle to fat. The metabolic rate largely depends on it. Excess weight always increases the number of heart contractions, even at rest. At the same time, the muscles’ need for oxygen and nutrients also increases. In obese people, lipid metabolism is often disrupted. This contributes to the development of diseases such as diabetes mellitus and hypertension, which are risk factors for the development of coronary artery disease. If a person’s body weight is above normal, he should resort to physical activity and proper nutrition. It is best to consult a doctor who will help you create the right diet and tell you which foods will be healthy and which will have to be excluded from your diet.

Massage for coronary heart disease

A patient with coronary artery disease can supplement treatment with massage and aromatherapy. A special lamp must be placed in the room where the patient sleeps. It will fill the air with various aromas of oils. Lavender, tangerine, ylang-ylang, lemon balm are best suited.

Chest massage does not need to be done every day, it should be occasional. Instead of massage oil, you should use peach, corn or olive oil.

A tablespoon of any of them is mixed with one of the following compositions (1 drop of each ingredient):

• geranium, marjoram and frankincense oils;
• neroli, ginger and bergamot oils;
• clary sage, bergamot and ylang-ylang oils.

The massage should be done by first applying the resulting mixture to the left pectoral muscle and on top of it. Movements should be light, smooth, without strong pressure.

Any method of surgical treatment of coronary artery disease is highly effective. The severity of shortness of breath decreases, angina decreases or completely disappears. Each method of surgical treatment has its own indications and contraindications. For the treatment of coronary artery disease, the following are used: coronary artery bypass grafting and...

Coronary heart disease is one of the most common pathologies of the cardiovascular system in developed countries. It is a heart lesion that is caused by an absolute or relative disruption of the blood supply resulting from a circulatory disorder in the coronary...

Insufficient oxygen supply to the heart due to narrowing of the arteries and their clogging with plaque leads to the development of coronary heart disease (CHD). There can be many reasons: alcohol abuse, poor diet, a sedentary lifestyle that contributes to the development of physical inactivity, constant stress and...

The principle of using ECG was first introduced into circulation in the 70s of the 19th century. This was done by an Englishman named W. Walter. Now, when almost 150 years have passed since that moment, the method of taking indicators of the electrical activity of the heart has changed significantly, becoming more reliable and informative, but the basic principles...

The principles of treatment and prevention are closely related to the use of herbal medicine and diet. Proper nutrition and folk remedies in the treatment of coronary heart disease can radically improve the patient’s condition. Principles of therapy The causes of IHD are different, but almost all are based on poor nutrition and unhealthy...

Characterized by attacks of sudden pain in the chest area. In most cases, the disease is caused by atherosclerosis of the coronary arteries and the development of a deficiency of blood supply to the myocardium, the worsening of which occurs with significant physical or emotional stress.

Treatment of the disease in the form of monolaser therapy is carried out during the non-attack period; During the period of acute manifestations, treatment is carried out in combination with medications.

Laser therapy for coronary heart disease is aimed at reducing psycho-emotional excitability, restoring the balance of autonomic regulation, increasing the activity of the erythrocyte component of the blood, eliminating deficient coronary blood supply with the subsequent elimination of metabolic disorders of the myocardium, normalizing the lipid spectrum of the blood with reducing the level of atherogenic lipids. In addition, when conducting pharmacolaser therapy, the effect of laser radiation on the body leads to a reduction in the side effects of drug therapy, in particular those associated with lipoprotein imbalance when taking b-blockers, and increases sensitivity to the medications used as a result of restoration of the structural and functional activity of the cell receptor apparatus.

Laser therapy tactics include zones of mandatory exposure and zones of secondary choice, which include the projection zone of the aortic arch and zones of final choice, connected after 3-4 procedures, positioned in the projection of the heart.

Rice. 86. Projection zones of the heart region. Legend: pos. “1” — projection of the left atrium, pos. “2”—projection of the left ventricle.

Irradiation of the heart is preferably using pulsed infrared lasers. The irradiation mode is performed with pulse power values ​​in the range of 6-8 W and a frequency of 1500 Hz (corresponds to myocardial relaxation by reducing its sympathetic dependence), exposure is 2-3 minutes for each field. The number of procedures during a course of treatment is at least 10.

As the main manifestations of the disease are relieved, the prescription includes effects on reflex zones: the area of ​​segmental innervation at the Th1-Th7 level, receptor zones in the projection of the inner surface of the shoulder and forearm, the palmar surface of the hand, the sternum area.

Rice. 87. Projection zone of influence on the area of ​​segmental innervation Th1-Th7.

Modes of laser exposure to areas of additional exposure

Stable angina pectoris

Stable exertional angina: Brief description

Stable angina pectoris voltage- one of the main manifestations of IHD. The main and most typical manifestation of angina pectoris is chest pain that occurs during physical activity, emotional stress, when going out into the cold, walking against the wind, or at rest after a heavy meal.

Pathogenesis

As a result of a discrepancy (imbalance) between the myocardial need for oxygen and its delivery through the coronary arteries due to atherosclerotic narrowing of the lumen of the coronary arteries, the following occur. Myocardial ischemia (clinically manifested by chest pain). Violations of the contractile function of the corresponding part of the heart muscle. Changes in biochemical and electrical processes in the heart muscle. In the absence of a sufficient amount of oxygen, cells switch to an anaerobic type of oxidation: glucose breaks down to lactate, intracellular pH decreases and energy reserves in cardiomyocytes are depleted. The subendocardial layers are primarily affected. The function of cardiomyocyte membranes is disrupted, which leads to a decrease in the intracellular concentration of potassium ions and an increase in the intracellular concentration of sodium ions. Depending on the duration of myocardial ischemia, changes can be reversible or irreversible (myocardial necrosis, i.e., infarction). Sequences of pathological changes during myocardial ischemia: impaired myocardial relaxation (impaired diastolic function) - impaired myocardial contraction (impaired systolic function) - ECG changes - pain syndrome.

Classification

Canadian Cardiovascular Society (1976). Class I - “ordinary physical activity does not cause an attack of angina.” Pain does not occur when walking or climbing stairs. Attacks occur with strong, rapid or prolonged stress at work. Class II - “mild limitation of usual activities.” Pain occurs when walking or quickly climbing stairs, walking uphill, walking or climbing stairs after eating, in the cold, against the wind, during emotional stress, or within a few hours of waking up. Walking more than 100-200 m on level ground or climbing more than 1 flight of stairs at a normal pace and under normal conditions. Class III - “significant limitation of usual physical activity.” Walking on level ground or climbing one flight of stairs at a normal pace under normal conditions provokes an attack of angina. Class IV - “impossibility of any physical activity without discomfort.” Seizures may occur at rest

Stable exertional angina: Signs, Symptoms

CLINICAL MANIFESTATIONS

Complaints. Characteristics of pain syndrome. Localization of pain is substernal. Conditions for the occurrence of pain are physical activity, strong emotions, large meals, cold, walking against the wind, smoking. Young people often have the so-called phenomenon of “passing through pain” (the “warm-up” phenomenon) - a decrease or disappearance of pain while increasing or maintaining the load (due to the opening of vascular collaterals). The duration of pain is from 1 to 15 minutes, and has an increasing character (“crescendo”). If the pain continues for more than 15 minutes, the development of MI should be assumed. Conditions for stopping pain are stopping physical activity and taking nitroglycerin. The nature of pain during angina pectoris (squeezing, pressing, bursting, etc.), as well as the fear of death, are very subjective and do not have serious diagnostic significance, since they largely depend on the physical and intellectual perception of the patient. Pain irradiates to both the left and right parts of the chest and neck. Classic irradiation - to the left arm, lower jaw.

Associated symptoms- nausea, vomiting, increased sweating, fatigue, shortness of breath, increased heart rate, increased (sometimes decreased) blood pressure.

Angina equivalents: shortness of breath (due to impaired diastolic relaxation) and severe fatigue during exercise (due to decreased cardiac output due to impaired systolic myocardial function with insufficient oxygen supply to skeletal muscles). In any case, symptoms should decrease when exposure to the provoking factor (physical activity, hypothermia, smoking) or nitroglycerin is stopped.

Physical data. During an attack of angina - pallor of the skin, immobility (patients “freeze” in one position, since any movement increases the pain), sweating, tachycardia (less often bradycardia), increased blood pressure (less often, its decrease). Extrasystoles and a “gallop rhythm” can be heard. systolic murmur arising from mitral valve insufficiency as a result of dysfunction of the papillary muscles. An ECG recorded during an attack of angina can detect changes in the final part of the ventricular complex (T wave and ST segment), as well as heart rhythm disturbances.

Stable angina pectoris: Diagnosis

Laboratory data

- auxiliary meaning; They can only determine the presence of dyslipidemia, identify concomitant diseases and a number of risk factors (DM), or exclude other causes of pain (inflammatory diseases, blood diseases, thyroid diseases).

Instrumental data

ECG during an attack of angina: repolarization disturbances in the form of changes in T waves and ST segment displacement up (subendocardial ischemia) or down from the isoline (transmural ischemia) or heart rhythm disturbances.

Daily ECG monitoring allows you to identify the presence of painful and non-painful episodes of myocardial ischemia in the usual conditions for patients, as well as possible heart rhythm disturbances throughout the day.

Bicycle ergometry or treadmill (stress test with simultaneous recording of ECG and blood pressure). Sensitivity - 50-80%, specificity - 80-95%. The criterion for a positive stress test during bicycle ergometry is ECG changes in the form of horizontal ST segment depression of more than 1 mm lasting more than 0.08 s. In addition, stress testing can reveal signs associated with an unfavorable prognosis for patients with exertional angina: . typical pain syndrome. ST segment depression more than 2 mm. persistence of ST segment depression for more than 6 minutes after cessation of exercise. the appearance of ST segment depression at a heart rate (HR) less than 120 per minute. the presence of ST depression in several leads, ST segment elevation in all leads, with the exception of aVR. absence of a rise in blood pressure or its decrease in response to physical activity. the occurrence of cardiac arrhythmias (especially ventricular tachycardia).

EchoCG at rest allows you to determine the contractility of the myocardium and conduct a differential diagnosis of pain syndrome (heart defects, pulmonary hypertension, cardiomyopathies, pericarditis, mitral valve prolapse, left ventricular hypertrophy with arterial hypertension).

Stress - EchoCG (EchoCG - assessment of the mobility of left ventricular segments with an increase in heart rate as a result of the administration of dobutamine, transesophageal pacemaker or under the influence of physical activity) is a more accurate method for identifying coronary artery insufficiency. Changes in local myocardial contractility precede other manifestations of ischemia (ECG changes, pain). The sensitivity of the method is 65-90%, specificity is 90-95%. Unlike bicycle ergometry, stress echocardiography can detect coronary artery insufficiency when one vessel is damaged. Indications for stress echocardiography are: . atypical angina pectoris tension (presence of angina equivalents or unclear description of the pain syndrome by the patient). difficulty or impossibility of performing stress tests. uninformativeness of bicycle ergometry in a typical clinical picture of angina pectoris. absence of changes in the ECG during stress tests due to His bundle branch block, signs of left ventricular hypertrophy, signs of Wolff-Parkinson-White syndrome with a typical clinical picture of exertional angina. positive stress test during bicycle ergometry in young women (since the likelihood of coronary artery disease is low).

Coronary angiography is the “gold standard” in the diagnosis of coronary artery disease, as it allows us to identify the presence, location and degree of narrowing of the coronary arteries. Indications (recommendations of the European Society of Cardiology; 1997): . angina pectoris voltages above functional class III in the absence of effect of drug therapy. angina pectoris voltage of I-II functional class after MI. angina pectoris tension with His bundle branch block in combination with signs of ischemia according to myocardial scintigraphy. severe ventricular arrhythmias. stable angina pectoris in patients undergoing vascular surgery (aorta, femoral, carotid arteries). myocardial revascularization (balloon dilatation, coronary artery bypass grafting). clarification of the diagnosis for clinical or professional (for example, pilots) reasons.

Myocardial scintigraphy is a method of visualizing the myocardium that allows identifying areas of ischemia. The method is very informative when it is impossible to evaluate the ECG due to blockades of the His bundle branches.

Diagnostics

In typical cases, stable angina pectoris is diagnosed based on a detailed history, a detailed physical examination of the patient, a resting ECG recording, and subsequent critical analysis of the data obtained. It is believed that these types of examinations (history, examination, auscultation, ECG) are sufficient to diagnose angina pectoris with its classic manifestation in 75% of cases. If there is any doubt about the diagnosis, 24-hour ECG monitoring, stress tests (veloergometry, stress - echocardiography) are performed consistently, and if appropriate conditions are present, myocardial scintigraphy is performed. At the final stage of diagnosis, coronary angiography is necessary.

Differential diagnosis

It should be borne in mind that chest pain syndrome can be a manifestation of a number of diseases. We should not forget that there can be several causes of chest pain at the same time. Diseases of the cardiovascular system. THEM. Angina pectoris. Other reasons. possibly of ischemic origin: aortic stenosis, aortic valve insufficiency, hypertrophic cardiomyopathy, arterial hypertension, pulmonary hypertension, severe anemia. non-ischemic: aortic dissection, pericarditis, mitral valve prolapse. Gastrointestinal diseases. Diseases of the esophagus - esophageal spasm, esophageal reflux, esophageal rupture. Stomach diseases - peptic ulcers. Diseases of the chest wall and spine. Anterior chest wall syndrome. Anterior scalene syndrome. Costal chondritis (Tietze syndrome). Damage to the ribs. Shingles. Lung diseases. Pneumothorax. Pneumonia involving the pleura. PE with or without pulmonary infarction. Diseases of the pleura.

Stable exertional angina: Treatment methods

Treatment

The goals are to improve the prognosis (prevention of MI and sudden cardiac death) and reduce the severity (elimination) of symptoms of the disease. Non-drug, medicinal (drug) and surgical treatment methods are used.

Non-drug treatment - impact on risk factors for coronary artery disease: dietary measures to reduce dyslipidemia and reduce body weight, smoking cessation, sufficient physical activity in the absence of contraindications. Normalization of blood pressure levels and correction of carbohydrate metabolism disorders are also necessary.

Drug therapy - three main groups of drugs are used: nitrates, b - adrenergic blockers and slow calcium channel blockers. Additionally, antiplatelet agents are prescribed.

Nitrates. When nitrates are administered, systemic venodilation occurs, leading to a decrease in blood flow to the heart (reduction in preload), a decrease in pressure in the chambers of the heart and a decrease in myocardial tension. Nitrates also cause a decrease in blood pressure, reduce resistance to blood flow and afterload. In addition, the expansion of large coronary arteries and an increase in collateral blood flow are important. This group of drugs is divided into short-acting nitrates (nitroglycerin) and long-acting nitrates (isosorbide dinitrate and isosorbide mononitrate).

To relieve an attack of angina, nitroglycerin is used (tablet forms sublingually in a dose of 0.3-0.6 mg and aerosol forms - spray - are used in a dose of 0.4 mg also sublingually). Short-acting nitrates relieve pain in 1-5 minutes. Repeated doses of nitroglycerin to relieve an attack of angina can be used at 5-minute intervals. Nitroglycerin in tablets for sublingual use loses its activity after 2 months from the moment the tube is opened due to the volatility of nitroglycerin, so regular replacement of the drug is necessary.

To prevent angina attacks that occur more than once a week, long-acting nitrates (isosorbide dinitrate and isosorbide mononitrate) are used. Isosorbide dinitrate in a dose of 10-20 mg 2-4 times a day (sometimes up to 6) 30-40 minutes before the expected physical activity. Retard forms of isosorbide dinitrate - in a dose of 40-120 mg 1-2 times / day before the expected physical activity. Isosorbide mononitrate in a dose of 10-40 mg 2-4 times / day, and retard forms - in a dose of 40-120 mg 1-2 times / day also 30-40 minutes before the expected physical activity.

Tolerance to nitrates (loss of sensitivity, addiction). Regular daily use of nitrates for 1-2 weeks or more can lead to a decrease or disappearance of the antianginal effect. The reason is a decrease in the formation of nitric oxide, acceleration of its inactivation due to increased activity of phosphodiesterases and increased formation of endothelin-1, which has a vasoconstrictor effect. Prevention - asymmetric (eccentric) administration of nitrates (for example, 8 a.m. and 3 p.m. for isosorbide dinitrate or only 8 a.m. for isosorbide mononitrate). Thus, a nitrate-free period lasting more than 6-8 hours is provided to restore the sensitivity of the SMC of the vascular wall to the action of nitrates. As a rule, a nitrate-free period is recommended for patients during a period of minimal physical activity and a minimal number of pain attacks (in each case individually). Other methods of preventing nitrate tolerance include the use of sulfhydryl group donors (acetylcysteine, methionine), ACE inhibitors (captopril, etc.), angiotensin II receptor blockers, diuretics, hydralazine, however, the incidence of nitrate tolerance with their use decreases to a small extent .

Molsidomin- close in effect to nitrates (nitro-containing vasodilator). After absorption, molsidomine is converted into an active substance that is converted into nitric oxide, which ultimately leads to relaxation of vascular smooth muscle. Molsidomine is used in a dose of 2-4 mg 2-3 times / day or 8 mg 1-2 times / day (long-acting forms).

b - Adrenergic blockers. The antianginal effect is due to a decrease in myocardial oxygen demand due to a decrease in heart rate and a decrease in myocardial contractility. For the treatment of angina pectoris the following is used:

Non-selective b - adrenergic blockers (act on b1 - and b2 - adrenergic receptors) - for the treatment of angina, propranolol is used in a dose of 10-40 mg 4 times / day, nadolol in a dose of 20-160 mg 1 time / day;

Cardioselective b - adrenergic blockers (act predominantly on b1 - adrenergic receptors of the heart) - atenolol at a dose of 25-200 mg/day, metoprolol 25-200 mg/day (in 2 doses), betaxolol (10-20 mg/day), bisoprolol (5 - 20 mg/day).

Recently, β-blockers have been used that cause dilatation of peripheral blood vessels, such as carvedilol.

Slow calcium channel blockers. The antianginal effect consists of moderate vasodilation (including coronary arteries), reducing myocardial oxygen demand (in representatives of the verapamil and diltiazem subgroups). They are used: verapamil - 80-120 mg 2-3 times / day, diltiazem - 30-90 mg 2-3 times / day.

Prevention of MI and sudden cardiac death

Clinical studies have shown that the use of acetylsalicylic acid at a dose of 75-325 mg/day significantly reduces the risk of developing MI and sudden cardiac death. Patients with angina pectoris should be prescribed acetylsalicylic acid in the absence of contraindications - peptic ulcer, liver disease, increased bleeding, intolerance to the drug.

The prognosis of patients with stable angina pectoris is also positively influenced by reducing the concentration of total cholesterol and LDL cholesterol using lipid-lowering drugs (simvastatin, pravastatin). Currently, optimal levels are considered to be no more than 5 mmol/l (190 mg%) for total cholesterol and no more than 3 mmol/l (115 mg%) for LDL cholesterol.

Surgery

When determining the tactics of surgical treatment of stable angina pectoris, it is necessary to take into account a number of factors: the number of affected coronary arteries, left ventricular ejection fraction, and the presence of concomitant diabetes. Thus, with one or two-vessel lesions with a normal left ventricular ejection fraction, myocardial revascularization is usually started with percutaneous transluminal coronary angioplasty and stenting. In the presence of two or three vessel lesions and a decrease in the left ventricular ejection fraction of less than 45% or the presence of concomitant diabetes, it is more advisable to perform coronary artery bypass grafting (see also Atherosclerosis of the coronary arteries).

Percutaneous angioplasty (balloon dilation) is the expansion of a section of the coronary artery narrowed by an atherosclerotic process with a miniature balloon under high pressure under visual control during angiography. The success of the procedure is achieved in 95% of cases. When performing angioplasty, complications are possible: . mortality is 0.2% for single-vessel disease and 0.5% for multi-vessel disease, MI occurs in 1% of cases, the need for coronary artery bypass grafting appears in 1% of cases; . Late complications include restenosis (in 35-40% of patients within 6 months after dilatation), as well as the appearance of angina (in 25% of patients within 6-12 months).

In parallel with the expansion of the lumen of the coronary artery, stenting has recently been used - implantation of stents (thin wire frames that prevent restenosis) at the site of narrowing.

Coronary artery bypass grafting is the creation of an anastomosis between the aorta (or internal mammary artery) and the coronary artery below (distal) the site of narrowing to restore effective blood supply to the myocardium. A section of the saphenous vein of the thigh, the left and right internal mammary arteries, the right gastroepiploic artery, and the inferior epigastric artery are used as a graft. Indications for coronary artery bypass grafting (recommendations of the European Society of Cardiology; 1997). Left ventricular ejection fraction less than 30%. Damage to the trunk of the left coronary artery. The only unaffected coronary artery. Left ventricular dysfunction in combination with three-vessel disease, especially with damage to the anterior interventricular branch of the left coronary artery in the proximal section. When performing coronary bypass surgery, complications are also possible - MI in 4-5% of cases (up to 10%). Mortality is 1% for single-vessel disease and 4-5% for multi-vessel disease. Late complications of coronary artery bypass grafting include restenosis (when using vein grafts in 10-20% of cases during the first year and 2% every year for 5-7 years). When arterial grafts are used, shunts remain open in 90% of patients for 10 years. Within 3 years angina pectoris resumes in 25% of patients.

Forecast

Stable angina pectoris with adequate therapy and monitoring of patients is relatively favorable: mortality is 2-3% per year, fatal MI develops in 2-3% of patients. A less favorable prognosis is for patients with a decrease in the ejection fraction of the left ventricle, a high functional class of stable angina pectoris, elderly patients, patients with multivessel disease of the coronary arteries, stenosis of the main trunk of the left coronary artery, proximal stenosis of the anterior interventricular branch of the left coronary artery.

Clinical protocol for the diagnosis and treatment of diseases “IHD stable angina pectoris”

I. INTRODUCTORY PART:

1.Name: IHD stable angina pectoris

2. Protocol code:

3. Codes according to MKB-10:

4. Abbreviations used in the protocol:

AG - arterial hypertension

AA - antianginal (therapy)

BP - blood pressure

CABG - coronary artery bypass grafting

ALT - alanine aminotransferase

AO - abdominal obesity

AST - aspartate aminotransferase

CCBs - calcium channel blockers

GPs - general practitioners

VPN - upper limit norm

VPU - Wolff-Parkinson-White syndrome

HCM - hypertrophic cardiomyopathy

LVH - left ventricular hypertrophy

DBP - diastolic blood pressure

DLP - dyslipidemia

PVC - ventricular extrasystole

IHD - coronary heart disease

BMI - body mass index

ICD - short-acting insulin

IMT—thickness of the intima-media complex

TSH - glucose tolerance test

U3DG - Doppler ultrasound

PA - physical activity

FC - functional class

RF - risk factors

COPD - chronic obstructive pulmonary disease

CHF - chronic heart failure

HDL cholesterol - high density lipoprotein cholesterol

LDL cholesterol - low density lipoprotein cholesterol

4KB - percutaneous coronary intervention

HR - heart rate

ECG - electrocardiography

ECS - electrical pacemaker

EchoCG - echocardiography

VE - minute volume of breathing

VCO2 is the amount of carbon dioxide released per unit of time;

RER (respiratory quotient) - VCO2/VO2 ratio;

BR - respiratory reserve.

BMS - non-drug eluting stent

DES - drug eluting stent

5. Date of development of the protocol: year 2013.

7. Protocol users: general practitioners, cardiologists, interventional cardiologists, cardiac surgeons.

8. Indication of the absence of conflict of interest: absent.

9. Definition.

IHD is an acute or chronic lesion of the heart caused by a decrease or cessation of blood supply to the myocardium due to a disease process in the coronary vessels (WHO definition 1959).

Angina pectoris is a clinical syndrome manifested by a feeling of discomfort or pain in the chest of a compressive, pressing nature, which is most often localized behind the sternum and can radiate to the left arm, neck, lower jaw, and epigastric region. Pain is provoked by physical activity, going out into the cold, eating a lot of food, and emotional stress; goes away with rest or is eliminated by taking sublingual nitroglycerin within a few seconds or minutes.

II. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSTICS AND

10. Clinical classification:

Table 1. - Classification of the severity of stable angina pectoris according to the classification of the Canadian Heart Association (Campeau L, 1976)