I21.9 Acute myocardial infarction, unspecified What is acute myocardial infarction Types of heart muscle necrosis other than AMI

About 43% of patients note the sudden development of myocardial infarction, while the majority of patients experience a period of unstable progressive angina of varying duration. Sharpest period.
Typical cases of myocardial infarction are characterized by an extremely intense pain syndrome with localization of pain in the chest and irradiation to the left shoulder, neck, teeth, ear, collarbone, lower jaw, interscapular zone. The nature of the pain can be compressive, arching, burning, pressing, sharp ("dagger"). The larger the zone of myocardial damage, the more pronounced the pain.
The pain attack proceeds in waves (sometimes intensifying, then weakening), lasts from 30 minutes to several hours, and sometimes days, is not stopped by repeated administration of nitroglycerin. The pain is associated with severe weakness, agitation, fear, shortness of breath.
Perhaps an atypical course of the most acute period of myocardial infarction.
Patients have a sharp pallor of the skin, sticky cold sweat, acrocyanosis, anxiety. Arterial pressure during an attack is increased, then moderately or sharply decreases compared to the initial one (systolic tachycardia, arrhythmia.
During this period, acute left ventricular failure (cardiac asthma, pulmonary edema) may develop. acute period.
In the acute period of myocardial infarction, the pain syndrome, as a rule, disappears. Preservation of pain is caused by a pronounced degree of ischemia of the near-infarction zone or the addition of pericarditis.
As a result of the processes of necrosis, myomalacia and perifocal inflammation, fever develops (from 3-5 to 10 or more days). The duration and height of the rise in temperature during fever depend on the area of ​​necrosis. Arterial hypotension and signs of heart failure persist and increase. Subacute period.
There are no pain sensations, the patient's condition improves, body temperature normalizes. Symptoms of acute heart failure become less pronounced. Disappears tachycardia, systolic murmur. Postinfarction period.
In the postinfarction period, there are no clinical manifestations, laboratory and physical data are practically without deviations. Atypical forms of myocardial infarction.
Sometimes there is an atypical course of myocardial infarction with localization of pain in atypical places (in the throat, fingers of the left hand, in the area of ​​the left shoulder blade or cervicothoracic spine, in the epigastrium, in the lower jaw) or painless forms, the leading symptoms of which may be cough and severe suffocation, collapse, edema, arrhythmias, dizziness and confusion.
Atypical forms of myocardial infarction are more common in elderly patients with severe signs of cardiosclerosis, circulatory failure, against the background of recurrent myocardial infarction.
However, only the most acute period usually proceeds atypically, the further development of myocardial infarction becomes typical.

It is a complication of coronary heart disease and is characterized by the development of acute insufficiency of blood supply to the myocardium with the occurrence of a focus of necrosis in the heart muscle. In addition to the typical form of the disease, there are also atypical forms. These include:

Ø Abdominal shape. It proceeds according to the type of pathology of the gastrointestinal tract with the registration of pain in the epigastric region, nausea and vomiting. Most often gastralgic (abdominal) form of myocardial infarction occurs with infarction of the posterior wall of the left ventricle.

Ø Asthmatic form: begins with cardiac asthma and provokes pulmonary edema. Pain may be absent. The asthmatic form occurs more often in older people with cardiosclerosis, with a second heart attack, or with extensive heart attacks.

Ø Brain form: in the foreground, symptoms of cerebrovascular accident by the type of stroke with loss of consciousness, occurs more often in older people with cerebral vascular sclerosis.

Ø Silent (painless) form is sometimes an accidental finding during clinical examination. Clinical symptoms manifest themselves in the form of a sudden disturbance of well-being, severe weakness, the appearance of sticky sweat; then all symptoms, except for weakness, disappear.

Ø Arrhythmic form: the main symptom is paroxysmal tachycardia, pain may be absent.

Laser therapy is aimed at increasing the effectiveness of drug therapy, reducing pain during the attack period, improving blood hemorheology and reducing its increased coagulation ability, preventing DIC, eliminating macro- and microcirculatory disorders of coronary hemodynamics in the ischemic zone, eliminating hypoxic and metabolic disorders in biological tissues, cardioprotective action by reducing the area of ​​necrosis, normalization of the autonomic regulation of the heart.

In the acute period of the disease, blood irradiation in the ILBI mode using the NIR-ILBI emitter is decisive; it is especially important to perform the procedure within the next 6 hours from the onset of the disease. The duration of the session is 15-20 minutes at a power of 3 mW. On the first day, it is allowed to perform 2 procedures with an interval of at least 4 hours.

Course treatment is 3-5 procedures.

MINISTRY OF HEALTH OF THE RUSSIAN FEDERATION

On the features of coding of some diseases of class IX ICD-10

The tenth revision of the International Statistical Classification of Diseases and Related Health Problems (hereinafter referred to as ICD-10) is a single regulatory document for the formation of a system for recording morbidity and causes of death, as well as a means to ensure the reliability and comparability of statistical data in health care.

Structure of the ICD-10

ICD-10 is built on a hierarchical principle: class, block, heading, subheading.

At the heart of the ICD-10 disease is the three-digit code, which is the required level of coding for mortality data for reporting to WHO as well as for international comparisons.

Unlike previous revisions, the ICD-10 uses an alphanumeric code instead of a numeric one, with the letter of the English alphabet as the first character and a number in the second, third and fourth characters of the code. The fourth character follows the decimal point. Code numbers range from A00.0 to Z99.9. The fourth character is not mandatory for reporting data at the international level, it is used in all medical organizations.

The three-digit ICD-10 code is called a three-digit heading, the fourth character is called a four-digit subheading. Replacing a digit with a letter in the ICD-10 code increased the number of three-digit categories from 999 to 2600, and four-digit subcategories from about 10,000 to 25,000, which expanded the classification possibilities.

ICD-10 consists of three volumes:

Volume 1- consists of two parts (in the English version - one) and contains:

- a complete list of three-digit rubrics and four-digit subcategories, including mainly statistical (nosological) formulations of diagnoses of diseases (conditions), injuries, external causes, factors affecting health, and appeals;

- coded nomenclature of neoplasm morphology;

- special lists of major diseases (conditions) for summary statistical developments of mortality and morbidity data.

Volume 2- contains basic information and rules for using the ICD-10, instructions for coding causes of death and morbidity, formats for presenting statistical data and the history of the development of the ICD.

Volume 3- is an alphabetical index of diseases, injuries and external causes, as well as a table of medicines and chemicals containing about 5.5 thousand terms.

ICD-10 is divided into 22 classes. The new XXII class was introduced in 2003. Each letter of the code corresponds to a particular class, with the exception of the letter D, which is used in classes II and III, and the letter H, which is used in classes VII and VIII. Four classes - I, II, XIX and XX use more than one letter in the first character of their codes.

Class is a grouped list of diseases that have common features. Each class contains a sufficient number of rubrics to cover all known diseases and conditions. A portion of free codes (disease-free) is intended for use in future revisions.

Classes I-XVII include diseases and pathological conditions.

Class XIX - injuries.

Class XVIII—Symptoms, signs, and abnormalities found in clinical and laboratory investigations.

Class XX - external causes of morbidity and mortality.

Unlike previous revisions, ICD-10 contains 2 new classes: Class XXI ("Factors influencing health status and visits to healthcare facilities"), designed to classify data explaining the reason for contacting a person who is not currently ill or different circumstances of receipt of medical care, as well as XXII class ("Codes for special purposes").

Classes are divided into heterogeneous blocks. representing various groupings of diseases (for example, according to the method of infection transmission, localization of neoplasms, etc.).

Blocks, in turn, consist of three-digit headings. which are a code consisting of 3 characters - a letter and 2 numbers. Some of the three-character rubrics are for only one disease. Others are for groups of diseases.

Most three-digit rubrics are further subdivided into four-digit ones. subheadings. those. have the 4th character. Subheadings have different content: these can be anatomical localizations, complications, variants of the course, forms of diseases, etc.

Four-digit sub-categories are represented by numbers from 0 to 9. A rubric may not contain all 9 digits that have different meanings. Most often, the number "8" means "other specified conditions" related to this heading, which in most cases are included in volume 3 of ICD-10, called the alphabetical index (hereinafter referred to as the Index). The sub-category with the number "9" denotes "unspecified conditions", i.e. this is the name of a three-character category without additional indications.

A number of three-character rubrics do not have four-character subcategories. This means that at the present stage of the development of medical science, these headings do not have a generally accepted division. Subheadings may be added in future updates and revisions.

The fourth sign is a kind of "quality mark", as it allows in most cases to identify diagnoses of diseases that have not been specified by a doctor. It helps to assess the quality of diagnostics, which is of great importance for solving economic issues in healthcare, improving the skills of specialists, assessing the availability of medical equipment and technology, etc.

The first volume uses various concepts, descriptions, conventions, which you should always pay attention to when coding.

it special terms, double coding and conventions .

To special terms relate:

— included terms;

— excluded terms;

- descriptions in the form of a glossary.

Double coding some states:

1. Coding system cross (┼) and asterisk (*).

Some formulations of diagnoses have two codes. The main one is the code of the main disease, marked with a cross (┼), an optional additional code related to the manifestation of the disease, marked with an asterisk (*). In official statistics, only one code is used - with a cross (┼). The asterisk (*) codes are given as separate three-character categories with four-character subcategories and are never used on their own.

2. Other types of double coding:

2.1. For local infections due to other specified pathogens, may be used additional codes B95-B97 to clarify infectious agents (for example, B97.0 - Adenoviruses).

2.2. For functionally active neoplasms from class II can be used to identify activity additional codes from class IV(e.g. E05.8, E07.0; E16-E31, E34.-).

2.3. To determine the type of tumor, the neoplasm code can be added additional morphological code(ICD-10, Volume 1, Part 2, pp. 579-599) (e.g. M8003/3 Malignant giant cell tumor).

2.4. Organic mental disorders (F00-F09) may have additional code to identify the underlying illness causing the psychiatric disorder (e.g. G30.1 Late Alzheimer's disease).

2.5. If the condition is a consequence of exposure to a toxic substance, then use additional code from class XX to identify that substance (eg Y49.4 Antipsychotics).

2.6. Used for injuries and poisoning double coding. one code from class XIX is a code for the nature of the injury, the second is a code for an external cause (class XX). In world statistics, the code of the external cause is considered the main one, and the code of the nature of the injury is considered additional. In the Russian Federation, for injuries and poisonings, both codes are used as equivalent. This methodology does not contradict world statistics and allows a detailed analysis of injuries (for example, S02.0 Fracture of the calvarium, V03.1 Pedestrian injured in a collision with a car, road accident).

Legend:

- round brackets ();

- square brackets ;

- colon (:);

— curly brackets ">";

- abbreviations ("NDU" - no further specification, "NKDR" - not classified elsewhere);

- the union "and" in the names;

— dot dash ".-".

The index contains "leading terms" located in the left column, and "modifying" (clarifying) terms located at different levels of indentation below them.

Definitions that do not affect the code are enclosed in parentheses. They may or may not be present in the formulation of the diagnosis.

Code numbers following the terms refer to the respective headings and subheadings. If the code is three-digit, then the rubric does not have a subcategory. In most cases, subheadings have a fourth character. If instead of the 4th character there is a dash, this means that the necessary subheadings can be found and specified in the full list (ICD-10, volume 1).

The conventions for the third volume include "conditions not elsewhere classified" (NCER) and cross-references.

Diagnosis coding algorithm

To assign a code to one or another formulation of the diagnosis, a special coding algorithm is used:

- In the medical record containing information about the disease or cause of death, it is necessary to determine the wording of the diagnosis to be coded.

- In the formulation of the diagnosis, it is necessary to determine the leading nosological term and search for it in the Index.

In the Index, the term is most often reflected in the form of a noun. However, it should be remembered that as leading terms in the Index there are names of some painful conditions in the form of an adjective or participle.

— Having found the leading nosological term in the Index, it is necessary to familiarize yourself with all the notes located under it and be guided by them.

— Next, read all the terms in parentheses after the leading term (these definitions do not affect the code number), as well as all the terms indented under the leading term (these definitions may affect the code number), to until all the words in the nosological formulation of the diagnosis are taken into account.

— Carefully follow any cross-references ("see" and "see also") found in the Index.

- To make sure that the code number chosen in the Index is correct, you should compare it with the headings of Volume 1 of the ICD-10 and take into account that the three-digit code in the Index with a dash in place of the fourth character means that in Volume 1 of the ICD-10 you can find the corresponding subheading with the fourth sign. Further subdivision of such headings by additional code characters is not given in the Index and, if used, should be indicated in Volume 1 of ICD-10.

- When using ICD-10 Volume 1, you must be guided by all included or excluded terms under the selected code or under the name of a class, block or heading.

— Then the formulation of the diagnosis must be assigned a code.

- It is important not to forget about the double coding of some states, or the symbol system with the signs (┼) and (*).

Ciphers with the symbol (*) are not used in official statistics and are used only for special purposes.

In hospital statistics, only the main disease is coded (complications of the main disease, background, competing and concomitant diseases are not coded). In outpatient statistics, in addition to the main disease, all other existing diseases are coded, except for complications of the main disease. In the event of death, all recorded conditions are coded, but only the initial cause of death is included in the mortality statistics, which sometimes does not coincide with the formulation of the final clinical or post-mortem (forensic) diagnosis. All other status codes are used for analysis of multiple causes of death.

Principles for coding diagnoses used in morbidity statistics by referrals

The practitioner, when preparing medical records for each case or episode of medical care, must first of all select the "main" disease (condition) for registration, as well as record concomitant diseases.

Properly completed medical documentation is necessary for the quality organization of patient care and is one of the valuable sources of epidemiological and other statistical information about morbidity and other problems associated with the provision of medical care.

Each "nosological" diagnostic formulation should be as informative as possible in order to classify the condition under the appropriate heading of the ICD-10.

If an accurate diagnosis has not been established by the end of the episode of medical care, then the information should be recorded that most allows you to get the most correct and accurate idea of ​​​​the condition for which the patient was treated or examined.

The "main" condition and the "other" (comorbid) conditions relevant to a given episode of care should be specified by the attending physician, and coding in such cases is not difficult, since the designated "main" condition should be taken for coding and data processing.

If the medical statistician or medical statistician has difficulty verifying the selection and coding of the "main" condition by the physician, i.e. there is a medical record with an apparently inconsistent or incorrectly recorded "main" condition, it should be returned to the physician for clarification of the diagnosis.

If this is not possible, the special rules set out in Volume 2 of ICD-10 apply.

"Other" conditions related to the episode of care should always be recorded in addition to the "main" condition, even in the case of a single cause morbidity analysis, as this information can assist in selecting the correct ICD-10 code for the "main" condition. .

Principles for coding causes of death

Cause of death statistics are based on the concept of "original cause of death", which was approved at the International Conference on the Sixth Revision in Paris in 1948.

The original cause of death is:

— illness or injury that triggered a chain of events leading directly to death;

— the circumstances of the accident or act of violence that caused the fatal injury.

This definition is dictated by the fact that, having built a chain of events that led to death, in some cases it is possible to influence it in order to prevent death.

In the event of death, a medical death certificate (hereinafter referred to as the Certificate) is issued by a doctor or paramedic. Filling out the Certificate is carried out according to certain rules.

Paragraph 19 of the section "Causes of death" of the Certificate must be completed on the basis of medical documentation - a "post-mortem epicrisis", in the final part of which the final diagnosis must be clearly reflected: the main clinical or pathoanatomical diagnosis with complications, background, competing and concomitant diseases.

Recording the causes of death is carried out in strict accordance with the established requirements (letter of the Ministry of Health and Social Development of Russia dated January 19, 2009 N 14-6 / 10 / 2-178):

in each subparagraph of Part I, only one cause of death is indicated, and the line of subparagraph a), lines of subparagraphs a) and b) or lines of subparagraphs a), b) and c) can be filled in. The line of subparagraph d) is filled in only if the cause of death is injury and poisoning;

Part I of paragraph 19 of the Certificate is filled in in reverse order to the main disease with complications: the wording of the main disease is entered, as a rule, on the line of subparagraph c). Then 1-2 complications are selected, of which they make up a "logical sequence" and write them down on the lines of subparagraphs a) and b). In this case, the state written in the line below must be the cause of the state written in the line above. It is allowed to select the causes of death for the Certificate in a different order, starting with the immediate cause;

in part I of paragraph 19, only one nosological unit can be recorded, unless this is stipulated by the special rules of ICD-10.

Part II of paragraph 19 includes other causes of death - these are other important diseases, conditions (background, competing and concomitant) that were not associated with the original cause of death, but contributed to the onset of death. In this case, only those conditions are selected that had an impact on this death (aggravated the underlying disease and accelerated death). This part also indicates the fact of the use of alcohol, narcotic drugs, psychotropic and other toxic substances, their content in the blood, as well as the operations performed or other medical interventions (name, date), which, in the opinion of the doctor, were related to death. The number of recorded states is not limited.

A number of diseases, such as certain cerebrovascular diseases, coronary heart disease, bronchial asthma, alcohol-related diseases, etc. often contribute to death, so if the deceased(s) had them during their lifetime, they should be included in part II of the paragraph 19 Testimonies.

It is not recommended that symptoms and conditions accompanying the mechanism of death be included on the Certificate as causes of death, such as cardiac or respiratory failure, which occur in all deceased.

Statistical developments should be made not only for the original, but also for multiple causes of death. Therefore, all recorded diseases (conditions), including section II, are coded in the Medical Certificate. If possible, the entire logical sequence of interrelated causes is indicated.

The ICD-10 underlying cause of death code is written in the "ICD-10 Code" column opposite the selected underlying cause of death and is underlined. Codes for other causes of death are written in the same column, opposite each line, without underlining.

In the column "Approximate period of time between the onset of the pathological process and death", opposite each selected cause, the period of time in minutes, hours, days, weeks, months, years is indicated. In this case, it should be taken into account that the period indicated on the line above cannot be greater than the period indicated on the line below. This information is necessary to obtain information about the average age of the dead in various diseases (conditions).

After filling in all the required lines of item 19 of the Medical Certificate of Death, it is necessary to assign a code to all recorded conditions and find the original cause of death.

If the Certificate is completed in accordance with the prescribed requirements and the logical sequence is observed, then in accordance with the "General Principle" the original cause of death will always be on the lowest completed line of Section I.

If the requirements are not met when filling out the Certificate, then the selection and modification rules set out in Volume 2 of ICD-10 should be applied.

Features of filling out medical documentation and coding diagnoses

The transition of all healthcare institutions of the Russian Federation since 1999 to the International Statistical Classification of Diseases and Related Health Problems, 10th revision, marked the adoption of new international terminology used in many countries of the world.

In this regard, in the practice of a doctor, sometimes there are difficulties in filling out medical documentation, correctly diagnosing and coding various diseases and conditions.

The main types of medical records of a polyclinic and a hospital include:

"Medical record of an outpatient" (form N 025 / y-04);

"Coupon for an outpatient" (form N 025-12 / y-04);

"Medical record of an inpatient" (form N 003 / y);

"Statistical card of the person who left the hospital" (form N 066 / y-02);

"Medical certificate of death" (form N 106 / y-08).

The main types of reporting medical documentation:

form of federal statistical observation N 12 "Information on the number of diseases registered in patients living in the service area of ​​a medical institution";

form of federal statistical observation N 14 "Information on the activities of the hospital".

In the accounting medical documentation, the diagnosis must be recorded in full, without abbreviations, corrections, in neat handwriting.

When formulating a clinical diagnosis, it should rubricate. that is, divided into sections. The following sections are generally recognized:

1. Main disease.

2. Complications of the underlying disease, which must be grouped according to severity.

3. Background and competing diseases.

4. Concomitant diseases.

The main disease (injury, poisoning) is considered to be the one that, in itself or through its complications, was the reason for seeking medical help, caused hospitalization and (or) death. If there is more than one disease, the "major" disease is considered to be the one that accounted for the largest share of the used medical resources.

The International Statistical Classification of Diseases is not a model for formulating a clinical diagnosis, but only serves to formalize it.

It is unacceptable to use the names of classes, blocks and groups of diseases as a diagnosis ("ischemic heart disease", "cerebrovascular disease", "general atherosclerosis", etc.). Only one specific nosological unit. Clinical diagnosis cannot be replaced by a list of syndromes or symptoms of the disease.

The diagnosis must be sufficient and formulated in such a way that it can be translated into an international statistical code used later to extract statistical data.

The coding of diseases is the responsibility of the attending physician. The statistician or medical statistician is responsible for quality control of coding, he must check the correctness of the coding of diagnoses by the doctor, and in case of inconsistency, correct the code; if it is impossible to fit the ICD-10 code to the recorded condition, the accounting statistical document should be returned to the attending physician for corrections to be made to it.

Filling in accounting and reporting documentation, as well as coding some diseases from class IX "Diseases of the circulatory system" can cause difficulties for doctors in their practice and have their own characteristics.

A. Outpatient organizations and divisions

1. "Outpatient card"- the main accounting document of the polyclinic, in which, for statistical accounting, the diagnosis must be correctly formulated and recorded and all conditions are coded, except for the complications of the main one.

If the patient asked for medical help, bypassing the clinic, to the hospital, then the "Outpatient Coupon" (hereinafter - the Coupon) is filled in the clinic after the patient is discharged from the hospital on the basis of the "Discharge summary". At the same time, if the patient came to the appointment, then in the Talon a mark is made on the registration of all diseases in order to include this information in the federal statistical observation form N 12 and a mark on the visit is entered. If the patient did not come to the appointment, then all diseases are recorded in the Talon without a mark on the visit.

The Talon must also record a treatment for illness, including one or more visits, as a result of which the purpose of the treatment is achieved.

A visit is a patient's contact with a doctor at an outpatient clinic (unit) or hospital (without subsequent hospitalization) for any reason, followed by an entry in the "Medical record of an outpatient", including complaints, anamnesis, objective data, diagnoses with their coding according to the ICD- 10, health group, examination and follow-up data, prescribed treatment, recommendations.

When filling out the Coupon, the doctor also makes notes on the date of the first detected underlying and concomitant diseases, taking and removing from the dispensary register. These data are required to fill out the Federal Statistical Observation Form No. 12.

1.1. Block "Acute rheumatic fever" (I00-I02).

"Acute rheumatic fever" is an acute illness lasting up to 3 months. Outcomes: recovery and transition to another disease - chronic rheumatic heart disease.

1.2. Block "Ischemic heart diseases" (I20-I25).

are acute forms of ischemic heart disease. If a myocardial infarction is diagnosed in a patient for the first time in his life, it is coded as "acute myocardial infarction" (I21), all subsequent myocardial infarctions in the same patient are coded as "repeated myocardial infarction", code I22.-, first detected.

The duration of myocardial infarctions is determined by ICD-10 and is 4 weeks or 28 days from the onset of the disease.

Myocardial infarction (acute or recurrent), defined as the underlying condition diagnosed at the end of an episode of care (outpatient or inpatient), is always recorded as an acute newly diagnosed disease (with a + sign).

Recurrent myocardial infarction of the posterior wall I22.8

Complications: cardiogenic shock

atrial fibrillation

pulmonary edema

Concomitant diseases: postinfarction cardiosclerosis

hypertensive disease with a primary lesion of the heart and heart failure.

If the patient was treated on an outpatient basis or admitted to a hospital with a diagnosis of acute or recurrent myocardial infarction, then within this episode of medical care, regardless of the duration of hospitalization, an acute or recurrent myocardial infarction is recorded.

In case of death, regardless of the duration of hospitalization, acute or recurrent myocardial infarction is also recorded.

The patient is deregistered after discharge from the hospital in connection with registration for another disease (postinfarction cardiosclerosis) or in connection with death.

1.3. Block "Cerebrovascular diseases" (I60-I69).

I60 Subarachnoid hemorrhage

I61 Intracerebral hemorrhage

I62 Other non-traumatic intracranial hemorrhage

I63 Cerebral infarction

I64 Stroke, not specified as haemorrhage or infarction

I65-I66 Blockage and stenosis of the precerebral and cerebral arteries, not leading to cerebral infarction (in cases of death, the codes for these diagnoses are replaced by the code I63.-).

There are acute forms of cerebrovascular diseases lasting up to 30 days (order of the Ministry of Health and Social Development of Russia dated 01.08.2007 N 513) - headings I60-I66, chronic forms are classified in heading I67. The consequences of cerebrovascular diseases (heading I69) are used only for registration of lethal outcomes.

Recurrent acute forms of cerebrovascular disease, defined as underlying conditions diagnosed during an episode of care (outpatient or inpatient, regardless of the length of hospitalization), are always recorded as acute newly diagnosed diseases (with a + sign).

The consequences of cerebrovascular diseases exist for a year or more from the onset of the acute form of the disease, include various conditions classified in other headings (ICD-10, vol. 1, part 1, p. 512).

In morbidity statistics, the heading of consequences (I69) should not be used, but it is necessary to indicate specific conditions that were the result of acute forms of cerebrovascular diseases, for example, encephalopathy, paralysis, etc. (ICD-10, vol. 2, pp. 115-116). However, no minimum time period has been set.

According to the rules of ICD-10, categories I65-I66 should not be used to register deaths. In mortality (mortality) statistics, codes of acute forms (headings I60-I64) and consequences of cerebrovascular diseases (heading I69) are used as the initial cause.

Approximate formulation of the final clinical diagnosis:

Cerebral infarction caused by thrombosis of the cerebral arteries I63.3

Complications: cerebral edema

right-sided hemiparesis

total aphasia

Concomitant diseases: atherosclerotic cardiosclerosis

arterial hypertension.

If the patient was treated on an outpatient basis or admitted to a hospital with a diagnosis of one of the acute forms of cerebrovascular disease, then, within this episode of medical care, regardless of its duration, an acute form of cerebrovascular disease is recorded; if the diagnosis was made later than 30 days from the onset of the disease, then registration is made according to the final clinical diagnosis - one of the chronic forms classified in heading I67, or conditions in the headings of specific neurological disorders, but not according to the consequences of cerebrovascular diseases (heading I69).

Deregistration is made after the end of the episode of medical care and in connection with registration under another nosological unit (chronic form, classified in heading I67, or conditions in the headings of specific neurological disorders) or in connection with death.

2. Form of federal statistical observation N 12- for this form, registration of diseases is carried out on a territorial basis when providing medical care in a polyclinic according to the Talon data (information for filling out the Talon after hospitalization is contained in the "Discharge summary").

2.1. Block "Acute rheumatic fever" (I00-I02).

2.1.1. Up to 3 months from the onset of the disease, "Acute rheumatic fever" is recorded in the corresponding line of tables 1000, 2000, 3000 and 4000 as a newly diagnosed disease (c +).

2.1.2. Since "Acute rheumatic fever" does not have a chronic form, it is not subject to re-registration (the data of the line in the columns "Registered in total" and "including with a diagnosis established for the first time in life" of tables 1000, 2000, 3000 and 4000 should be equal).

2.1.3. "Acute rheumatic fever" is subject to dispensary registration within 3 months (the data in the column "Consists of dispensary supervision" of tables 1000, 2000, 3000 and 4000 should be equal to approximately 25% of the number of newly diagnosed cases).

2.1.4. In case of recovery, if further observation is necessary from the doctor's point of view, then use the codes of class XXI "Factors influencing the state of health of the population and visits to health care institutions" (Z54 State of recovery; Z86.7 Personal history of circulatory system disease; Z91 B personal history of risk factors). Information is reflected in tables 1100, 2100, 3100 and 4100.

2.1.5. If the outcome of "Acute rheumatic fever" was chronic rheumatic heart disease, then the registration of chronic rheumatic heart disease is carried out according to the line of the same name, as a newly diagnosed disease (another nosological unit), and subsequently re-registered in the prescribed manner (1 time per year from -) in during the entire follow-up period. At the same time, the patient is removed from the register on the line "Acute rheumatic fever".

2.1.6. In the event of a patient's death from "acute rheumatic fever" (if the patient was observed in a polyclinic or there is relevant medical documentation), a "Medical death certificate" is issued (registration form N 106 / y-08. approved by order of the Ministry of Health and Social Development of Russia dated December 26, 2008 N 782n ).

2.2. Block "Ischemic heart diseases" (I20-I25).

Categories "Acute and repeated myocardial infarctions" (I21-I22)- in accordance with ICD-10, registration of myocardial infarction (acute or repeated) is carried out up to 28 days from the date of the disease.

2.2.1. Within an episode of medical care, if the diagnosis is established before 28 days from the onset of the disease, then an acute or recurrent myocardial infarction is recorded, regardless of the duration of hospitalization.

2.2.2. If the episode of medical care began later than 28 days from the date of onset of the disease, then postinfarction cardiosclerosis is recorded (I25.8). If within 28 days the first hospitalization ended and the second one began, then post-infarction cardiosclerosis (code I25.8) is recorded during the second hospitalization.

2.2.3. Since acute diseases are not subject to re-registration, the data of the corresponding lines in the columns "Registered in total" and "including those with a diagnosis established for the first time in life" of tables 3000 and 4000 of the reporting form N 12 should be equal.

2.2.4. Acute and repeated myocardial infarctions are subject to dispensary observation within 28 days, and therefore, in the column "Is under dispensary observation" of tables 3000 and 4000, only those myocardial infarctions that were registered during this period for form N 12, i.e., should be shown. e. in December of the reporting year.

2.2.5. In the event of death from acute or recurrent myocardial infarction, it should be remembered that not all cases of myocardial infarction are coded I21-I22:

- in case of a combination of acute or repeated myocardial infarction with a malignant neoplasm, diabetes mellitus or bronchial asthma, these diseases are considered the initial cause of death, and myocardial infarctions are their complications (ICD-10, vol. 2, p. 75), these combinations must be correctly reflected in the final post-mortem diagnosis, the time interval is maintained - no later than 28 days from the onset of a heart attack or within an episode of medical care;

- in other cases, the underlying cause of death should be considered acute or recurrent myocardial infarction (codes I21-I22) within a period of time up to 28 days or within an episode of medical care (even if the episode ended after 28 days);

- if the diagnosis of myocardial infarction was established after 28 days from its occurrence, the initial cause of death should be considered postinfarction cardiosclerosis, code I25.8 (ICD-10, vol. 1, part 1, p. 492);

- code I25.2 is not used as the initial cause of death, this condition indicates a myocardial infarction, transferred in the past and diagnosed by ECG, in the current period - asymptomatic. If there is a record in the primary medical records of a past myocardial infarction as a single condition and no diagnoses of other diseases, the initial cause of death should be considered postinfarction cardiosclerosis, code I25.8;

- codes I23 and I24.0 also do not apply as the initial cause of death, codes I21-I22 must be used (ICD-10, v.2, p.61);

- when myocardial infarction (acute or repeated) is combined with diseases characterized by high blood pressure, priority in choosing the initial cause of death is always given to myocardial infarction (ICD-10, vol. 2, pp. 59-61).

2.2.6. In the event of a patient's death from "acute or repeated myocardial infarction" (due to the initial or immediate cause of death), a "Medical death certificate" is issued (registration form N 106 / y-08. approved by order of the Ministry of Health and Social Development of Russia dated December 26, 2008 N 782n).

Heart attack is one of the leading causes of death in most developed countries. The promotion of a healthy lifestyle as a way to prevent heart disease leads to a decrease in mortality.

Risk factors

Smoking, eating fatty foods, not exercising, being overweight.
The risk of developing the disease increases with age. Before the age of 60, a heart attack often develops in men; at an older age, the number of cases in men and women evens out. Sometimes there is a family predisposition. The risk group includes people in whose family there were cases of coronary heart disease, especially if one or two family members were diagnosed with coronary artery disease or had a heart attack before the age of 55 years.

Etiology

Myocardial infarction usually develops against the background. With this disease, there is a narrowing of the coronary arteries that supply the heart with oxygenated blood. The cause of the narrowing is usually in which cholesterol settles and accumulates on the walls of the arteries. Deposits form, called atherosclerotic plaques. Irregularities and damaged places on the walls of the arteries trap platelets, the accumulation of which triggers the formation of blood clots. A thrombus can completely block the lumen of the artery, which leads to a heart attack.

Symptoms

Usually appear suddenly. Among them:

  • severe pressing and squeezing pain in the center of the chest, which spreads to the neck or left arm;
  • pallor and sweating;
  • dyspnea;
  • nausea and sometimes vomiting;
  • restlessness, which is sometimes accompanied by fear of death;
  • excitation.

If the patient has these symptoms, an ambulance should be called immediately - any delay can be fatal. Before the doctor arrives, you need to take half a tablet of aspirin, which will prevent the formation of other blood clots.

Sometimes a heart attack gives a different pattern of symptoms. If the patient suffers from seizures, then chest pain may persist during rest, not only during exertion. When angina attacks do not go away after taking medication or last more than 10 minutes, a heart attack is possible, and the patient needs urgent medical care in a hospital setting.

In about 1 in 5 cases, the disease does not cause chest pain. Only other symptoms are present: shortness of breath, loss of consciousness, pallor and sweating. These are, perhaps, signs of the so-called. "silent" heart attack. It is more characteristic of diabetics or hypertensive patients, as well as the elderly.

Complications

In the first few hours and days, the biggest danger in a heart attack is the development of life-threatening arrhythmia and cardiac arrest. Depending on the severity and location of damage to the heart muscle, other disorders may develop. For example, in the weeks and months following a heart attack, the heart muscle will be so weak that heart failure will set in. Its symptoms are weakness, shortness of breath and swelling of the legs. A more rare complication is damage to one of the heart valves or inflammation of the inner lining of the heart (endocardium), both conditions also lead to the development of heart failure.

Diagnostics

In most cases, the diagnosis is obvious. An ECG (recording of the electrical activity of the heart) often shows changes that confirm myocardial infarction. An ECG is necessary to assess the location and extent of damage to the heart muscle, as well as to predict possible heart rhythm disturbances. To confirm the diagnosis, blood tests are carried out, with the help of which the content of special substances that enter the blood from the damaged heart muscle is determined.

The main goal of treatment is to relieve pain, restore normal blood supply to the heart, minimize damage, and prevent subsequent complications. This can be achieved in the intensive care unit, where continuous monitoring of heart rate and vital signs is possible. For very severe chest pain, injections of a strong analgesic are indicated.

In some cases, urgent coronary angioplasty is needed to clear the blockage. During this procedure, a stent is placed inside the clogged artery, and drugs are injected intravenously to improve blood flow and prevent blood from clotting.

During the stay in the intensive care unit, the work of the heart is constantly monitored and treated for arrhythmias and / or heart failure. With a favorable post-infarction period, the patient may be allowed to get out of bed after about 24-48 hours. Soon after, a rehabilitation program will begin, during which it is recommended to spend more time on your feet.

Post-rehabilitation activities

At the end of rehabilitation measures for a heart attack, the condition of the coronary arteries and heart muscle is assessed. To determine the strategy for further treatment, exercise electrocardiography and echocardiography are performed. For example, with a decrease in the strength of contractions of the heart, the patient will be prescribed and / or. With complete blockage of the coronary artery, coronary bypass surgery is performed. If studies have shown a persistent heart rhythm disorder, then implantation of an artificial pacemaker is possible.

A number of drugs are prescribed for a long time to reduce the risk of developing a second heart attack. Usually prescribed, and / or aspirin. In addition, you should follow a low-fat diet and take to lower cholesterol levels. These drugs will be of great benefit after a heart attack, even with normal cholesterol levels.

After a heart attack, anxiety about one's own health very often arises, so cases of mild depression are possible. Most heart centers provide outpatient rehabilitation programs that help people gain self-confidence.

If the patient had the first heart attack, and the correct and timely treatment was carried out and there were no complications, then the prognosis will be favorable. After 2 weeks, the risk of developing a second heart attack is greatly reduced, and the patient has a good chance of living another 10 years or more. The prognosis will only improve if the patient quits smoking, reduces alcohol consumption, exercises regularly and switches to a healthy diet.

If the heart attack is not the first, then the prognosis depends on the extent of damage to the heart muscle and the complications that have developed. But in most cases, after surgery or angioplasty, most patients live another 10 years or more.

Lifestyle changes help speed recovery from a heart attack and reduce the risk of another heart attack.

After recovery, the patient will gradually be able to return to normal life: perhaps after 6 weeks or earlier to return to work (initially on a part-time basis); after about 6 weeks the patient will be able to drive a car.

Precautionary measures

  • you need to quit smoking. This is the main measure of prevention of recurrent heart attack;
  • switch to a healthy diet and maintain a normal weight;
  • drastically reduce alcohol consumption;
  • work with the doctor to develop a program of physical activity that the patient can withstand (for example, swimming for 30 minutes or more);
  • avoid stressful situations.

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

Acute transmural myocardial infarction, unspecified (I21.3)

Cardiology

general information

Short description

Protocol approved
Expert Commission on Health Development
June 28, 2013


Term "acute myocardial infarction"(acute myocardial infarction) (MI/AMI) should be used when there is clinical evidence of myocardial necrosis due to myocardial ischemia. Under these conditions, in any of the following cases, a diagnosis of myocardial infarction is made.
Detection of an increase and/or decrease in the level(s) of cardiac biomarkers (preferably troponin), provided that at least one value is above the 99th percentile of the upper reference limit, and this increase in the biomarker level is associated with at least one of the following signs:
- symptoms of ischemia;
- new or likely new significant changes in the ST segment and the T wave or the appearance of a left bundle branch block;
- the appearance of pathological Q waves on the ECG;
- detection of new foci of non-viable myocardium or new foci of wall motion disorders with various methods of myocardial imaging;
- detection of an intracoronary thrombus during coronary angiography or autopsy.

Cardiac death with symptoms suggestive of myocardial ischemia and possibly new ischemic ECG changes or new left bundle branch block (LBBB) in conditions where death occurred before blood tests were taken or before levels of biomarkers of myocardial necrosis may have increased.

Myocardial infarction associated with percutaneous coronary intervention is by convention defined as an increase in cardiac troponin levels greater than 5 times the level of the 99th percentile upper relative limit, or a troponin level increase of more than 20% if there was an increase in baseline level at its stable value or decrease in dynamics. In addition to changes in troponin levels, one of the following signs should be observed:
- symptoms of myocardial ischemia;
- new signs of ischemia on the ECG or new LBBB;
- angiographically proven violation of the patency of the main coronary vessels or branches;
- pronounced slowing of blood flow or embolism;
- detection of new foci of non-viable myocardium or new foci of wall motion disorders with various methods of myocardial imaging.

Myocardial infarction associated with stent thrombosis on angiography or autopsy, with evidence of ischemia and an increase and/or decrease in cardiac biomarkers such that at least one value is above the 99th percentile of the upper reference limit, but death occurred before how the cardiac biomarkers were released into the blood or before the cardiac biomarkers increased.

Myocardial infarction associated with coronary artery bypass grafting is by convention defined as an increase in cardiac troponin levels greater than 10 times the level of the 99th percentile upper relative limit in patients with initially normal troponin levels (≤99th percentile).
In addition to elevated troponins, one of the following should be observed:
- new pathological Q wave or new blockade of LBH;
- angiographically documented occlusion of the shunt or new artery;
- detection of new foci of non-viable myocardium or new foci of wall motion disorders with various methods of myocardial imaging.

I. INTRODUCTION

Protocol name: Clinical protocol for the diagnosis and treatment of ST-segment elevation myocardial infarction, with Q wave (transmural)
Protocol code:

ICD-10 code(s):
I 21 - Acute myocardial infarction
I 21.0 - Acute transmural infarction of the anterior wall of the myocardium
I 21.1 - Acute transmural infarction of the lower wall of the myocardium
I 21.2 - Acute transmural myocardial infarction of other specified localizations
I 21.3 - Acute transmural myocardial infarction of unspecified localization
I 22 - Recurrent myocardial infarction
I 22.0 - Repeated infarction of the anterior wall of the myocardium
I 22.1 - Repeated infarction of the lower wall of the myocardium
I 22.8 - Repeated myocardial infarction of another specified localization

Abbreviations used in the protocol:
AH - arterial hypertension
BP - blood pressure
CABG - coronary artery bypass grafting
ALT - alanine aminotransferase
AO - abdominal obesity
BAC - biochemical blood test
CCB - calcium channel blockers
LBBB - left bundle branch block
HCM - hypertrophic cardiomyopathy
LVH - left ventricular hypertrophy
DLP - dyslipidemia
ESC - European Society of Cardiology
PVC - ventricular extrasystole
IHD - ischemic heart disease
BMI - body mass index
CAG - coronary angiography
CA - coefficient of thetherogenicity
CPK - creatine phosphokinase
MS - metabolic syndrome
THC - total cholesterol
OKCbnST - Non-ST Elevation Acute Coronary Syndrome
OKCspST - 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
TSH - thyroid stimulating hormone
UZDG - ultrasonic dopplerography
FK - functional class
TFN - exercise tolerance
RF - risk factors
COPD - chronic obstructive pulmonary disease
CHF - chronic heart failure
HDL-C - high-density lipoprotein cholesterol
HSLNP - low-density lipoprotein cholesterol
PKB - percutaneous coronary intervention
HR - heart rate
ECG - electrocardiography
EchoCG - echocardiography

Protocol development date: year 2013.
Patient category: patients with suspected ST-segment elevation ACS.
Protocol Users: emergency doctors, resuscitators, therapists, cardiologists, interventional cardiologists, cardiac surgeons.

Classification


Clinical classification

Table 1 - Classification of types of myocardial infarction (ECS/ACCF/AHA/WHR 2007)

Types Characteristic
1 type Spontaneous myocardial infarction associated with rupture, ulceration, damage, erosion or dissection of an atherosclerotic plaque with the development of thrombosis of one or more coronary arteries, which leads to a deterioration in myocardial blood supply or to embolism of the distal bed, followed by necrosis of cardiomyocytes.
type 2 Myocardial injury with necrosis, in conditions other than coronary heart disease, leading to an imbalance between myocardial oxygen demand and delivery, for example, due to endothelial dysfunction of the coronary vessels, coronary vasospasm, coronary embolism, tachy-brady arrhythmia, anemia, respiratory failure, hypotension, hypertension with or without LV hypertrophy.
3 type Cardiac death with evidence of possible myocardial ischemia and suspected new ECG evidence of ischemia or new LBBB, in circumstances where death occurred before blood samples were taken or before myocardial necrosis biomarker levels could rise, or in rare cases, when biomarkers were not identified.
4a type Myocardial infarction associated with percutaneous coronary intervention is by convention defined as an increase in cardiac troponin levels greater than 5 times the level of the 99th percentile upper relative limit, or a troponin level increase of more than 20% if there was an increase in baseline level at its stable value or decrease in dynamics. In addition to the dynamics of the level of troponins, one of the following signs should be observed: 1) symptoms of myocardial ischemia, 2) new signs of ischemia on the ECG or new blockade of LBH 3) angiographically proven violation of the patency of the main coronary vessels or branches 4) a pronounced slowing of blood flow or embolism 5) detection of new foci of non-viable myocardium or new foci of wall motion disorder in various myocardial imaging methods.
4b type Myocardial infarction associated with stent thrombosis on angiography or autopsy, with evidence of ischemia and an increase and/or decrease in cardiac biomarkers such that at least one value is above the 99th percentile of the upper reference limit
5 type Myocardial infarction associated with coronary artery bypass grafting is defined by agreement when the level of cardiac troponins increases more than 10 times the level of the 99th percentile of the upper relative limit in patients with initially normal troponin levels (≤99th percentile) In addition to an increase in the level of troponins one of the following must be observed: 1) new pathological Q wave or new LBBB, 2) angiographically documented graft or new artery occlusion, 3) detection of new foci of nonviable myocardium or new foci of wall motion disorder on various myocardial imaging modalities


Table 2 - Classification of acute heart failure according to Killip (Killip T, Kimballe J, 1967)


Diagnostics


II. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

List of basic and additional diagnostic measures

Main researches:
1. Complete blood count
2. Determination of glucose
3. Determination of creatinine
4. Determination of creatinine clearance
5. Determination of troponin
6. Definition of ALT
7. Definition of CRP
8. Definition of ABC
9. Definition of APTT
10. Definition of PTI
11. Determination of fibrinogen
12. Determination of total cholesterol
13. Definition of LDL
14. Definition of HDL
15. Determination of triglycerides
16. Determination of potassium/sodium
17. Urinalysis
18. HIV testing
19. Determination of markers of viral hepatitis B and C
20. Determination of blood group and Rh factor
21. Microreaction
22. Feces on worm eggs
23. ECG
24. 12-lead ECG monitoring
25. ECHOCG
26. Coronary angiography
27. Chest x-ray

Additional research:
1. Glycemic profile
2. Glycated hemoglobin
3. Oral glucose loading test
4.NT-proBNP
5. D-dimer
6. Definition of MV-CPK
7. Definition of MHO
8. Determination of magnesium
9. Determination of the acid-base state
10. Determination of myoglobin
11. Determination of alpha-amylase
12. Definition of ACT
13. Determination of alkaline phosphatase
14. Determination of platelet aggregation
15. ECG exercise test (VEM/treadmill)
16. Stress echocardiography with dobutamine
17. Myocardial perfusion scintigraphy/SPECT
18. CT, MRI, PET

Diagnostic criteria

Complaints and anamnesis:
The diagnosis of myocardial infarction is usually based on the presence of chest pain/discomfort lasting 20 minutes or more, not relieved by nitroglycerin, characterized by pain radiating to the neck, lower jaw, and left arm. Some patients may have less typical symptoms such as nausea, vomiting, shortness of breath, weakness, palpitations, or loss of consciousness. In the diagnosis, information about the presence of coronary heart disease in history is important.

Physical examination
Evaluation of patients with chest pain includes examination of the chest, auscultation, and measurement of heart rate and blood pressure. There are no individual physical signs of ST elevation MI, but many patients have signs of sympathetic nervous system activation (pallor, severe sweating) and either arterial hypotension or low pulse pressure, pulse wave irregularity, bradycardia, tachycardia, III tone can also be observed. heart and rales in the lower parts of the lungs. An important goal of the examination is to exclude CVD of a non-ischemic nature (pulmonary embolism, aortic dissection, pericarditis, heart disease) and possible non-cardiac diseases (pneumothorax, pneumonia, pleural effusion).

Instrumental Research
Mandatory instrumental studies in ACS are ECG (within 10 minutes after the initial medical contact - PMK), echocardiography (ECHOCG) - can help in the diagnosis in unclear cases, but should not delay angiography.

Diagnostic ECG criteria:
- ST segment elevation, measured at point J, in two adjacent leads in leads V2-V3;
- ≥0.25 mV in men under 40;
- ≥0.2 mV in men over 40;
- ≥0.15 mV in women in other leads;
- ≥0D mV (in the absence of left ventricular hypertrophy (LV) or left bundle branch block (LBBB));
- with lower myocardial infarction, ST elevation in the right chest leads (V3R-V4R) is a sign of right ventricular MI;
- ST-segment depression in leads V1-V3 suggests myocardial ischemia, especially with positive T-wave, and can be confirmed by concomitant ST elevation ≥0.1 mV in leads V7-V9.

Deciphering the ECG is difficult in the following cases
Bundle branch block (BBB): in LBBB, the presence of a concordant ST segment elevation (i.e., in leads with positive QRS deviations) is one of the indicators of a developed myocardial infarction. A previous ECG may be useful in determining whether LBBB is acute. Newly arisen blockade, as a rule, often accompanies acute current myocardial infarction. In patients with clinical signs of myocardial ischemia with new or suspected new LBBB, reperfusion therapy should be considered.
Blockade of RBBB usually does not interfere with the interpretation of ST-segment elevation.
A ventricular pacemaker may also interfere with the interpretation of ST segment changes and may require urgent angiography to confirm the diagnosis and initiate therapy.
If a patient with acute coronary occlusion does not have ST-segment elevation, there are tall and peaked T waves that usually precede ST-segment elevation, a repeat ECG or ST-segment monitoring is necessary. Lack of ST elevation may be present in patients with left circumflex coronary artery occlusion, acute vein graft thrombosis, or left main coronary artery disease. Despite the high diagnostic value, ECG recording in additional V7-9 leads does not always help to identify patients with acute occlusion and is an indication for emergency coronary angiography for myocardial revascularization.
Isolated posterior myocardial infarction (inferior-basal), often due to damage to the circumflex branch of the left coronary artery and electrocardiographically manifested only by isolated depression of the ST segment ≥0.05 mV in leads V 1-3, should be observed and treated as MI with ST segment elevation . In such cases, it is advisable to remove the ECG in additional postero-thoracic V 7-9 leads, which will allow you to detect ST segment elevation ≥0.05 mV (≥0.1 mV in men) characteristic of lower basal myocardial infarction<40 лет).
Left main coronary artery obstruction electrocardiographically manifesting as ST-segment elevation in lead aVR and ST-segment depression in posterolateral leads suggests multivessel coronary disease or left coronary artery obstruction, especially if the patient has hemodynamic compromise. The ECG should be repeated after PCI 1 hour later, and within 24 hours after the initial PCI, monitoring of the ECG in the cardiac intensive care unit is necessary, the ECG is recorded at each recurrence of symptoms.

Table 5 - Diagnosis of acute myocardial infarction based on the criteria for electrocardiogram recordings with angiograsic correlation

Localization Anatomy of occlusion ECG 30-day mortality, % Mortality within 1 year (%)
Extensive anterior infarction Anterior descending artery proximal to the first septal branch ST V1-V6, I, aVL or BLN PG 1.9,6 25,6
Big front Proximal to the major diagonal but distal to the first septal perforation ST V1-V6, I, aVL 9,2 12,4
Anterior-apical or anterior-lateral Distal to the major diagonal or to the very diagonal ST v1-v4 or
ST I, V5, V6 or aVL, V5, V6
6,8 10,2
Large lower with damage to the right ventricle, inferolateral and posterior Proximal right coronary artery or left circumflex ST II, ​​III, aVF and Any of the following: Vl, V3R, V4R V5,V6 R>S in V1,V2 6,4 8,4
Small inferior infarction Occlusion of the distal right coronary artery or branch of the left circumflex ST only II, III, aVF 4,5 6,7

*Based on GUSTO-I data.

echocardiography
In medical institutions that do not have the ability to perform emergency coronary angiography, in order to resolve the issue of transferring a patient to a clinic where he can angiographically confirm the diagnosis and perform primary PCI, it is advisable to perform two-dimensional echocardiography, which makes it possible to detect segmental violations of myocardial wall contractility. It has been established that regional violations of myocardial contractility occur within a few minutes after coronary occlusion, that is, long before the development of necrosis. Two-dimensional echocardiography is performed only if it does not delay the transfer of the patient to the clinic, where they can urgently perform emergency coronary angiography. It must also be remembered that regional disorders of myocardial wall contractility are not specific only for myocardial infarction, but can be in patients with myocardial ischemia, cicatricial changes after previous heart attacks, or intraventricular conduction disorders. Two-dimensional echocardiography can diagnose or rule out diseases such as pericarditis, massive pulmonary embolism, and ascending aortic dissection that can cause chest pain. The absence of signs of impaired myocardial wall mobility in two-dimensional echocardiography excludes the possibility of extensive myocardial infarction. In emergency situations, computed tomography is used to differentiate between acute aortic dissection and pulmonary embolism.

Recommendations class a level b
When the patient is taken to the hospital
In the acute phase, when the diagnosis is unclear, emergency echocardiography may be helpful. If it is unavailable or inconclusive and there is persistent doubt, urgent angiography should be considered. I FROM -
After the acute phase
All patients should undergo echocardiography to assess infarct size and left ventricular function at rest. I AT
If echocardiography is not possible, magnetic resonance imaging can be used as an alternative IIb C -
Before or after discharge
For patients with multivessel disease or when revascularization of other vessels is being considered, stress testing or imaging (eg, using myocardial stress perfusion scintigraphy, stress echocardiography, positron emission tomography, or MRI) is indicated to evaluate ischemia and viability. I BUT
Computed tomographic angiography plays no role in the routine management of patients with ST-segment elevation ACS III FROM -

Indications for expert advice:
- cardiac surgeon- determination of indications for surgical revascularization within the framework of a collegial decision (cardiologist + cardiac surgeon + anesthesiologist + interventional cardiologist).
- Endocrinologist- diagnosis and treatment of glycemic status disorders, treatment of obesity, etc., teaching the patient the principles of dietary nutrition, switching to short-acting insulin treatment before planned surgical revascularization.
- Neurologist- the presence of symptoms of brain damage (acute disorders of cerebral circulation, transient disorders of cerebral circulation, 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.
- Other narrow specialists- according to indications.


Laboratory diagnostics


The mandatory minimum of initial tests should include: troponin, CPK MB, OAK, hematocrit, hemoglobin, platelets, coagulogram (ABC, APTT, MHO), biochemical blood test (BAC), electrolytes (potassium, sodium, magnesium), TAM.

Troponin (T or I). In patients with MI, the initial rise in troponins occurs within ~4 hours of onset of symptoms. Elevated troponin levels may persist for up to 2 weeks due to proteolysis of the contractile apparatus. In ACS BP ST, a slight increase in troponin levels usually resolves within 48-72 hours. There are no significant differences between troponin T and troponin I. Detection is impossible only at a very early stage. With a second test within 3 hours of symptom onset, sensitivity to MI approaches 100%.

Table 3 - Biochemical markers of myocardial necrosis

Markers Specificity Sensitivity First rise after MI Peak after MI Return to normal
MV-KFK ++ + 4 h 24 hours 72 h
myoglobin + + 2 h 6-8 h 24 hours
Troponin T +++ +++ 4 h 24-48 hours 5-21 cyt
Troponin I +++ +++ 3-4 h 24-36 hours 5-14 days

Clinical blood test with platelet count. Against the background of treatment with heparin, the determination of hemoglobin (Hb), hematocrit (Ht) and counting the number of platelets should be carried out daily.

Biochemical blood test includes determination of creatinine, creatinine clearance, ALT, highly sensitive CRP, glucose, lipid spectrum. It is important to determine the glomerular filtration rate as soon as possible after the patient's admission to the hospital.
Approximately 20-30% of patients with ACS BP ST have diabetes, and about the same number of patients have undiagnosed diabetes or impaired glucose tolerance. Diabetes mellitus is an independent predictor of mortality among patients with ACS BP ST. Hyperglycemia on admission or later during hospital stay is an important independent marker of poor prognosis in ACS, whether the patient is diabetic or not, and may be an even more reliable marker of risk than diagnosed diabetes.

Coagulogram - includes APTT, PTI, fibrinogen A, INR.

Electrolytes - include potassium, magnesium, sodium.

Lipid Spectrum (Total Cholesterol, HDL, LDL, Triglycerides) All patients should have risk factors assessed upon admission to the hospital, including total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein cholesterol, triglycerides, and fasting plasma glucose. Since LDL levels tend to decrease during the first days after a myocardial infarction, it is best to measure them as soon as possible after hospitalization.

Table 4 - Assessment of lipid spectrum indicators

Lipids Normal level (mmol/l) Target level for coronary artery disease and diabetes (mmol/l)
Total cholesterol <5,0 <4,0
LDL cholesterol <3,0 <1,8
HDL cholesterol ≥1.0 in men, ≥1.2 in women
Triglycerides <1,5

With ALT > 3 TPN, CPK > 5 TPN, statins are canceled or not prescribed.
OAM - initially and according to indications.

Additional laboratory tests:
Glycemic profile - in the diagnosis of diabetes mellitus (DM). Hyperglycemia on hospitalization is an important predictor of mortality and heart failure, even in non-diabetic patients.
NT-proBNP is a highly sensitive and fairly specific marker used to detect left ventricular dysfunction.
D-dimer.

Differential Diagnosis


Differential Diagnosis

Table 7 - Differential diagnosis of ACS with other cardiac and non-cardiac diseases

cardiac Pulmonary Hematological
Myocarditis
Pericarditis
cardiomyopathy
Valvular heart disease
Apical enlargement of the apex of the heart (Takotsubo syndrome)
Thromboembolism of the branches of the pulmonary artery
Lung infarction
Pneumonia
Pleurisy
Pneumothorax
sickle cell anemia
Vascular Gastrointestinal Orthopedic
Aortic dissection
aortic aneurysm
Coarctation of the aorta
Cerebrovascular diseases
Esophageal spasms
Ulcer of the stomach and duodenum
pancreatitis
Cholecystitis
cervical discopathy
rib fracture
Muscle inflammation damage
Costal chondritis

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Treatment


Treatment Goals
Timely elimination of ischemia with subsequent prevention of serious complications such as death, recurrent MI and life-threatening arrhythmias.

Treatment tactics

Non-drug treatment
Patients with significant left ventricular involvement should be prescribed bed rest until the extent and severity of myocardial infarction can be assessed to detect early heart failure and arrhythmias. In uncomplicated cases, the patient can sit up in bed for the first few days, use the chair-toilet and take care of himself and eat on his own. Patients often begin to get up early (especially patients who have had radial access).

Recommended diet:
- the use of a wide range of products;
- 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, and reduce total fat (of which less than one-third should be saturated) to less than 30% of total calories consumed;
- decrease in salt intake, with an increase in blood pressure. Most semi-finished and ready-made meals contain high levels of salt and fats of dubious quality;
- a body mass index (BMI) of less than 25 kg/m2 is considered normal and weight reduction is recommended for BMIs of 30 kg/m2 or more, as well as for waist circumferences greater than 102 cm in men or weight gain can improve many obesity-related risk factors.

Medical treatment

Recommendations class a level b
1 2 3
For pain relief, intravenous administration of titratable opioids is indicated. I FROM
Oxygen in the event of shortness of breath and symptoms of acute heart failure and hypoxia with a decrease in SaO 2<95% I FROM
When patients have very high anxiety, tranquilizers are prescribed IIa FROM

IV = intravenously; SaO 2:= saturated saturated oxygen.

Titratable opioids are indicated for pain relief (1C)
Morphine - with ongoing pain 4-8 mg IV with an additional injection of 2 mg every 5-15 minutes, depending on the intensity of pain, until pain is relieved or side effects occur.
Side effects of morphine administration:
- nausea, vomiting, hypotension with bradycardia, and respiratory depression;
- in parallel with opioids to minimize nausea, antiemetics (metoclopramide 5-10 mg IV) can be administered;
- hypotension and bradycardia usually respond to atropine;
- in case of respiratory depression, inject naloxone (0.1-0.2 mg IV every 15 minutes, if indicated);
- these drugs should always be available.

Primary coronary intervention- emergency percutaneous catheterization for ST elevation myocardial infarction on ECG without prior fibrinolytic therapy is the preferred reperfusion tactic, provided it is performed within the established time frame, regardless of whether the patient is admitted to a PCI hospital. If the patient is admitted to a center that does not perform PCI, transport via ambulance to the catheterization laboratory should take place immediately. Preferred time frame from first medical contact to primary PCI ≤ 90 min and ≤ 60 min for early patient admission<2 часов с момента возникновения симптомов заболевания и обширной зоной инфаркта.
Primary PCI is the recommended reperfusion therapy, compared to fibrinolytic therapy, if performed within 120 min of PUMP by an experienced team (≤90 min for early admission with large ischemic risk area) - IA.
Primary PCI is indicated in patients with severe acute heart failure or cardiogenic shock, unless the expected delay associated with PCI is too long and the patient presents early after symptom onset - IB.
Stenting is recommended as a primary PCI (rather than balloon angioplasty alone) - IA.

Coronary drug eluting stent
1. Balloon expandable everolimus drug eluting stent on a 143 cm quick change delivery system. Material cobalt-chromium alloy L-605, wall thickness 0.0032". Material balloon - 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 from 8 to 38 mm. Diameters from 2.25 to 4.0 mm.
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 mh (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, L5 atm for 4.0 mm diameter Sizes: diameter from 2.25 to 4.00 and stent length (mm) from 8 to 38.
3. The material of the stent is platinum-chromium alloy. The wall thickness of the stent is 0.0032". The drug coating of the stent consists of two polymers and the drug everolimus. 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 diameters - from 2.25 to 4.00 mm. The length of the stents is from 8 to 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 144 cm.
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"). The crossing profile of the stent is 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. Diameter of the distal end part (entry profile) - 0.017 "(0.4318 mm). Working length of the catheter - 140 cm. Nominal pressure 8 atm. Design balloon burst pressure 16 atm. Stent diameter 2.25 mm at a pressure of 8 atmospheres: 2.0 mm. Diameter stent 2.25 mm at a pressure of 14 atmospheres: 2.43 mm.

Coronary stent without drug coating
1. Balloon expandable stent on a 143 cm rapid delivery system. Stent material: non-magnetic cobalt-chromium alloy L-605. Tank material - Pebax. Wall thickness: 0.0032" (0.0813 mm). Diameter: 2.0 to 4.0 mm. Length: 8 to 28 mm. Balloon stent profile 0.040" (3.0x18 mm stent). 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 (NBP) 9 atm., design burst pressure (RBP) 16 arnl.
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 Sizes: diameter from 2.25 to 4.00 and stent length (mm) from 8 to 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. Low profile 0.038" for 3.0 mm stent. Nominal balloon pressure 9 atm for 4 mm diameter and 10 atm for diameters 2.0 to 3.5 mm; burst pressure 14 atm. Proximal shaft diameter - 2.0 Fr, distal -2.7 Fr Diameters: 2.0 to 4.0 Lengths 8 to 30 mm.

Primary PCI should be limited to the infarct-related artery, except in cases of cardiogenic shock and persistent ischemia after PCI-IIa B.
If performed by an experienced radial operator, radial access should be preferred over femoral access - IIa B.
If the patient has no contraindications to long-term DAPT (an indication for oral anticoagulation or a high risk of bleeding on the CRUSADE scale) and is likely to comply with the recommendations, a drug-eluting stent should be preferred over an uncoated metal stent - IIa A.
Routine thrombus aspiration should be considered - IIa B.
Routine use of distal guards is not recommended - III C.
Routine use of IABP (in patients without shock) is not recommended - III B.
Immediate angiography with primary PCI is recommended in patients resuscitated after cardiac arrest with evidence of ST MI on EG-I B.
Immediate angiography with primary PCI should be considered in cardiac arrest survivors without diagnostic ST segment elevation on the ECG but with significant suspicion of current infarction - IIa B.
Therapeutic hypothermia is indicated early after resuscitation from cardiac arrest in patients in a coma or deep sedation - IB.
Primary coronary intervention is the optimal treatment strategy in case of contraindications to fibrinolytic therapy, the presence of an experienced team of interventional cardiologists and qualified personnel of the cardiac intensive care units, a hospital with a developed intervention program (24/7), performing primary PCI as a routine method in patients with ST ACS as early as possible ( within 30-60 minutes from the moment the patient first contacted (IB).
Routine anticoagulant therapy after a primary PCI procedure is not indicated, except in some clinical situations where there are special indications for anticoagulation (atrial fibrillation, presence of mechanical valves, LV thrombus, delayed removal of the stent shield) or for the prevention of venous thromboembolism in patients requiring long-term aftercare mode.

Table 9 - Antithrombotic therapy in primary PCI

Recommendations class a level b
Antiplatelet therapy
Oral or IV aspirin recommended (if unable to swallow) I AT
An ADP-receptor blocker is recommended in addition to aspirin. The following options: I BUT
. Ticagrelor I AT
. Clopidogrel when prasugrel or ticagrelor is not available or contraindicated I FROM -
Anticoagulant therapy
Injectable anticoagulants should be used in primary PCI I FROM -
Bivalirudin is recommended over unfractionated heparin with glycoprotein IIb/IIIa inhibitors I AT
Enoxaparin may be preferred over unfractionated heparin IIb AT
Unfractionated heparin should be used in patients not receiving bivalirudin or enoxaparin I FROM
Fondaparinux is not recommended for primary PCI III AT
The use of fibrinolysis prior to planned primary PCI is not recommended. III BUT
Table 10 - Antiplatelet and anticoagulant doses for primary PCI
Doses of antiplatelet therapy
Aspirin Loading dose of 150–300 mg orally or 80–150 mg IV if oral administration is not possible, followed by a maintenance dose of 75–100 mg/day
Clopidogrel Loading dose of 600 mg orally, followed by a maintenance dose of 75 mg/day
Ticagrelor Loading dose of 180 mg orally followed by a maintenance dose of 90 mg twice daily.
Unfractionated heparin 70-100 U/kg IV bolus unless glycoprotein IIb/IIIa inhibitors are planned. 50-60 U/kg IV bolus with glycoprotein IIb/IIIa inhibitors
Enoxaparin 0.5 mg/kg IV bolus
Bivalirudin 0.75 mg/kg IV bolus, followed by 1.75 mg/kg/hour IV drip up to 4 hours after the procedure, as clinically warranted treatment. After stopping the 1.75 mg/kg/h infusion, a reduced dose of 0.25 mg/kg/h infusion may be continued for 4-12 hours as clinically necessary.

Fibrinolysis and subsequent interventions
Fibrinolysis is an important reperfusion strategy when primary PCI cannot be performed within the recommended time frame in patients with ST sp MI. In the absence of contraindications, it is necessary to start fibrinolytic therapy in the prehospital stage (II a A), especially if transport to the hospital takes more than 30 minutes, under the following conditions:
1. If the time from the onset of an anginal attack is 4-6 hours, at least it does not exceed 12 hours;
2. ECG shows ST-segment elevation > 0.1 mV in at least 2 consecutive chest leads or 2 limb leads, or new left bundle branch block (LBBB) and other ECG changes noted above.
3. The introduction of thrombolytics is justified at the same time with ECG signs of true posterior MI (high R waves in the right precordial leads V 1 -V 2 and depression of the ST segment in leads V 1 -V 4 ​​with an upward T wave).
4. Fibrinolytic therapy is recommended within 12 hours of symptom onset if primary PCI cannot be performed within 90 minutes if fibrinolysis is possible, and within 120 minutes of first medical contact if there are no contraindications. In late delivery of patients (particularly after 6 hours), primary PCI is preferred (as opposed to fibrinolytic therapy), as the effect and clinical benefit of fibrinolysis declines over time.

Table 11 - Contraindications to fibrinolytic therapy

Absolute
Previous intracranial hemorrhages or strokes of unknown origin at any time
Ischemic stroke in the previous 6 months
CNS injury or neoplasms or atrioventricular malformations
Recent major trauma/surgery/head trauma (within the previous 3 weeks)
Gastrointestinal bleeding within the last month
Known bleeding disorder (excluding menses)
Aortic dissection
Non-compressible wound/puncture in the last 24 hours (eg, liver biopsy, lumbar puncture)
relative
Transient ischemic attack in the previous 6 months
Oral anticoagulant therapy
Pregnancy or within 1 week postpartum
Arterial refractory hypertension (systolic blood pressure >180 mmHg and/or diastolic blood pressure >110 mmHg)
Severe liver disease
Infective endocarditis
Active peptic ulcer
Prolonged or traumatic resuscitation
Table 12 - Fibrinolytic therapy
Recommendations class a level b
Fibrinolytic therapy is recommended within 4 to 6 hours no more than 12 hours from the onset of symptoms in patients without contraindications, if it is not possible; primary PCB by an experienced team within 120 minutes from the first medical contact I BUT
With early delivery of the patient (<2 часов после появления симптомов) с обширным инфарктом и низким риском кровотечения, фибринолиз должен быть рассмотрен, если время от первого медицинского контакта до надувания баллона >90 minutes IIa AT
If possible, fibrinolysis should be initiated in the prehospital setting. IIa BUT
Fibrin-specific drugs (tenecteplase, alteplase, reteplase) are recommended I AT
Antiplatelet therapy for fibrinolysis
Oral or IV aspirin should be given I AT
Clopidogrel is indicated in addition to aspirin I BUT
Anticoagulant therapy for fibrinolysis
Anticoagulation is recommended in STEMI patients treated with fibrinolytics prior to revascularization (if indicated) or during the entire hospital stay, up to 8 days Anticoagulants may include: I BUT
. IV enoxaparin followed by SC (mode listed below) (preferably over unfractionated heparin) I BUT
. Unfractionated heparin is given as a weight-adjusted IV bolus or drip (under APTT monitoring)* I FROM
In patients treated with streptokinase, fondaparinux is given by IV bolus followed by a dose s.c. 24 hours later IIa AT

Table 13 - Doses of antiplatelet and anticoagulant therapy for fibrinolysis
Doses of antiplatelet therapy
Aspirin
Clopidogrel 75 mg/day orally
Doses of anticoagulant therapy
Unfractionated heparin 60 U/kg intravenously by bolus with a maximum of 4000 U, followed by intravenous drip of 12 U/kg with a maximum of 1000 U/hour for 24-48 hours. Target APTT: 50-70 sec or 1.5-2.0 times higher than baseline and control at 3, 6, 12 and 24 hours.
Enoxaparin Patients<75 лет: 30 мг в/в струйно, через 15 минут и далее 1 мг/кг п/к каждые 12 часов до выписки из стационара, максимально в течение 8 дней. Первые две дозы не должны превышать 100 мг.
Patients >
<30 мл/мин, независимо от возраста, п/к дозы вводятся 1 раз в 24 часа.
Fondaparinux* (for streptokinase) 2.5 mg IV bolus followed by 2.5 mg s.c. once daily for up to 8 days or until hospital discharge.

*patients without reperfusion therapy delivered after 24 hours from the onset of an attack (IA)


Thrombolytic drugs
Alteplaza

It is administered intravenously (previously the drug is dissolved in 100-200 ml of distilled water or 0.9% sodium chloride solution) according to the "bolus + infusion" scheme. Dose of the drug 1 mg / kg body weight (but not more than 100 mg): 15 mg is administered as a bolus; subsequent infusion of 0.75 mg/kg body weight over 30 minutes (but not more than 50 mg), then 0.5 mg/kg (but not more than 35 mg) over 60 minutes (total duration of infusion - 1.5 hours). Or
Tenecteplase- intravenously 30 mg at body weight< 60 кг, 35 мг при 60-70 кг, 40 мг при 70-80 кг: 45 мг при 80-90 кг и 50 мг при массе тела >90 kg, the required dose is given as a bolus over 5-10 seconds. Given the longer half-life from the body, the drug is used as a single bolus, which is especially convenient for pre-hospital thrombolysis. Or
Streptokinase- administered in / in a dose of 1500000 ME for 30-60 minutes in a small amount of 0.9% sodium chloride solution. The development of hypotension, acute allergic reactions is often noted. You can not enter repeatedly (specify anamnesis).
Transportation to a hospital where PCI is performed is indicated for all patients after fibrinolysis.

Table 14 - Interventions after fibrinolysis

Emergency PCI is indicated immediately when fibrinolysis fails (<50% снижение сегмента ST на 60-й минуте) I BUT 165, 166
Emergency PCI is indicated in cases of recurrent ischemia or evidence of re-occlusion after initial successful fibrinolysis. I AT 165
Urgent angiography followed by revascularization is indicated in patients with heart failure/shock I BUT 167
Angiography for subsequent revascularization (associated with arterial infarction) is indicated after successful fibrinolysis I BUT 168-171
Optimal angiography time for stable patients after successful lysis: 3-24 hours Pa BUT 172

PCV after fibrinolysis(pharmacoinvasive strategy) should be performed within 3 to 24 hours of successful fibrinolysis (with resolution of chest pain/discomfort and decreased ST elevation on the ECG) (I A).

PKB is not recommended patients with a fully formed myocardial infarction with a Q wave without ongoing symptoms / signs of ischemia or without signs of viability of myocardial sites in the area of ​​damage, upon admission to a medical institution later than 24 hours from the onset of the disease (III B).
Such patients are shown electoral CHKB before discharge from the hospital with positive provocative tests (stress-induced myocardial ischemia) (I B).

Among patients delivered several days after an acute event with a completed myocardial infarction, only those patients who present with recurrent angina or documented residual ischemia and have demonstrated large myocardial viability on non-invasive imaging may be considered for revascularization for an occluded infarct artery.
Reperfusion therapy with primary PCI may be considered for stable patients admitted to the hospital within 12–24 hours of symptom onset (IIb B).

Table 15 - Doses of antiplatelet and anticoagulant therapy in situations without reperfusion

Without reperfusion therapy
Aspirin Starting dose 150-500 mg orally
Clopidogrel 75 mg/day orally
Without reperfusion therapy
Unfractionated heparin
60 U/kg intravenously by bolus with a maximum of 4000 U, followed by intravenous drip of 12 U/kg with a maximum of 1000 U/hour for 24-48 hours. Target APTT: 50-70 sec or 1.5-2.0 times higher than baseline and control at 3, 6, L2 and 24 hours.
Enoxaparin Same dose as with fibrinolytic therapy
Patients<75 лет: 30 мг в/в струйно, через 15 минут и далее 1 мг/кг п/к каждые 12 часов до выписки из стационара, максимально в течение 8 дней. Первые две дозы не должны превышать 100 мг.
Patients >75 years: no IV bolus; start with the first sc dose of 0.75 mg/kg, maximum 75 mg for the first two sc doses.
In patients with creatinine clearance<30 мл/мин, независимо от возраста, п/к дозы вводятся 1 раз в 24 часа.
Fondaparinux Same dose as with fibrinolytic therapy
2.5 mg IV bolus followed by 2.5 mg s.c. once daily for up to 8 days or until hospital discharge.


Given the proven role of aspirin in secondary prevention, it should be used in all patients with STEMI. For long-term therapy, usually low doses (70-100 mg) are used. Dual antiplatelet therapy, the combination of aspirin with an ADP receptor blocker (clopidogrel or ticagrelor), is recommended in STEMI patients who have undergone primary PCI (up to 12 months). Pending results from ongoing studies, the recommended duration of dual antiplatelet therapy is 9-12 months, with a strict minimum of one month for patients with a bare metal stent and six months for patients with a drug-eluting stent. It is important to inform patients and their physicians of the need to avoid premature discontinuation of dual antiplatelet therapy.
For patients with STEMI and atrial fibrillation, and requiring continued use of anticoagulants after primary PCI [if ≥2 points on CHADS score)], "triple therapy", a combination of aspirin, ADP receptor antagonists, and oral anticoagulants, is recommended to reduce thromboembolic complications associated with atrial fibrillation and to minimize the risk of stent thrombosis. In STEMI patients with an indication for the use of anticoagulants and the need for stents, non-drug eluting stents should be preferred, as this may minimize the duration of triple therapy and therefore reduce the risk of bleeding.
Gastroprotective drugs, preferably proton pump inhibitors, should be given to patients with a history of gastrointestinal bleeding who have multiple risk factors for bleeding, including older age, concomitant use of anticoagulants, steroids, or non-steroidal anti-inflammatory drugs, including high doses of aspirin, and infection with Helicobaster pyori.
The role of new anticoagulants in combination with dual antiplatelet therapy in the secondary prevention of STEMI remains under discussion. The significant reduction in mortality seen with low-dose rivaroxaban in combination with aspirin and clopidogrel allows this combination to be recommended for selected patient groups with a low risk of bleeding.
The benefits of long-term treatment with beta-blockers after STEMI are well known. Oral use of beta-blockers has been shown to be highly effective. Early intravenous use of beta-blockers is contraindicated in patients with clinical signs of hypotension or congestive heart failure. Early use may be associated with modest benefit in low-risk, hemodynamically stable patients. In most cases, it is considered reasonable to start therapy with beta-blockers after the patient's condition has stabilized, and oral administration of the drug should be prescribed rather than intravenous.
Statins should be given to all patients with acute myocardial infarction, regardless of cholesterol levels. This treatment should be started immediately on admission as it increases patient adherence to treatment after discharge, and high dose statins should be given as this leads to early and sustained clinical benefit. The goal of treatment is to achieve a concentration of LDL cholesterol< 1,8 ммоль/л. Использование терапии низкой интенсивности статинами должно рассматриваться у пациентов с повышенным риском возникновения побочных эффектов от приема статинов (например, пожилые люди, пациенты с печеночной или почечной недостаточностью, с предыдущим развитием побочных эффектов от применения статинов или при наличии высокой вероятности взаимодействия с препаратами сопутствующей терапии). Повторное определение уровня липидов крови следует провести через 4-6 недель после ОКС, для того, чтобы оценить достигнуты ли целевые уровни, и безопасность терапии; после получения результатов дозу статинов следует скорректировать. У пациентов с известной непереносимостью статинов в любой дозе, необходимо рассмотреть возможность лечения эзетимибом.
Routine use of nitrates in STEMI has not been shown to benefit patients, and for this reason, their use is not recommended. Intravenous nitrates may be useful during the acute phase in patients with hypertension or heart failure, provided there has been no hypotension, right ventricular infarction, or use of phosphodiesterase-5 inhibitors in the previous 48 hours. In the acute and stable phase, nitrates remain valuable drugs for controlling angina symptoms.
For patients who are contraindicated in the use of beta-blockers, especially those with chronic obstructive pulmonary disease, calcium antagonists may be prescribed, which is a reasonable solution for patients without heart failure.
Angiotensin-converting enzyme (ACE) inhibitors should be given to patients with impaired ejection fraction (< 40%) или пациентам с острой сердечной недостаточностью на ранней стадии. Использование ингибиторов АПФ следует рассмотреть для всех пациентов с атеросклерозом long-term use is not necessary in post-STEMI patients with normal blood pressure, without heart failure, or without LV systolic dysfunction and without diabetes mellitus. Patients who cannot tolerate ACE inhibitors should be treated with angiotensin receptor blockers (ARBs). Valsartan is (text is given in accordance with the original) alternative to ACE inhibitors, in patients with clinical signs of heart failure and / or with an ejection fraction ≤ 40%.
Aldosterone blockers may be considered in post-STEMI patients with an ejection fraction ≤ 40% and heart failure or diabetes, provided that the creatinine level is< 221 мкмоль/л (2,5 мг/дл) у мужчин и < 177 мкмоль/л (2,0 мг/дл) у женщин, а калия < 5,0 мг-экв/л. Необходим регулярный мониторинг уровня калия в сыворотке крови.

Basic medicines:
Narcotic analgesics:
- Morphine hydrochloride in amp. 1% 1 ml
Thrombolytic agents:
- Alteplase 1 vial, 50 mg
Antithrombotic agents:
- Bivalirudin* 250 mg - 1 vial
- Enoxaparin syringe tube 0.3 ml, 0.6 ml, 1 ml
Nitrates:
- Nitroglycerin tab. 0.5 mg
- Nitroglycerin amp. 10 ml
- Isosorbide mononitrate cape. 40 mg
Beta blockers:
- Metoprolol tartrate tab. 25 mg, 50 mg
- Metoprolol tartrate amp. 5 ml
ACE inhibitors:
- Captopril 6.25 mg, 12.5 mg, 25 mg
- Zofenopril 7.5 mg (preferred for CKD patients with GFR< 30 мл/мин)
Antiplatelet agents:
- Acetylsalicylic acid tab. 75 mg, 150 mg. Starting dose 500 mg uncoated
- Ticagrelor tab. 90 mg
Lipid-lowering agents:
- Atorvastatin tab. 40 mg

Additional medicines
Antithrombotic agents:
- Heparin solution for and 5000IU / ml vial.
- Fondaparinux 2.5 mg (for non-invasive strategy)
Nitrates:
- Isosorbide dinitrate cape. 20 mg
- Isosorbide dinitrate aeroz. dose
Beta blockers:
- Carvedilol 6.25 mg, 25 mg
calcium antagonists:
- Diltiazem cape. 90 mg
- Verapamil tab. 40 mg
AIF inhibitors:
- Ramipril tab. 10 mg
Angiotensin-II receptor antagonists:
- Valsartan tab 80 mg, 160 mg
Antiplatelet agents:
- Clopidogrel tab. 75 mg, 300 mg
Lipid-lowering agents:
- Rosuvastatin tab. 10 mg
- Naloxone solution for injections 1 ml/400 mcg
- Atropine injection solution 0.1% 1 ml
- Metoclopramide hydrochloride monohydrate amp. 1 ml
- Tofisopam tab. 50 mg
- Diazepam tab. 5 mg
- Diazepam amp. 2 ml
- Dobutamine*40 mg/50 ml
- Spironolactone tab. 25 mg
- Rivaroxaban 10 mg
Proton pump inhibitors:
- Esomeprazole lyophilisate amp. 40 mg
- Pantoprazole tab., 40 mg
- Esomeprazole tab. 40 mg
- Sodium chloride 0.9% solution 200 ml, 400 ml
- Dextrose 5% solution 200 ml, 400 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”).

Other treatments

Surgical intervention
PCI on non-infarct arteries in the acute setting is generally not recommended, except in extreme cases with cardiogenic shock, and in patients with ongoing ischemia after the suspected culprit vessel has been opened. The optimal management strategy for STEMI patients with multivessel disease who have undergone primary PCI on an infarct-related artery in the acute phase with persistent multivessel disease has not yet been established.
Of all the possible strategies, two are most commonly used: conservative approach- with the use of medical therapy after primary PCI and revascularization of other arteries, only if there are symptoms or evidence of ischemia in provocative tests; stepwise revascularization approach- with PCI or coronary artery bypass grafting of non-infarcted arteries days or weeks after primary PCI, often after confirming the severity of the stenosis by measuring fractional blood flow reserve, a multidisciplinary approach is often needed, including a cardiac team and appropriate informed consent from the patient.
In cases where angioplasty with PCI is not possible, CABG is indicated, provided that the patency of the infarct-dependent coronary artery is preserved, because time is needed to transfer the patient to the hands of the surgical team. CABG may be indicated in patients with cardiogenic shock if it is impossible to perform angioplasty in PCI and in cases of technical complications during PCI.
The benefit of CABG is uncertain in patients with failed PCI, those with coronary artery occlusion not eligible for angioplasty in PCI, and those with refractory symptoms after PCI, as in most of these cases surgical reperfusion will take a long time to complete and the risks associated with surgery are high.

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
Acute Coronary Syndrome (ACS) occurs twice as often in smokers than in non-smokers, suggesting a strong prothrombotic effect of smoking. Studies have found that patients who quit smoking have reduced their mortality compared to those who continued to smoke. Smoking cessation is the most effective of all secondary preventive measures and therefore every effort should be made to achieve this. It is ideal for health professionals to help patients quit smoking that patients do not smoke during the acute phase of AMI, as well as during the recovery period. 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. The use of nicotine patches has been shown to be safe in patients with AMI. 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 an increasing problem in AMI patients. 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
Therapeutic exercise has long been used for rehabilitation purposes after AMI. Regular exercise has also been found to improve 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
In hypertensive patients with AMI, blood pressure should be well controlled. Pharmacotherapy (beta-blockers, ACE inhibitors, or angiotensin receptor blocker ARBs) recommended after an MI, 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.

Physical rehabilitation.
It was found that dosed physical activity contributed to a decrease in mortality and the risk of recurrent heart attack. Expansion of the motor regimen must be considered individually for each patient, depending on the function of the left ventricle, the amount of revascularization performed and heart rate control. Extended sick leave is generally perceived negatively, so light to moderate exercise should be encouraged after discharge. Sexual activity can be resumed earlier if adaptation to physical capabilities has occurred. Long-distance air walks should be limited for 4–6 weeks in residual ischemia or left ventricular dysfunction.

Stationary rehabilitation program.
An individual rehabilitation program is drawn up for each patient. Rehabilitation treatment should be started when the patient is still in bed, regular passive movements in the joints of the limbs, breathing exercises will allow the patient to avoid complications such as muscle weakness, muscle atrophy, pneumonia, etc.
The tasks of inpatient treatment and rehabilitation of patients with MI are the prevention and treatment of complications, the achievement of an optimal condition for the patient, the stabilization of clinical, laboratory and instrumental data, the achievement of such a level of physical activity of the patient at which he could serve himself, climb the 1st floor, take walks 2-3 km in 2-3 steps.
The final goal of inpatient treatment and rehabilitation of patients is to prepare them for transfer to the rehabilitation department of the local cardiological sanatorium. Follow-up treatment is sent no earlier than 20 days for small-focal myocardial infarction, and after 30 days for large-focal myocardial infarction.
At the stationary stage, physical and psychological aspects are used. Physical rehabilitation was developed by L.F. Nikolaeva, D.M. Aronov (1988).

Rehabilitation measures are performed depending on the class of clinical severity of myocardial infarction. There are 4 classes of severity of myocardial infarction.
The classification is based on: the size of necrosis (small-focal, large-focal, subenocardial, circular, apical), the severity of complications divided into 3 groups, age, the presence of arterial hypertension, diabetes mellitus.

Classification of complications of myocardial infarction:
Complications of the 1st group:
1. rare extrasystole
2. atrioventricular blockade of the 1st stage, which existed before the development of myocardial infarction
3. atraoventricular blockade 1 stage, with posterior myocardial infarction
4. sinus bradycardia
5. circulatory failure not higher than 1 tbsp.
6. epistenocarditis pericarditis
7. blockade of the legs of the bundle of His

Complications of the 2nd group:
1. reflex shock (hypotension)
2. atrioventricular blockade of the 1st degree, with posterior myocardial infarction, atrioventricular blockade of the 1st degree, with anterior myocardial infarction or against the background of blockade of the legs of the His bundle.
3. paroxysmal arrhythmias, with the exception of paroxysmal ventricular tachycardia.
4. Migration of the pacemaker.
5. extrasystole: parts (more than 1 extrasystole per minute, and (or) polytopic, and (or) group, and (or) early ("R on T") long-term (during observation) or frequently recurring episodes.
6. circulatory failure stage IIA.
7. Dressler's syndrome.
8. hypertensive crisis.
9. stable arterial hypertension (systolic blood pressure 200 mmHg, diastolic blood pressure 200 mmHg).

Complications of group III:
1. recurrent or prolonged course of myocardial infarction
2. state of clinical death
3. complete atrioventricular block
4. atrioventricular blockade of the 1st stage, with anterior myocardial infarction.
5. acute aneurysm of the heart
6. thromboembolism in various organs
7. true cardiogenic shock
8. pulmonary edema
9. circulatory failure refractory to treatment
10. thromboendocarditis
11. gastrointestinal bleeding
12. ventricular paroxysmal tachycardia
13. combination of two or more complications of the 2nd group.

Complications of the 1st group practically do not lengthen the rehabilitation period. Complications of the 2nd group do not prevent rehabilitation, but the rate of expansion of the regime slows down. Complications of the 3rd group significantly impede rehabilitation and require medical treatment.
The terms of activation and the rehabilitation program are carried out depending on the severity class. When expanding the regimen of a patient with myocardial infarction, it is necessary to monitor his condition.

Indicators of an adequate response of the patient to physical activity and expansion of the regimen are:
- an increase in the pulse rate at the height of the load and in the first 3 minutes after it up to 20 minutes, the number of breaths - up to 6-8 minutes, systolic blood pressure - by 20-40 mm Hg, diastolic blood pressure - by 10-20 mm. Hg compared with the original values;
- or a decrease in heart rate for no more than an hour for 10 minutes, a decrease in systolic blood pressure by no more than 10 mm Hg.

To assess the functional capabilities of a patient who has had a myocardial infarction, and to select the optimal physical activity, an early bicycle ergometry test (VEM) is used, usually performed on the 11-21st day of illness. In the presence of complications and a high class of severity, the activation time is extended by 3-4 days.
The patient is invited to perform continuous stepwise increasing physical activity. The initial load power is 25 W - 1 stage, 2 stage - 50 W, 3 stage - 100 W. The duration of each step is 3 minutes. The test must be stopped when a submaximal heart rate is reached, or when signs appear that are an indication for termination: an attack of angina pectoris, an ischemic ST segment displacement of 1 mm or more, an increase in systolic blood pressure of more than 200 mm Hg. or its decrease by 10-20 mmHg, the development of arrhythmias and disorders of atrioventricular and intraventricular conduction.

When conducting VEM, the office should be equipped with everything necessary for providing emergency assistance: a defibrillator, a ventilator, a pacemaker, and medications.

To increase the effectiveness of rehabilitation treatment at the inpatient stage, it is advisable to prescribe physical training for small muscle groups using expanders for 3-8 days along with a set of therapeutic exercises No. 1, as well as training dosed walking and exercise bikes.

Physical training of small muscle groups is carried out under the guidance and supervision of a physical therapy methodologist. Heart rate and blood pressure are measured every 5 minutes. Exercise should be stopped when systolic blood pressure increases by 40 mm Hg, diastolic blood pressure by 15 mm Hg, heart rate by 30 beats per minute.
Physical training of small muscle groups is carried out daily during the period of mastering the second stage of physical activity.

When transferring to the III level of activity, along with physical training of small muscle groups, dosed walking along the corridor is allowed. After the transfer to stage III, when the patients have mastered walking along the corridor, VEM is performed in order to determine the individual tolerance of physical activity at this stage.
Tolerance to physical activity is estimated by the maximum power of the mastered load, at which signs of intolerance appeared.
Training on a bicycle ergometer is carried out 3 times a week every other day, in the first half of the day, not earlier than 1.5 hours after eating, dosed walking and training of small muscle groups - 2 times a week.

Dosed walking is an integral part of the physical training program at the stationary stage. The distance during dosed walking is determined by the threshold power level. At a threshold power of 50 W, patients are invited to carry out up to 3 km per day in 3-6 doses, with a threshold power above 50 W - 5 km in 5-10 doses.
The complex of physical training continues at the IV degree of physical activity, up to discharge from the hospital.

Contraindications for physical training in patients with myocardial infarction:
1. Angina at rest
2. Circulatory failure IIB and IIIst
3. Severe respiratory failure
4. High blood pressure (systolic blood pressure above 180 mmHg, diastolic blood pressure above 120 mmHg)
5. Increased body temperature
6. ESR above 25 mm/h
7. Acute thrombophlebitis
8. Frequent extrasystole
9. Atrioventricular block II and III stage
10. Blockade of the legs of the bundle of His and atrial fibrillation

Great importance is attached to the psychological rehabilitation of patients with myocardial infarction at the stationary stage. Psychological rehabilitation is carried out by a cardiologist, a psychotherapist.
The system of rehabilitation measures, rehabilitation treatment carried out in a hospital are also considered as the beginning of secondary prevention of myocardial infarction. The implementation of rehabilitation measures in the hospital is controlled by a doctor.

The tasks of the sanatorium stage of rehabilitation of patients with myocardial infarction are:
- restoration of physical performance;
- psychological readaptation;
- preparation for further independent life and production activities.
Patients with I-III classes of severity of the disease are transferred to the rehabilitation department of sanatoriums with their satisfactory adaptation to the IV degree of physical activity.
For physical rehabilitation at the sanatorium stage, therapeutic exercises, dosed walking, training walking up the stairs with a gradual increase in the intensity of physical activity are used. The volume of physical activity is determined taking into account the functional classes of IHD.

Rehabilitation part secondary prevention myocardial infarction (post-hospital rehabilitation) is important for eliminating all the consequences of a myocardial infarction and its complications, for normalizing metabolism in the part of the heart muscle unaffected by a heart attack, which is important for preventing (reducing the risk) the possibility of a second heart attack in the future. One of the most important areas of secondary prevention is the stabilization of atherosclerosis (in particular, coronary vessels) and the possible achievement of reverse development (decrease in degree) of coronary atherosclerosis.

After the sanatorium stage of treatment and rehabilitation of myocardial infarction or immediately after discharge from the hospital (where sanatorium treatment was not carried out), a patient with postinfarction cardiosclerosis comes under the supervision of a general practitioner of the clinic or under the supervision of a cardiologist in the cardiology office of the polyclinic (or a cardiologist from a specialized cardiological polyclinic or cardiological dispensary). The frequency of medical supervision and correction of the selected rehabilitation regimen is determined by the attending physician and is initially repeated on average 1 time per week, then 1 time in 2 weeks, and after 3-4 months (upon the patient returns to work) and during the first year - approximately 1 time in 3-4 weeks. In the second year after myocardial infarction, control is carried out very individually, most often once every 2-3 months.

Individually selected regimens of physical training with simultaneous long-term (within 3-4 months) use of special drugs in the post-stationary period, aimed at stimulating reparative processes in the heart muscle, give a high therapeutic effect, causing a high level of return of patients to work, as well as a significant decrease in the frequency repeated myocardial infarctions. Today, thanks to advances in the treatment and rehabilitation of patients with myocardial infarction, 65-80% of patients of working age return to work.

Further management

Table 16 - Routine therapy for acute, pre-acute and long-term STEMI therapy

Recommendations Class (a) Level (b)
Active smokers with STEMI should receive counseling and be involved in a smoking cessation program. I AT
Every hospital involved in the management of STEMI patients should have a smoking cessation protocol. I FROM
Recommended physical rehabilitation of patients with STEMI I AT
Antiplatelet therapy using low dose aspirin (75-100 mg) is indicated indefinitely after STEMI. I BUT
In patients with aspirin intolerance, clopidogril is indicated as an alternative to aspirin. I AT
Dual antiplatelet therapy in combination with aspirin and prasugrel or aspirin and ticagrelor (more than aspirin and clopidogrel) is recommended in patients with PCI. I BUT
Dual antiplatelet therapy with aspirin and oral ADP antagonists should be used up to 12 months after STEMI, with a strict minimum for: I FROM
. patients with uncoated stent - 1 month I FROM
. patients with a drug-eluting stent - 6 months IIb AT
In patients with left ventricular thrombosis, anticoagulant therapy should be given for at least 3 months. IIa AT
In patients with strong indications for the use of oral anticoagulants (atrial fibrillation according to the CHA 2 DS 2 -VASc ≥2 scale or the presence of a mechanical valve prosthesis), they should be used in addition to antiplatelet therapy. I FROM
If patients require triple antithrombotic therapy, a combination of dual antiplatelet therapy and OAT, for example, after stent implantation in patients with a strong indication for OAT, the duration of dual antiplatelet therapy should be minimized to reduce the risk of bleeding. I FROM
In selected patients at low risk of bleeding who are receiving aspirin and clopidogrel, low-dose rivaroxaban (2.5 mg twice daily) may be considered. IIb AT
Dual antiplatelet therapy should be continued for 1 year in STEMI patients who have not received stenting. IIa FROM
Gastroprotective therapy with proton pump inhibitors should be considered in patients with: a high risk of bleeding during the entire period of receiving dual antiplatelet therapy IIa FROM
Oral beta-blocker treatment should be initiated during hospitalization and continued after discharge in all patients with STEMI unless contraindicated. IIa AT "
The use of oral beta-blockers is indicated in patients with heart failure or with left ventricular dysfunction. I BUT
IV beta-blockers should not be given to patients with hypotension or heart failure III AT
For intravenous admission, the use of beta-blockers is indicated in patients without contraindications with high blood pressure, tachycardia and no signs of heart failure. IIa AT
Fasting lipid profile measurements in all STEMI patients should be performed as soon as possible after admission. I FROM
It is recommended that high-dose statins be started or continued immediately upon admission in all STEMI patients with no contraindications or no history of statin intolerance, regardless of baseline cholesterol levels. I BUT
Re-measurement of LDL cholesterol levels is done every 4-6 weeks to ensure that the target level is ≤ 1.8 mmol/L (70 mg/dL). IIa FROM
Verapamil may be indicated for secondary prevention in patients in whom beta-blockers are contraindicated and in the absence of heart failure. IIb AT
ACE inhibitors should be started within the first 24 hours of STEMI in patients with evidence of heart failure, left ventricular systolic dysfunction, diabetes mellitus, or anterior myocardial infarction. I BUT
ARBs, preferably valsartan, are an alternative to ACE inhibitors for patients with heart failure or LV systolic dysfunction, especially those who are intolerant to ACE inhibitors. I AT
ACE inhibitors should be given to all patients, provided there are no contraindications. IIa BUT
Aldosterone antagonists, such as eplerenone, are indicated in patients with ejection fraction ≤40%, heart failure, or diabetes mellitus, provided there is no renal failure or hyperkalemia. I AT

Indicators of treatment efficacy and safety of diagnostic and treatment methods described in the protocol

Table 17 - Criteria for the effectiveness of rehabilitation treatment of patients with a cardiological and cardiac surgical profile in inpatient rehabilitation departments of medical institutions (assessed by a set of signs 1-8)

Criteria Significant improvement Improvement no change Deterioration
1 Clinical classification of the severity of the condition Transition to an easier class. Preservation of class I No speakers Upgrading to a heavier class
2 angina pectoris Disappeared Lessening of seizures, the occurrence of seizures at high loads No speakers More frequent or worse seizures
3 Signs of heart failure Disappeared Decreased No speakers increased
4 6-minute walk test results Transition to an easier class >500 m Transition to an easier class. Preservation of class I No speakers Transition to a heavier class.
5 Achieved degree of motor activity by the time of discharge. Achievement of the VII stage of physical activity Achievement of the V-VI stage of physical activity Achievement of the IV stage of physical activity Transfer to I-III stages of physical activity
6 exercise tolerance An increase of at least 1 step (according to load tests) No speakers Decrease
7 ECG dynamics ECG is stable or positive ECG stable or positive dynamics No speakers Negative dynamics
8 Dynamics of echocardiography Improving EchoCG parameters Improving EchoCG parameters No speakers Negative dynamics

Hospitalization


Indications for hospitalization indicating the type of hospitalization
Emergency hospitalization - a patient with ACS with ST elevation on the ECG should be taken to the angiography laboratory on the catheterization table, bypassing the cardiac intensive care unit or the emergency cardiology department (I A).

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. Algorithm for the treatment of acute coronary syndrome with persistent ST segment elevation (Protocol of the Expert Council of the Ministry of Health of the Republic of Kazakhstan dated January 8, 2013 No. 1). 2. ESC guidelines for the management of acute myocardial infarction with ST-segment elevation 2012. 3. Diseases of the heart and blood vessels. Guidelines of the European Society of Cardiology, "Geotar-Media", Moscow, 2011. 4. 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. Tokhtasunova S.V. - Junior Researcher, Department of Cardiology, Research Institute of Cardiology and Internal Diseases.
5. Mekebekova D.M. - Junior Researcher, Department of Cardiology, Research Institute of Cardiology and Internal Diseases.

Reviewers:
1. Abseitova S.R. - 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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There are 3 stages of hypertension. Hypertension of the 3rd degree is very difficult to compensate. To stabilize blood pressure in this case, the patient should undergo complex treatment and take antihypertensive drugs on an ongoing basis.

Without fail, hypertension must follow a diet and lead a healthy lifestyle. Increased physical activity is contraindicated, so it is quite possible to get by with exercise therapy or walking.

If hypertension occurs with many complications, the patient may be assigned a disability. To obtain it, you must undergo a series of medical examinations.

Definition and causes of hypertension

Hypertension (ICD-10 code I10) is a disease of the cardiovascular system, which is characterized by a persistent increase in blood pressure above 140/90 mm Hg.

It is necessary to distinguish between such a thing as hypertension and hypertension. Arterial hypertension can be secondary, that is, be the result of pathologies of the kidneys or other internal organs.

Hypertension is not completely curable. The disease can be compensated, that is, to improve the patient's quality of life and stabilize blood pressure within acceptable limits.

Why patients develop essential (primary) hypertension is still unknown to science. Doctors suggest that there are a number of factors that increase the likelihood of disease progression.

These factors are:

  • Atherosclerosis, coronary heart disease and other pathologies of the cardiovascular system.
  • Regular stress.
  • Brain injury.
  • Obesity and unbalanced nutrition.
  • Elderly age.
  • Climax.
  • Smoking, drug addiction, drinking alcohol.
  • Cravings for drinks that are high in caffeine. These are energy drinks, black tea and coffee.
  • Excessive salt intake.
  • Hypodynamia (lack of physical activity).

Hypertension of the 3rd degree most often develops due to the lack of adequate therapy for milder forms of the disease.

Risk and symptoms of hypertension

Often patients ask doctors, I have hypertension stage 3 stage 3 risk 4 what is it? This abbreviation refers to the severity of the disease and the level of risk.

What is risk? There is a specialized risk classification that displays the prevalence of target organ damage. When making a diagnosis, this classification must be used. In total, there are 4 degrees of risk, we will consider each of them separately:

  1. Risk I degree. In this case, there are no complications, and the prognosis is generally favorable.
  2. Risk II degree. In this case, we are talking about at least 3 factors that significantly aggravate the course of hypertension. The prognosis is less favorable. Target organs are affected by no more than 20%.
  3. Risk III degree. There are many complicating factors. The prognosis is unfavorable. Target organs are affected by 30%.
  4. Risk IV degree. The prognosis is unfavorable. There are lesions of the heart, kidneys and brain. Target organs are affected by 30-40%.

In the third degree of hypertension, most often the risk is III or IV degree. In the vast majority of patients, the heart muscle thickens, the kidneys decrease in size, and the renal tubules become sclerosed. In severe cases, the kidney tissue is scarred, and the walls of the vessels from the inside are affected by cholesterol plaques.

Consider the signs of hypertension of the 3rd degree. Of course, the disease has a pronounced symptomatology. Only in the first stage of the disease can be asymptomatic. So, the characteristic features are:

  1. Headache. They become chronic and have a "dull" character. The pain syndrome radiates to the temples, jaw, eyeballs, temples.
  2. Nausea. With jumps in blood pressure, vomiting occurs.
  3. Noise in ears.
  4. Pain in the chest area. For hypertension of the 3rd degree, angina pectoris is characteristic, that is, a pronounced pain syndrome in the region of the heart, accompanied by shortness of breath and panic attacks.
  5. Numbness of the extremities, muscle weakness, convulsions. In some cases, the disease is accompanied by swelling of the limbs.
  6. Decreased mental activity. The patient perceives information much worse, memory impairment develops. Such symptoms are caused by the fact that cerebral ischemia gradually progresses.
  7. Deterioration of visual acuity. The reason for this is chronic vasospasm of the retina.

Against the background of stage 3 hypertension, heart or kidney failure often develops.

Treatment and disability for grade 3 hypertension

End-stage hypertension is treated with medication. The basis of therapy is pills for high blood pressure. ACE inhibitors, diuretics, calcium antagonists, beta-1-blockers, diuretics, centrally acting antihypertensives, combined drugs can be used.

With this severity of hypertension, it is customary to use several drugs at once. Various combinations of 2 or 3 drugs may be used. The patient will have to take the pills for life. If this rule is neglected, then hypertensive crises will regularly develop with all the ensuing consequences.

Antihypertensive pills should not be taken during pregnancy and lactation. Some drugs in this group are contraindicated in the presence of renal failure, diabetes mellitus and liver failure.

In addition to taking medications, the patient should:

  • Refuse once and for all from smoking, alcohol, drugs.
  • Try to spend more time outdoors. Of course, it is impossible to give the body increased loads in this case. It is optimal to do exercise therapy or go for walks. With the permission of the doctor, you can use the pool.
  • Eat properly. Table 10 diet of hypertensive patients is shown. Completely remove fatty, fried, spicy foods from the diet. Refusal of sweets and carbonated drinks is shown. It is necessary to follow a diet for life - this is a prerequisite for treatment.

With stage 3 hypertension, the patient can get a disability. To do this, he needs to undergo a medical examination. The first or second group of disability can be assigned. Most often, benefits are given to hypertensive patients who have recently suffered a stroke, and, accordingly, are disabled.

Patients with stage 3 hypertension should be registered at the dispensary and undergo periodic examinations.

Prevention and complications of GB

The best prevention of stage 3 essential hypertension is to treat the disease in time at stages 1-2. It is much easier to achieve compensation in the initial stages, when GB does not affect target organs.

Also, in order to avoid grade 3 hypertension, you should regularly exercise, refrain from drinking alcohol and smoking, eat right, treat pathologies of the cardiovascular system in a timely manner, and do not drink a lot of coffee and other drinks that contain caffeine.

If there is a predisposition to atherosclerosis, it is imperative to monitor the level of low and high density lipoproteins, total cholesterol and triglycerides. If there are deviations, undergo treatment with statins and fibrates.

Possible complications of hypertension:

  1. Stroke.
  2. Myocardial infarction.
  3. Renal failure.
  4. Heart failure.
  5. Hypertensive crisis.
  6. Cardiac ischemia.
  7. cardiac asthma.
  8. Aortic aneurysm.
  9. Uremia.
  10. Retinal detachment.

As you can see, stage 3 hypertension is fraught with many complications, and poses a great danger to the patient's life.

It is much easier to seek compensation for the disease in the initial stages. Therefore, it is strongly recommended that when the first signs of GB appear (headaches, dizziness, nosebleeds, "flies" before the eyes), you should immediately contact a cardiologist.

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Types of atherosclerosis. Disease classification

Atherosclerotic vascular lesions and associated circulatory disorders are one of the leading causes of death. That is why great attention is paid to its study and the search for effective methods of treatment. The classification of atherosclerosis is extensive, it concerns the causes, course, stages and localization of atherosclerotic lesions.

Classification of atherosclerosis by etiology

The division of types of atherosclerosis by origin is proposed by the World Health Organization. It is supported by domestic cardiologists, vascular surgeons and phlebologists.

Hemodynamic form

Its development is provoked by high blood pressure. The branching sites of the arteries are most at risk, it is in them that the protective layer of the vascular endothelium (glycocalix) is damaged under the action of hemodynamic pressure.

The inner lining of the vessels (intima) becomes permeable to lipoproteins. In the future, a thrombus or cholesterol plaque forms at this place. Also, the cause of atherosclerosis can be thrombosis, varicose veins or thrombophlebitis. Another reason is vasospasm.

metabolic form

This form is also called alimentary. Atherosclerosis develops as a result of a violation of carbohydrate or fat metabolism. This occurs with improper and unbalanced nutrition or as a result of a lack of minerals in food.

This also includes atherosclerosis caused by autoimmune disorders - hypothyroidism, diabetes mellitus or a decrease in the level of sex hormones.

mixed form

The combination of hemodynamic and metabolic causes of atherosclerosis cause a mixed form of the disease. The processes that provoke atherosclerosis resemble a vicious circle. Formed blood clots lead to circulatory disorders and negatively affect metabolism.

In turn, improper fat metabolism leads to increased blood clotting and, as a result, provokes the formation of blood clots. On the inner lining of the vessels, fatty stripes and spots begin to form - harbingers of future atherosclerotic plaques. But fatty spots are not yet a disease; at this stage, the condition lends itself well to correction, subject to early detection.

Types of atherosclerosis by localization

Another classification divides atherosclerosis according to the location of the damage:

  • coronary atherosclerosis (affects the vessels of the heart);
  • cerebral (affects cerebral arteries);
  • obliterating sclerosis of the lower extremities;
  • damage to the aorta;
  • atherosclerosis of the renal arteries;
  • atherosclerosis of brachiocephalic arteries;
  • multifocal atherosclerosis.

Each of them has its own symptoms, prognosis and course.

Atherosclerosis of the coronary arteries

Atherosclerotic lesions of the heart vessels are characterized by a long latent (hidden) course. More than one year may pass from the beginning of formation to the development of a “full-fledged” atherosclerotic plaque.

Symptoms can occur when the blood flow in them is disturbed so noticeably that cardiac ischemia develops. It is accompanied by angina attacks, arrhythmias, swelling of the legs. The function of the left ventricle of the heart decreases, body weight increases. The most severe consequence is myocardial infarction.

Atherosclerosis of the arteries of the brain

Cerebral atherosclerosis is divided into stages (or degrees of damage):

  • initial, when the symptoms appear only under the influence of provoking factors, and the violations are functional in nature;
  • at the second stage, morphological disorders join the functional disorders, and the manifestations of the disease become more persistent;
  • the third degree is characterized by ischemic attacks, leading to necrosis of certain parts of the brain and loss of their functions.

Among the main symptoms are emotional instability, sleep deterioration, memory and intellectual abilities decrease. As a result of microstrokes, paresis and paralysis can develop.

Atherosclerosis of the vessels of the legs

The main provoking factors in the development of sclerotic lesions of the vessels of the legs are varicose veins and diabetes mellitus. Cholesterol plaques block the lumen of the femoral artery. At the initial stage, there are symptoms such as numbness and chills in the lower extremities. Next comes intermittent claudication.

As obliterating atherosclerosis develops, the color of the feet changes - they become pale. Hair growth on the affected leg gradually stops, and nail growth slows down. At the last stage, areas of necrosis appear. The most severe consequence is gangrene.

Aortic lesion

The aorta is the largest and at the same time the most vulnerable vessel for atherosclerosis in the human body.

The thoracic aorta contains the most damaging factors - pathogenic microorganisms and viruses that destroy the endothelium. Here, most of all fatty deposits, from which atherosclerotic plaques are formed.

Due to the large diameter of the vessel, the clinical manifestations of atherosclerosis occur mainly in old age, when the artery loses its elasticity and thickens due to calcium deposits. Depending on the place in which the lumen of the thoracic aorta is blocked, the heart or brain suffers. Accordingly, the symptoms appear.

atherosclerosis of the abdomen

In the abdominal region, the aorta divides into two large arteries. The branching site is the “favorite” area of ​​​​atherosclerotic deposits. Plaque occlusion of the mesenteric arteries disrupts the blood supply to the intestines and pelvic organs.

The first symptoms are variable "wandering" pain around the navel, weight loss and constant bloating and constipation. Intestinal ischemia is accompanied by intense pain, gradually increasing poisoning of the body, tension in the abdominal muscles and profuse vomiting.

Violation of the nutrition of the genital organs causes infertility, in men - problems with sexual life. Atherosclerosis of the abdominal region is fraught with intestinal gangrene, intestinal obstruction and bleeding.

Atherosclerosis of the kidney vessels

At the first stage of the development of atherosclerosis, fatty spots appear in the renal arteries, which then turn into fibrous plaques. These stages proceed without obvious symptoms. The plaques gradually overgrow with connective tissue, blocking the lumen of the vessels. And only then the signs of defeat begin to appear.

One of the most formidable consequences of renal artery sclerosis is renovascular hypertension. She quickly passes the 1st degree, taking a course of moderate severity with consistently high blood pressure.

If both arteries are captured by the pathological process, hypertension becomes malignant. Problems with urination, weakness and constant headaches join high pressure numbers. Can hurt the lower back and stomach.

Atherosclerosis of the brachiocephalic arteries (BCA)

The brachiocephalic trunk is a group of blood vessels that supply the brain and shoulder girdle. This includes in particular the carotid, subclavian and vertebral arteries. BCA atherosclerosis in terms of prevalence occupies one of the leading places among all atherosclerotic lesions.

There are two types of BCA sclerosis:

  • non-stenosing, that is, not reducing the lumen of the vessel;
  • stenosing, when the vessel narrows by 70% or is completely blocked by an atherosclerotic plaque.

A non-stenosing variant is the formation of fatty bands in the arteries, which only slow down the flow of blood. Stenosing with the formation of plaques inevitably leads to cerebral ischemia and stroke and requires urgent medical attention.

Non-stenosing atherosclerosis of the BCA may be asymptomatic as long as less than 50% of the vessel diameter is occluded. Or it can be symptoms that the patient does not attach much importance to - chronic fatigue, absent-mindedness, dizziness, numbness of the fingers. However, over time, the symptoms become more pronounced. This means that the pathological process deepens and passes into the stenosing stage.

Multifocal atherosclerosis

So in medicine is called a generalized atherosclerotic lesion of the arteries. Pathology captures almost all vascular pools. In almost half of the cases, it is not accompanied by obvious symptoms, and this is the main danger of the multifocal form.

At first, the disease is localized in one place, gradually capturing all new sections of the arteries. It is this period of distribution that is practically not manifested by any specific signs. This is due to the protective reaction of the body, which creates bypass routes for blood flow - collaterals. If the "reserve" vascular network is well developed, the asymptomatic period lasts a long time.

But with the spread of atherosclerosis, symptoms characteristic of damage to the coronary, cerebral arteries and vessels of the legs begin to appear. With all the ensuing consequences described above.

Classification according to ICD-10 and A.L. Myasnikov

In the international classification of diseases, atherosclerosis is usually divided into periods or stages of development:

  1. The pathological process is fully compensated by the inclusion of internal reserves of the body. Symptoms may only appear in response to intense physical exertion. There is shortness of breath, a feeling of fatigue, mild paresis.
  2. Incomplete compensation begins at the second stage of the disease, when its signs are felt regardless of physical exertion.
  3. The subcompensated stage is manifested at rest by chills, convulsions, and morning edema. This means that the body loses its protective resource.
  4. The decompensated stage is manifested by impaired blood flow, intoxication and tissue ischemia. Severe pains begin in the suffering organs. Immunity is reduced and pathogenic flora is activated.

Soviet cardiologist A.L. Myasnikov classified atherosclerosis in a similar way, describing the processes occurring in the vessels:

  1. The period until the disease makes itself felt is preclinical. Changes can only be detected with the help of instrumental studies.
  2. The fatty spots formed in the vessels begin to become inflamed, and the sites of inflammation become overgrown with connective tissue, forming a scar. The ischemic period of the disease begins. The lumen of the arteries narrows, the blood supply and the performance of the organs deteriorate.
  3. Blood clots form on the inflamed fatty spot, forming a thrombus or embolus. They block the lumen of the vessel even more. There is a constant danger of a blood clot breaking off. The stage is called thrombonecrotic. The risk of heart attack and stroke increases.
  4. The sclerotic stage is marked by the formation of a scar at the site of inflammation of the vascular wall. The arteries do not cope with the nutrition of the organs, ischemia and necrosis of their tissue occurs.

The first stage of atherosclerosis - the formation of fatty spots - can begin at a very young age. Do not neglect its first signs. At this stage, the disease is completely curable. And if you keep the process under control, atherosclerosis will not bother even in old age.

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