Extensive myocardial infarction: is there life after it? What is a major myocardial infarction?

Problems caused by contractions of the chaotic nature of the myocardial muscle are called atrial fibrillation. Pathology acts as both an independent problem and a consequence of previous cardiovascular diseases, the consequences of which are serious threat for human life. It is required to know the symptoms of occurrence, the causes of the disease and methods of effectively combating the pathology to ensure the normal functioning of the body.

Types of pathology

Flickering arrhythmia is a chaotic contraction of myocardial muscle tissue with an interval of 350-600 pulse oscillations per minute. Atrial contraction does not proceed fully, which forms blood stagnation, causing the risk of thrombotic plaques, provoking an ischemic stroke. This type pathology has a diverse classification. The characteristic course of arrhythmia varies:

Chronic (stable or permanent). Flow chronic pathology continues until surgery, treatment by other methods is ineffective;
Persistent. The duration of the attack exceeds a week and is recurrent;
Transient (paroxysmal). The duration does not exceed 1-6 days and is recurrent in nature.

According to the type of rhythmic disorder, atrial fibrillation (atrial fibrillation) is distinguished. There is a scattered contraction of different muscle filaments of the myocardium, which eliminates the coordinated rhythm in atrial fibrillation and leads to an abnormal discharge of blood flow into the aorta. Frequent flickering leads to the risk of myocardial muscle arrest. The next type is atrial flutter; the rhythm of contractions up to 400 beats becomes characteristic, while maintaining the correct contraction of the atrium. The continuous contractions caused interfere with the normal blood flow in the ventricles, therefore, the blood flow into the aorta is disrupted. Based on the frequency of ventricular compressions, atrial fibrillation is classified into the tachysystolic form, the normosystolic form, and the bradysystolic form.

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Causes of pathology

Causes of atrial fibrillation provoked by cardiogenic factors:

sclerosis of the myocardial muscle of diverse etiology;
acute myocarditis;
congenital or acquired pathologies of the cardiovascular system;
injury to the heart muscle during surgery;
valvular dysfunction;
heart attack;
hypertension and hypertension;
development of myocardial tumors.

Causes of atrial fibrillation from non-cardiac factors:

thyroid problems;
psycho-emotional overload;
drug overdose;
transferred viral and infectious diseases;
electric shock;
VSD (rare phenomena);
toxic effects on the body;
hormonal imbalance in the body.

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Symptoms of atrial fibrillation

When the heart rhythm is disrupted, blood output decreases.

At the initial stage, there are practically no symptomatic signs. Diagnosis of flickering arrhythmia is carried out only through examinations, and sometimes manifests itself during physical activity. As the pathology progresses, symptoms and signs characteristic of the disease appear, depending on the form and stage of development. When arrhythmia develops, the symptoms are as follows:

difficulty breathing;
feeling of a “stone” on the heart;
variable flutter of the heart muscle;
lethargy;
state of chills;
increased sweating;
decreased temperature of the extremities;
panic attacks;
frequent urge to go to the toilet;
myocardial rhythm disturbance.

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Risks of atrial fibrillation

An attack of atrial fibrillation of long duration can cause ischemic stroke, as well as thromboembolism. Manifestations of atrial fibrillation lead to blockage by a blood clot, causing death. Development arrhythmogenic shock becomes one of the most dangerous manifestations myocardial failure in atrial fibrillation. The transition of atrial fibrillation to the stage of ventricular fibrillation becomes dangerous, which causes death.

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Diagnostic measures

To make a diagnosis of atrial fibrillation, the following diagnostic measures are carried out:

Name	Description
Initial examination and interview with the patient	clarification of complaints and initial examination allow us to determine the presence of violations; The pulse is measured; its irregularity will help the specialist suspect fibrillation.
ECG	simple and accessible technique determination of atrial fibrillation; readings are taken by ambulance workers or in a clinic.
Determine indications for hospitalization	examinations are carried out in the cardiology department; After collecting all the data, the patient is sent for additional diagnostics.
Daily examination using an ECG device	The slightest deviations that were not recorded by the cardiogram are measured to check the correctness of treatment.
Cardiac ultrasound	determines characteristic failures in the contractile work of the myocardium, structural disorders.
ChPEFI	held artificial stimulation, causing atrial fibrillation to record a clinical arrhythmia that was not reflected on the ECG.
X-ray of the chest organs	used to determine the presence of thrombotic congestion.
Blood tests	the hormonal level of the thyroid gland is studied; helps in diagnosing cardiomeopathy.

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Medicines

The treatment method for paroxysmal and permanent forms of atrial fibrillation differs. The difference arises against the background of different stages of the two forms of pathology. The difference is that the first pathology consists of treatment for the purpose of providing first aid, and flows into rhythm-restoring therapy. The second is treated with medications to provoke a cut heart rate.

Drugs for the treatment of atrial fibrillation do not themselves affect the heart rhythm: they prevent the ventricles from contracting.

Treatment of atrial fibrillation in the manifestation of heart failure occurs more actively with specific medications:

when treated and for prophylactic purposes, cardiac glycosides are used;
stagnation of blood circulation is treated with beta blockers;
Anticoagulants are used to thin the blood;
treatment with thrombolytic enzymes begins when thrombosis is diagnosed;
diuretics eliminate swelling of the lung tissue and cardiac asthma.

Treatment of atrial fibrillation to prevent recurrent factors is carried out comprehensively over several years. The patient must strictly follow the instructions prescribed by the doctor, apply the prescribed medication, do physical exercise to improve myocardial function. It is possible to stop using any drug only if you are intolerant of its components, or if the drug is diagnosed as ineffective.

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Other methods

After recovery sinus rhythm, therapy is recommended breathing exercises, which, filling the body with oxygen, will restore the heartbeat and improve conductivity. Recommended use therapeutic exercises, active physical exercise is prohibited until the absence of relapse is confirmed. Surgical intervention is prescribed in case of ineffectiveness drug treatment.

An important point in the treatment of atrial fibrillation is the correct diet. Changing the type of diet can improve clinical picture diseases. It is recommended to give up sweets, spicy foods, and butter, smoked products, fatty. You should eat fermented milk products, lean meat, vegetables and fruits, 4-6 meals a day, in small portions.

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Forecasts and preventive measures

The positive prognosis for a diagnosis of atrial fibrillation depends on the severity of the arrhythmia and the causes that provoked it. Recovery for myocardial defects with development acute failure, acquires favorable prognosis only after surgical intervention. Without surgery, the patient survives only until the acute form of the disease develops. In the absence of organic pathologies, the prognosis for recovery is favorable.

Prevention of the disease involves the following measures:

timely treatment of CVS pathologies;
stop bad habits;
stop excessive physical activity;
work to reduce psycho-emotional stress;
do not neglect sedatives;
Carry out regular monitoring of cholesterol and blood glucose levels.

Atrial fibrillation is becoming a serious threat to the lives of people susceptible to both cardiovascular diseases and non-cardiac diseases. It is important to know the symptoms, causes, causing disease and timely contact with the attending physician for assistance and prescription quality treatment. Strict adherence to prescribed instructions and carrying out preventive measures will help cope with pathology.

Treatment of dyscirculatory encephalopathy: causes, clinical signs, treatment

At the first stage of the disease, neurological deficit affects only certain areas mental activity. This is expressed in the appearance of memory or behavior disorders. Subsequently, memory loss gradually increases and intelligence decreases. In addition, there is also an increasing decrease in the affective sphere, characteristic of chronic phase psychoorganic process and almost indistinguishable from vascular dementia.

Especially with this disease, complex mental processes that are associated with information processing suffer. In patients diagnosed with dyscirculatory encephalopathy mixed origin there is a disorder in the program of actions, gait, orientation in time, place, and even one’s own personality. Paroxysmal disorders of consciousness, counting, writing, and generalized thinking may occur.

In addition to the slowly progressive course of discirculatory encephalopathy, there is also a “galloping” and remitting course with the presence of periodic breakdowns and compensations. Usually, stressful situations, infections, injuries, intoxications cause relapse of this disease.

Clinical signs

As a rule, functional neurodynamic symptoms appear in the first stages of the disease. Subsequently, there is a progression of an organic neuropsychic defect with a disorder of memory, motivation, drives, and emotions.

The patient's complaints include fatigue, irritability, absent-mindedness, memory loss, and headaches with mental or physical stress. Symptoms of the disease increase in the afternoon, after sleepless night etc. It is worth noting that the patient’s own assessment of the decline in his performance does not coincide with positive characteristic those around you. Asthenic syndrome may be regressive with long-term rest, treatment, changes in the environment at home or at work, and regression can last a relatively long time.

At the second stage of the disease, the neuropsychic defect deepens. The patient is not critical enough of his condition and overestimates his capabilities and performance. A transition from self-doubt to attempts to find “objective reasons” for one’s failures is also characteristic. In addition, such patients experience a narrowing of the scope of perception, rapid exhaustion, refusal to complete tasks and their replacement with easier primitive forms.

Treatment of dyscirculatory encephalopathy

Among the main directions drug therapy slowly progressive type of failure cerebral circulation There are several separate stages. Therapeutic measures aimed at strengthening cerebral blood flow and metabolism of brain tissue, relief of neurasthenic symptoms, normalization of sleep, limitation of the volume of mental and physical activity, exception stressful situations, normalization of rest and work conditions.

As for medications, wide use received drugs in the treatment of dyscirculatory encephalopathy nicotinic acid, nootropic drugs, calcium channel blockers.

In addition, the patient needs psychotherapeutic conversations, autogenic training, selection of a rational diet, moderate physical activity, walks in the fresh air, physical labor. If symptoms increase, consultation with a neuropsychiatrist is necessary.

Features of stage 3 hypertension

What is stage 3 hypertension?
Risk groups of patients with hypertension
What to pay attention to
Reasons for the development of stage 3 hypertension

Hypertension is a fairly common problem. The most dangerous option is stage 3 of this disease, but when making a diagnosis, the stage and degree of risk are indicated.

People who have high blood pressure should understand the dangers of this in order to take adequate measures in time and not increase the already high risk of complications. For example, if the diagnosis is hypertension risk 3, what is it, what do these numbers mean?

They mean that a person with such a diagnosis has a 20 to 30% risk of developing a complication due to hypertension. If this indicator is exceeded, a diagnosis of stage 3 hypertension is made, risk 4. Both diagnoses mean the need urgent measures on treatment.

What is stage 3 hypertension?

This degree of the disease is considered severe. It is determined by blood pressure indicators, which look like this:

Systolic pressure 180 or more mmHg;
Diastolic – 110 mmHg. and higher.

In this case, the blood pressure level is always elevated and almost constantly remains at levels that are considered critical.

Risk groups of patients with hypertension

In total, it is customary to distinguish 4 such groups depending on the likelihood of damage to the heart, blood vessels and other target organs, as well as the presence of aggravating factors:

1 risk – less than 15%, no aggravating factors;
2 risk – from 15 to 20%, no more than three aggravating factors;
3 risk – 20-30%, more than three aggravating factors;
4 risk – above 30%, more than three aggravating factors, target organ damage.

Aggravating factors include smoking, insufficient physical activity, excess weight, condition chronic stress, poor nutrition, diabetes, endocrine disorders.

With hypertension of 3 degrees with risk 3, a health threat arises. Many patients are in risk group 4. High risk is also possible at lower blood pressure levels, since each organism is individual and has its own margin of safety.

In addition to the degree and risk group, the stage of hypertension is also determined:

1 – no changes or damage in target organs;
2 – changes in several target organs;
3 – except for target organ damage plus complications: heart attack, stroke.

When hypertension develops to grade 3 with risks 3 and 4, it is impossible not to notice the symptoms, because they manifest themselves quite clearly. The main symptom is critical levels of blood pressure, which causes all other manifestations of the disease.

Possible manifestations:

Dizziness and headaches with throbbing;
Flashing “flies” before the eyes;
General deterioration of condition;
Weakness in the arms and legs;
Vision problems.

Why do these symptoms occur? The main problem with hypertension is damage to vascular tissue. High blood pressure increases the load on the vascular wall.

In response to this, the inner layer is damaged, and the muscle layer of the vessels increases, which is why their lumen narrows. For the same reason, the vessels become less elastic; cholesterol plaques, the lumen of the vessels narrows even more, and blood circulation becomes even more difficult.

In general, the health risk is very high, and grade 3 hypertension with a risk of grade 3 threatens disability quite realistically. Target organs are especially affected:

Heart;
Kidneys;
Brain;
Retina.

What happens in the heart

The left ventricle of the heart expands, the muscle layer in its walls grows, and the elastic properties of the myocardium deteriorate. Over time, the left ventricle is not able to fully cope with its functions, which threatens the development of heart failure if timely and adequate measures are not taken.

Kidney damage

The kidneys are an organ that is abundantly supplied with blood, so they often suffer from high blood pressure. Damage to the renal vessels impairs their blood supply.

The result is chronic renal failure, since destructive processes in blood vessels lead to changes in tissues, for this reason the functions of the organ are disrupted. Kidney damage is possible with stage 2 hypertension, stage 3, risk 3.

With hypertension, the brain also suffers from blood supply disturbances. This is due to sclerosis and decreased tone of blood vessels, the brain itself, as well as the arteries running along the spine.

The situation is aggravated if the patient’s vessels are highly tortuous, which often happens in this area of the body, since tortuosity contributes to the formation of blood clots. As a result, with hypertension, without timely and adequate help, the brain does not receive enough nutrition and oxygen.

The patient's memory deteriorates and attention decreases. Encephalopathy may develop, accompanied by a decrease in intelligence. This is very unpleasant consequences, so they can lead to loss of performance.

The formation of blood clots in the vessels supplying the brain increases the likelihood ischemic stroke, and the rupture of a blood clot can lead to hemorrhagic stroke. The consequences of such conditions can be catastrophic for the body.

Effects on the organs of vision

In some patients with grade 3 hypertension with grade 3 risk, damage to the vessels of the retina occurs. This negatively affects visual acuity, it decreases, and “spots” may also appear before the eyes. Sometimes a person feels pressure on eyeballs, in this state he constantly feels drowsy, his performance decreases.

Another danger is hemorrhage.

One of dangerous complications hypertension grade 3 with risk 3 – hemorrhages in various organs. This happens for two reasons.

Firstly, the thickening walls of blood vessels lose their elasticity so much that they become brittle.
Secondly, hemorrhages are possible at the site of the aneurysm, because here the walls of the vessels become thinner from overflow and are easily torn.

Minor bleeding as a result of a ruptured vessel or aneurysm leads to the formation of hematomas; in the case of large ruptures, hematomas can be large-scale and damaging internal organs. It is also possible heavy bleeding, which require immediate medical attention to stop.

There is an opinion that high blood pressure a person immediately feels it, but this does not always happen. Everyone has their own individual sensitivity threshold.

The most common variant of the development of hypertension is the absence of symptoms until the onset of a hypertensive crisis. This already means the presence of hypertension stage 2, stage 3, since this state indicates organ damage.

The period of asymptomatic disease can be quite long. If a hypertensive crisis does not occur, then the first symptoms gradually appear, to which the patient often does not pay attention, attributing everything to fatigue or stress. This period can even last until the development of arterial hypertension of degree 2 with a risk of 3.

What to pay attention to

Regular dizziness and headaches;
Feeling of tightness in the temples and heaviness in the head;
Noise in ears;
"Floaters" before the eyes;
General decrease in tone4
Sleep disorders.

If you do not pay attention to these symptoms, then the process continues, and increased load the vessels are gradually damaged, they cope with their work worse and worse, and the risks grow. The disease progresses to next stage and the next degree. Arterial hypertension grade 3, risk 3, can progress very quickly.

This results in more severe symptoms:

Irritability;
Decreased memory;
Shortness of breath with little physical exertion;
Visual impairment;
Interruptions in the functioning of the heart.

With grade 3 hypertension, risk 3, the likelihood of disability is high due to large-scale vascular damage.

Reasons for the development of stage 3 hypertension

The main reason why such a serious condition as stage 3 hypertension develops is the lack of treatment or insufficient therapy. This can happen both through the fault of the doctor and the patient himself.

If the doctor is inexperienced or inattentive and has developed an inappropriate treatment regimen, then it will not be possible to lower blood pressure and stop the destructive processes. The same problem awaits patients who are inattentive to themselves and do not follow the specialist’s instructions.

For correct diagnosis Anamnesis is very important, that is, information obtained during examination, acquaintance with documents and from the patient himself. Complaints, blood pressure indicators, and the presence of complications are taken into account. Blood pressure should be measured regularly.

To make a diagnosis, the doctor needs data for dynamic observation. To do this, you need to measure this indicator twice a day for two weeks. Blood pressure measurement data allows you to assess the condition of blood vessels.

Other diagnostic measures

Listening to lungs and heart sounds;
Percussion of the vascular bundle;
Determination of heart configuration;
Electrocardiogram;
Ultrasound of the heart, kidneys and other organs.

To clarify the state of the body, it is necessary to do tests:

Blood plasma glucose levels;
General blood and urine analysis;
Creatinine level uric acid, potassium;
Determination of creatinine clearance.

In addition, the doctor may prescribe additional examinations necessary for a particular patient. In patients with stage 3 hypertension, stage 3, risk 3, there are additional aggravating factors that require even more careful attention.

Treatment of stage 3 hypertension, risk 3, involves a set of measures that includes drug therapy, diet and active lifestyle. It is mandatory to give up bad habits - smoking and drinking alcohol. These factors significantly aggravate the condition of blood vessels and increase risks.

For the treatment of hypertension with risks 3 and 4, drug treatment with one drug will not be enough. A combination of drugs from different groups is required.

To ensure stability of blood pressure, long-acting drugs are mainly prescribed, which last up to 24 hours. The selection of drugs for the treatment of stage 3 hypertension is carried out based not only on blood pressure indicators, but also on the presence of complications and other diseases. The prescribed drugs should not have side effects undesirable for a particular patient.

Main groups of drugs

Diuretics;
ACE inhibitors;
β-blockers;
Calcium channel blockers;
AT2 receptor blockers.

In addition to drug therapy, it is necessary to adhere to a diet, work and rest, and give yourself feasible exercise. The results of treatment may not be noticeable immediately after it begins. It takes a long time for symptoms to begin to improve.

Adequate nutrition for hypertension is an important part of treatment.

You will have to exclude foods that contribute to a rise in blood pressure and the accumulation of cholesterol in the blood vessels.

Salt consumption should be kept to a minimum, ideally no more than half a teaspoon per day.

Prohibited Products

Smoked meats;
Pickles;
Spicy dishes;
Coffee;
Semi-finished products;
Strong tea.

It is impossible to completely cure arterial hypertension of the 3rd degree, risk 3, but it is possible to stop the destructive processes and help the body recover. The life expectancy of patients with stage 3 hypertension depends on the degree of development of the disease, the timeliness and quality of treatment, and the patient’s compliance with the recommendations of the attending physician.

The prognosis may be unfavorable. Most alarming diagnosis— hypertension stage 3, degree 3, with risk 4, since there are also unfavorable factors, and critical blood pressure, and target organ damage.

To keep blood vessels under control, you need to undergo regular examinations, regardless of how you feel. It necessarily includes taking tests and ECG from 1 to 3 times a year. The patient's blood pressure should be measured regularly. You can do this yourself using a convenient tonometer.

3. 1. Large focal (transmural). Q infarction.

3. 2. Finely focal. Not Q heart attack.

4. Post-infarction cardiosclerosis.

The diagnosis is made no earlier than 2 months after the onset of myocardial infarction. The diagnosis indicates the presence of a chronic cardiac aneurysm, internal myocardial ruptures, dysfunction of the papillary muscles of the heart, intracardiac thrombosis, the nature of conduction and heart rhythm disturbances, the form and stages of heart failure. If the ECG does not show signs of a previous myocardial infarction, the diagnosis can be made by typical ECG changes or enzyme changes in the anamnesis (based on medical documentation).

5. Heart rhythm disturbances (indicating the form).

Typically, conduction and heart rhythm disturbances complicate other forms of coronary artery disease, but sometimes they can be the only manifestation of the disease. In these cases, the diagnosis of IHD requires clarification using functional stress tests and selective coronary angiography.

6. Heart failure.

Heart failure can complicate any form of coronary artery disease. If patients with heart failure do not have clinical or electrocardiographic evidence of CAD (current or history), the diagnosis of CAD becomes questionable.

Note: in case of successful resuscitation of a patient with coronary artery disease, it is better to use the term “SCA - sudden (primary) circulatory arrest,” and in case of “biological” death, you can use the term “sudden coronary death”

Functional severity classes of stable angina pectoris according to the Canadian Heart Association classification

I fk. – Normal daily physical activity (walking or climbing stairs) does not cause angina attacks. An attack of angina occurs when performing very fast or prolonged physical work.

II fk. – Slight limitation of usual physical activity – the occurrence of angina as a result of fast walking or quickly climbing stairs, after eating, in the cold in windy weather, under the influence of emotional stress, in the first few hours after getting out of bed, while walking more than 200 meters (two blocks) on level ground or while climbing more than one flight of stairs at a normal pace under normal conditions.

III fk. – Marked limitation of usual physical activity – an attack of angina occurs as a result of walking one to two blocks (100-200 m) on level ground or when climbing one flight of stairs at a normal pace under normal conditions.

IV fk. – Inability to perform any type of physical work without causing discomfort– an attack of angina may occur at rest

CLASSIFICATION OF UNSTABLE ANGINA (National Guidelines for Cardiology, 2007)

Clinical forms of unstable angina

-New-onset angina– the occurrence of angina attacks during the last two months

- Progressive angina– an increase in the frequency and/or duration of anginal attacks, a decrease in exercise tolerance, the appearance of attacks at rest, as well as a decrease in the effectiveness of antianginal drugs.

-Angina at rest– attacks at rest lasting more than 20 minutes for 2 months.

Classification of unstable angina(S. W. Hamm, E. Braunwald, 2000)

	And it develops in the presence of extracardiac factors that increase myocardial ischemia. Secondary NS	INdevelops without extracardiac factors Primary NS	WITH- occurs within 2 weeks after a heart attack Post-infarction NS
1 - First appearance of severe angina, progressive angina; without angina at rest
II - Angina at rest in the previous month, but not in the next 48 hours; (angina pectoris, subacute
III- Angina at rest in the previous 48 hours (angina at rest,		IIIB - Troponin – IIIB - Troponin +

CLASSIFICATION OF ACUTE CORONARY SYNDROME (National Guidelines on Cardiology, 2007)

Acute coronary syndrome - acute phase IHD. Acute coronary syndrome is a temporary “working” diagnosis, which is necessary for initial assessment, risk stratification, and choice of treatment tactics in patients with exacerbation of coronary artery disease. From the point of view of the peculiarities of the development of the process, the possibility of rapid diagnosis, and the development of treatment tactics, acute coronary syndrome is conveniently divided into 2 groups depending on changes in the initial ECG:

Acute coronary syndrome with segment elevation ST;

ST.

In acute coronary syndrome with ST segment elevation, in most cases, large focal MI subsequently develops. In patients with acute coronary syndrome without segment elevation ST Usually the diagnosis is unstable angina or small focal MI. With the widespread introduction into clinical practice of the determination of cardiac troponins (markers of myocardial damage) in patients with acute coronary syndrome, the division of acute coronary syndrome without segment elevation ST for unstable angina and small focal MI has become widespread.

Acute coronary syndrome without segment elevation ST

DEFINITIONS

Acute coronary syndrome without segment elevation ST characterized by anginal attacks and the absence of segment elevation on the ECG ST. To acute coronary syndrome without segment elevation ST include unstable angina and non-elevation myocardial infarction ST.

Unstable angina is a worsening of the course of angina, expressed in an increase in the frequency and duration of attacks, a decrease in exercise tolerance, and a decrease in the effectiveness of antianginal therapy.

Unstable angina includes any variants of new-onset angina (last 2 months), worsening of existing angina (transition from class I-II to class III or IV), and the appearance of angina attacks at night. The severity and duration of an attack with unstable angina are insufficient for the development of myocardial necrosis. Usually there are no elevations on the ECG ST. There is no release of biomarkers of myocardial necrosis into the bloodstream in quantities sufficient to diagnose MI.

Myocardial infarction without segment elevation ST- acute myocardial ischemia, leading to necrotic damage. There are no segment elevations on the initial ECG ST. In the majority of patients whose disease begins as non-elevation myocardial infarction ST, Q_waves do not appear and, as a result, small focal MI without Q waves is diagnosed. MI without ST segment elevation differs from unstable angina by the appearance or increase in the levels of markers of myocardial necrosis, which are absent in unstable angina.

CLASSIFICATION OF MYOCARDIAL INFARCTION (National Guidelines for Cardiology, 2007)

Initial changes on the ECG:

MI with ST segment elevation (this group also includes acute blockade of the left His bundle branch);

Non-ST segment elevation MI

Subsequent changes on the ECG:

MI with the formation of pathological Q waves (usually MI with ST segment elevation corresponds to developing large-focal MI with the subsequent formation of pathological Q waves);

MI without the formation of pathological Q waves.

Dimensions of the necrosis focus:

large-focal (transmural) MI;

small focal MI.

Localization of the necrosis focus:

MI of the anterior wall of the left ventricle (anterior MI)

MI of the lateral wall of the left ventricle (lateral MI)

isolated apex myocardial infarction

MI of the inferior wall of the left ventricle (inferior MI)

THEM back wall left ventricle

MI of the interventricular septum

Right ventricular MI

Atrial MI

Combined localizations are possible: posteroinferior, anterolateral, etc.

History of MI:

primary MI;

recurrent MI;

recurrent MI.

MI period:

the most acute period: from the beginning pain attack before the formation of a focus of necrosis (the first 4-6 hours);

acute period: final formation of a necrosis focus (up to 2 weeks);

subacute period: scar formation (up to 2 months)

post-infarction period: complete scarring and scar consolidation (after 2 months)

CLASSIFICATION OF CLINICAL FORMS AND COURSE OF MYOCARDIAL INFARCTION ACCORDING TO THEODORI M.I. WITH ADDENDUMS

“Classic” (retrosternal pain)

With a typical onset in the form of an acute, prolonged painful attack and a cyclic course with clearly defined three periods: acute, subacute and functional-restorative

Erased (reduced) forms

With typical, but mildly expressed symptoms or only with individual symptoms characteristic of myocardial infarction.

Atypical forms:

a) peripheral

With the occurrence or primary localization of pain not in the heart area, but on the periphery: left-scapular, left-hand, upper vertebral, mandibular and ear, laryngeal-pharyngeal.

b) abdominal

With a picture of an acute abdominal catastrophe: perforated gastric ulcer, gastric bleeding, intestinal obstruction.

c) painless

“Asthmatic” - with cardiac asthma syndrome, sometimes with the development of pulmonary edema. With acute development of heart failure (right ventricular or biventricular).

"Collaptoid"

"Arrhythmic" with a picture severe violation heart rate and conduction (in the presence of complete atrioventricular block - often with Morgagni-Adams-Stokes syndrome).

“Asymptomatic” - without pronounced clinical manifestations, detected only by electrocardiographic examination.

d) cerebral

With a picture acute disorder cerebral circulation:

fainting form;

the onset of clinical myocardial infarction masked by a hypertensive crisis;

hemiplegic form

e) combined

When combined, for example, pulmonary edema and cardiogenic shock;

retrosternal pain form and acute cerebrovascular accident, etc.

By localization

Anterior, anterolateral, anteroseptal, posterior, posterolateral, posteroseptal, septal, anteroposterior, involving the papillary muscles, involving the atria (if there are clinical data for damage to the papillary muscles or electrocardiographic data for damage to the atria) .

According to the depth of the lesion Transmural, subepicardial, subendocardial, intramural

By prevalence Widespread (extensive), limited.

According to the number of myocardial infarctions suffered Primary, repeated (indicating, if possible, which one).

Note: repeated (as opposed to recurrent) myocardial infarction should be understood as one that developed at different times after the previous one, but always after completion of the repair processes from the previous lesion

Flow:

a) typical

With pronounced periods - acute, subacute and functional-restorative, the terms of which do not deviate from the usual ones.

b) recurrent

With repeated infarctions of the heart muscle, occurring at different periods of the disease, but always before the completion of the repair processes from the previous infarction.

c) protracted

With a slow pace of development of reparative processes and prolongation of certain periods of the disease.

d) latent (subclinical)

Without any pronounced clinical symptoms, but with typical electrocardiographic dynamics.

According to the presence of complications:

a) uncomplicated

b) complicated

Acute vascular insufficiency - cardiogenic shock-collapse (true cardiogenic collapse; reflex-type collapse; arrhythmic-type collapse; collapse due to rupture of the heart muscle).

Acute heart failure (left ventricular, right ventricular, biventricular).

Rhythm and conduction disturbances (extrasystole, paroxysmal tachycardia, atrial fibrillation and flutter, blockades (intraventricular and atrioventricular), ventricular fibrillation.

Diffuse fibrinous or effusion pericarditis. Acute cardiac aneurysm. Heartbreak. Rupture of the interventricular septum. Avulsion of the papillary muscle. Acute dilatation stomach. Intestinal paresis. Gastric bleeding (due to acute ulcer or erosive gastritis).

Spicy diabetic syndrome with hyperosmotic or acidotic coma.

Acute renal failure. Thromboendocarditis (usually parietal, aseptic or septic).

Thromboembolic complications:

a) early (from loose parietal thrombi in the ventricles of the heart);

b) late (venous thrombosis with pulmonary embolism, thromboembolism in the arterial system).

Post-infarction syndrome.

Myocardial abscess (purulent melting of a necrotic focus with the development purulent pericarditis or rupture of an abscess into the pericardium and hemotamponade).

Chronic cardiac aneurysm.

Progressive chronic heart failure.

Examples of diagnosis formulation

IHD. New onset angina pectoris. CHF 0 st -FC 0

IHD. Stable angina pectoris functional class III. CHF I stage – FC I

IHD. Stable angina pectoris IIfk, post-infarction (large focal) cardiosclerosis (AMI in 1991) CHF IIa. –FC III

IHD. Spontaneous angina. CHF I stage - FC II.

IHD. Unstable angina IV. HSNIst.-FKI.

IHD. Unstable angina IIС. HSNIst. – FKI.

IHD. transmural myocardial infarction of the anteroseptal region with transition to the apex, the most acute period. Ventricular extrasystole, class II according to Lown, OSNIIIst. by Killip.

IHD. Paroxysm of atrial fibrillation, tachysystolic form, cholesterol level H 1 - FC I.

IHD. Complete atrioventricular block. Adams-Stokes-Morgagni attacks, II degree of severity, CHF IIb - FC III

Classification of hyperlipoproteinemia

	Increased lipoproteins	Increased lipids
	Chylomicrons	Triglycerides, cholesterol
		Cholesterol (normal triglycerides)
	LDL and VLDL	Same
	β-VLDL (floating β)	Cholesterol, triglycerides
	VLDL	Triglycerides, cholesterol
	Chylomicrons, VLDL	Triglycerides (normal cholesterol)

CLASSIFICATION OF ARTERIAL HYPERTENSION (HYPERTENSION) (Russian recommendations, 2008)

Classification of blood pressure levels

	SBP, mmHg	DBP, mm Hg.
Optimal blood pressure
Normal blood pressure
High normal blood pressure
AH I degree of severity (mild)
AH II degree of severity (moderate)
AG III degree severity (heavy)
PI-isolated systolic hypertension

Threshold blood pressure levels (mmHg) for diagnosing arterial hypertension according to various measurement methods

In addition, classification according to the stages of the disease is used

Stage I hypertension - absence of target organ damage.

Stage II hypertension - the presence of changes in one or more target organs.

Stage III hypertension - the presence of associated clinical conditions.

Of great importance is the assessment of overall cardiovascular risk, the degree of which depends on concomitant risk factors, target organ damage and associated clinical conditions.

Risk stratification criteria

Risk factors

▪ pulse blood pressure value (in the elderly)

men over 55 years old;

women over 65 years of age;

dyslipidemia (total cholesterol >5.0 mmol/l (>190 mg/dl) or LDL cholesterol >3.0 mmol/l (>115 mg/dl) or HDL cholesterol<1,0 ммоль/л (40 мг/дл) для мужчин и <1,2 ммоль/л (46 мг/дл) для женщин; или ТГ >1.7 mmol/l(150 mg/dl)
fasting plasma glucose 5.6 – 6.9 mmol/l (102-125 mg/dl)
Impaired glucose tolerance
family history of early cardiovascular disease (women under 65 years of age, men under 55 years of age);
abdominal obesity (waist circumference > 102 cm for men or > 88 cm for women) in the absence of metabolic syndrome;

Target organ damage

LV hypertrophy:

ECG: Sokolov-Lyon sign >38 mm; Cornell product >2440 mm-ms;

EchoCG: LV myocardial mass index >125 g/m2 for men and >110 g/m2 for women.

Vessels

▪Ultrasound signs of atherosclerotic plaques or thickening of the artery wall(thickness of the intima-media layer carotid artery>0.9 mm) or atherosclerotic plaques of the great vessels.

▪pulse wave speed from the carotid to the femoral artery > 12 m/s

▪ ankle/brachial index< 0,9

Kidneys

▪ Small increase in serum creatinine 115-133 µmol/L (1.3-1.5 mg/dL) for men or 107-124 µmol/L (1.2-1.4 mg/dL) for women.

▪ Low GFR< 60 мл/ мин/1,73 м2 (MDRD формула) или низкий клиренс креатинина < 60 мл/ мин (формула Кокрофта-Гаулта)

▪ Microalbuminuria: 30-300 mg/day;

▪ urine albumin/creatinine ratio ≥22 mg/g (2.5 mg/mmol) for men and ≥31 mg/g (3.5 mg/mmol) for women.

Associated (concomitant) clinical conditions

Cerebrovascular diseases:

ischemic stroke;

hemorrhagic stroke;

transient ischemic attack.

Heart diseases:

myocardial infarction;

angina pectoris;

coronary revascularization;

chronic heart failure.

Kidney diseases:

diabetic nephropathy;

renal failure (serum creatinine >133 µmol/L (>1.5 mg/dL) for men or >124 µmol/L (>1.4 mg/dL) for women);

proteinuria (>300 mg/day).

Peripheral arterial diseases:

dissecting aortic aneurysm;

symptomatic damage to peripheral arteries.

Hypertensive retinopathy (hemorrhages or exudates, papilledema).

Diabetes : fasting plasma glucose ≥7 mmol/L (126 mg/dL) with repeated measurements;

blood plasma glucose after a meal or 2 hours after taking 75 g of glucose ≥11 mmol/l (198 mg/dl).

Metabolic syndrome

The main criterion is AO (OT > 94 cm for men and > 80 cm for women)

Additional criteria: blood pressure≥ 140 and 90 mmHg.

LDL cholesterol > 3.0 mmol/l, HDL cholesterol< 1,0 ммоль/л для мужчин или < 1,2 ммоль/л для женщин, ТГ >1.7 mmol/l, fasting hyperglycemia≥ 6.1 mmolk, IGT – plasma glucose 2 hours after taking 75 g of glucose≥ 7.8 and≤ 11.1 mmol/l

▪ The combination of the main and 2 of the additional criteria indicates the presence of MS

Depending on the degree of increase in blood pressure, the presence of risk factors, target organ damage and associated clinical conditions, all patients with hypertension can be classified into one of four risk groups:

Low risk;

Moderate level of risk;

High level of risk;

Very high level of risk.

According to the European SCORE system, the risk of death from diseases associated with atherosclerosis within 10 years is assessed in patients who do not have proven coronary heart disease: low risk corresponds to a value of less than 5%; moderate - 5-9%; high - 10-14% and very high - more than 15%.

Risk stratification in patients with hypertension*

Risk factors, target organ damage and comorbidities	High normal 130-139 /85-89 mmHg.	AG I degree 140 -159 /. .90 – 99 mmHg	AH II degree 160 – 179 / 100 -109 mmHg.	AH III degree ≥180 /110 mmHg
	Insignificant	Low additional risk	Average extra risk	High add. risk
	Low add. risk	Average extra risk	Average extra risk	Very high add. risk
≥3 FR, POM, MS or diabetes mellitus	High add. risk	High add. risk	High add. risk	Very high add. risk
Associated clinical conditions	Very high add. risk	Very high add. risk	Very high add. risk	Very high add. risk

Note* the accuracy of determining the overall cardiovascular risk directly depends on how completely the clinical, instrumental and biochemical examination of the patient is carried out. Without cardiac and vascular ultrasound data to diagnose LVH and carotid artery wall thickening (or plaque), up to 50% of hypertensive patients may be erroneously classified as low or moderate risk instead of high or very high; ** add. – additional risk.

High and very high risk patients

SBP ≥ 180 mmHg. and/or DBP ≥110 mmHg

SBP > 160 mmHg with low DBP (<70 мм.рт.ст.)

Diabetes

Metabolic syndrome

≥3 risk factors

Target organ damage

LVH according to ECG or EchoCG

Ultrasound signs of carotid artery wall thickening (IMT >0.9) mm or atherosclerotic plaques

Increased arterial wall stiffness

Moderate increase in serum creatinine

Decreased GFR or creatinine clearance

Microalbuminuria or proteinuria

Associated clinical conditions.

Formulation of diagnosis

When formulating a diagnosis, the presence of risk factors, target organ damage, associated clinical conditions, and cardiovascular risk should be reflected as fully as possible. The degree of increase in blood pressure is necessarily indicated in patients with newly diagnosed arterial hypertension; in other patients, the achieved degree of arterial hypertension is written. It is also necessary to indicate the stage of the disease.

Examples of diagnostic reports

Stage I hypertension. Degree of hypertension 2. Dyslipidemia. Risk 2 (medium)

Stage II hypertension. Degree of hypertension 3. Dyslipidemia. LVH. Risk 4 (very high).

Stage III hypertension. Degree AG2.. IHD. Angina pectoris II FC. Risk 4 (very high).

Stage III hypertension. Achieved degree of hypertension 1. Obliterating atherosclerosis of the vessels of the lower extremities. Intermittent claudication. Risk 4 (very high).

Stage I hypertension. Degree of hypertension 1. Diabetes mellitus type 2. Risk 3 (high).

IHD. Post-infarction (large focal) cardiosclerosis. Stage III hypertension. The achieved degree of hypertension is 1. Risk 4 (very high).

Obesity I degree. Impaired glucose tolerance. Stage 3 hypertension.. Risk 4 (very high).

Pheochromocytoma of the right adrenal gland. AH 3 degrees. LVH. Risk 4 (very high)...

CLASSIFICATION OF HYPERTENSIVE CRISES

International recommendations suggest clinical classification, based on the severity of clinical symptoms and the risk of developing severe (even fatal) life-threatening complications. These conditions are divided into complicated (emergency) and uncomplicated GC (urgency).

A complicated hypertensive crisis (critical, emergency, life-threatening, emergency) is accompanied by the development of acute clinically significant and potentially fatal damage to target organs, which requires emergency hospitalization (usually in a block). intensive care) and immediate reduction of blood pressure using parenteral antihypertensive drugs.

An uncomplicated hypertensive crisis (non-critical, urgent, urgency) occurs with minimal subjective and objective symptoms against the background of a significant increase in blood pressure. It is not accompanied by acute development of target organ damage. Requires a decrease in blood pressure within several hours. Does not require emergency hospitalization.

Classification of hypertensive crises (Russian recommendations, 2008)

Complicated

Accompanied by signs of acute life-threatening damage to target organs.

1. Arterial hypertension or symptomatic hypertension benign and malignant course, complicated by acute damage to target organs;

Acute hypertensive encephalopathy;

Brain stroke;

Acute coronary syndrome;

Acute left ventricular failure

▪ dissecting aortic aneurysm.

2. Preeclampsia or eclampsia in pregnant women.

3. Crisis with pheochromocytoma.

4. Severe hypertension associated with subarachnoid hemorrhage or brain injury.

5. Arterial hypertension in postoperative patients and with the threat of bleeding.

6. Crisis due to the use of amphetamines, cocaine, etc.

Uncomplicated

Despite the pronounced clinical symptoms, an uncomplicated hypertensive crisis is not accompanied by clinically significant dysfunction of target organs.

Classification of arterial hypertension according to etiology ( National leadership in Cardiology, 2007).

Symptomatic renal hypertension

♦ Hypertension in chronic kidney diseases:

chronic glomerulonephritis, chronic pyelonephritis, diabetic nephropathy (glomerulosclerosis), chronic urate tubulointerstitial nephritis, analgesic nephropathy, polycystic kidney disease, kidney damage with systemic vasculitis, amyloidosis of the kidneys, tuberculosis of the kidneys, tumors and injuries of the kidneys, nephropathy of pregnancy (primary and secondary), congenital anomalies of the number/location, shape of the kidneys (hypoplasia, duplication, kidney dystopia, hydronephrosis, horseshoe kidney)

● Vasorenal hypertension: atherosclerosis, fibromuscular dysplasia, nonspecific aortoarteritis, hematomas and tumors compressing the renal arteries, congenital pathology (atresia and hypoplasia of the renal arteries, angiomas and arteriovenous fistulas, aneurysms).

Endocrine hypertension:

♦ hypersecretion of mineralcorticoids (primary and idiopathic aldosteronism, familial form of hyperaldosteronism type I);

♦ hypersecretion of glucocorticoids (Itsenko-Cushing syndrome);

♦ damage to the adrenal medulla: hypersecretion of catecholamines (pheochromocytoma);

♦ dysfunction of the thyroid gland: hyperthyroidism, hypothyroidism; hyperparathyroidism;

♦ damage to the pituitary gland: Itsenko-Cushing’s disease; acromegaly.

● Hypertension caused by damage to large arterial vessels: atherosclerosis of the aorta; coarctation of the aorta; stenosing lesions of the aorta and brachiocephalic arteries in nonspecific aortoarteritis.

Centrogenic hypertension:

♦ with organic lesions of the central nervous system;

♦ when increasing intracranial pressure(tumors, injuries, encephalitis, poliomyelitis, focal ischemic lesions), with sleep apnea syndrome, lead intoxication, acute porphyria.

● Medicines and exogenous substances that can cause hypertension: hormonal contraceptives, corticosteroids, sympathomimetics, mineralcorticoids, cocaine, foods containing tyramine or monoamine oxidase inhibitors, NSAIDs, cyclosporine, erythropoietin.

Examples of diagnosis formulation

Atherosclerosis of the right renal artery. Vasorenal hypertension, stage III hypertension. LVH.Risk 4 (very high).

Atherosclerosis of the left carotid artery, stage II hypertension. LVH. Risk 3 (high).

Chronic pyelonephritis, phase of latent inflammation. AH II degree. LVH. Risk 3 (high). CKD stage 2 – CRF 1 st.

CLASSIFICATION CARDIOGENIC SHOKA (CHAZOV E.I. 1971.

Reflex shock is caused mainly by reflex disorders due to changes in vascular tone, which lead to shifts in the adequate regulation of general and regional blood circulation.

True cardiogenic shock - in its development, the main role is played by a sharp drop in the propulsive function of the left ventricle, which leads to a significant decrease in cardiac output and a decrease in blood pressure.

Arrhythmic shock develops in connection with the occurrence of rhythm disturbances, predominantly ventricular paroxysmal tachycardia or complete transverse block.

Areactive shock can be diagnosed if, within 15-20 minutes, the administration of increasing doses of norepinephrine or hypertensin does not cause an increase in blood pressure.

CLASSIFICATION OF DEGREES OF SEVERITY OF CARDIOGENIC SHOCK, V. N. Vinogradov, V. G. Popov, A. S. Smetnev, 1961.

I degree : 3-5 hours, blood pressure within 90 and 50 mm Hg. Art. - 60 and 40 mm Hg. Art., pulse pressure 40-25 mm Hg. Art. Symptoms of heart failure are mild. Rapid sustained pressor reaction (30-60 minutes after a set of measures). Mortality 6.9%.

II degree : duration from 5 to 10 hours, blood pressure within 80 and 50 mm Hg. Art. - 40 and 20 mm Hg. Art., pulse pressure 30-15 mm Hg. Art. Peripheral signs of shock are expressed, in most cases - symptoms of acute heart failure (shortness of breath at rest, acrocyanosis, congestive wheezing in the lungs). The pressor response to treatment is slow and unstable.

III degree : extremely difficult and long course against the background of steadily progressing peripheral signs and a sharp drop in blood pressure, pulse pressure below 15 mm Hg. Art. Acute heart failure, 70% have alveolar pulmonary edema. There is no pressor response to adrenomimetics or this reaction is unstable and short-term. Mortality - 91%.

CLASSIFICATION OF FUNCTIONAL DISEASES OF THE CARDIOVASCULAR SYSTEM according to N. N. Savitsky, 1952

How long people live after a myocardial infarction depends on a number of factors. A person’s age and type of disease play a big role. When the patient is young and the pathology is not severe, the prospects are quite encouraging. Survival rate of elderly people who have had similar pathology heart rate, especially with its transmural variety, is quite low. Concomitant pathologies, such as aneurysm, diabetes mellitus or arterial hypertension, are often detected in elderly patients. It is these ailments that are considered criteria that significantly reduce the life expectancy of these patients. Statistics show that myocardial infarction often leads to fatal outcome, so you should try to do everything possible to prevent this.

All complications are divided by doctors into early and late.

Acute (early) consequences:

the occurrence of pulmonary edema;
heart rhythm disorder;
acute heart failure;
thrombosis formed in the systemic circulation.

If the heart attack is small-focal, then the likelihood of complications is reduced. Since as a result of such a destructive process, damage to the left ventricle of the organ occurs more often, insufficiency of this particular section is observed. A symptom of such a disorder is breathing problems; the patient cannot inhale air normally. Against the background of such a disorder and insufficiency of the left ventricle, swelling of the lung tissue occurs.

Another serious consequence of myocardial infarction is considered to be dangerous forms of arrhythmia, including ventricular fibrillation. The pathologies themselves are serious, some people cannot live long if they occur, and if such a situation develops after a heart attack, the prognosis is often disappointing. When such damage to the heart is detected, the localization of which is located in the endocardial zone from below, then there is a significant likelihood of thrombosis in the area great circle blood circulation If a blood clot breaks off and enters the vascular bed of the brain, the lumen of these arteries becomes blocked, causing a stroke.

Long-term complications are considered less dangerous than acute ones, but they appear much more often than early consequences.

Long-term complications:

pericarditis;
all types of arrhythmia;
development of cardiosclerosis;
damage to the lung tissue or pleurisy.

If we talk about cardiosclerosis, then this disorder is detected in all patients who have suffered such a heart disease. It affects how long you can live after a heart attack. Similar conditions have a direct connection with the formation connective fibers to form a scar on the organ. If cardiosclerosis has diffuse form, then deviations in the functioning of the heart muscle may be observed. If the conductivity of an organ is disrupted, then interruptions in its contractions occur, and heart failure often appears. The processes that can appear during the heart attack itself are varied and deadly.

Complications during the death of heart cells:

organ tamponade, causing hemorrhage to the pericardial zone;
acute cardiac aneurysm;
thromboembolism affecting the lung;
development of thromboendocarditis;
rupture of one of the ventricles of the organ and death.

This is why it is difficult for doctors to answer questions regarding how long such a patient will live; many factors play a role here. associated factors. Those patients whose condition is not burdened by additional ailments have a chance. It is important to follow the recommendations of your doctor during the recovery phase; this will help reduce the likelihood of severe consequences or the development of a second heart attack. The effectiveness of the therapy also affects the prognosis. The treatment method, surgical or medicinal, should help the person’s heart resume its activity. If doctors managed to achieve this, it means that the patient’s life expectancy will increase. Stenting is another way to help patients live long lives. If this intervention has been applied, the wall of the artery, in which there are atherosclerotic plaques, is cleared of them, then blood flow is restored, helping to improve the functioning of the main organ.

How long do they live after a massive heart attack?

During myocardial infarction, part of the heart tissue dies. If we're talking about If there is an extensive type of disease, then a large area of the organ is susceptible to necrosis, significantly disrupting its activity. Necrotic changes most often affect the anterior wall of the left ventricle, since it is this area that is more functionally loaded than others. From this zone, blood is released into the aorta under high pressure. Statistics show that in a small proportion of patients, a destructive process is observed in the right ventricle, and an even smaller number of heart attack victims are exposed to atrial pathology.

If developed massive heart attack myocardium, then damage to all layers of the muscle tissue of the organ, epicardium, myocardium, and endocardium is detected.

The necrosis zone can measure up to 8-9 cm in width. This large area of cell death is caused by critical level nutrients and oxygen to the heart. Such deviations are usually the result of long-term disruption of blood flow in the coronary artery.

Problems with blood flow in this area are often associated with atherosclerotic lesions of the vessel walls. As the plaques begin to increase in size, they gradually close this gap until it becomes completely obstructed. The danger of this condition is that any external influence in the form of excessive physical activity or emotional overload can contribute to plaque detachment and damage the fibers of the vascular wall. The restoration process in the tissues of the artery walls occurs due to the formation of a blood clot, which gradually increases in size and closes the lumen of the artery, which leads to a stop in blood supply.

Among other things, a growing blood clot releases special substances that can cause vessel spasm. Such narrowing of the lumen can be observed both in small sections of the arteries and affect it completely. During the period of spasm, blood flow is often disrupted, and sometimes it is completely blocked, preventing nutrients from entering the heart. This process entails the death of organ cells, which usually occurs 15-18 minutes after the onset of such pathology. When another 6 to 8 hours pass, extensive myocardial infarction occurs, after which life expectancy is significantly reduced.

What causes blood blockage:

Arterial hypertension. Under the influence of high pressure, thickening occurs blood arteries, more precisely, their walls, they become less flexible and thick. During periods of stress, such vessels are not able to provide the main organs with all nutrients and oxygen.
Genetic predisposition. A person may develop a tendency to form blood clots, develop atherosclerotic lesions and high blood pressure as a result of heredity. On average, such causes cause myocardial infarction in a third of all cases.
Diabetes. This pathology increases the growth of atherosclerotic plaques. In addition, the disease destroys vascular tissue and disrupts the body's metabolic processes. The combination of such factors often leads to serious illnesses hearts.
Age criteria. Young people are less likely to suffer from this pathology.
Bad habits. Inhaling tobacco smoke negatively affects the condition of blood vessels, causing them to narrow. Alcohol contributes to the development of disorders in the liver, the organ responsible for the breakdown of fats. Due to the inability of the liver to perform this function normally, fat accumulates and is deposited on the walls of the arteries.
Being male. In men, myocardial infarction occurs much more often than in women, approximately 3-4 times.
Insufficient or complete lack of physical activity affects the elasticity of the vascular walls, leading to loss of flexibility.
Failure in kidney function. Failure of this organ provokes a disorder metabolic processes concerning calcium and phosphorus. If on vascular walls calcium will begin to be deposited, the risk of myocardial infarction increases significantly as thrombosis develops.

Excess weight. Extra kilos create heavy load to the entire cardiovascular system.
Intense sports or physical activity. During periods of such intensive training myocardium requires a large number of nutrients and oxygen. If a person’s arteries are inelastic, then their spasm during intense activity can result in a heart attack.
Surgeries or injuries. Narrowing of the lumen of the coronary arteries often occurs as a result of surgical intervention in this area.

Statistics on how many years people live after a myocardial infarction are disappointing. Doctors' manipulations in case of a large heart attack should be quick, and decisions should be made in a matter of minutes, then you can count on a favorable prognosis.

Probability of another heart attack

Second attack of myocardial infarction more dangerous than the first. Relapse is more often observed in elderly males who suffer from arterial hypertension accompanying a person during the first year after myocardial infarction, and the Q wave was absent. Such a disease can occur with the presence of multiple asthmatic disorders, organ rhythm disorders, and heart failure. The clinical picture of a recurrent attack appears less pronounced relative to the intensity of the pain, which is due to a decrease in the sensitivity of areas of the heart that were previously susceptible to necrosis.

Symptoms of a recurrent heart attack:

difficulty breathing;
pain radiating to the neck, arm or shoulder on the left;
decrease in blood pressure;
severe suffocation;
cyanosis (blue skin);
impaired consciousness or fainting.

Such symptoms are a consequence of serious swelling of the lung tissue, which occurs as a result of the patient’s terminal conditions.

No one can accurately predict whether there will be a second myocardial infarction and how long people live after it. Some patients follow all the recommendations of the attending physician and protect themselves from negative impacts stress and take all the prescribed medications, but the attack overtakes them again. Other patients refuse to take medications, lead their previous lifestyle without limiting themselves in any way, and their health remains good.

Doctors divide repeated heart attack and its recurrent type. The difference is that a repeated attack of the disease occurs more than 2 months after the first, and a recurrent attack appears earlier, less than 2 months after the previous one. The second time, the pathology can be large-focal or small-focal. In addition, the lesion can cover the same areas as before, or be localized in another part of the myocardium.

Causes re-development This disease usually lies in the same atherosclerosis. Plaques can grow into coronary vessels, causing them to narrow.

Atherosclerosis does not disappear anywhere, even after a heart attack, so you need to carefully monitor the level of cholesterol in the blood and try to reduce it with the help of medications prescribed by the doctor.

In order to live long life after heart attack, people need to reduce low-density lipoproteins (bad cholesterol) and protect themselves from emotional and physical stress, establish a proper diet and give up bad habits.

Rehabilitation period

The recovery stage after myocardial infarction can last differently. This process is influenced by many factors.

What determines the duration and nature of rehabilitation:

concomitant diseases;
severity of the attack;
presence of complications;
the patient's occupation;
age data.

During the recovery period, a person needs to reconsider his lifestyle, habits and preferences.

Rehabilitation includes:

proper nutrition;
absence of stressful situations and worries;
physical activity that needs to be developed gradually;
visits to a psychologist;
taking all medications prescribed by a doctor;
weight loss, if it is excess;
rejection of bad habits;
regular examinations and consultations with the treating doctor.

Nutrition for patients who have suffered a myocardial infarction is divided into 3 stages. A general description of the diet can be seen in diet menu No. 10.

The first step is the table of a person who is in an acute period of illness. Meals include dishes without added salt, boiled or cooked in a double boiler. It is better to eat pureed food, in small amounts, but often, 5-6 times a day. Liquid is also limited, 0.8 liters per day is enough.
In the second or third week of the post-infarction period, the patient's menu changes slightly. You need to prepare food in the same way, but you can eat it not pureed, but lightly chopped. The diet is fractional, and water is allowed in a volume of about 1 liter.
The scarring stage may allow inhibitions to be slightly reduced. The method of preparing dishes remains the same, but it is permissible to eat them in pieces, and the doctor often allows salt, but in the amount of 4 grams per day, and only for some patients. Eating should be done frequently, up to 5-4 times a day.

There is a special menu preferred for such patients. These foods and dishes contain large amounts useful elements, especially necessary for people who have suffered a myocardial infarction. When discharged from the hospital, you should ask your doctor to draw up a similar memo, with the help of which it will be easier for patients to navigate when developing a personal diet.

Recommended menu:

low-fat fish;
lean meat, preferably chicken or veal;
soups made from pureed vegetables and cereals;
fermented milk drinks with a low fat content;
egg white omelet;
bread, crackers;
butter is acceptable to a minimum, and by the 3rd stage up to 10 grams is possible;
boiled vegetables, stew;
baked fruits;
drinks in the form of fruit drinks, compotes, loosely brewed teas, rose hips;
natural honey

There are many dietary restrictions; you need to exclude from your diet a large number of foods that can negatively affect the health and activity of the human heart.

What is prohibited:

When the body recovers, dietary restrictions can be lifted, but this must be done gradually and only under the supervision of a doctor.

Emotional overload often provokes serious violations health, especially with heart disease. After a myocardial infarction, the patient should absolutely not be nervous, since any excitement can cause a rhythm disorder in the main organ and lead to vasospasm, which provokes a repeat attack. To cope with emotions and survive the illness, the patient is prescribed a course of therapy with a psychologist. The doctor will help you recover, without manifestations of nervousness and fear.

Physical activity is necessary for such people, but all actions are coordinated with the doctor. Within a few days after the attack, patients are allowed to get out of bed and walk around the ward a little. Walking in the fresh air allows a little later, and the distance that such a person can walk increases gradually. With the help of physical activity, it is possible to restore normal blood circulation and heart function. It is important during sports warm-ups not to bring the situation to the point of pain or other unpleasant sensations, this can provoke a recurrent attack. Exercise therapy procedures are prescribed to many patients after a heart attack. During these sessions, all stress on a person is controlled by a specialist.

Rehabilitation measures should not fade into the background if your health has improved. The duration of this period is regulated only by doctors, and you cannot stop these actions on your own.

Traditional treatment

Plants and other medicines can help recover from such an illness. homemade. But before using any of these remedies, you need to coordinate your actions with your doctor.

Methods of traditional therapy:

Sprouted wheat. Take several glasses of wheat and soak them in gauze with water. Wait until sprouts appear (it will take several days). Break off these sprouts and eat 1 teaspoon in the morning on an empty stomach.
Hawthorn. Pour one tablespoon of dried hawthorn fruit into a glass of boiling water, leave for half an hour, strain and drink. You need to take 2 glasses of this drink per day.
Honey and rowan. Take 2 kg of honey and 1 kg of fresh rowan fruits. Grind the berries and mix with honey. Eat 1 tablespoon throughout the day.

The prognosis for myocardial infarction is impossible to predict, but every person is able to help himself. By following all the doctor’s recommendations and additionally using folk therapy, people improve their well-being and heart activity, thereby reducing the risk of death and recurrent attack.

Some people who have had a heart attack die immediately or almost immediately, others suffer three, four, or even five heart attacks. Why does this happen and how do people live after a heart attack? Let's talk about this on the pages of our website.

Why do people have multiple heart attacks?

And, perhaps, luck. More strong body A person who leads a predominantly healthy lifestyle can survive several heart attacks. While a person with poor health, a weakened psyche, weak nerves and a sick cardiovascular system may not survive even one heart attack.

The more you eat, the more likely you are to have another heart attack. concomitant diseases and predisposing conditions. , hereditary predisposition, poor nutrition, excess body weight, as well as psycho-emotional and physical overload - all this affects the condition of the diseased core. And there is no point in hoping that he might be lucky and be able to suffer three more heart attacks - the risk is very high. Moreover, men are more vulnerable to repeated heart attacks than women.

How should a person who has had a heart attack behave?

A patient who has had a myocardial infarction is at risk, so he must adhere to some unshakable rules if he does not want to have another heart attack.

First of all, you should give up bad habits, quit smoking - this is a categorical requirement. A heart attack patient who persistently continues to smoke may consider himself suicidal. The fact is that the fat content in a smoker’s blood is much higher than in the blood of a non-smoker, and this is a direct threat to atherosclerosis. When smoking, the clotting time accelerates, which leads to the formation of blood clots and to another attack.

The second most important risk factor is obesity. There is only one recommendation here, long known to everyone - eat less and move more. As for physical activity, no matter how hard it is for a heart attack patient, he needs to move as much as possible.

Atherosclerosis is treated with physical exercise. 30 minutes three times a week is enough to improve general state blood according to fat indicators, decreased, developed circulatory system, nourishing the myocardium, cholesterol normalized, fatty plaques resolved. All this can be proven using angiography of the heart vessels. Moreover, the sooner a heart attack patient begins to load the heart after a heart attack, the better. But the loads should increase gradually.

Patients should not refuse medications prescribed by their doctor. After all, we are talking about, and therefore about life and death. Many do not follow the recommendations at all, do not receive treatment, or are treated sporadically. If you want to avoid a heart attack, follow your doctor's advice.

They carry the disease on their legs, however, until a certain time, until the disease causes complications. If some forms of heart attack respond well to treatment, then an extensive one threatens the patient with death.

Is it possible to avoid it? Yes, if you know everything about the risk factors and treatment of extensive myocardial infarction.

Features of the disease

A massive heart attack is perhaps the most dangerous form of pathology. If in a small-focal form the blood flow is disrupted in small areas of the heart, then in a widespread form it is covered big square heart muscle. According to statistics, men suffer from a heart attack approximately 4 times more often than women.

After a major myocardial infarction, patients may be given a third group of disability if they lose their ability to work or they still have symptoms. In some cases, patients are entitled permanent disability, If further treatment has a poor prognosis.

Classification and forms

Extensive in itself is a form of myocardial infarction, and therefore has no specific classification. The disease is classified by location, so most often an extensive form of myocardial infarction affects:

anterior wall of the left ventricle of the heart;
interventricular septum;
posterior wall of the myocardium;

There are several stages of the condition:

acute - up to 2 hours. from the onset of a heart attack;
acute - up to 10 days. from the onset of a heart attack;
subacute - from 10 days. up to 8 months;
scarring period - from approximately 8 weeks to 6 months;

Also, the pathology can occur with or without pulmonary edema, which happens more often. Read about the symptoms and first signs of a massive heart attack below.

Causes of extensive myocardial infarction

The main cause of a heart attack is atherosclerotic plaques, which form due to the disease of the same name, atherosclerosis. Atherosclerotic plaques constrict blood vessels, which leads to insufficient blood flow and lack of oxygen in the heart.

There are several risk factors that greatly increase the risk of a heart attack. The most aggressive factor is smoking, since it itself constricts blood vessels. No less serious factors can be considered alcohol consumption and genetic disposition, while others include:

diabetes;
ischemia;
chronic kidney disease;

Second-degree obesity is also a risk factor.

Symptoms

Symptoms largely depend on the location of the lesion and the stage of the disease. An indicative symptom is pain in the sternum, which radiates to the shoulder blades, shoulder, lower jaw, and can lead to numbness of the left arm. The pain is compressive and acute in nature and is not relieved by nitroglycerin.

Typically, a heart attack is accompanied by:

cough;
dyspnea;
blue discoloration of the skin;
cold sweat;
cardiac asthma if pulmonary edema occurs;

If the posterior wall is damaged, symptoms of poisoning may appear: heartburn, vomiting, diarrhea, pain in the abdominal area. In very rare cases, a heart attack can be suffered with virtually no symptoms, or with atypical symptoms, for example, in the right arm.

The following will tell you what nutrition should be like in the event of a major myocardial infarction:

Diagnostics

A doctor can make a primary diagnosis even during the patient’s first visit, since myocardial infarction has symptoms characteristic of the condition. First, the doctor collects a history of complaints and life, finding out when the patient began to feel pain, what accompanies these conditions, and whether he has addictions to bad habits and fatty foods. Next, the patient undergoes a physical examination and auscultation, where the skin tone is assessed, and murmurs in the heart and lungs are detected, blood pressure and pulse are determined.

Based on these studies, the doctor prescribes symptomatic treatment, which most often turns out to be correct, and prescribes further, already hardware, examinations, for example:

General an-z of urine. Helps identify concomitant pathologies and complications of the disease.
General an-z blood. Helps determine increased erythrocyte sedimentation rate and detect leukocytosis.
Biochemical analysis of blood. Necessary to determine whether the patient has risk factors for myocardial development, e.g. increased content cholesterol, sugar and triglycerides.
Blood enzyme tests, which detect the presence of protein enzymes in the blood. These enzymes are released due to the destruction of heart cells during a heart attack.
ECG. A fundamental study, since it not only confirms the presence of a heart attack, but also shows its localization, extent and duration of its course.
EchoCG. Necessary to assess the condition of blood vessels, as well as the size and structure of the heart.
Coagulogram. Needed to select optimal doses of medications.
Breast X-ray. Shows the condition of the aorta, the presence of complications of a heart attack.
Coronary angiography. Determines the location and location of narrowing of the artery.

Depending on the presence of complications, accompanying pathologies, as well as equipment in the hospital, the patient may undergo other tests. For example, expensive MSCT, which visualizes the entire heart muscle.

Treatment

Treatment of a large heart attack is carried out in a hospital, since the patient’s condition must be constantly monitored. In the first stages, treatment consists of a combination medicinal method with therapeutic.

However, drug therapy is often not enough, so surgery is required.

Therapeutic

The basis of therapy is restriction of any physical activity. The patient must remain calm both physically and emotionally, since the opposite can worsen the course of the disease.

During the entire treatment it is recommended with limited consumption animal fats, alcohol, salt and caffeine. A special place in dietary nutrition allocated to products that help restore the body, that is, cereal crops, fish, lean meat, vegetables and fruits.

If necessary, the patient may be given oxygen through a mask.

Medication

Drug therapy is aimed at stabilizing the patient's condition and preventing the development of complications. For this purpose they use

Aspirin, Plavix, Ticlopedine and similar drugs that activate blood flow to the affected area.
Narcotic and non-narcotic analgesics to relieve pain symptoms.
Lidocaine, Amiodarone and analogues for elimination.
Anticoagulants for prevention.
Thrombolytics for resolving blood clots.

Calcium antagonists and beta-blockers have shown good effectiveness. Read below about what types of operations are performed for a large heart attack.

Operation

Large infarctions often respond poorly to drug therapy. In this case, the patient is prescribed:

Coronary angioplasty, which involves installing a stent in a vessel to maintain normal lumen in it.
Coronary artery bypass surgery. Complex operation, in which a bridge is created from a healthy vein, ensuring optimal blood delivery above the narrowing.

Sometimes operations also do not work positive effect and the lesion begins to develop and become more complicated. In such cases, a heart transplant is indicated.

You can see how stenting is performed in case of extensive myocardial infarction in the following video:

Disease prevention

Preventive measures are aimed at preventing the development of heart disease. For this:

, which increases the risk of heart attack by almost 50%.
Form a daily and rest routine in which at least 7 hours will be allocated for sleep.
Limit the volume of animals and vegetable fats in the diet.
Eat more protein foods, beans, fruits, lean meats and fish.
Exercise and do cardio exercises.

If you snore at night, check to see if you have apnea. To do this, you can visit any sleep center.

Along with the above, it is necessary to constantly monitor blood pressure and cholesterol levels and lower the levels as they increase.

Read on to learn how life can turn out after a major myocardial infarction and what the consequences are for the heart.

Complications

A large heart attack often causes complications even with timely treatment. Among them are:

local necrotization and scarring of left ventricular tissue;
myocardial rupture at the site of infarction;
arrhythmias;
inflammation in serosa hearts;
autoimmune complications;
pulmonary edema with extensive myocardial infarction;
blood clot formation, thromboembolism;

Nonspecific complications associated with circulatory disorders may also be observed. Read below about how long people live after resuscitation of a major myocardial infarction, and what the general prognosis is for its consequences.

Forecast

The prognosis for treatment of extensive myocardial infarction is extremely unfavorable.

With this form, slightly more than 50% of patients survive.
Moreover, more than 10% do not survive more than a year and die from complications of the disease.

The statistics are average, since in hospital conditions the mortality rate is very low, however, many patients simply do not live to see it.

About how to provide first aid in case of extensive myocardial infarction, the video below will tell you: