Ischemic heart disease according to ICD 10. Causes of these diseases. Large-focal postinfarction cardiosclerosis

Against the background of the development of necrosis of the heart muscle and the formation of scar tissue, patients develop postinfarction cardiosclerosis, the ICD-10 code of which is I2020. - I2525.

This condition affects the functioning of the cardiovascular system and the body as a whole.

The essence of the disease

According to statistics, this pathology tends to develop in people after 50 years.

Unfortunately, specialists have not yet been able to develop an accurate method of therapeutic therapy that could permanently save the patient from the development of an anomaly.

A distinctive feature of the disease is that its development occurs gradually.

At the site of necrosis as a result of scarring, connective tissues are replaced by scar tissue. This reduces the functionality of the myocardium: it becomes less elastic.

In addition, there is a change in the structure of the heart valves, as well as tissues and fibers of the heart muscle are replaced by pathogenic tissue.

In patients who suffer from other diseases of the cardiovascular system, the likelihood of developing PICS is significantly increased.

The reasons

Experts identify several reasons that can provoke the occurrence of postinfarction cardiosclerosis. One of the first places among this list is occupied by the consequences of a myocardial infarction suffered by a patient.

After a patient has had an MI, the process of replacing dead tissue with scar tissue takes several months (2–4). The newly formed tissues cannot take part in the contraction of the heart and myocardium. In addition, they are not able to transmit electrical impulses.

As a result, the cavities of the heart gradually increase in volume and deform. This is the main cause of dysfunction of the heart and system.

Among the factors that provoke pathology, one can also name myocardial dystrophy, the essence of which is that the violation of the metabolic process and blood circulation in the heart muscle leads to the loss of the possibility of its contraction.

Mechanical injury to the chest, which is accompanied by a violation of the integrity of the heart or valves. But this reason is quite rare.

Postinfarction cardiosclerosis leads to disruption of the CCC. Patients who are exposed to one or more of the above factors are at risk.

Symptoms and classification

The disease has quite a variety of manifestations.

Among them are the following:

In modern medicine, the PICS classification is used, which is based on the size of the area of ​​damage to cardiac tissues:

The manifestation of symptoms of the disease is directly dependent on the localization of the pathology, as well as on its type.

Diagnosis

The effectiveness of the treatment process depends on the timeliness and correctness of the diagnosis. For this, the following methods are used:

Treatment

According to the international classification, PICS refers to rather dangerous pathologies of the cardiovascular system, which can lead to the death of the patient. That is why it is extremely important to choose the most correct method of treatment.

Specialists use two main methods:

• diuretics;
• aspirin;
• ACE inhibitors;
• beta blockers.

As a rule, specialists prescribe not one, but a whole complex of drugs.

1. Surgical. The operation is prescribed for patients who are in the process of aneurysm formation or in the zone of necrosis development there is a living tissue of the heart muscle. In this case, coronary artery bypass grafting is used. In parallel with shunting, the dead tissue is also removed. The operation is performed under general anesthesia, as well as with the obligatory presence of a heart-lung machine.

Regardless of the method of treatment chosen by the specialist, the patient is necessarily under his supervision. He needs to change his lifestyle and go to rehab.

It is necessary to be attentive to the manifestation of various signs indicating a violation of cardiac activity. This can help prevent the development of a serious illness or its complications.

2. DIAGNOSTICS OF CHRONIC CAD

2.1. The diagnosis of IHD is formed on the basis of:

• Questioning and collecting anamnesis;
• Physical examination;
• Instrumental research;
• Laboratory research.

2.2. Tasks of the doctor during the diagnostic search:

• Make a diagnosis and determine the form of IHD;
• Determine the prognosis of the disease - the likelihood of complications;
• Based on the degree of risk, determine the tactics of treatment (medical, surgical), the frequency and volume of subsequent outpatient examinations.

In practice, diagnostic and prognostic evaluations are carried out simultaneously, and many diagnostic methods contain important prognostic information.

The degree of risk of complications in chronic coronary artery disease is determined by the following main indicators:

• Clinical picture (severity of myocardial ischemia) of the disease
• Anatomical prevalence and severity of atherosclerosis of large and medium coronary arteries;
• Systolic function of the left ventricle;
• General health, presence of comorbidities and additional risk factors.

2.3. IHD classifications

There are several classifications of IBS. In Russian clinical practice, a classification based on the International Classification of Diseases IX revision and the recommendations of the WHO Expert Committee (1979) is widely used. In 1984, with the amendments of the VKNTs AMS of the USSR, this classification was adopted in our country.

IHD classification (according to ICD-IX 410-414.418)

1. Angina pectoris:
1.1. First-time angina pectoris;
1.2. Stable exertional angina with indication of the functional class (I-IV);
1.3. Angina pectoris progressive;
1.4. Spontaneous angina (vasospastic, special, variant, Prinzmetal);
2. Acute focal myocardial dystrophy;
3. Myocardial infarction:
3.1. Large focal (transmural) - primary, repeated (date);
3.2. Small-focal - primary, repeated (date);
4. Postinfarction focal cardiosclerosis;
5. Violation of the heart rhythm (indicating the form);
6. Heart failure (indicating the form and stage);
7. Painless form of coronary artery disease;
8. Sudden coronary death.

Notes:

Sudden coronary death- death in the presence of witnesses, occurring instantly or within 6 hours from the onset of a heart attack.

New onset angina pectoris- the duration of the disease up to 1 month. since its inception.

stable angina- the duration of the disease is more than 1 month.

Progressive angina- an increase in the frequency, severity and duration of seizures in response to the usual load for this patient, a decrease in the effectiveness of nitroglycerin; sometimes changes on the ECG.

Spontaneous (vasospastic, variant) angina pectoris- attacks occur at rest, are difficult to respond to nitroglycerin, can be combined with angina pectoris.

Postinfarction cardiosclerosis- is placed no earlier than 2 months after the development of myocardial infarction.

Cardiac arrhythmias and conduction disorders(indicating the form, degree).

Circulatory failure(indicating the form, stage) - is made after the diagnosis of "postinfarction cardiosclerosis".

2.4. Examples of the formulation of the diagnosis

1. IHD, atherosclerosis of the coronary arteries. First-time angina pectoris.
2. IHD, atherosclerosis of the coronary arteries. Angina pectoris and (or) rest, FC IV, ventricular extrasystole. HK0.
3. ischemic heart disease. Vasospastic angina.
4. IHD, atherosclerosis of the coronary arteries. Angina pectoris, functional class III, postinfarction cardiosclerosis (date), violation of intracardiac conduction: atrioventricular block I degree, left bundle branch block. Circulatory insufficiency II B stage.

In the International Classification of Diseases X revision, stable coronary artery disease is in 2 headings.

In clinical practice, it is more convenient to use the WHO classification, since it takes into account different forms of the disease. For statistical needs in health care, ICD-10 is used.

2.5. Forms of chronic ischemic heart disease

2.5.1. Angina pectoris;

Symptoms

Signs of typical (undoubted) exertional angina (all 3 signs):

1. pain in the sternum, possibly radiating to the left arm, back or lower jaw, lasting 2-5 minutes. Pain equivalents are shortness of breath, a feeling of "heaviness", "burning".
2. The pain described above occurs during times of severe emotional stress or physical exertion;
3. The above pain quickly disappears after the cessation of physical activity or after taking nitroglycerin.

There are atypical variants of irradiation (to the epigastric region, to the shoulder blade, to the right half of the chest). The main symptom of angina pectoris is a clear dependence of the onset of symptoms on physical activity.

The equivalent of angina pectoris can be shortness of breath (up to suffocation), a feeling of "heat" in the sternum, attacks of arrhythmia during exercise.

The equivalent of physical activity can be a crisis increase in blood pressure with an increase in the load on the myocardium, as well as a heavy meal.

Signs of atypical (possible) angina pectoris

The diagnosis of atypical angina is made if the patient has any 2 of the 3 above signs of typical angina.

Nonanginal (nonanginal) chest pain

1. Pain is localized to the right and left of the sternum;
2. The pains are local, "point" in nature;
3. After the onset of pain lasts more than 30 minutes (up to several hours or days), it can be constant or “suddenly piercing”;
4. Pain is not associated with walking or other physical activity, however, it occurs when tilting and turning the body, in the prone position, with a long stay of the body in an uncomfortable position, with deep breathing at the height of inhalation;
5. Pain does not change after taking nitroglycerin;
6. Pain is aggravated by palpation of the sternum and / or chest along the intercostal spaces.

2.5.1.1. Functional classes of angina pectoris

During the questioning, depending on the physical activity tolerated, 4 functional classes of angina pectoris are distinguished (according to the classification of the Canadian Society of Cardiology):

Table 2. "Functional classes of angina pectoris"

2.5.1.2. Differential diagnosis in angina pectoris

• Cardiovascular diseases: severe myocardial hypertrophy in arterial hypertension, aortic stenosis, hypertrophic cardiomyopathy, coronaritis, dissecting aortic aneurysm, vasospastic angina pectoris, pulmonary embolism, pericarditis
• Acute and chronic diseases of the upper gastrointestinal tract: reflux esophagitis, spasm of the esophagus, erosive lesions, peptic ulcer and tumors of the esophagus, stomach and duodenum, hiatal hernia, cholecystitis, pancreatitis;
• Acute and chronic diseases of the upper respiratory tract: acute bronchitis, tracheitis, bronchial asthma;
• Lung diseases: pleurisy, pneumonia, pneumothorax, lung cancer;
• Injuries and post-traumatic diseases of the chest, osteochondrosis of the cervicothoracic spine with radicular syndrome;
• Psychogenic disorders: neurocirculatory dystonia, hyperventilation syndrome, panic disorders, psychogenic cardialgia, depression;
• Intercostal neuralgia, myalgia;
• Arthritis of the sternocostal joints (Tietze's syndrome);
• Acute infectious diseases (herpes zoster)

2.5.2. Painless myocardial ischemia

A significant part of episodes of myocardial ischemia occurs in the absence of symptoms of angina pectoris or its equivalents - up to the development of painless MI.

Within the framework of chronic coronary artery disease, 2 types of painless myocardial ischemia (SIMI) are distinguished:

Type I - completely painless myocardial ischemia
Type II - a combination of painless and painful episodes of myocardial ischemia

Episodes of MIMS are usually identified during exercise testing and 24-hour ECG monitoring.

Completely painless myocardial ischemia is detected in approximately 18-25% of individuals with proven coronary artery atherosclerosis. With concomitant diabetes mellitus, the likelihood of type I and type II MIMS is higher. According to 24-hour ECG monitoring, most episodes of MIMS occur during the day, which is explained by an increased average heart rate during vigorous activity. At the same time, episodes of MIMS often occur at night, against the background of normal and even reduced heart rate, which, apparently, reflects the role of dynamic coronary artery stenoses (spasms). It is believed that if BBMI occurs both at night and in the morning, this is a characteristic sign of multivessel atherosclerosis, or damage to the trunk of the left coronary artery.

Diagnostic tests for painless myocardial ischemia

In the diagnosis and evaluation of IMIM, stress tests and 24-hour ECG monitoring complement each other.

Treadmill test, VEM, CPES - allow you to actively identify IMIM and characterize its relationship with blood pressure, heart rate, physical activity. Simultaneous perfusion myocardial scintigraphy and echocardiography can detect concomitant hypoperfusion and impaired myocardial contractile function.

ECG monitoring allows you to determine the total number and duration of episodes of MIMS, as well as to identify MIMS at night and without regard to exercise.

Painless type II ischemia is much more common than type I MI. Even in individuals with typical angina, about 50% of ischemic episodes are asymptomatic. With concomitant diabetes mellitus, this figure is somewhat higher. It should be remembered that MIMI, as well as oligosymptomatic and asymptomatic MI, are often found in people with diabetes mellitus, sometimes being the only indication for coronary artery disease. In this disease, neuropathy with a violation of superficial and deep sensitivity is very common.

Forecast

The damaging effect of ischemia on the myocardium is determined not by the presence of pain, but by the severity and duration of hypoperfusion. Therefore, painless myocardial ischemia of both types is a poor prognostic sign. The number, severity and duration of episodes of myocardial ischemia, regardless of whether they are painful or painless, have an unfavorable prognostic value. Individuals with type 1 MIMI identified during exercise testing have a 4- to 5-fold higher risk of cardiovascular death than healthy individuals. Identification of episodes of MIMD during daily ECG monitoring is also an unfavorable predictor. Concomitant MIMD cardiovascular risk factors (diabetes mellitus, history of myocardial infarction, smoking) further worsen the prognosis.

2.5.3. Vasospastic angina

Described in 1959 as a type (variant) of a pain attack in the chest caused by myocardial ischemia at rest, without regard to physical and emotional stress, accompanied by ST segment elevations on the ECG. Often such angina is called variant.

Vasospastic angina may be accompanied by threatening arrhythmias (ventricular tachycardia, ventricular fibrillation), occasionally leading to the development of MI and even sudden death.

It has been proven that this type of angina pectoris is caused by spasm of the coronary arteries. With “typical” vasospastic angina, ischemia occurs due to a significant decrease in the diameter of the lumen of the coronary arteries and a decrease in blood flow distal to the site of spasm, but not as a result of an increase in myocardial oxygen demand.

As a rule, spasm develops locally, in one of the large coronary arteries, which may be intact or contain atherosclerotic plaques.

The reasons for the increased sensitivity of local areas of the coronary arteries to vasoconstrictor stimuli are unclear. Among the main promising areas of research are endothelial dysfunction, damage to the vascular wall during the early formation of atheroma, and hyperinsulinemia.

Among the established risk factors for vasospastic angina are cold, smoking, severe electrolyte disturbances, the use of cocaine, ergot alkaloids, autoimmune diseases.

Perhaps vasospastic angina is associated with the precursors of aspirin bronchial asthma, as well as other vasospastic disorders - Raynaud's syndrome and migraine.

Symptoms

Vasospastic angina usually occurs at a younger age than exertional angina due to coronary artery atherosclerosis. It is not uncommon for patients with vasospastic angina to fail to identify many of the typical risk factors for atherosclerosis (with the exception of smoking).

The pain attack in vasospastic angina is usually very strong, localized in a "typical" place - in the sternum. In cases where the attack is accompanied by syncope, concomitant ventricular arrhythmias should be suspected. Often such attacks occur at night and early in the morning.

Unlike unstable angina and exertional angina, the intensity of attacks of vasospastic angina does not increase over time, and exercise tolerance in patients is preserved. At the same time, it should be remembered that in some patients, vasospastic angina pectoris develops against the background of atherosclerosis of the coronary arteries, so they may have positive exercise tests with ST segment depression during or after exercise, as well as ST segment elevations during spontaneous coronary artery spasms outside physical activity. loads.

Differential diagnosis between exertional angina and vasospastic angina based on the description of a painful attack is not easy. Physical examination is most often nonspecific.

The basis of non-invasive diagnosis of vasospastic angina is the ECG changes recorded during an attack. Vasospastic angina is accompanied by marked ST segment elevations. Simultaneous inversion of the T waves and an increase in the amplitude of the R waves may be harbingers of threatening ventricular arrhythmias. Simultaneous detection of ST segment elevations in many leads (extensive ischemic zone) is an unfavorable predictor of sudden death. Along with ST-segment elevations detected against the background of pain, 24-hour ECG monitoring often reveals similar pain-free changes. Sometimes vasospastic angina is accompanied by transient disturbances of intracardiac conduction. Ventricular extrasystole usually occurs against the background of prolonged ischemia. Ventricular arrhythmias in vasospastic angina can be caused by both hypoperfusion against the background of vasospasm and subsequent reperfusion after its disappearance. Sometimes the consequence of prolonged spasm of the coronary arteries may be an increase in the activity of cardiospecific plasma enzymes. Cases of the development of transmural MI after severe spasms of the coronary arteries are described.

Stress testing of individuals with vasospastic angina is not very informative. In the course of stress tests, the following are detected in approximately equal amounts: 1) ST segment depression (against the background of concomitant coronary artery atherosclerosis), 2) ST segment elevation, 3) absence of diagnostic ECG changes.

On echocardiography during an attack of vasospastic angina pectoris, a violation of local myocardial contractility in the ischemic zone is noted.

The main diagnostic criterion for vasospastic angina is considered to be coronary artery spasm verified during CAG - spontaneous, or during a pharmacological test.

The majority of patients with vasospastic angina pectoris in coronary artery hypertension have hemodynamically significant stenosis in at least one large coronary artery. In this case, the site of spasm development is usually within 1 cm of the stenosis. Sometimes spasms develop in several parts of the coronary bed at once. Angina pectoris in such patients is associated with physical activity, while ECG changes are recorded more often in precordial leads (V1-V6).

In some individuals with CAG, completely intact coronary arteries are detected. In such cases of vasospastic angina, ST-segment elevation is noted in leads II, III, aVF and is not related to exercise in any way.

Diagnostic tests for vasospastic angina

They are used to call a typical pain attack for the patient. They are unsafe, so they are carried out in the conditions of the ward (department) of intensive observation or angiographic laboratory through a central venous or intracoronary catheter. Considering that a prolonged spasm of damaged coronary arteries can cause MI, provocative tests are usually carried out in persons with intact or slightly changed coronary arteries based on the results of a previous angiographic study.

The main tests for detecting vasospastic angina pectoris are a cold test, intracoronary administration of acetylcholine, methacholine, histamine, dopamine.

Forecast

Mortality from cardiovascular complications in vasospastic angina in the absence of angiographic signs of stenosing coronary atherosclerosis is about 0.5% per year. However, when a spasm of the coronary arteries is combined with atherosclerotic stenosis, the prognosis is worse.

2.5.4. Microvascular angina

Synonymous with this type of angina is the term "coronary syndrome X". It is characterized by a combination of 3 features:

• Typical or atypical angina pectoris;
• Identification of signs of myocardial ischemia based on the results of stress ECG tests (treadmill, VEM, PEES) and imaging studies ((in most cases - myocardial scintigraphy; or - stress echocardiography). The most sensitive method for diagnosing myocardial ischemia in these patients is the use of pharmacological tests ( with ATP / adenosine / dipyridamole / dobutamine) or VEM test in combination with single photon emission computed tomography of the myocardium with the introduction of 99mTc-MIBI (analogue of Thallium-201);
• Detection of normal or slightly changed large and medium coronary arteries in CAG, and normal function of the left ventricle in ventriculography.

The cause of microvascular angina is considered to be dysfunction of small coronary arteries with a diameter of 100-200 microns in the pre-arteriolar segment of the coronary bed. The CAG method does not allow to detect damage to arteries, the diameter of which is less than 400 microns. Dysfunction of these arteries is characterized by excessive vasoconstriction (microvascular spasm) and an inappropriate vasodilation response (decreased coronary reserve) in response to exercise. Ischemic changes on the ECG and defects in myocardial capture of the radiopharmaceutical during stress tests are identical in patients with microvascular angina (MVS) and obstructive atherosclerosis of the epicardial coronary arteries, but differ in the absence of hypokinesis zones in microvascular angina, which is due to small volumes of ischemic foci, their frequent localization in the subendocardial zone.

Microvascular angina may coexist with classic angina in patients with atherosclerotic stenosis (more than 70% of cases).

In some patients with angina pectoris syndrome with "normal" large and medium coronary arteries, myocardial hypertrophy is often detected against the background of arterial hypertension. The "hypertensive heart" syndrome is characterized by endothelial dysfunction of the coronary arteries, changes in the ultrastructure of the myocardium and the coronary bed with a simultaneous decrease in the coronary reserve.

Diagnostic tests for microvascular angina pectoris

• Exercise echocardiography with exercise or intravenous dobutamine to detect segmental disorders of myocardial contractility.

Prognosis for microvascular angina

As recent studies have shown, the long-term prognosis is unfavorable: according to long-term observations, cardiovascular events develop in 5-15% of patients.

2.6. General non-invasive diagnostics

When examining all patients with suspected CAD, as well as before changing the treatment of patients with proven CAD, the doctor conducts a general health assessment (Table 3).

Table 3. "Diagnostic measures for suspected chronic ischemic heart disease and for optimizing treatment in people with proven chronic ischemic heart disease"

2.6.1 Physical examination

In most cases, physical examination in chronic coronary artery disease is of little specificity. Signs of risk factors and symptoms of coronary heart disease complications can be identified. The symptoms of heart failure (shortness of breath, wheezing in the lungs, cardiomegaly, gallop rhythm, swelling of the jugular veins, hepatomegaly, swelling of the legs), atherosclerosis of peripheral arteries (intermittent claudication, weakening of the pulsation of the arteries and atrophy of the muscles of the lower extremities), arterial hypertension, arrhythmia, noise over the carotid arteries.

In addition, attention should be paid to overweight and external symptoms of anemia, diabetes mellitus (scratching, dryness and flabbiness of the skin, decreased skin sensitivity, skin trophic disorders). In patients with familial forms of hypercholesterolemia, a careful examination can reveal xanthomas on the hands, elbows, buttocks, knees and tendons, as well as xanthelasmas on the eyelids.

Be sure to calculate the body mass index, waist circumference, determine the heart rate, measure blood pressure (BP) on both arms. All patients should conduct palpation of the peripheral pulse, auscultation of the carotid, subclavian and femoral arteries. If intermittent claudication is suspected, the ankle-brachial systolic BP index should be calculated. In atypical angina pectoris, pain points of the parasternal region and intercostal spaces are palpated.

2.6.2. EKG at rest

Recording a 12-lead ECG at rest is mandatory for all patients.

In uncomplicated chronic coronary artery disease outside the load, specific ECG signs of myocardial ischemia are usually absent. The only specific sign of IHD on the resting ECG is large-focal cicatricial changes in the myocardium after myocardial infarction. Isolated changes in the T wave, as a rule, are not very specific and require comparison with the clinic of the disease and data from other studies.

Registration of an ECG during a pain attack in the chest is of much greater importance. If there are no ECG changes during pain, the probability of coronary artery disease in such patients is low, although it is not completely excluded. The appearance of any ECG changes during a pain attack or immediately after it significantly increases the likelihood of coronary artery disease. Ischemic ECG changes in several leads at once are an unfavorable prognostic sign.

In patients with initially altered ECG due to postinfarction cardiosclerosis during an attack, even typical angina pectoris, ECG changes may be absent, be of little specificity or false positive (decrease in amplitude and reversion of initially negative T waves). It should be remembered that against the background of intraventricular blockades, ECG registration during a pain attack is uninformative. In this case, the doctor decides on the nature of the attack and the tactics of treatment according to the accompanying clinical symptoms.

2.6.3. ECG monitoring

ECG monitoring is indicated for all patients with CIHD with suspected concomitant arrhythmias, as well as when it is impossible to perform a stress test due to concomitant diseases (diseases of the musculoskeletal system, intermittent claudication, a tendency to a pronounced increase in blood pressure during dynamic physical exertion, detraining, respiratory failure) .

Allows you to determine the incidence of pain and painless myocardial ischemia, as well as to conduct a differential diagnosis with vasospastic angina.

The sensitivity of ECG monitoring in the diagnosis of coronary artery disease is 44-81%, the specificity is 61-85%. This diagnostic method is less informative for detecting transient myocardial ischemia than exercise tests.

Prognostically unfavorable findings during daily ECG monitoring:

• Large total duration of myocardial ischemia;
• Episodes of ventricular arrhythmias during myocardial ischemia;
• Myocardial ischemia with low heart rate (<70 уд./мин).

The detection of the total duration of myocardial ischemia during ECG monitoring > 60 min per day serves as a good reason for referring the patient to CAG and subsequent myocardial revascularization, since it indicates severe damage to the coronary arteries.

2.6.4. Ultrasound examination of the carotid arteries

The study is carried out in patients with a diagnosis of coronary artery disease and a moderate risk of severe complications to assess the severity and prevalence of atherosclerosis. The detection of multiple hemodynamically significant stenoses in the carotid arteries forces us to reclassify the risk of complications as high, even with moderate clinical symptoms. In addition, ultrasound of the carotid arteries is performed in all patients with coronary artery disease who are scheduled for surgical myocardial revascularization.

2.6.5. X-ray examination in chronic ischemic heart disease

X-ray examination of the chest is performed in all patients with coronary artery disease. However, this study is most valuable in patients with postinfarction cardiosclerosis, heart defects, pericarditis and other causes of concomitant heart failure, as well as in cases of suspected aneurysm of the ascending aortic arch. In such patients, on radiographs, it is possible to assess the increase in the heart and aortic arch, the presence and severity of intrapulmonary hemodynamic disorders (venous congestion, pulmonary arterial hypertension).

2.6.6. Echocardiographic study

The study is carried out in all patients with a suspected and proven diagnosis of chronic coronary artery disease. The main purpose of echocardiography (EchoCG) at rest is the differential diagnosis of angina pectoris with non-coronary chest pain in aortic valve defects, pericarditis, ascending aortic aneurysms, hypertrophic cardiomyopathy, mitral valve prolapse and other diseases. In addition, echocardiography is the main way to detect and stratify myocardial hypertrophy and left ventricular dysfunction.

2.6.7. Laboratory research

Few laboratory studies have independent prognostic value in chronic CAD. The most important parameter is the lipid spectrum. Other laboratory tests of blood and urine reveal previously hidden concomitant diseases and syndromes (DM, heart failure, anemia, erythremia, and other blood diseases), which worsen the prognosis of coronary artery disease and require consideration in the possible referral of the patient for surgical treatment.

Lipid spectrum of blood

Dyslipoproteinemia, a violation of the ratio of the main classes of lipids in plasma, is a leading risk factor for atherosclerosis. With a very high cholesterol content, coronary artery disease develops even in young people. Hypertriglyceridemia is also a significant predictor of atherosclerosis complications.

RCHD (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical Protocols of the Ministry of Health of the Republic of Kazakhstan - 2013

Other forms of angina pectoris (I20.8)

Cardiology

general information

Short description

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

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

angina pectoris- this 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, epigastric region. The pain is provoked by physical activity, exposure to cold, heavy meals, emotional stress; resolves with rest or resolves with sublingual nitroglycerin for a few seconds to minutes.

I. INTRODUCTION

Name: IHD stable exertional angina
Protocol code:

Codes for MKB-10:
I20.8 - Other forms of angina pectoris

Abbreviations used in the protocol:
AH - arterial hypertension
AA - antianginal (therapy)
BP - blood pressure
CABG - coronary artery bypass grafting
ALT - alanine aminotransferase
AO - abdominal obesity
ACT - aspartate aminotransferase
CCB - calcium channel blockers
General practitioners - general practitioners
VPN - upper limit norm
WPW - Wolff-Parkinson-White Syndrome
HCM - hypertrophic cardiomyopathy
LVH - left ventricular hypertrophy
DBP - diastolic blood pressure
DLP - dyslipidemia
PVC - ventricular extrasystole
IHD - ischemic 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 - non-ST elevation acute coronary syndrome
ACS SPST - acute coronary syndrome with ST segment elevation
OT - waist size
SBP - systolic blood pressure
DM - diabetes mellitus
GFR - glomerular filtration rate
ABPM - ambulatory blood pressure monitoring
TG - triglycerides
TIM - thickness of the intima-media complex
TSH - glucose tolerance test
U3DG - ultrasonic dopplerography
FA - physical activity
FK - 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
EKS - pacemaker
EchoCG - echocardiography
VE - minute volume of breathing
VCO2 - the amount of carbon dioxide released per unit of time;
RER (respiratory ratio) - VCO2/VO2 ratio;
BR - respiratory reserve.
BMS - non-drug coated stent
DES - drug eluting stent

Protocol development date: year 2013.
Patient category: adult patients who are hospitalized with a diagnosis of coronary artery disease stable angina pectoris.
Protocol Users: general practitioners, cardiologists, interventional cardiologists, cardiac surgeons.

Classification

Clinical classification

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

Diagnostics

II. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

Laboratory tests:
1. OAK
2. OAM
3. Blood sugar
4. Blood creatinine
5. Total Protein
6. ALT
7. Blood electrolytes
8. Blood lipid spectrum
9. Coagulogram
10. ELISA for HIV (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. Echocardiography
3. FG/radiography of chest
4. EFGDS (as indicated)
5. ECG with exercise (VEM, treadmill test)
6. Stress echocardiography (according to indications)
7. 24-hour Holter ECG monitoring (according to indications)
8. Coronary angiography

Diagnostic criteria

Complaints and anamnesis
The main symptom of stable angina pectoris is 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, epigastric region.
The main factors that provoke chest pain: physical activity - brisk walking, climbing uphill or stairs, carrying heavy loads; increase in blood pressure; cold; plentiful food intake; emotional stress. The pain usually resolves at rest in 3-5 minutes. or within seconds to minutes of sublingual nitroglycerin tablets or spray.

table 2 - Symptom complex of angina pectoris

When taking an anamnesis, it is necessary to note the risk factors for coronary artery disease: male gender, older age, dyslipidemia, hypertension, smoking, diabetes mellitus, increased heart rate, low physical activity, overweight, 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 disease, tachycardia.
reducing the supply of oxygen
- 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 the body mass index (BMI) and waist circumference, determine the heart rate, pulse parameters, blood pressure on both arms;
- signs of lipid metabolism disorders can be detected: xanthoma, xanthelasma, marginal opacification of the cornea of ​​the eye (“senile arch”) and stenosing lesions of the main arteries (carotid, subclavian peripheral arteries of the lower extremities, etc.);
- during physical activity, sometimes at rest, during auscultation, the 3rd or 4th heart sounds can be heard, 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 an aneurysm of the heart or expansion of the boundaries of the heart due to severe hypertrophy or dilatation of the myocardium.

Instrumental Research

Electrocardiography in 12 leads is a mandatory method: the diagnosis of myocardial ischemia in stable angina pectoris. Even in patients with severe angina, resting ECG changes are often absent, which does not exclude the diagnosis of myocardial ischemia. However, the ECG may show signs of coronary heart disease, such as 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 during myocardial ischemia or signs of pericardial damage. ECG registration during stool and pain is especially indicated if vasospasm is suspected. Other changes can be detected on the ECG, such as left ventricular hypertrophy (LVH), bundle branch block, ventricular preexcitation syndrome, arrhythmias, or conduction abnormalities.

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

Recommendations for 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. Past myocardial infarction (B)
4. Left bundle branch block, Q waves, or other significant pathological changes on the ECG (C)

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

The criterion for myocardial ischemia during daily monitoring (SM) of the ECG is ST segment depression > 2 mm with a duration of at least 1 min. The duration of ischemic changes according to the SM ECG is important. If the total duration of the ST segment decrease 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 exercise: The exercise test is a more sensitive and specific method for diagnosing myocardial ischemia than resting ECG.
Recommendations for exercise testing in patients with stable angina pectoris
Class I:
1. The test should be performed in the presence of symptoms of angina pectoris and moderate / high probability of coronary heart disease (taking into account age, sex and clinical manifestations) unless the test cannot be performed due to exercise intolerance or the presence of changes in the ECG at rest (AT).
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 nature of clinical manifestations (B).

Reasons for terminating a stress test:
1. Onset of symptoms such as chest pain, fatigue, shortness of breath, or intermittent claudication.
2. The combination of symptoms (eg, pain) with marked changes in the ST segment.
3. Patient safety:
a) severe ST segment depression (> 2 mm; if the ST segment depression is 4 mm or more, then this is an absolute indication to stop the test);
b) ST segment elevation ≥2 mm;
c) the appearance of a threatening violation of the rhythm;
d) persistent decrease in systolic blood pressure by more than 10 mm Hg. Art.;
e) high arterial hypertension (systolic blood pressure over 250 mm Hg or diastolic blood pressure over 115 mm Hg).
4. Achieving the maximum heart rate may also serve as a basis for terminating the test in patients with excellent exercise tolerance who do not have 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 FC in patients with coronary artery disease with stable angina pectoris according to the results of a test with FN (Aronov D.M., Lupanov V.P. et al. 1980, 1982).

Stress echocardiography surpasses stress ECG in predictive 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 amounts proportional to the coronary fraction of cardiac output and reflects the regional distribution of perfusion. The FN test is a more physiological and preferred method for reproducing myocardial ischemia, but pharmacological tests can be used.

Recommendations for stress echocardiography and myocardial scintigraphy in patients with stable angina pectoris
Class I:
1. Resting ECG changes, left bundle branch block, ST-segment depression greater than 1 mm, pacemaker, or Wolff-Parkinson-White syndrome that prevent interpretation of exercise ECG results (B).
2. Inconclusive results of exercise ECG with acceptable exercise tolerance in a patient with a low probability of coronary heart disease, if the diagnosis is in doubt (B)
Class IIa:
1. Localization of myocardial ischemia before myocardial revascularization (percutaneous intervention on the coronary arteries or coronary artery bypass grafting) (B).
2. Alternative to exercise ECG with appropriate equipment, personnel and facilities (B).
3. An alternative to exercise ECG when there is a low likelihood of coronary heart disease, for example, in women with atypical chest pain (B).
4. Evaluation of the functional significance of moderate coronary artery stenosis detected by angiography (C).
5. Determining the localization of myocardial ischemia when choosing the method of revascularization in patients who underwent angiography (C).

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 an adequate load.

Multislice computed tomography of the heart and coronary vessels:
- is prescribed when examining men aged 45-65 years and women aged 55-75 years without established CVD in order to detect early signs of coronary atherosclerosis;
- as an initial outpatient diagnostic test in patients aged< 65 лет с атипичными болями в грудной клетке при отсутствии установленного диагноза ИБС;
- as an additional diagnostic test in patients aged< 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 genesis (cardiopathies, 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 disorders. The technique is recent and therefore less well understood than other non-invasive imaging techniques. The sensitivity and specificity of LV contractility disorders detected by MRI are 83% and 86%, respectively, and perfusion disorders are 91% and 81%. Stress perfusion MRI has a similarly high sensitivity but reduced specificity.

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

Coronary angiography (CAT)- the main method for diagnosing the state of the coronary bed. CAG allows you to choose the optimal method of treatment: medication or myocardial revascularization.
Indications for prescribing CAG to a patient with stable angina when deciding whether to perform PCI or CABG:
- severe angina pectoris III-IV FC, which persists 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 myocardial infarction and myocardial revascularization (up to 1 month);
- doubtful results of non-invasive tests in persons with socially significant professions (public transport drivers, pilots, etc.).

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

Recommendations for chest x-ray in patients with stable angina
Class I:
1. Chest X-ray is indicated in the presence of symptoms of heart failure (C).
2. Chest X-ray is justified in the presence of evidence of lung involvement (B).

Fibrogastroduodenoscopy (FGDS) (according to indications), a study on Helicobtrcter Pylori (according to indications).

Indications for expert advice
Endocrinologist- diagnosis and treatment of glycemic status disorders, treatment of obesity, etc., teaching the patient the principles of dietary nutrition, switching to treatment with short-acting insulin before planned surgical revascularization;
Neurologist- the presence of symptoms of brain damage (acute cerebrovascular accidents, transient cerebrovascular accidents, chronic forms of vascular pathology of the brain, etc.);
Optometrist- the presence of symptoms of retinopathy (according to indications);
Angiosurgeon- diagnostics 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. Complete blood count, including determination of hemoglobin and leukocyte formula (B)
4. Creatinine level (C), calculation of creatinine clearance
5. Indicators of thyroid function (as indicated) (C)

Class IIa
Oral glucose loading test (B)

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

Table 4 - Assessment of lipid spectrum indicators

List of basic and additional diagnostic measures

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

Additional Research
1. Glycemic profile
2. Chest x-ray
3. EFGDS
4. Glycated hemoglobin
5. Oral glucose challenge
6.NT-proBNP
7. Definition of hs-CRP
8. Definition of ABC
9. Definition of APTT
10. Determination of magnesium
11. Determination of total bilirubin
12. SM AD
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

The clinical picture suggests the presence of three signs:
- typical angina pectoris that occurs during exercise (less often - angina pectoris or shortness of breath at rest);
- positive result of ECG with FN 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 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. Informing and educating the patient.

2. Stop smoking.

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

4. Recommended diet: eating a wide range of foods; control over the calorie content of food, in order to avoid obesity; increased consumption of fruits and vegetables, as well as whole grains 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, as well as reduce total fat (of which less than one-third should be saturated) to less than 30% of total calories, 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 BMIs of 30 kg/m2 or more and for waist circumferences greater than 102 cm in men or greater than 88 cm in women, as weight loss may improve many obesity-related risk factors.

5. Alcohol abuse is unacceptable.

6. Treatment of concomitant diseases: in case of hypertension - achievement of the target level of blood pressure<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.

Medical treatment
Drugs that improve prognosis in patients with angina pectoris:
1. Antiplatelet drugs:
- acetylsalicylic acid (dose 75-100 mg / day - long-term).
- in patients with aspirin intolerance, clopidogrel 75 mg daily is indicated as an alternative to aspirin
- dual antiplatelet therapy with aspirin and oral ADP receptor antagonists (clopidogrel, ticagrelor) should be used 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 considered 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 ≥2 scale or the presence of a mechanical valve prosthesis), they should be used in addition to antiplatelet therapy.

2. Lipid-lowering drugs that reduce the level of LDL:
- Statins. The most studied statins for IHD are atorvastatin 10-40 mg and rosuvastatin 5-40 mg. It is necessary to increase the dose of any of the statins, observing an interval of 2-3 weeks, since during this period the optimal effect of the drug is achieved. The target level is determined by CHLP - less than 1.8 mmol / l. Monitoring indicators in the treatment of statins:
- it is necessary to initially take a blood test for lipid profile, ACT, 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 the dose, they are primarily guided by the tolerability and safety of treatment, and secondly, by achieving target lipid levels.
- with an increase in the activity of liver transaminases more than 3 ULN, it is necessary to repeat the blood test again. It is necessary to exclude other causes of hyperfermentemia: alcohol intake the day before, cholelithiasis, exacerbation of chronic hepatitis, or other primary and secondary liver diseases. The reason for the increase in CPK activity can be damage to the skeletal muscles: intense physical activity the day before, intramuscular injections, polymyositis, muscular dystrophy, trauma, surgery, myocardial damage (MI, myocarditis), hypothyroidism, CHF.
- with ACT, ALT > 3 UL, CPK > 5 UL, statins are canceled.
- Inhibitor of intestinal absorption of cholesterol - 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 appointment of ezetimibe:
- in the form of monotherapy for the treatment of patients with heterozygous form of FH who do not tolerate statins;
- in combination with statins in patients with heterozygous form of FH, if the level of LDL-C remains high (more than 2.5 mmol / l) against the background of the highest possible doses of statins (simvastatin 80 mg / day, atorvastatin 80 mg / day) or poor tolerance to high doses of statins. The fixed combination is the drug Inegy, which contains - ezetimibe 10 mg and simvastatin 20 mg in one tablet.

3. β-blockers
The positive effects of the use of this group of drugs are based on a decrease in 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 heart disease in: 1) the presence of heart failure or left ventricular dysfunction; 2) concomitant arterial hypertension; 3) supraventricular or ventricular arrhythmias; 4) myocardial infarction; 5) the presence of a clear relationship between physical activity and the development of an angina attack
The effect of these drugs in stable angina pectoris can only be expected if, when they are prescribed, a clear blockade of β-adrenergic receptors is achieved. To do this, it is necessary to maintain resting heart rate within 55-60 beats / min. In patients with more severe angina, 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 two doses.
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, with a single appointment.
Carvedilol - a starting dose of 6.25 mg (with 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 appointment of beta-blockers for coronary artery disease - severe bradycardia (heart rate less than 48-50 per minute), atrioventricular blockade of 2-3 degrees, sick sinus syndrome.

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

4. ACE inhibitors or ARA II
ACE inhibitors are prescribed to patients with coronary artery disease in the presence of signs of heart failure, arterial hypertension, diabetes mellitus and the absence of absolute contraindications to their appointment. Drugs with a proven effect on the long-term prognosis are used (ramipril 2.5-10 mg once a day, perindopril 5-10 mg once a day, fosinopril 10-20 mg per day, zofenopril 5-10 mg, etc.). In case of intolerance to ACE inhibitors, angiotensin II receptor antagonists with a proven positive effect on the long-term prognosis in 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, unlike beta-blockers, has not been proven. They are prescribed for contraindications to the appointment of b-blockers or their insufficient effectiveness in combination with them (with dihydropyridines, except for short-acting nifedipine). Another indication is vasospastic angina.
Currently, for the treatment of stable angina pectoris, mainly long-acting CCBs (amlodipine) are recommended; they are used as second-line drugs if symptoms are not relieved by b-blockers and nitrates. CCB should be preferred for concomitant: 1) obstructive pulmonary diseases; 2) sinus bradycardia and severe disorders of atrioventricular conduction; 3) variant angina (Prinzmetal).

6. Combination therapy (fixed combinations) patients with stable angina II-IV FC is carried out according to the following indications: the impossibility of selecting effective monotherapy; the need to enhance the effect of ongoing monotherapy (for example, during a period of increased physical activity of the patient); correction of adverse hemodynamic changes (for example, tachycardia caused by BCC of the dihydropyridine group or nitrates); with a combination of angina pectoris with hypertension or cardiac arrhythmias that are not compensated in cases of monotherapy; in case of intolerance to patients of conventional doses of AA drugs in monotherapy (at the same time, to achieve the necessary AA effect, small doses of drugs can be combined, other drugs are sometimes prescribed to the main AA drugs (potassium channel activators, ACE inhibitors, antiplatelet agents).
When conducting AA therapy, one should strive to almost completely eliminate anginal pain and return the patient to normal activity. However, therapeutic tactics do not give the desired effect in all patients. In some patients with exacerbation of coronary artery disease, there is sometimes an aggravation of the severity of the condition. In these cases, it is necessary to consult cardiac surgeons in order to provide the patient with cardiac surgery.

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

Nitrates and nitrate-like. With the development of an attack of angina pectoris, the patient should stop physical activity. The drug of choice is nitroglycerin (IGT and its inhaled forms) or short-acting isosorbide dinitrate taken sublingually. Prevention of angina pectoris is achieved with various forms of nitrates, including isosorbide di- or mononitrate tablets for oral administration or (less commonly) a once-daily transdermal nitroglycerin 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 a sharp cessation of taking drugs (symptoms of exacerbation of coronary artery disease).
The undesirable effect of developing tolerance can be prevented by creating 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 retarded mononitrates.

Inhibitors of If channels.
Inhibitors of If channels of the cells of the sinus node - Ivabradine, selectively slowing down the sinus rhythm, has a pronounced antianginal effect, comparable to the effect of b-blockers. It is 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 pectoris
Class I:
1. Acetylsalicylic acid 75 mg / day. in all patients in the absence of contraindications (active gastrointestinal bleeding, aspirin allergy or intolerance) (A).
2. Statins in all patients with ischemic heart disease (A).
3. ACE inhibitors in the presence of arterial hypertension, heart failure, left ventricular dysfunction, myocardial infarction with left ventricular dysfunction, or diabetes mellitus (A).
4. β-AB by mouth in patients with a history of myocardial infarction or with heart failure (A).
Class IIa:
1. ACE inhibitors 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 because of allergies (B).
3. High-dose statins for high risk (cardiovascular mortality > 2% per year) in patients with proven coronary artery disease (B).
Class IIb:
1. Fibrates for low HDL or high triglycerides in patients with diabetes mellitus or metabolic syndrome (B).

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

Essential drugs
Nitrates
- Nitroglycerin tab. 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
ACE inhibitors
- Ramipril tab. 5 mg, 10 mg
- Zofenopril 7.5 mg (preferably for CKD - ​​GFR less than 30 ml/min)
Antiplatelet agents
- Acetylsalicylic acid tab. coated 75, 100 mg
Lipid-lowering drugs
- Rosuvastatin tab. 10 mg

Additional medicines
Nitrates
- Isosorbide dinitrate tab. 20 mg
- Isosorbide dinitrate aeroz dose
Beta blockers
- Carvedilol 6.25 mg, 25 mg
calcium antagonists
- Amlodipine tab. 2.5 mg
- Diltiazem cape. 90 mg, 180 mg
- Verapamil tab. 40 mg
- Nifedipine tab. 20 mg
ACE inhibitors
- Perindopril tab. 5 mg, 10 mg
- Captopril tab. 25 mg
Angiotensin-II receptor antagonists
- Valsartan tab. 80 mg, 160 mg
- Candesartan tab. 8 mg, 16 mg
Antiplatelet agents
- Clopidogrel tab. 75 mg
Lipid-lowering drugs
- Atorvastatin tab. 40 mg
- Fenofibrate tab. 145 mg
- Tofisopam tab. 50mg
- Diazepam tab. 5mg
- Diazepam amp 2ml
- Spironolactone tab. 25 mg, 50 mg
- Ivabradin tab. 5 mg
- Trimetazidine tab. 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 single import permit (Order of the Ministry of Health of the Republic of Kazakhstan dated December 27, 2012 No. 903 “On approval of marginal prices for medicines purchased within the guaranteed volume of free medical care for 2013”).

Surgical intervention
Invasive treatment of stable angina is indicated primarily in patients with a high risk of complications, because. revascularization and medical treatment do not differ in the incidence of myocardial infarction and mortality. The efficacy of PCI (stenting) and medical therapy has been compared in several meta-analyses and a large RCT. In most meta-analyses, there was no reduction in mortality, an increase in the risk of non-fatal periprocedural MI, and a decrease in the 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 frequency of restenosis and repeated revascularization.
It is recommended to use stents that meet the following specifications:
Coronary drug eluting stent
1. Everolimus baolon-expandable drug-eluting stent on a quick-change delivery system, 143 cm long. Material 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. Length 8, 12, 15, 18, 23, 28, 33, 38 mm. Diameters 2.25, 2.5, 2.75, 3.0, 3.5, 4.0 mm. Dimensions on request.
2. The material of the stent is cobalt-chromium alloy L-605. Tank material - Fulcrum. Coated with a mixture of zotarolimus drug 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 4.0 mm diameter Dimensions: 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. The material of the stent is platinum-chromium alloy. The share of platinum in the alloy is not less than 33%. The share of nickel in the alloy - no more than 9%. The thickness of the walls of the stent 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). Stents diameter - 2.25 mm; 2.50mm; 2.75mm; 3.00mm; 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. Limiting pressure - not less than 18 atm. The balloon tip profile of the stent delivery system is no more than 0.017". The working length of the balloon catheter on which the stent is mounted is at least 144 cm. The length of the balloon tip of the delivery system is 1.75 mm. -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 stent diameter: 2.25/2.5/2.75/3.0/3.5/4.0 mm. Distal end diameter (entrance profile) - 0.017" (0.4318 mm). The working length of the catheter is 140 cm. The nominal pressure is 8 atm. Estimated burst pressure of the cylinder is 16 atm. Stent diameter 2.25 mm at 8 atmospheres: 2.0 mm. Stent diameter 2.25 mm at 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. Tank 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 balloon 0.040" (stent 3.0x18mm). The length of the working surface of the balloon beyond the edges of the stent (balloon overhang) is not more than 0.69 mm. Compliance: nominal pressure (NP) 9 atm., design burst pressure (RBP) 16 atm.
2. The material of the stent 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 4.0 mm diameter Dimensions: 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. The material of the stent is 316L stainless steel on a fast delivery system 145 cm long. The presence of M coating of the distal shaft (except for the stent). The design of the delivery system is a three-lobed balloon boat. Stent wall thickness, no more than 0.08 mm. The design of the stent is open cell. 0.038" low profile for 3.0 mm stent. 0.056"/1.42 mm id guiding catheter available. Nominal cylinder pressure 9 atm for diameter 4 mm and 10 atm for diameters from 2.0 to 3.5 mm; burst pressure 14 atm. Proximal shaft diameter - 2.0 Fr, distal - 2.7 Fr, Diameters: 2.0; 2.25; 2.5; 3.0; 3.5; 4.0 Length 8; ten; 13; fifteen; eighteen; twenty; 23; 25; 30 mm.
Compared with medical therapy, dilatation of the coronary arteries does not lead to a decrease in mortality and the risk of myocardial infarction in patients with stable angina pectoris, but increases exercise tolerance, reduces the incidence of angina pectoris and hospitalizations. 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 is continued 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, corticosteroids / NSAIDs, dyspepsia or heartburn) requires the prophylactic administration of proton pump inhibitors (for example, rabeprazole, pantoprazole, etc.).

Contraindications for myocardial revascularization.
- Borderline stenosis (50-70%) of the CA, except for the trunk of the LCA, and the absence of signs of myocardial ischemia in a non-invasive study.
- Insignificant stenosis of the coronary artery (< 50%).
- Patients with stenosis of 1 or 2 CAs without pronounced proximal narrowing of the anterior descending artery, who have mild or no symptoms of angina pectoris, and who have not received adequate medical therapy.
- High operational 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: improved prognosis and reduced symptoms. The reduction in mortality and the risk of MI has not been convincingly proven.
A consultation with a cardiac surgeon is necessary to determine the indications for surgical revascularization as part of a collegiate decision (cardiologist + cardiac surgeon + anesthesiologist + interventional cardiologist).

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

OMT = optimal drug therapy;

FFR = fractional flow reserve;
ANA = anterior descending artery;
LCA = left coronary artery;
PCB = percutaneous coronary intervention.

Recommendations for myocardial revascularization to improve prognosis in patients with stable angina
Class I:
1. Coronary artery bypass grafting in 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 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 2 coronary arteries in combination with severe 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 in severe stenosis of the coronary arteries in combination with impaired left ventricular function and the presence of a viable myocardium filed by non-invasive tests (B).
Class II a:
1. Coronary artery bypass grafting for stenosis of one or 2 coronary arteries without marked narrowing of the left anterior descending artery in patients with sudden death or persistent ventricular tachycardia (B).
2. Coronary artery bypass grafting for severe stenosis of 3 coronary arteries in diabetic patients who have signs of reversible myocardial ischemia in functional tests (C).

Preventive actions
Key lifestyle interventions include smoking cessation and tight control of blood pressure, advice on diet and weight control, and encouragement of physical activity. Although general practitioners will be responsible for the long-term management of this group of patients, these interventions are more likely to be implemented if initiated during the patient's hospital stay. In addition, the benefits and importance of lifestyle changes should be explained and offered to the patient - who is a key player - prior to discharge. However, life habits are not easy to change, and the implementation and follow-up of these changes is a long-term challenge. In this regard, close collaboration between the cardiologist and general practitioner, nurses, rehabilitation specialists, pharmacists, nutritionists, physiotherapists is critical.

To give up smoking
Patients who quit smoking reduced their mortality compared to those who continued to smoke. Smoking cessation is the most effective of all secondary prevention 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 counseling is needed during the rehabilitation period. The use of nicotine substitutes, buproprion, and antidepressants may be helpful. A smoking cessation protocol must be adopted by every hospital.

Diet and weight control
The prevention guide currently recommends:
1. rational balanced nutrition;
2. control of caloric content of foods to avoid obesity;
3. increased consumption of fruits and vegetables, as well as whole grains, fish (especially fatty varieties), lean meats 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 calories;
5. restriction of salt intake with concomitant arterial hypertension and heart failure.

Obesity is a growing problem. The current ESC guidelines define a body mass index (BMI) of less than 25 kg/m 2 as the optimal level, and recommend weight loss if a BMI is 30 kg/m 2 or more and if a waist circumference is greater than 102 cm in men or greater than 88 cm in women, as weight loss can improve many of the risk factors associated with obesity. However, weight loss alone has not been found to reduce mortality. Body mass index \u003d weight (kg): height (m 2).

Physical activity
Regular exercise brings improvement in patients with stable CAD. In patients, it can reduce feelings of anxiety associated with life-threatening illnesses and increase self-confidence. It is recommended that you do moderate-intensity aerobic exercise for thirty minutes at least five times a week. Each step of increasing peak exercise power results in a reduction in the risk of all-cause mortality in the range of 8-14%.

Blood pressure control
Pharmacotherapy (beta-blockers, ACE inhibitors or ARBs - angiotensin receptor blockers) in addition to lifestyle changes (reducing salt intake, increasing physical activity and weight loss) usually helps to 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-service capabilities;
- reduce doses of antianginal drugs;
- improve the patient's well-being and quality of life.

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

Psychological rehabilitation.
Virtually every patient with stable angina needs psychological rehabilitation. In an outpatient setting, with the presence of specialists, 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.
With intimacy in patients with stable angina pectoris, 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 FC angina pectoris (III-IV) should adequately assess their capabilities in this regard and take into account the risk of developing CVC. Patients with erectile dysfunction, after consulting a doctor, can use phosphodiesterase type 5 inhibitors: sildenafil, vardanafil, tardanafil, but taking into account contraindications: taking prolonged nitrates, low blood pressure, TFN.

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

Dispensary supervision.
All patients with stable angina pectoris, regardless of age and the presence of concomitant diseases, must be registered at the dispensary. Among them, it is advisable to single out a high-risk group: a history of myocardial infarction, periods of unstable ischemic heart disease, frequent episodes of painless myocardial ischemia, serious cardiac arrhythmias, heart failure, severe concomitant diseases: diabetes, cerebrovascular accident, etc. Dispensary observation implies systematic visits to a cardiologist ( therapist) 1 time in 6 months with mandatory instrumental methods of examination: ECG, Echo KG, stress tests, lipid profile determination, as well as Holter ECG monitoring, ABPM according to indications. An essential point is the appointment of adequate drug therapy and correction of RF.

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

Hospitalization

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

Information

Sources and literature

1. Minutes of the 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 pectoris. Russian recommendations (second revision). Cardiovascular. ter. and profilak. 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 Diseases.
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 Cardiology Department of the Research Institute of Cardiology and Internal Diseases.
4. Salikhova Z.I. - Junior Researcher, Department of Cardiology, Research Institute of Cardiology and Internal Diseases.
5. Amantayeva A.N. - Junior Researcher, Department of Cardiology, Research Institute of Cardiology and Internal Diseases.

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

Indication of no conflict of interest: missing.

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

Attached files

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This condition affects the functioning of the cardiovascular system and the body as a whole.

The essence of the disease

According to statistics, this pathology tends to develop in people after 50 years.

Unfortunately, specialists have not yet been able to develop an accurate method of therapeutic therapy that could permanently save the patient from the development of an anomaly.

A distinctive feature of the disease is that its development occurs gradually.

At the site of necrosis as a result of scarring, connective tissues are replaced by scar tissue. This reduces the functionality of the myocardium: it becomes less elastic.

In addition, there is a change in the structure of the heart valves, as well as tissues and fibers of the heart muscle are replaced by pathogenic tissue.

In patients who suffer from other diseases of the cardiovascular system, the likelihood of developing PICS is significantly increased.

The reasons

Experts identify several reasons that can provoke the occurrence of postinfarction cardiosclerosis. One of the first places among this list is occupied by the consequences of a myocardial infarction suffered by a patient.

After a patient has had an MI, the process of replacing dead tissue with scar tissue takes several months (2–4). The newly formed tissues cannot take part in the contraction of the heart and myocardium. In addition, they are not able to transmit electrical impulses.

As a result, the cavities of the heart gradually increase in volume and deform. This is the main cause of dysfunction of the heart and system.

Among the factors that provoke pathology, one can also name myocardial dystrophy, the essence of which is that the violation of the metabolic process and blood circulation in the heart muscle leads to the loss of the possibility of its contraction.

Mechanical injury to the chest, which is accompanied by a violation of the integrity of the heart or valves. But this reason is quite rare.

Postinfarction cardiosclerosis leads to disruption of the CCC. Patients who are exposed to one or more of the above factors are at risk.

Symptoms and classification

The disease has quite a variety of manifestations.

Among them are the following:

• violation of the rhythm of contraction of the heart and myocardium;
• shortness of breath, which tends to manifest itself at night or with an increase in physical activity. Such attacks last no more than 5-20 minutes. In order to remove the attack, the patient must immediately take a vertical position. Otherwise, the patient is more likely to experience pulmonary edema;
• fast fatiguability;
• cardiopalmus;
• angina;
• swelling of the hands or feet;
• swelling of the veins in the neck, as well as their strong pulsation, which can be seen visually;
• accumulation of excess fluid in the pleural cavity or heart shirt;
• stagnant processes in the liver or spleen. Perhaps their increase in size.

In modern medicine, the PICS classification is used, which is based on the size of the area of ​​damage to cardiac tissues:

1. Large focal. This type of pathology is particularly dangerous. This is due to the large area of ​​the lesion, as well as the likelihood of aneurysm formation, which can burst at any time.
2. Small focal. In this case, small white stripes form on the surface of the heart or myocardium. The reason for the development of small-focal postinfarction cardiosclerosis is that atrophy of the heart tissue or its degeneration occurs. There is a high probability of occurrence of such processes in an insufficient amount of oxygen, which enters the heart and valves with the blood.
3. diffuse. The surface of the heart muscle is covered with connective tissue, which leads to its coarsening and loss of elasticity.

The manifestation of symptoms of the disease is directly dependent on the localization of the pathology, as well as on its type.

Diagnosis

The effectiveness of the treatment process depends on the timeliness and correctness of the diagnosis. For this, the following methods are used:

1. Echocardiogram. This technique allows you to accurately determine the localization of the affected area. In addition, specialists can identify the presence of an aneurysm. You can calculate the volume and size of the cavities of the heart. Using special calculations, you can calculate the volume of regurgitation.
2. Electrocardiogram. According to its results, it is possible to accurately determine the myocardial infarction suffered by the patient, violations of the frequency of contraction of the heart and heart muscle.
3. X-ray. Allows you to identify the state in which the left ventricle of the heart is at the time of the examination (whether there is a stretch or an increase in volume). This method has a low success rate.
4. Positron emission tomography. For this examination, a special liquid is used, which is injected into the vessels of the heart. As a result of this, specialists can determine the area of ​​the lesion, as well as the degree of severity of the course of metabolic processes.

Treatment

According to the international classification, PICS refers to rather dangerous pathologies of the cardiovascular system, which can lead to the death of the patient. That is why it is extremely important to choose the most correct method of treatment.

Specialists use two main methods:

1. Medical therapy. The main direction of this method is to eliminate the signs of the manifestation of the disease. For this, drugs of the following groups are used:

• diuretics;
• aspirin;
• ACE inhibitors;
• beta blockers.

As a rule, specialists prescribe not one, but a whole complex of drugs.

1. Surgical. The operation is prescribed for patients who are in the process of aneurysm formation or in the zone of necrosis development there is a living tissue of the heart muscle. In this case, coronary artery bypass grafting is used. In parallel with shunting, the dead tissue is also removed. The operation is performed under general anesthesia, as well as with the obligatory presence of a heart-lung machine.

Regardless of the method of treatment chosen by the specialist, the patient is necessarily under his supervision. He needs to change his lifestyle and go to rehab.

It is necessary to be attentive to the manifestation of various signs indicating a violation of cardiac activity. This can help prevent the development of a serious illness or its complications.

IBS progressive angina pectoris code 10

Defects in the structure or functioning of the heart muscle of a congenital nature or the so-called congenital heart defects are considered to be certain deformations in the structure of the coronary vessels or the heart that have been present since the birth of the child.

Moreover, each congenital defect almost always disrupts (to one degree or another) the blood flow inside the heart muscle, affecting the functionality of the systemic and / or pulmonary circulation of the newborn child.

• General information
• Possible types of pathology
• Reasons for the development of defects
• Symptoms of the problem
• Diagnostics
• Treatment

It is impossible not to notice that congenital defects of the heart muscle are considered one of the most common problems among developmental defects that form at the embryonic stage.

In addition, it is congenital heart defects that are considered the most common cause of death in children under the age of 10 years, from anomalies of intrauterine development.

What is a congenital malformation of the heart muscle? What code, according to the modern classifier - ICD 10, does this pathology have? What are the signs of the development of defects in the structure of the heart muscle? How dangerous is the diagnosis - congenital heart disease in a newly born child? How are these pathologies detected and treated? These and many other questions covering congenital heart defects will be answered by our publication.

General information

First of all, I would like to recall that the ICD-10 is the currently accepted international medical classifier of existing diseases and pathological conditions of the 10th revision.

The ICD-10 pathology classifier is a globally accepted coder for the diagnoses of modern medicine, developed by specialists from the World Health Organization.

At the same time, the classifier (ICD) of the 10th revision is represented by twenty-one sections, with subsections storing information (codes) about various diseases or pathological conditions. To understand which code has a particular congenital heart disease, you should, in the specified classifier, go through the following path:

• open class XVII with congenital anomalies (malformations), including various kinds of deformities or chromosomal disorders;
• select subsection Q20-Q28, with congenital anomalies affecting the circulatory system, describing congenital malformations in the development of the heart and coronary vessels;
• also, certain congenital malformations of the heart muscle may be classified under Q90-99, which describes abnormalities of chromosomal origin not elsewhere classified.

Note that the most common congenital heart muscle defects in a child, according to the described 10th revision classifier, may have the Q24 code. (3.4, 6, 8 or 9).

The main goal of creating the classifier described above (10th revision) was to create the necessary conditions for a unified international systematized registration, analysis of the data obtained regarding the incidence and mortality of people in different regions.

The 10th revision classifier allows you to convert verbal diagnoses into an alphanumeric code that is recognizable by doctors from different countries speaking different languages.

Possible types of pathology

What are congenital malformations of the heart muscle of a child, which are coded using the international classifier of the 10th revision?

By this term, physicians define such defects in the cardiac or vascular structures that are present in a child from the moment of birth and allow the blood to fully circulate inside the organ.

Today, there are a huge number of definitions and varieties of pathologies that fall under the concept of congenital heart muscle disease. First of all, congenital heart defects in children can be defined as:

Pathologies of the white type. Not associated with mixing of arterial and venous blood flow. Such pathologies are classified into problems characterized by:

Problems associated with the fact that in the pulmonary circulation there is an excess or enrichment of blood. Such defects include: incomplete closure of the arterial duct, deformations of the cardiac septa, atrioventricular communications.

Pathological conditions of the blue type. In which there is a mixture of arterial venous blood flow, characterized by:

The occurrence of enrichment, excess blood flow in the pulmonary circulation. These are states of complete transposition of the main vascular bed, for example.

Reasons for the development of defects

The reasons for the development of certain congenital heart defects in a child can be hidden in a variety of factors of a genetic or environmental type. In some cases, there is a combination of both types of causative factors.

To genetic factors that can provoke the development of congenital heart anomalies in a child, physicians include:

• point type gene changes;
• specific mutations, chromosomal type.

The causative factors of the ecological type, often provoking the development of intrauterine cardiac pathology in a child, are usually attributed to:

• the effect of ionizing radiation on the body of a pregnant woman;
• negative impact on pregnancy of chemical irritants - paints and varnishes, phenols, pesticides, nitrates, medications, etc .;
• abuse by a pregnant woman of alcohol or tobacco;
• diseases that overtook a pregnant woman - for example, such as rubella, lupus, diabetes, syphilis, etc.

Symptoms of the problem

Symptoms of congenital heart defects in a child can be radically different, from minimal or absent manifestations of the defect, to the most serious manifestations leading to the development of emergency conditions.

The signs of such violations of the structure of the heart muscle depend on the type of defect itself, its severity, and the general condition of the small patient.

Compensated heart defects may not manifest themselves in any way, without affecting the quality of life of the patient and go unnoticed or simply fixed throughout his life.

Sometimes more severe birth defects in the structure of the heart muscle can have the following symptoms:

• the appearance of shortness of breath at rest;
• the occurrence of cyanosis;
• delays in growth or development;
• frequent fainting;
• the appearance of deviations in the indicators of the pulse.

It is impossible not to notice that in some cases the signs of pathology can be so intense that the defect leads to the development of a state of acute heart failure, acute or chronic hypoxia, even to cardiac arrest.

Diagnostics

As a rule, signs of congenital heart disease are observed in the first days of a child's life. That is why, often such a pathology in newborns is diagnosed even in the maternity hospital. When making a diagnosis, doctors always take into account the data obtained with standard laboratory and instrumental research methods.

The most informative diagnostic methods that allow making the correct diagnosis are:

• electrocardiogram;
• x-ray studies - an overview picture, angiography, ventriculography;
• echocardiography, on which it is possible to notice the morphology of defects, to determine the functional state of the organ;
• doppler echocardiography, clearly determining the direction of blood flow.

It is not possible to independently determine which variant of violations of the structure of the heart takes place!

Treatment

Initially, doctors divide the treatment of defects in the structure of the heart into surgical and medical.

Unfortunately, conservative treatment, with the appointment of certain medications, as a rule, is not effective for congenital defects in the structure of the heart, since it is not able to eliminate the causes of the pathology.

Such treatment is often used as an auxiliary or restorative.

Surgical treatment for severe decompensated malformations of the heart muscle is considered radical, the only possible one. Moreover, many doctors are convinced that the sooner an operation is performed to eliminate one or another heart defect, the more likely the patient is to fully recover and lead a full life in the future.

Clinics in which such surgical treatment of pathology can be carried out will be presented in the table below.

Unfortunately, it is extremely difficult to predict or assume how one or another defect in the development of the heart will behave. Sometimes the pathology practically does not bother the patient, does not interfere with his growth and development, does not affect the usefulness of later adult life. Sometimes, congenital malformations can quickly become complicated: heart failure, endocarditis, pneumonia, angina pectoris, anemia, etc.

It is quite clear that in cases where the defect is detected late, when the pathology progresses rapidly, and surgical treatment is impossible for some reason, the survival prognosis for such patients may be doubtful or even negative.

If heart defects are not too complex and compensated, if the pathology is detected early and the patient is successfully operated on, then the prognosis of his future life becomes as positive as possible.

In more than sixty percent of cases, after a successful heart operation, the patient gets the opportunity to live a long, fulfilling life!

• Do you often experience discomfort in the area of ​​the heart (pain, tingling, squeezing)?
• You may suddenly feel weak and tired...
• Feeling high pressure all the time...
• There is nothing to say about shortness of breath after the slightest physical exertion ...
• And you have been taking a bunch of medications for a long time, dieting and watching your weight ...

Postinfarction cardiosclerosis: causes, symptoms, diagnosis, how to treat, consequences

Postinfarction cardiosclerosis is one of the forms of chronic coronary heart disease, expressed in the formation of scar tissue in the myocardium (heart muscle) after suffering necrosis due to obstruction of the coronary arteries.

The growth of connective tissue in a limited area of ​​the myocardium leads to a violation of the contractile function in it, which inevitably affects both intracardiac and general hemodynamics. A decrease in contractility entails a decrease in the volume of blood ejected by the heart into the systemic circulation during systole, which is why the internal organs experience hypoxia and undergo changes characteristic of this state.

Postinfarction cardiosclerosis, like other forms of coronary disease, is quite common, because the number of heart attacks is constantly growing. Acquired non-communicable pathology of the heart is still the leader in the number of cases and deaths from cardiovascular pathology worldwide. Even in developed countries with a high level of medical care, the problem of chronic heart and vascular diseases remains quite relevant.

Lifestyle, a high level of stress, especially among residents of megacities, poor quality food and individual eating habits contribute to changes in the vessels of the heart and its muscles, which are very difficult to deal with even with the most modern methods of treatment.

Active preventive work is also not able to improve statistical indicators, because doctors cannot force patients to move more or give up their favorite fried foods and bad habits. In most cases, the fault for the occurrence of a heart attack and subsequent cardiosclerosis lies with the patients themselves, and the realization of this fact can come when it is necessary to move from prevention to active lifelong treatment.

Among those diagnosed with postinfarction cardiosclerosis, men predominate, and often of working age. This is not surprising, since myocardial infarction also shows a clear trend towards “rejuvenation”, affecting more and more people as they age. In women, the vessels of the heart are affected later, during menopause, due to the protective effect of sex hormones, therefore, both formed atherosclerotic and postinfarction cardiosclerosis are detected in them later - in years.

Coronary artery disease and postinfarction cardiosclerosis are classified as class I20-25 according to the international classification of diseases, including the ischemic disease itself and its specific forms. Postinfarction cardiosclerosis is coded under the heading of chronic ischemic disease - I25, as a heart attack in the past.

Cardiologists consider postinfarction cardiosclerosis an independent form of coronary heart disease (ICD code 10 - I25.2), as well as heart attack, angina pectoris, arrhythmias and other types of ischemic lesions. It takes about 6-8 weeks to form a scar, that is, already after one and a half to two months after muscle necrosis, we can talk about the presence of a formed scar.

The diagnosis in the case of a post-infarction scar sounds something like this: IHD (coronary heart disease): post-infarction cardiosclerosis. The following are the manifestations of the pathology in the form of arrhythmias, chronic heart failure (CHF), indicating the stage, severity, varieties, etc.

Causes of postinfarction cardiosclerosis

The causes of postinfarction cardiosclerosis are:

• Transferred acute heart attack on the background of atherosclerosis and subsequent scarring;
• Myocardial dystrophy;
• Necrosis due to arteriospasm.

Necrosis in the heart muscle, in turn, occurs due to organic damage to the arteries of the heart by the atherosclerotic process. In rare cases, a violation of blood flow occurs due to vasospasm or against the background of myocardial dystrophy, and then the cardiac arteries can be quite passable. Cardiosclerosis as a form of coronary heart disease occurs in connection with atherosclerosis of the arteries, in other cases it will be coded according to the ICD as another pathology.

Restoration of the myocardium after the death of muscle cells is possible only due to the newly formed connective tissue, because cardiomyocytes are not able to multiply again and make up for the defect that has appeared. The focus of sclerosis replaces necrosis after several weeks, during which the cellular composition at the site of scarring changes from neutrophils, designed to limit the area of ​​necrosis and break down cell decay products, to macrophages that absorb tissue detritus.

Hypoxia in the area of ​​the destroyed myocardium stimulates the migration of not only blood cells, but also an increase in the activity of connective tissue elements - fibroblasts that produce collagen fibers. These fibers will subsequently become the basis of a dense scar.

The formed focus of postinfarction cardiosclerosis has the appearance of a dense whitish tissue, the size and location of which are determined by the localization of the previous infarction. The consequences and depth of the disorder of the heart directly depend on the size and location of the scar. Actually, cardiosclerosis happens:

The larger the scar, the more pronounced will be the violation of hemodynamics, since the connective tissue cannot contract and does not conduct electrical impulses. It is the impossibility of conducting that becomes the cause of intracardiac blockades and pathology of the rhythm.

If necrosis occupied a significant area, and most often this occurs with transmural infarcts that “penetrate” the entire thickness of the myocardium, then they speak of large-focal postinfarction cardiosclerosis. After a small necrosis, the focus of connective tissue growth will also be small - small-focal cardiosclerosis.

Against the background of the formed scar, the heart will try to compensate for the decrease in myocardial contractility by hypertrophy of its cells, however, such compensatory hypertrophy cannot exist for a long time, because the muscle does not receive sufficient nutrition and experiences an increased load.

Sooner or later, hypertrophy will be replaced by an expansion of the chambers of the heart due to the weakening and depletion of cardiomyocytes, resulting in heart failure, which has a chronic progressive course. Structural changes will appear in other organs experiencing insufficient blood flow.

Large-focal cardiosclerosis, in which the scar replaces one of the walls of the left ventricle, is fraught with the formation of a chronic aneurysm, when there is no contraction of the corresponding part of the myocardium, but instead only dense connective tissue fluctuates. Chronic aneurysm of the heart early and fairly quickly can lead to severe organ failure.

Since heart attacks usually occur in the walls of the left ventricle, as the most involved part of the heart, the subsequent cardiosclerosis will also be there. For the same reason, hemodynamic disturbances will inevitably affect other organs supplied by the aorta and its branches, because it is the left ventricle that supplies the entire large circle with blood.

Manifestations and complications of postinfarction cardiosclerosis

Symptoms of postinfarction cardiosclerosis depend on the volume and location of the scar, but almost always it consists of:

• Increasing organ failure;
• Pathology of the conduction of nerve impulses.

If the scar is barely noticeable and arose after small-focal necrosis, then there may not be any symptoms at all, but such a phenomenon is rather an exception to the rule. In the vast majority of cases, it is impossible to avoid circulatory failure.

The most common symptoms of postinfarction cardiosclerosis are:

1. Dyspnea;
2. Increased heart rate or irregularity;
3. Rapid fatigue and weakness;
4. Edema.

As myocardial contractility decreases, shortness of breath increases, which increases in the supine position and with physical effort. Patients tend to take a semi-sitting position in order to relieve the load on the venous vascular bed and lungs.

Weakness, fatigue are characteristic, and in advanced cases of CHF, it is difficult for the patient to perform even simple household tasks, go outside, cook food, take a shower, etc. These actions provoke increased shortness of breath, possibly dizziness, aggravation of arrhythmias.

A specific sign of heart failure are bouts of dry cough and shortness of breath at night, when the patient is sleeping lying down. This phenomenon is called cardiac asthma, which occurs due to stagnation of blood in the lungs. These symptoms make you wake up and sit or stand up. Blood rushes into the veins of the lower half of the body, somewhat unloading the lungs and heart, so the patient feels relief after about a quarter of an hour or even earlier.

Cardiac asthma is especially dangerous with concomitant hypertension, since pressure loading on the left ventricle further impairs its contractility, resulting in acute left ventricular failure and pulmonary edema, a potentially fatal complication.

Pain syndrome is not considered an indispensable companion of cardiosclerosis after a heart attack, but most often patients are concerned about pain of the type of angina pectoris - behind the sternum, on the left in the chest, spreading to the left arm or under the shoulder blade. The larger the scar, the more likely the pain attack. If there is diffuse sclerosis of the myocardium, then the effects of angina pectoris are almost inevitable.

The expansion of the chambers of the heart disrupts the activity of its right half, impedes venous return, provokes stagnation in the veins, which is manifested by edema. At first, they are noticeable only at the end of the day, they are localized on the feet and legs, but the increase in CHF exacerbates them, and in case of severe heart failure, the edema no longer disappears by morning, rising up - to the arms, abdominal wall, face.

Over time, there is an accumulation of fluid in the cavities - abdominal, thoracic, pericardial. The advanced stages of the disease are characterized by cyanosis of the skin, swelling of the veins of the neck, an increase in the size of the liver, and total swelling.

Rhythm disturbances are a characteristic symptom even in small areas of sclerosis in the myocardium. An impulse traveling through the conducting system encounters an obstacle in its path in the form of scar tissue and either stops or changes its direction. This is how tachycardia, blockades, atrial fibrillation, extrasystoles occur.

Arrhythmias are manifested by a feeling of discomfort, a feeling of increased heartbeat or fading in the chest, weakness, with blockades, dizziness and fainting are not uncommon.

A great danger is atrioventricular blockade and paroxysmal tachycardia, in which the pulse can reach 200 or more beats per minute. With a complete blockade, on the contrary, severe bradycardia develops, and the heart can stop at any time.

With chronic aneurysm, the likelihood of intracardiac thrombosis increases sharply, and blood clots are able to break away and migrate into a large circle - thromboembolic syndrome. Such a complication can manifest itself as kidney failure, circulatory disorders in the brain with a stroke clinic. An aneurysm rupture will lead to acute heart failure against the background of pericardial hemotamponade and death of the patient.

Complications such as:

• Decompensated heart failure;
• thromboembolic syndrome;
• ventricular fibrillation or cardiac arrest;
• Myocardial rupture in the scar area.

Diagnostics

Diagnosis of postinfarction cardiosclerosis is based on information regarding previous diseases, the patient's lifestyle, and the presence of cardiac pathology in close relatives. If the diagnosis of a heart attack was established in a timely manner, then the cause of the growing organ failure or arrhythmia is much easier to assume, and an additional examination only confirms the guesses of the attending physician.

In some cases, cardiologists deal with a heart attack that was not diagnosed in the past, which the patient suffered, as they say, on his feet. Such patients need a comprehensive examination, including:

1. electrocardiography;
2. echocardiography;
3. chest x-ray;
4. X-ray contrast examination of the patency of the coronary vessels;
5. Tomography of the heart;
6. Biochemical analysis of blood with the study of the lipid spectrum, etc.

On examination, the doctor pays attention to the color of the skin, the severity of edema. During the examination, displacement of the borders of the heart, weakening of tones, the appearance of additional noises and changes in rhythm can be detected. X-ray will show an increase in heart size.

ECG gives only indirect signs of ischemic changes in the myocardium - hypertrophy of the left sections, blockade of the conduction pathways, extrasystoles, etc. Ischemia is usually shown by the ST segment, which shifts downward from the isoline.

If little time has passed since the formation of the scar or it is relatively small, then additional tests with a load are used - treadmill, bicycle ergometry, daily monitoring.

Ultrasound is recognized as the most informative diagnostic method, which detects aneurysms, determines the volume of the heart chambers and the thickness of their walls, reveals foci of impaired cardiomyocyte contractility and abnormal mobility of individual muscle sections.

Treatment

Treatment of postinfarction cardiosclerosis can be conservative or surgical. It is not aimed at eliminating the scar, which is completely impossible to remove either with drugs or with the surgeon's scalpel, but at preventing the progression of CHF, eliminating rhythm anomalies, and preventing recurrent necrosis.

Lifestyle, work and rest regimen are reviewed already at the stage of diagnosing an acute infarction. Bad habits must be eliminated. Patients are recommended to limit physical activity and emotional overload, diet and regular intake of medications prescribed by a cardiologist.

To reduce the load on the heart and slow down atherosclerosis, you should limit the amount of fluid and salt you drink, change your diet towards vegetables, fruits, lean meats and fish, giving up animal fat in any form, pickles, smoked foods, fried foods, semi-finished products.

In the treatment of postinfarction cardiosclerosis, the patient takes a number of drugs from different groups. Usually this:

• ACE inhibitors - enalapril, lisinopril, etc., which normalize blood pressure and blood flow in organs;
• Nitrates - long or fast action - nitroglycerin, isosorbide dinitrate, which help relieve angina attacks and improve the contractile function of the heart;
• Beta-blockers - metoprolol, bisoprolol, atenolol - eliminate tachycardia, reduce the load on the diseased heart, improve organ perfusion;
• Diuretics - furosemide, veroshpiron, aldactone - fight edema, reduce the load on the heart by removing excess fluid;
• Means for improving metabolism and increasing tissue resistance to hypoxia - inosine, ATP preparations, potassium-polarizing mixture, mildronate, thiotriazoline;
• Vitamins and trace elements (especially - group B, magnesium, potassium);
• Anticoagulants and antiplatelet agents - aspirin cardio, cardiomagnyl and other aspirin-containing drugs, warfarin.

Most drugs patients must take for life. This is especially true of antiarrhythmics, antihypertensives, acetylsalicylic acid.

Early initiation of active prevention of severe CHF can help prolong active life and work capacity, and also reduces the risk of the most dangerous complications.

In severe forms of chronic coronary artery disease, surgery may be required. It may consist in the implantation of a pacemaker or cardioverter-defibrillator, coronary artery bypass grafting, stenting, vascular plasty in case of severe occlusion of the arteries of the heart by atherosclerotic plaques. Large aneurysms can be resected.

The prognosis for postinfarction cardiosclerosis is always serious, since its complications pose a direct threat to the life of the patient. To slow down the progression of the pathology, it is important to take the prescribed drugs, avoid stressful situations, and most importantly, treat a heart attack in a timely manner, without trying to leave the clinic as soon as possible and start the usual level of duties and work.

The patient needs to take care of himself, but it is not worth refusing moderate exercise in the form of walking in the fresh air, visiting the pool, spa treatment if the attending physician considers them safe. Disability is indicated for patients with advanced chronic heart failure, which makes it difficult to work. The group is established based on the degree of disability and the results of a comprehensive examination.

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Postinfarction cardiosclerosis - what is it, causes, symptoms, treatment, causes of death, survival prognosis, microbial-10

Postinfarction cardiosclerosis is a focus consisting of connective tissue, which is formed in the area of ​​death of cardiomyocytes during a heart attack.

If the blood supply to a certain part of the heart is disturbed, this area dies off. Necrosis can have different sizes and locations.

To compensate for the lost muscle tissue, the heart is forced to produce more connective tissue fibers. Therefore, postinfarction cardiosclerosis is considered the only outcome of a heart attack, if the patient does not die.

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According to ICD-10, this pathology is coded under the code I25.1 “Atherosclerotic heart disease. Coronary (th) (arteries): atheroma, atherosclerosis, disease, sclerosis.

The reasons

The main cause of this disorder is myocardial infarction. Cardiologists detect postinfarction cardiosclerosis 2-4 months after the attack. It is this period that is required to complete the scarring process.

Replacement of the affected cells is carried out by scar-connective tissue. Depending on the location and degree of the disorder, various problems develop in the work of the heart.

Connective tissues cannot contract and transmit electrical impulses, which causes disturbances.

As a result, the heart tissue is stretched and deformed. Depending on the location of the foci, the valves of the heart are sometimes affected.

Another factor influencing the development of pathology is myocardial dystrophy. This deviation appears as a result of a violation of metabolic processes. As a result, there are problems with blood circulation, as the contractility of the heart muscle decreases.

Traumatic injury can also provoke the development of this pathology.

There are also rarer mechanisms for the appearance of pathology. However, their role is still not well understood. These include the following:

• It can penetrate into tissues and lead to disruption in the functioning of organs and systems.
• When the heart is irradiated, the structure of its cells is disrupted.
• After a certain time, this provokes an increased formation of connective tissue.
• If the dose of radiation was high, the process takes place within a few months. At a low dose, it takes years.

• This term is understood as a systemic pathology in which inflammatory granulomas form in the myocardium.
• Under the condition of treatment, they disappear, but connective tissue is formed in this place, which leads to focal cardiosclerosis.

• With this problem, a lot of iron is deposited in the tissue of the organ.
• After a certain time, this will give a toxic effect, which is accompanied by the development of inflammation and an increase in connective tissue.
• In this case, cardiosclerosis affects the entire muscle, and sometimes affects the endocardium.

• In this case, the violation develops for no apparent reason.
• Scientists suspect that hereditary predisposition plays an important role in this process.

• With this diagnosis, the growth of connective tissue begins with the capillaries.
• In this case, the heart increases in size, but there are no symptoms of inflammation.

Establishing the exact causes of the development of the disease can be quite difficult. However, it is very important for the successful treatment of the disease. Only after the elimination of the root cause will it be possible to stop the development of the pathological process.

Symptoms

With the gradual development of cardiosclerosis, the disease has no obvious symptoms. With a moderate growth of the connective tissue, the walls of the heart do not lose their elasticity, and the strength of the muscle is not weakened.

There are no symptoms even if the focus of connective tissue is on the surface and has a small area.

In other cases, disruption of the heart is accompanied by the following manifestations:

• This is one of the signs of a chronic form of heart failure, which often accompanies severe cardiosclerosis. It can appear years after the proliferation of connective tissue.
• A more rapid onset of a symptom occurs after a heart attack or myocarditis - in this case, cardiosclerosis develops more intensively.
• Shortness of breath is manifested as a violation of breathing, in which a person fails to normalize the rhythm of inhalation and exhalation. Most often, this symptom appears during physical exertion, in stressful situations or in a horizontal position.
• It is not possible to completely cope with this violation, since irreversible changes occur in the heart muscle.

• This symptom appears due to stagnation of blood in the lungs. In this case, the walls of the bronchi are filled with fluid and their thickening occurs.
• This feature provokes irritation of cough receptors.
• As a rule, with this diagnosis, the cough is dry and appears in the same situations as shortness of breath.
• With adequate treatment, it can completely disappear or become much less common.

• Problems with heart rhythm appear when the conduction system of the heart is damaged.
• The fibers, which are supposed to conduct impulses evenly, are damaged.
• Due to this feature, some areas of the heart contract later. This provokes a deterioration in blood flow.
• In addition, uneven contraction of the heart muscle provokes increased mixing of blood in the heart chamber, which increases the risk of thrombosis. As a rule, arrhythmias are characteristic of people with severe cardiosclerosis.

• This symptom is a consequence of rhythm disturbance or lack of synchrony.
• Sometimes this condition indicates frequent extrasystole.
• In such situations, a person feels a heartbeat in the neck or abdomen.

• Problems in the work of the heart lead to a decrease in the release of blood with each push. In addition, the weakening of the contractions of the heart does not make it possible to maintain normal blood pressure.
• Rapid fatigue is observed both during physical and intellectual stress.
• In the first case, there are problems with the work of muscles that suffer from a lack of oxygen. When the brain is starving, a person complains of a deterioration in concentration, memory and attention.

• The appearance of edema is considered a rather late manifestation of cardiosclerosis.
• This symptom is a consequence of stagnation in the systemic circulation.
• Most often, edema affects the lower extremities, which can swell and expand.
• At first, they appear only in the morning, but as the disease develops, they persist throughout the day.

• This symptom appears in the later stages of the development of the disease and manifests itself in the form of episodic fainting.
• Such disorders are the result of acute cerebral hypoxia, which is associated with a violation of the rhythm of the heart contraction and a sharp decrease in pressure.

Diagnostics

At an early stage in the development of the disease, diagnosing cardiosclerosis can be quite difficult. Most techniques fail to detect a small accumulation of connective tissue in the heart. In addition, patients rarely go to the doctors, because there are no symptoms of the disease.

That is why cardiosclerosis is diagnosed in the later stages, when manifestations of heart failure occur or complications develop. Targeted diagnosis is carried out exclusively in people who have suffered a heart attack or myocarditis.

To identify cardiosclerosis, perform the following studies:

• This first stage of diagnosis is carried out by a cardiologist or therapist.
• This examination does not make it possible to detect cardiosclerosis, however, it allows to identify chronic heart failure.

• Using this technique, it is possible to assess the bioelectrical activity of the heart.
• After the appearance of an impulse in the sinus node, it propagates along the fibers of the conducting system.
• With the help of an ECG, it is possible to assess the direction of its movement, which will give the doctor information regarding the functions and structure of the heart.

• This study does not reveal changes in the heart muscle.
• However, it is sometimes carried out to make a preliminary diagnosis.
• In the later stages of cardiosclerosis, a significant increase in the heart can be seen.

• These studies have approximately the same diagnostic value.
• In the images obtained during the research, it is possible to identify small areas of connective tissue.

• This method involves the introduction into the blood of special substances that help to identify a certain type of cell.
• Thus, less contrast accumulates in damaged cells.
• In healthy people, this substance is distributed evenly, while in cardiosclerosis, you can see areas in which there is no contrast.

• Cardiosclerosis does not provoke significant changes in the analysis of blood or urine.
• However, laboratory studies sometimes allow us to establish the causes of this violation.
• So, with myocarditis in the blood test, you can see the symptoms of the inflammatory process, and atherosclerosis is accompanied by an increase in cholesterol.

Treatment of postinfarction cardiosclerosis

Currently, there is no effective treatment for cardiosclerosis, since there are no drugs that can make functional cardiomyocytes from connective tissue. Therefore, the process of therapy should continue throughout life.

• elimination of the cause of the disease;
• elimination of aggravating factors;
• prevention of complications;
• improving the quality of human life;
• elimination of manifestations of heart failure and coronary artery disease.

Cardinal surgery

Cardinal method of surgical intervention is heart transplantation.

Only by complete organ replacement can symptoms be managed and oxygen supply to the organs restored.

Of course, such an operation is performed with the defeat of most of the heart after a serious heart attack. In milder cases, a heart transplant is considered an unjustified risk, so medical treatment is selected.

Today, a heart transplant is not considered an exceptionally complex procedure. It is successfully used in many countries of the world to treat severe patients with heart failure. The main indications for a heart transplant include:

Contraindications include the lack of an accurate diagnosis. If the cause of cardiosclerosis is an undetermined systemic pathology or infection, transplantation will not give stable results.

Without adequate therapy for the underlying disease, the new heart muscle will also be susceptible to cardiosclerosis.

Palliative Surgery

Such treatment is carried out to combat the signs or consequences of cardiosclerosis without eliminating the disease itself. This measure allows you to extend the life of the patient and improve its quality.

Palliative care includes the following procedures:

• It is carried out in the event that cardiosclerosis is provoked by a narrowing of the coronary vessels, which gradually progresses.
• With the help of surgical intervention, it is possible to expand their lumen and restore blood flow.
• Thanks to this, it is possible to leave the death of cardiomyocytes and prevent the subsequent progression of the growth of connective tissue.

• This is a fairly serious complication of postinfarction cardiosclerosis.
• During the operation, the protrusion is removed or its weak area is strengthened.
• Due to this, rupture of muscle tissue can be prevented.

• This term is understood as conventional pacemakers, which are implanted in complex forms of arrhythmia.
• They provide a stronger impulse, which allows you to suppress the natural bioelectric discharge of the sinus node.
• This can prevent arrhythmias and reduce the risk of sudden cardiac arrest.

Medicines

The use of drugs depends on the severity of manifestations of cardiosclerosis. The choice of medications should be carried out by the doctor after a detailed examination.

Many drugs for correcting the work of the heart have side effects and are difficult to combine with other drugs. Therefore, self-medication is a real danger to life.

To eliminate chronic heart failure, the following drugs are used:

• They affect the enzyme that affects the production of angiotensin II.
• Due to this, it is possible to reduce the load on the heart and cope with the acute symptoms of the disease.
• These products are effective in dealing with high blood pressure.
• This category includes enalapril, captopril.

• Such drugs block the hormone aldosterone, which is involved in the regulation of blood pressure and affects the functioning of the heart.
• Such drugs are often combined with the use of ACE inhibitors and beta-blockers.
• In the first weeks, fairly high doses are prescribed, which help to quickly compensate for the work of the organ.
• Then supportive therapy is carried out. As a rule, the drug spironolactone is prescribed.

• They help stabilize the heart rhythm and reduce the risk of complications that are associated with this symptom.
• In addition, they reduce the heart's need for oxygen.
• Drugs in this category are initially prescribed in small doses, after which the amount is gradually increased.
• This group includes drugs such as metoprolol, carvedilol.

• Such funds contribute to increased contractions of the heart, which affects the performance of the pumping function.
• Such drugs should be prescribed with great care so as not to provoke an overdose.
• Digoxin is usually used to relieve symptoms.

• Such funds are indicated for the appearance of edema.
• With their help, it is possible to modify the functioning of the kidneys and increase the volume of urine released.
• Due to this, the load on the heart is reduced and the symptoms of the disease disappear.
• Your doctor may prescribe drugs such as furosemide or bumetanide in the morning on an empty stomach.

As symptoms develop, a specialist may prescribe various medications to normalize a person's condition.

Antiplatelet agents, which thin the blood and prevent platelets from sticking together, may be used to prevent blood clots.

There are also many antiarrhythmic drugs that eliminate rhythm disturbances in the early stages of the disease.

Prevention

1. eat a nutritious and balanced diet; the diet should contain a lot of vitamins and minerals; it is especially important to include foods with magnesium and potassium in the menu; portions should be small, while it is recommended to eat 5-6 times a day;
2. control body weight;
3. avoid increased physical activity;
4. fully rest and sleep;
5. avoid stressful situations;
6. timely treat myocardial infarction;
7. engage in physical therapy;
8. regularly examined by a doctor;
9. practice spa treatment;
10. walk every day before going to bed, be in a ventilated room;
11. have a positive attitude towards life;
12. do preventive massages.

It is very important to exclude the use of coffee and alcoholic beverages.

Also, do not consume foods that excite the cells of the nervous and cardiovascular systems. These include cocoa and strong tea, fatty meats and fish.

From the menu you need to remove foods that lead to increased gas formation in the intestines. These include radishes, radishes, legumes, cabbage.

Do not eat offal, which provoke the deposition of cholesterol on the vessels. The diet should not contain spicy and smoked foods. In addition, stabilizers, dyes, emulsifiers are prohibited.

Forecast

The prognosis of survival in postinfarction cardiosclerosis largely depends on the location of the changes and the severity of the disease.

If the left ventricle is affected and blood flow is reduced by more than 20%, the patient's quality of life is seriously affected.

In this case, drug therapy helps maintain the patient's condition, but it will not be possible to completely get rid of the disease. If a heart transplant is not performed, survival usually does not exceed 5 years.

Possible Complications

Progressive postinfarction cardiosclerosis provokes the development of such complications:

• atrial fibrillation;
• the appearance of an aneurysm of the left ventricle, which can lead to a chronic condition;
• diverse blockades;
• increased risk of thrombosis and thromboembolic symptoms;
• sick sinus syndrome;
• paroxysmal ventricular tachycardia;
• ventricular extrasystole;
• complete atrioventricular block;
• tamponade of the pericardial cavity.

The cause of death in postinfarction cardiosclerosis may be an aneurysm rupture. Also, a fatal outcome can be a consequence of asystole or cardiogenic shock.

Ventricular fibrillation, which consists in a disparate contraction of bundles of myocardial fibers, can also provoke the death of a patient.

Postinfarction cardiosclerosis is an extremely dangerous disorder that can lead to death.

All available signs of cardiosclerosis of the heart are listed below.

Read here about the treatment of cardiosclerosis drugs.

Unfortunately, it is impossible to completely recover from this pathology, but it is quite possible to maintain the patient's condition in the normal range. To do this, you need to consult a doctor in time, who will select effective medications.

A scar on the heart is not just a figurative expression that people like to use when they are experiencing another separation from a loved one or mental suffering. Scars on the heart, indeed, take place in some patients who have had a myocardial infarction.

In medical terminology, such changes in the myocardium in the form of scars on the heart are called: cardiosclerosis. Accordingly, cicatricial post-infarction changes in the myocardium - post-infarction cardiosclerosis.

To understand how post-infarction cardiosclerosis occurs and how cicatricial post-infarction changes in the myocardium are formed, one should understand what happens during a heart attack. Myocardial infarction in its development goes through several stages.

The first stage of ischemia, when cells experience oxygen "hunger". This is the most acute stage, usually very short, passing into the second stage - the stage of necrosis. This is the stage at which irreversible changes occur - the death of the muscle tissue of the heart. Then comes the subacute stage, and after it - cicatricial. It is in the cicatricial stage that connective tissue begins to form at the site of the focus of necrosis.

Nature does not tolerate emptiness and seems to be trying to compensate for the dead muscle fibers of the heart with connective tissue. But young connective tissue does not have the functions of contractility, conductivity, excitability, which were characteristic of heart cells. Therefore, such a "replacement" is not at all equivalent. Connective tissue, growing at the site of necrosis, forms a scar.

Postinfarction cardiosclerosis develops on average 2 months after a heart attack. The size of the scar depends on the size of the damage to the heart muscle, therefore, both large-focal cardiosclerosis and small-focal cardiosclerosis are distinguished. Small-focal cardiosclerosis is more often represented by individual inclusions of connective tissue elements that have grown into the muscle tissue of the heart.

Postinfarction cardiosclerosis carries a lot of problems and complications from the work of the heart. Since scar tissue does not have the ability to contract and excite, postinfarction cardiosclerosis can lead to the development of dangerous arrhythmias, the occurrence of aneurysms, worsen the contractility and conduction of the heart, increasing the load on it. The consequence of such changes inevitably becomes heart failure. Also, life-threatening conditions include dangerous arrhythmias, the presence of aneurysms, blood clots in the heart cavities.

Symptoms of postinfarction cardiosclerosis

Postinfarction cardiosclerosis can manifest itself in different ways, depending on the prevalence of cicatricial changes and their localization. Patients will present with complaints characteristic of heart failure. With the development of left ventricular failure, patients will complain of shortness of breath with little physical exertion, or at rest, low tolerance for physical activity, dry, raw cough, often with an admixture of blood.

With insufficiency of the right sections, there may be complaints of swelling of the feet, legs, ankles, enlargement of the liver, neck veins, an increase in the size of the abdomen - ascites. For patients suffering from cicatricial changes in the heart, the following complaints are also characteristic: palpitations, impaired heartbeat, interruptions, "failures", accelerations in the work of the heart - various arrhythmias. There may be pain in the region of the heart, different in intensity and duration, general weakness, fatigue, decreased performance.

Post-infarction cardiosclerosis is established on the basis of anamnesis data (past myocardial infarction), laboratory and instrumental diagnostic methods:

1. ECG - signs of a previous heart attack: a Q or QR wave may be observed, the T wave may be negative, or smoothed, weakly positive. Various rhythm disturbances, conduction disturbances, signs of an aneurysm can also be observed on the ECG;
2. Radiography - expansion of the shadow of the heart mainly on the left (enlargement of the left chambers);
3. Echocardiography - zones of akinesia are observed - areas of non-contracting tissue, other contractility disorders, chronic aneurysm, valve defects, an increase in the size of the heart chambers can be visualized;
4. Positron emission tomography of the heart. Areas of reduced blood supply are diagnosed - myocardial hypoperfusion;
5. Coronary angiography - conflicting information: the arteries may not be changed at all, or their blockage may be observed;
6. Ventriculography - provides information about the work of the left ventricle: allows you to determine the ejection fraction and the percentage of cicatricial changes. Ejection fraction is an important indicator of the work of the heart, with a decrease in this indicator below 25%, the prognosis for life is extremely unfavorable: the quality of life of patients worsens significantly, survival without a heart transplant is no more than five years.

Scars on the heart, as a rule, remain for life, therefore, it is not the scars on the heart that need to be treated, but the complications that they cause: it is necessary to stop the further aggravation of heart failure, reduce its clinical manifestations, and correct rhythm and conduction disturbances. All therapeutic measures taken by a patient with postinfarction cardiosclerosis should have one goal - to improve the quality of life and increase its duration. Treatment can be either medical or surgical.

In the treatment of heart failure against the background of postinfarction cardiosclerosis, apply:

1. Diuretic drugs. With the development of edema, diuretics or diuretic drugs are prescribed: furosemide, hydrochlorothiazide, indapamide, spironolactone. Diuretic therapy is recommended to prescribe with low doses of thiazide-like diuretics in compensated myocardial heart failure. With persistent, pronounced edema, loop diuretics are used. With long-term treatment with diuretics, monitoring of the electrolyte balance of the blood is mandatory.
2. Nitrates. To reduce the load on the heart, expand the coronaries, nitrates are used: molsilodomine, isosorbide dinitrate, monolong. Nitrates contribute to the unloading of the pulmonary circulation.
3. ACE inhibitors. The drugs cause the expansion of arteries and veins, reduce the pre- and afterload on the heart, which improves its work. The following drugs are widely used: lisinopril, perindopril, enalapril, ramipril. Dose selection begins with a minimum, with good tolerance, you can increase the dosage. The most common side effect of this group of drugs is the appearance of a dry cough.

Drug treatment of postinfarction cardiosclerosis, or rather its manifestations: heart failure, arrhythmias, is a very complex process that requires deep knowledge and experience from the attending physician, since combinations of three or more medicines from different groups are used when prescribing treatment. The doctor needs to clearly know the mechanism of their action, indications and contraindications, individual characteristics of tolerance. And self-medication with such a serious disease is simply life-threatening!

If drug therapy is not effective, severe rhythm disturbances persist, cardiac surgeons may install a pacemaker. If frequent angina attacks persist after myocardial infarction, coronary angiography, coronary artery bypass grafting, or stenting may be performed. In the presence of a chronic aneurysm, its resection can also be performed. Indications for surgical operations are determined by the cardiac surgeon.

To improve general well-being, patients with postinfarction cardiosclerosis should follow a salt-free hypocholesterol diet, give up bad habits (alcohol, smoking), observe a work and rest schedule, and strictly follow all the recommendations of their doctor.

Stay healthy and take care of your heart!

IHD is the most common disease in the world, as they say, "the disease of the century." To date, there are no methods that can reverse the development of coronary artery disease back. A complete cure is also impossible. But with timely and systematic treatment, the development of the disease can be slowed down a little, and life expectancy can be increased - this is also possible.

What is ischemic heart disease?

IHD is an acute or chronic dysfunction of the heart. It occurs due to insufficient supply of nutrients from the coronary arteries directly to the heart muscle. The main reason is atherosclerosis, plaques form, which eventually narrow the lumen in the arteries.

The blood flow decreases, the balance between: needs and capabilities of the heart to supply him with the food he needs for life.

IHD is included in the ICD code 10. This is the International Classification of Certain Diseases 10 revision. ICD-10 includes 21 classes of diseases, among which there is coronary artery disease. IHD code: I20-I25.

Classification

Acute:

• unexpected coronary death of the patient;
• acute heart attack;
• angina pectoris (vasospastic, variant);
• angina (unstable).

Chronic:

• strenuous angina (indicates the functionality of the class and rest);
• postinfarction cardiosclerosis, disturbed heart rhythm and its conduction;
• aneurysm;
• painless ischemia.

Symptoms

Mental symptoms:

1. panic, almost animal fear;
2. inexplicable apathy;
3. causeless anxiety.

Diagnostics

Purpose of diagnosis:

1. find existing risk factors: previously undiagnosed diabetes mellitus, bad cholesterol, kidney disease, etc .;
2. according to the results of the diagnosis, the condition of the heart muscle and arteries should be assessed;
3. choose the right treatment;
4. to understand whether surgery is needed, or conservative treatment can still be carried out.

First, you need to consult a specialist cardiologist. If operation is shown then the cardiosurgeon is necessary. With elevated sugar, treatment is first carried out by an endocrinologist.

Blood tests ordered:

• general;
• blood for sugar;
• overall lipid profile;
• urea, creatine (assesses the performance of the kidneys).

Urinalysis:

• microalbuminuria (MAU) - for the presence of a protein called albumin.
• proteinuria - determines the health of the kidneys.

Other diagnostics:

• measurement of blood pressure;
• radiography;
• ECG without load;
• ECG with exercise;
• determination of the level of bad cholesterol in the blood;
• Echo KG - ultrasound of the heart;
• coronary angiography.

When diagnosing, it is necessary to take into account the forms of IHD, there are five of them:

1. Angina pectoris.
2. Vasospastic angina.
3. Myocardial infarction.
4. Postinfarction cardiosclerosis.
5. Heart failure.

The reasons

There are two reasons:

1. It is called a disease - "heat". This is when the liver overproduces cholesterol. This is called the imbalance of the regulatory system Mkhris-pa.
2. This is a disease - "cold", associated with digestion. With an abnormal slowdown in digestion and a violation of fat metabolism, an imbalance of the Bad-kan regulatory system occurs.

Excess blood cholesterol accumulates in the vascular walls in the form of atherosclerotic plaques. Gradually, the lumen in the vessels narrows, as a result of which there can be no normal blood circulation, so the blood supply to the heart worsens.

Development mechanism

• The heart is known, pumps blood, but it also desperately needs a good blood supply, which means nutrients and oxygen delivery.
• The heart muscle is nourished by blood coming from two arteries. They pass from the aortic root and go around the heart in the form of a crown. Therefore, they have such a name - coronary vessels.
• Then the arteries divide into several branches, smaller ones. Moreover, each of them should nourish only its part of the heart.

  If the lumen of even one vessel narrows a little, the muscle will begin to experience a lack of nutrition. But if it is completely clogged, then the development of many serious diseases is inevitable.

• Initially under heavy load the person will experience a slight pain behind the sternum - this is called exertional angina. But the metabolism of the muscle will worsen over time, the lumens of the arteries will narrow. Therefore, pain will now appear more often even: with a slight load, then in a horizontal position of the body.
• Together with exertional angina can form along the way chronic heart failure. It is manifested by shortness of breath, severe edema. If a sudden rupture of the plaque occurs, it will lead to the occlusion of the remaining lumen of the artery, then myocardial infarction inevitable.
  It can lead to cardiac arrest and even death, if you do not provide emergency assistance to a person. The severity of the lesion will depend only on where exactly the blockage occurred. In the artery or its branching, and which one. The larger it is, the more serious the consequences for a person.
• For the development of a heart attack The lumen should narrow by at least 70%. If this happens gradually, then the heart can still adapt to the decrease in blood volume. But a sharp blockage is very dangerous, it often leads to the death of the patient.

Risk factors

Treatment

There are many treatments for this serious disease. Proper treatment will not only improve the quality of life, but even significantly extend it.

Treatment methods:

1. conservative- life-long medication, physiotherapy exercises, healthy nutrition are indicated, bad habits are completely unacceptable now, it is desirable to lead only a healthy lifestyle.
2. surgical- restores the patency of blood vessels.

Conservative treatment

A significant role will be played by: reduction in consumption animal fats, only healthy foods should be present in the diet, leisurely walking is good.

Thus, the affected myocardium will be able to quickly adapt to the functionality of the vessels supplying the myocardium with blood.

Medical therapy- administration of antianginal drugs. They prevent or completely remove angina attacks. But often conservative treatment is not always effective, then surgical methods of correction are used.

Surgery

Treatment is selected depending on the degree of damage to the coronary vessels:

1. Coronary artery bypass grafting- take a vessel (artery, vein) from the patient and sutured to the coronary artery. Thus, they create a bypass blood supply. Blood now in sufficient volume will flow into the myocardium, eliminating ischemia and angina attacks.
2. - a tube (stent) is inserted into the affected vessel, which from now on will prevent further narrowing of the vessel. The patient after the installation of the stent will have to undergo long-term antiplatelet therapy. In the first two years, control coronary angiography is indicated.

In severe cases, they may offer transmyocardial laser myocardial revascularization. The surgeon directs the laser to the affected area, thereby creating many additional channels less than 1 ml. The channels, in turn, will promote the growth of new blood vessels. This operation is done separately, but can also be combined with aortic coronary bypass surgery.

Medicines

Medicines should be prescribed only by a doctor.

Their arsenal is quite large, and often it is required to take several drugs of different groups at once:

• nitrates- this is the well-known nitroglycerin, it not only expands the coronary arteries, but also the delivery of blood to the myocardium will improve significantly. Apply with unbearable pain, prevention of seizures;
• antiplatelet agents- for the prevention of thrombosis, dissolution of blood clots: Cardiomagnyl, Heparin, Laspirin, etc.;
• beta blockers- the need for oxygen decreases, normalizes the rhythm, is endowed with antiplatelet effects: Vero-Atenolol Metoprolol, Atenolol-Ubfi, Atenolol, etc.;
• calcium antagonists- have a wide spectrum of action: hypotensive, antianginal, improves tolerance to small physical exertion: Nifedipine, Isoptin, Verapamil, Veracard, Verapamil-LekT, etc.;
• fibrates and statins- lower blood cholesterol: Simvastatin, Lovastatin, Rosuvastatin, etc.;
• drugs that improve metabolism in the heart muscle - Inosin-Eskom, Riboxin, Inosie-F, etc.

Folk remedies

Before treatment, be sure to consult with your doctor.

Folk remedies:

Most popular recipes:

1. 1 st. l. flattened hawthorn fruits;
2. 400 ml of boiling water.

At night, put the fruits in a thermos, pour boiling water over it. Let them insist until the morning. Drink 3-4 times a day, 30 ml before meals for 1 hour. Reception 1 month, then take a break for a month and you can repeat.

1. crush the hawthorn;
2. motherwort herb.

Mix in equal proportions: take 5-6 tbsp. l. and pour 1.5 liters of boiling water, wrap and let it brew until warm. Take 0.5 cup 2-4 times a day, preferably before meals, for half an hour.

1. white mistletoe leaves - 1 tbsp. l.;
2. buckwheat flowers - 1 tbsp. l.

Pour 500 ml of boiling water and leave for 9-10 hours. Drink 2-4 tbsp. l. 3-5 times a day.

1. field horsetail - 20 gr.;
2. hawthorn flowers - 20 gr.;
3. grass of the bird mountaineer - 10 gr.

Pour 250 ml of boiling water, leave for about an hour, be sure to strain. Drink in small sips throughout the day can be taken every week.

1. corn root - 40 gr.;
2. medicinal lovage - 30 gr.

Pour boiling water (cover with water) and cook for 5-10 minutes, insist for an hour. Take 1/4 tbsp. 2-3 times a day, always after meals.

Modern methods of treatment

• Treatment methods are improving, but the principle of treatment remains the same - it is the restoration of blood flow.
  This is achieved in 2 ways: medical, surgical. Drug therapy is the basic basis of treatment, especially for chronic coronary artery disease.
• Treatment prevents the development of some serious forms of coronary artery disease: sudden death, heart attack, unstable angina. Cardiologists use various drugs: reducing "bad" cholesterol, antiarrhythmic, blood thinning, etc.
  In severe cases, surgical methods are used:
  • The most modern method of treatment- this is endovascular surgery. This is the latest trend in medicine that allows you to replace surgery with a bloodless one without incisions. They are less painful, never cause complications.
    The operation is performed without incisions., catheter and other instruments are inserted through small punctures in the skin and carried out under the control of radiation imaging techniques. Such an operation is performed on an outpatient basis, even anesthesia is not used in most cases.

Complications and consequences

Complications include:

• the formation of focal cardiosclerosis and diffuse atherosclerotic cardiosclerosis - there is a decrease in functioning cardiomyocytes. In their place, a rough connective tissue (scar) is formed;
• "Sleeping" or "stunned" myocardium - the contractility of the left ventricle is disturbed;
• diastolic, systolic function is disturbed;
• other functions are also impaired: automatism, excitability, contractility, etc.;
• inferiority - cardiomyocytes (energy metabolism of myocardial cells).

Effects:

1. According to statistics, 1/4 of deaths occur precisely because of coronary heart disease.
2. A frequently diagnosed consequence is diffuse, post-infarction cardiosclerosis. The connective tissue, growing, is replaced by a pathogenic fibrous scar with valvular deformity.
3. Myocardial hibernation is an adaptive reaction. The heart tries to adapt to the existing blood supply, adapts to the existing blood flow.
4. Angina - begins with insufficient coronary circulation.
5. Diastolic, or systolic left ventricular dysfunction - impaired contractility of the left ventricle. Or it is normal, but the ratio between: the filling of diastole and atrial systole is broken.
6. Conduction is disturbed and arrhythmia has developed - the initiating myocardial contraction does not function correctly.
7. Heart failure is preceded by: myocardial infarction.

The most dangerous types of coronary artery disease and angina pectoris, which are spontaneous in nature, they can instantly disappear and reappear. They can transform into a heart attack or simply copy.

IHD diagnosis- This is not a sentence, but a reason not to lose heart. It is necessary to act and not to miss precious time, but to choose the optimal treatment tactics. A cardiologist will help you with this. This will not only save your life, but also help you stay active for years to come. Health to all and longevity!