Infarction: concept, types, causes and mechanism of development, morphological characteristics, outcomes. Heart attack: what it is, causes, first signs, diagnosis and treatment. Types of heart attacks Classification of the disease: idiopathic, pulmonary, drug

Cardiovascular diseases are practically the first cause of death in many countries. One of the most common pathologies is a heart attack. What kind of disease is this, for what reason does it develop, is it possible to prevent the disease and how to help the patient? We will try to answer all these questions in detail.

Heart attack - what is it?

Almost everyone knows that this is a dangerous condition, but the mechanism and causes of development are not always of interest, although this must be known in order to prevent such a pathology. A heart attack develops as a result of a disruption in the blood supply to areas of the heart muscle.

This pathology is also called one of the forms of the heart. If the blood supply is disrupted for more than 15-20 minutes, then necrosis of living tissue occurs, which is accompanied by severe pain and can be fatal.

Cardiologists note that in the male population, heart attacks occur much more often, because in the female body, estrogens control the level of cholesterol in the blood. If before the development of a heart attack was 55-60 years, now it is relatively younger. Cases of pathology are diagnosed even in young people.

A heart attack does not always end in death for a person, but you need to know that after an incident there is always a scar left on the heart, so many patients become disabled after suffering such a disease.

How does a heart attack develop?

The formation of a heart attack begins long before its manifestation. It all starts with the formation of atherosclerotic plaques, which begin to form in blood vessels from bad cholesterol. The culprits of its appearance in the blood are dietary errors and a sedentary lifestyle. These plaques gradually narrow the lumen of the blood vessels, disrupting normal blood circulation.

The process gradually worsens, the plaques become so large that any pathological impact on them leads to rupture. At this point, the blood coagulates, forming a blood clot, which clogs the vessel, preventing blood from passing further. This is exactly the process that occurs in the heart area during a heart attack.

Reasons for the development of pathology

If a heart attack develops, the causes may be different, but the main one is the cessation of blood flow to certain areas of the heart muscle. This most often occurs due to:

• Atherosclerosis, as a result of which the walls of blood vessels lose their elasticity, the lumen is narrowed by atherosclerotic plaques.
• which can occur due to stress, for example, or exposure to other external factors.
• Arterial thrombosis, if a plaque breaks off and is carried through the bloodstream to the heart.

Factors that can provoke such conditions include:

• Hereditary predisposition to heart pathologies.
• High levels of “bad” cholesterol in the blood.
• Having a bad habit such as smoking.
• Too much body weight.
• Arterial hypertension.

• Diabetes.
• A large amount of fatty foods in the diet.
• Chronic stress.
• Some doctors also note the influence of psychosomatics, when the cause of a heart attack is excessive aggression and intolerance.
• Belonging to the stronger sex.
• Low physical activity.
• Age after 40 years.

It is necessary to take into account that if there is a combination of several factors, the risk of developing a heart attack increases.

Types of disease

If we look at a pathology such as a heart attack (we have already found out what it is), then cardiologists distinguish several forms of pathology depending on several criteria.

If we consider the stages of the disease, there are four of them, each of which is characterized by its own symptoms. The size of the affected area is also taken into account in the classification. Highlight:

• Large-focal infarction, when tissue necrosis covers the entire thickness of the myocardium.
• Finely focal, a small part is affected.

By location they are distinguished:

• Right ventricular infarction.
• Left ventricle.
• Interventricular septum.
• Side wall.
• Rear wall.
• Anterior wall of the ventricle.

A heart attack can occur with or without complications, so cardiologists distinguish:

• Complicated heart attack.
• Uncomplicated.

The localization of pain can also be different, so the following types of heart attacks are distinguished:

• Typical form with chest pain.
• The atypical form can be manifested by abdominal pain, shortness of breath, heart rhythm disturbances, dizziness and headache. Sometimes a heart attack develops in the absence of pain.

Types of heart attacks are also distinguished depending on the frequency of development:

• Primary pathology.
• Recurrent
• Repeated.

Life after a heart attack will depend on the severity of the pathology, its form and timely assistance provided.

Stages of heart attack development

Necrotic changes in the heart muscle develop in some sequence, therefore the following stages of infarction are distinguished:

1. Pre-infarction condition. The duration of this period ranges from several hours to several weeks, at which time small foci of necrosis are already forming in the heart muscle, and in their place a heart attack then develops.
2. The most acute period can last from several minutes to 2 hours. Myocardial ischemia increases.
3. The acute stage of a heart attack lasts several days. During this period, a focus of necrosis forms in the heart and partial resorption of damaged muscle tissue is observed.
4. The post-infarction stage can last up to six months; the connective tissue scar is completely formed.

Diagnosis of myocardial infarction

Making a diagnosis begins with a conversation with the patient. The doctor finds out when the pain began, what nature it has, how long it lasts, how the patient relieves heart attacks, and whether there is any result from taking medications.

Then risk factors are necessarily identified; for this, the doctor clarifies the features of lifestyle, culinary preferences, and the presence of bad habits. A family history is analyzed - the doctor finds out if anyone in the family has heart disease, or whether there have been cases of heart attack.

1. A general blood test is done, it allows you to detect an increased level of leukocytes, a high erythrocyte sedimentation rate, signs of anemia - all this begins to appear when the cells of the heart muscle are destroyed.
2. A urine test will help detect concomitant pathologies that can provoke heart attacks.
3. A biochemical blood test is performed to determine:

• cholesterol content;
• the ratio of “bad” and “good” cholesterol;
• presence of triglycerides;
• blood sugar levels to assess the risk due to vascular atherosclerosis.

If there is a suspicion of a heart attack, then a study of specific blood enzymes is carried out.

A coagulogram is done; it gives indicators of blood clotting, which help to choose the correct dosage of drugs for treatment.

Diagnosis of myocardial infarction is impossible without electrocardiography. Based on the results, a specialist can determine the localization of the pathology, how long ago it developed and the degree of damage.

An ultrasound examination of the heart is performed to study the structure and size of the heart muscle, to assess the degree of damage to blood vessels by atherosclerotic plaques.

X-rays help identify changes in the thoracic aorta, lungs and detect complications.

Coronary angiography is used to clarify the diagnosis; it allows you to accurately determine the location and degree of vasoconstriction.

With contrast, it allows you to obtain an accurate image of the heart, identify defects in its walls, valves, abnormalities in functioning and narrowing of blood vessels.

After all the research, you may need to consult a therapist.

Only after the diagnosis has been clarified, the patient is prescribed effective therapy, which will help bring life back to normal after a heart attack.

Symptoms of pathology

As a rule, a heart attack does not develop out of nowhere; usually the patient has already been diagnosed with angina or other cardiac pathologies. If a heart attack develops, the symptoms and first signs in women and men may be as follows:

• Chest pain becomes more intense and prolonged. The pain has a burning character, squeezing and squeezing is felt, and can radiate to the shoulder, arm or neck.

• Irradiation and expansion of the pain zone appears.
• The patient cannot tolerate physical activity.
• Taking Nitroglycerin no longer gives such an effect.
• Even at rest, shortness of breath, weakness and dizziness appear.
• There may be discomfort in the stomach.
• The heart rhythm is disturbed.
• Breathing becomes difficult.
• Cold sweat appears, the skin turns pale.

If at least some of the listed symptoms appear, you should urgently call a doctor.

First aid to a patient

If there is a suspicion of a heart attack, the symptoms and first signs in women will only progress if emergency assistance is not provided. It is as follows:

• The person must be seated or placed in a comfortable position.

• Unfasten tight clothing.
• Provide air access.
• Give a Nitroglycerin tablet under the tongue, if the attack is severe, then two are possible.
• If there is no Nitroglycerin, then you can use Corvalol or Aspirin.

Emergency care for a heart attack will help relieve pain during an attack and reduce the risk of complications.

Complications after a heart attack

It very rarely happens that a heart attack goes away without complications; there are almost always consequences. They reduce life expectancy after suffering from pathology. The most commonly diagnosed complications are:

• Heart failure.
• Rupture of the heart muscle.
• Aneurysm.
• Cardiogenic shock.
• Heart rhythm disturbances.

• Post-infarction angina.
• Pericarditis.

A heart attack can also have late consequences, for example:

• After a few weeks, post-infarction syndrome may develop.
• Thromboembolic complications are common.
• Neurotrophic disorders of the nervous system.

Many patients are interested in the question of how long can one live after a heart attack? The answer will depend on several factors: the degree of damage to the heart muscle, the timeliness of first aid, the effectiveness and correctness of therapy, and the development of complications.

According to statistics, about 35% of patients die, most of them, without even reaching a medical facility. Those patients who have suffered a heart attack are most often forced to change their field of activity or leave work altogether; many receive disability.

How to prevent another heart attack or even prevent its occurrence

Everyone now understands about a heart attack that it is a very serious disease that can result in death or leave you disabled. But everything is in the hands of the person himself - if you follow some recommendations, you can significantly reduce the risk of developing this pathology:

1. Keep your blood pressure level under control at all times, especially if it increases periodically.
2. Monitor your blood sugar levels.
3. In summer, avoid being in direct sunlight for long periods of time.
4. It is necessary to reconsider your diet, reduce the consumption of fatty foods, processed foods and add fresh vegetables and fruits.
5. Increase physical activity, you don’t have to go to the gym, it’s enough to take walks every day, walk a lot, ride a bike.
6. If health is more important, then you will have to give up smoking and alcohol abuse, and also not get carried away with coffee.
7. Keep your weight normal; if you can’t reduce it on your own, you can visit a nutritionist who will help you create an individual nutrition program.
8. If you have chronic diseases, they need to be treated periodically, especially for heart pathologies and vascular diseases.
9. If your relatives have been diagnosed with myocardial infarction, then you should take your health more seriously and avoid heavy physical labor.
10. Every year you need to arrange a good rest for yourself away from the bustle of the city; you can go to the mountains or to the sea coast.
11. Expose yourself to psycho-emotional stress as little as possible, learn relaxation techniques.
12. Be regularly examined and take all necessary tests to promptly detect elevated blood sugar or cholesterol levels.

If a heart attack could not be avoided, then every effort must be made to prevent another attack. To do this, you must follow all the doctor’s recommendations, take prescribed medications and change your lifestyle.

Aspirin (acetylsalicylic acid) has been used for decades to prevent thrombosis and coronary artery disease, but long-term use of it can lead to problems with the gastrointestinal tract, such as heartburn, gastritis, nausea, stomach pain, etc.

To reduce the risk of such undesirable consequences, it is necessary to take drugs in a special enteric coating. For example, you can use the drug "Trombo ACC®"*, each tablet of which is coated with an enteric film coating that is resistant to the effects of stomach hydrochloric acid and dissolves only in the intestines. This avoids direct contact with the gastric mucosa and reduces the risk of developing heartburn, ulcers, gastritis, bleeding, etc.

* There are contraindications; before use, you must consult a specialist.

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Heart attack- a focus of necrosis that developed as a result of circulatory disorders.

Heart attack also called circulatory or angiogenic necrosis.

The term “infarction” (from the Latin to stuff) was proposed by Virchow for a form of necrosis in which a dead area of ​​tissue becomes saturated with blood.

The size and morphological features of the infarction are determined by the caliber of the obstructed vessel and the presence of other circulatory disorders against which it develops.

With the main type of branching of the artery, the infarction in its outline resembles a cone, the narrow part of which (apex) faces the hilum of the organ, and the base is oriented to the periphery, to the zone of terminal branching of the intraorgan arteries. Heart attacks of this form are usually detected in the spleen, kidney, and lungs.

In organs with a predominance of scattered type of branching of the artery, for example in the brain, intestines, heart, the territory supplied with blood does not form cone-shaped contours and infarcts do not have a specific shape.

Types of heart attack

The infarction zone can occupy the entire organ or most of it (total and subtotal infarction) or can be detected only under a microscope (microinfarction).

Based on macroscopic features, there are 3 types of infarction: white, white with hemorrhagic rim and red .

White (ischemic) infarction is formed when the main arterial trunk is obstructed and the entire vascular bed in its basin is empty due to insufficient development of vascular anastomoses and collaterals. Most often detected in the spleen, sometimes in the brain and liver.

The necrosis zone is clearly visible upon macroscopic examination approximately 24 hours after the blood supply is disrupted. Under a microscope, the tissue is compacted, pale yellow in color, the structure of the tissue is indistinguishable, and its constituent elements merge into a homogeneous mass. Along the periphery, the infarction zone is limited by an inflammatory demarcation shaft.

White infarction with hemorrhagic rim appears as a whitish-yellow area surrounded by a dark red area of ​​hemorrhage. Such a heart attack develops in cases where the compensatory inclusion of collaterals and reactive arterial hyperemia of the vessels of the peripheral zone is preceded by vasospasm, followed by paralytic dilation.

As a result, a sharp congestion of blood vessels is accompanied by phenomena of blood stasis and diapedetic hemorrhages into necrotic tissue.

A white infarction with a hemorrhagic rim develops in the heart, spleen, and sometimes in the kidneys.

Red (hemorrhagic) infarction usually detected in the lungs, which is due to the characteristics of their blood supply.

Sometimes hemorrhagic infarction occurs against the background of severe hyperemia in other organs: intestines, brain, kidneys. With a red infarction, the ischemic zone is saturated with blood and acquires a dark red color and clear boundaries.

This effect occurs if, following a blockage of the artery, the peripheral vessels of the dead tissue become overfilled with blood flowing through the collaterals. With venous stagnation, the retrograde flow of blood from the veins into the ischemic zone also leads to the saturation of necrotic tissue with blood.

Hemorrhagic infarction can also develop as a result of pronounced venous stagnation with the rapid cessation of blood outflow through large venous trunks or the simultaneous exclusion of a large number of small veins from the bloodstream. Venous congestive infarctions are detected in the spleen with thrombosis of the vein draining blood from it, in the brain - with obstruction of the patency of the dural sinuses or jugular veins, in the heart - with obstruction of the coronary sinus by thrombotic masses, in the tissues of the lower extremities - with ligation of the femoral vein.

Microscopically, in the focus of a hemorrhagic infarction, masses of hemolyzed erythrocytes infiltrating necrotic tissue are noted.

General patterns of infarction formation and healing

Stage of ischemia and necrosis

The development of a heart attack is preceded by ischemia. The first changes caused by impaired blood supply are determined by inhibition of tissue respiration, compensatory activation of anaerobic glycolysis, and rapid accumulation of metabolites in cells in toxic concentrations.

Insufficient energy reproduction and the histotoxic effect of ischemia disrupt cell electrolyte homeostasis and suppress plastic processes, which leads to progressive dissociation of cytomembranes, acidification of the intracellular environment, protein denaturation, cell death and destruction.

Electron microscopy during ischemia reveals intracellular edema or, conversely, dehydration of the cytoplasmic matrix. Cell organelles swell, their membranes undergo homogenization and fragmentation, granules of labile glycogen disappear, accumulation of lipids in the form of droplets is noted due to their release from dissociating phospholipids of cytomembranes and disturbances in lipid metabolism.

Intracellular breakdown products accumulate in lysosomes.

Redistribution, condensation or washout of nuclear chromatin and destruction of nucleoli, melting of cytoplasmic ribosomes and organelles of non-membrane structure occur. Histochemically and biochemically in ischemic tissue, a decrease in the level of high-energy phosphates, the activity of redox enzymes, the accumulation of under-oxidized metabolites, disturbances in electrolyte metabolism, a decrease in the content of glycogen, RNA and DNA are determined, and over time, the accumulation of decay products of stromal structures.

At the necrotic stage of the infarction, upon microscopic examination, the cell nuclei are not stained, all structural elements of the tissue merge into a homogeneous mass.

The stage of reparative changes occurs after the formation of necrosis.

Along the periphery of a heart attack there is always a zone of dystrophic changes and reactive inflammation - the so-called demarcation shaft. Microscopically, the inflammatory reaction is observed within a few hours, and its maximum development occurs on the 3rd–5th day.

Inflammation in the zone of the demarcation shaft is accompanied by the release of blood cells from the capillaries. Necrotic masses gradually partially melt under the action of proteolytic enzymes emerging from neutrophilic leukocytes, partially undergo phagocytosis or are resorbed by the lymphatic network and excreted through its vessels.

Organization of the necrosis zone is the replacement of necrotic masses with connective tissue, which grows from the side of the demarcation shaft and by 7–10 days is transformed into granulation (young) connective tissue, and over time matures into scar tissue.

Features of the development of infarction in various organs

The morphology of the infarction largely depends on the organ architectonics of the vascular system

In clinical practice, infarctions of the heart (myocardium), brain, intestines, lungs, kidneys and spleen are most often noted.

The time required for the development of a heart attack in different organs is not the same and depends on functional energy consumption and phylogenetically established metabolism, which determines the tissue's need for oxygen supply.

For the development of MI, a complete cessation of its blood supply for 20–25 minutes is sufficient, but ischemia lasting 5 minutes already leads to the death of individual muscle cells.

In real life, the formation of a cardiac muscle infarction requires a slightly longer period of time, since in the ischemic zone, blood flow through vascular anastomoses and collaterals is always partially preserved. It is not sufficient to completely prevent necrosis, but it somewhat increases the period of its development and limits its size.

The infarction is usually localized in the left ventricle, most often in the anterior wall.

By type, it is a white infarction with a hemorrhagic rim and an irregular shape.

Depending on the volume and location of the affected myocardial tissue, small- and large-focal, subepicardial, intramural, subendocardial and transmural MI are distinguished, covering all layers of the heart wall.

In the zone of transition of the infarction to the epicardium or endocardium, reactive inflammation develops, in the first case leading to fibrous pericarditis (effusion of fibrin-enriched blood plasma into the pericardial cavity and the formation of fibrinous deposits on the epicardium), in the second - to thromboendocarditis (parietal thrombosis, corresponding to the zone heart attack).

The formation of MI begins with the ischemic stage.

Along with progressive metabolic disorders and disintegration of cell membranes, fragmentation, stretching and disintegration of cardiomyocyte myofibrils are noted. As a result, the activity of intracellular enzymes decreases, the nature of cell staining changes when using basic or acidic histological dyes, and the ability of cells to be refracted in polarized light and luminescent microscopic properties are disrupted.

These phenomena are used for early diagnosis of metabolic and ischemic heart damage. Histological signs of cell death - wrinkling, swelling and destruction of the cell nucleus, disappearance of longitudinal and transverse striations, homogenization of sarcoplasm are detected after 12 hours (Fig. 2.1).

Rice. 2.1. Acute MI

In parallel with the destructive changes in the working cells of the myocardium, a vascular-tissue reaction occurs, characterized by spasm and paretic dilatation of intramural arteries and arterioles, plasma impregnation and increased permeability of their walls, as well as impaired microcirculation with intravascular aggregation of erythrocytes, interstitial edema.

With the development of necrosis, blood flow in the necrotic zone stops, and in the peri-infarction zone it increases.

Along with diapedetic hemorrhages, extravasation of leukocytes occurs in it and a leukocyte bank is formed.

In the thickness of the necrotic zone around the preserved vessels, islands of viable tissue are sometimes detected, along the periphery of which the same phenomena are observed as in the zone surrounding the infarction.

During the first 18–24 hours from the onset of the pathological process, the myocardium in the affected artery is pallor against the background of a markedly uneven blood supply to the rest of the tissue.

At the end of the 1st day, the area of ​​necrosis becomes macroscopically visible.

Due to the continuous activity of the heart and the high activity of enzymes released from leukocytes, softening (myomalacia) of the dead tissue begins on the 3rd–5th day. Gradual resorption (resorption) of the necrotic mass is carried out with the active participation of microphage cells, which appear on the 4th day outward from the leukocyte shaft.

The fibroplastic reaction of the interstitium also occurs on the 4th–5th day, and the first fibrous elements of the newly formed connective tissue in the infarction zone appear after another 3 days.

Over the next week, the necrosis zone is represented by disintegrating muscle fibers, saturated with edematous fluid and infiltrated with disintegrating leukocytes. Along its periphery and around the perivascular islands of the preserved myocardium, new formation of connective tissue occurs.

The organization process lasts 2–2.5 months. Subsequently, the connective tissue formed at the site of necrotic masses becomes denser, its vessels become empty and obliterated, and a scar forms at the site of necrosis (Fig. 2.2).

Rice. 2.2.

The conduction system of the heart is more resistant to hypoxia compared to the working myocardium and is able to persist longer in ischemic areas, which is important for restoring rhythmic heart function after emergency invasive anti-ischemic therapy.

A white infarction with a hemorrhagic rim usually develops in the kidneys.

Due to the good development of vascular anastomoses and collaterals, infarction occurs only when the patency of vessels of a larger caliber than the lobular artery is impaired. The characteristic location of the infarction is the anterior lateral surface of the organ, since in this zone the renal arteries branch not along the main, but according to the scattered type, in which the intervascular collaterals are much less pronounced.

Typically, a renal infarction resembles a cone in shape, with its base facing the capsule and its apex facing the renal pelvis.

However, sometimes the process is limited only to the cortex, without affecting the pyramids, and the lesion approaches the shape of a square.

Kidney infarction often accompanied by hematuria due to blood entering the urinary tubules when small vessels rupture. The ischemic stage of renal infarction develops according to general patterns.

Necrosis of all structures of the renal parenchyma occurs within 24 hours, but damage to the epithelium of the renal tubules occurs much earlier.

Thus, after 6 hours, the death of the epithelium of the convoluted nephron tubules is observed, and after 12 hours - of the straight tubules of the nephron.

By this time, reactive inflammation develops along the periphery of the infarction, reaching its maximum around the 3rd day of the process.

The formation of a demarcation zone is accompanied by disturbances in blood flow in microvessels, symptoms of edema, plasmorrhagia and diapedetic hemorrhages, and active migration of leukocytes. This leads a day later to the formation of a peripheral hemorrhagic zone of infarction and a leukocyte shaft.

Around the same time, macrophages appear and the process of resorption of necrotic masses begins.

On the 7th day, destructive-resorptive processes are combined with clearly expressed phenomena of organization, which after a few weeks ends in the formation of a dense connective tissue scar, less often - a cyst.

In the spleen, the usual morphological type of infarction is white (ischemic).

In conditions of pronounced venous stagnation, splenic infarction can be hemorrhagic, acquiring a gray or white color within a few days. Ischemic infarction of the spleen is conical in shape, pale yellow in color. On the surface of the organ capsule in the area of ​​the wide part of this cone, as well as on the border of the infarction zone, reactive inflammation, processes of lysis, resorption and organization of necrotic masses develop.

Directly in the zone of necrosis, the red pulp is first destroyed, then the follicles and trabeculae.

The organization of a heart attack is carried out according to general laws. The maturation of the post-infarction scar is accompanied by deformation of the spleen.

Cerebral infarction is white in 85–90% of cases, in the rest - red or mixed.

White infarction can affect any part of the brain. Initially, it is a poorly demarcated area of ​​flabby or crumbling consistency, reddish-gray in color, with an erased natural pattern of the basal ganglia or cerebral cortex.

Hemorrhagic infarctions in the form of small red foci are localized mainly within accumulations of gray matter, most often in the cortex. Mixed infarcts consist of white and red areas, the latter located in the gray matter.

The topography of various morphological types of cerebral infarctions is predetermined by the characteristics of the blood supply to its various areas.

Most often they occur in the middle cerebral artery, less often in the vertebral and basilar arteries.

Hemorrhagic infarctions form in well-vascularized areas - accumulations of gray matter or in the cerebral cortex.

The development of cerebral infarction includes ischemic and necrotic stages.

The ischemic stage is characterized by dystrophic changes in nervous tissue, hemorrhages and destruction of cell membranes with irreversible disorganization of metabolic processes and electrolyte homeostasis of nerve cells. Microscopic examination reveals lysis of basophilic lumps, clearing of the cytoplasm, hyperchromatosis and deformation of the nucleus.

As a result, nerve cells and their nuclei acquire an angular shape, and the cytoplasm is homogenized, loses basophilic inclusions and becomes clear. Impaired blood circulation in microvessels is combined with pericellular edema - the appearance of a light gap between the capillary wall or neuron body and the surrounding tissue.

Around the capillaries, edema and swelling of the processes of the surrounding glial cells are noted.

The necrotic stage of the infarction is the stage of increasing autolysis of ischemic brain tissue. The death of neurons is preceded by their sharp clearing or compaction and transformation into pycnomorphic (compacted dehydrated) cells, and then into a homogeneous structureless mass.

Together with neurocytes, glial cells are also involved in destructive changes.

Diapedetic hemorrhages occur from small vessels, small and single in the foci of white infarction, multiple and merging with each other in hemorrhagic infarction.

By the beginning of the 2nd day, resorption of necrotic nervous tissue begins.

Leukocytes accumulate at the border with the focus of ischemic damage.

Together with them, numerous activated astrocytes penetrate into the necrosis zone and granular balls with lipid inclusions appear. Some astrocytes lose their cytoplasmic processes; numerous fibrils are detected in their cytoplasm, acquiring the ability to form fibrous structures.

New formation of vessels, capillaries and vascular loops begins around the focus of necrosis.

Both glial and connective tissue cells - fibroblasts - participate in the organization of necrotic masses.

However, at the final stage of the process, with small infarct sizes, the products of mesodermal proliferation are completely replaced by gliofibrous structures that form a scar. In large foci, the middle zone of the established infarction remains connective tissue, and in the center of the formed scar one or more cavities are formed, surrounded on the outside by glial growths.

Pulmonary infarction , as a rule, is hemorrhagic in nature, caused by double blood supply to the lungs and venous stagnation.

Blood enters the lungs both through the bronchial arteries, which are part of the systemic circulation system, and through the arteries of the pulmonary circulation. There are numerous anastomoses between the PA and the bronchial arteries, which have the structure of closing arteries and do not function under normal conditions.

When a sufficiently large branch of the pulmonary artery is obstructed, blood from the bronchial arteries rushes into its basin under high pressure through reflexively opened anastomoses.

The pulmonary capillaries, overflowing with blood, sharply dilate, their walls rupture, blood pours into the interstitium of the alveolar septa and into the cavities of the alveoli, imbibing the corresponding area of ​​​​tissue flow. Thanks to the autonomous arterial blood supply, the bronchi in the infarction zone remain viable.

Often, a hemorrhagic infarction in the lung develops against the background of chronic venous hyperemia, since an increase in pressure in large veins contributes to the retrograde flow of blood into the infarction zone. Infarction most often develops in the peripheral zones of the middle and small parts of the lungs. In this case, macroscopically, foci of a denser consistency than the surrounding tissue are detected, cone-shaped, with their base facing the pleura, which is covered with fibrinous plaque and becomes hyperemic due to reactive inflammation.

On the section, the necrotic tissue is dark red in color, slightly granular, and bulges above the surface. On the 1st day, in the infarction area, swelling and hemorrhages are microscopically determined in the form of accumulations of partially hemolyzed red blood cells in the interstitial tissue, in the lumens of the alveoli and small bronchi, which is accompanied by hemoptysis.

Then signs of necrosis of the alveolar walls appear and siderophages accumulate. On the 3rd–4th day, the infarction is a homogenized mass of destroyed red blood cells, against which traces of necrotic alveolar septa are visible.

Melting of necrotic tissue and shed blood, their resorption and organization begin from the periphery and from the preserved perivascular and peribronchial zones.

After 2–8 months, a scar or cyst remains at the site of the heart attack.

White infarction in the lung is rarely detected.

Occurs when blood flow in the bronchial arteries is disrupted against the background of obstruction of capillary blood flow, for example due to compression by intra-alveolar exudate or compaction (hepatization) of the lung tissue caused by pneumonia. In the intestine, a heart attack develops as a hemorrhagic one.

The most typical localization is the basin of the superior mesenteric artery, which, due to its large length, is more often subject to obstruction. Macroscopically, intestinal infarction has the appearance of a dark red area, which is quite clearly demarcated from the unaffected intestine.

The serous membrane in the area of ​​intestinal infarction becomes dull and fibrinous deposits appear on it.

The intestinal wall is thickened, the mucous membrane is bluish.

Necrotic and reactive changes in the ischemic segment of the intestine develop quickly.

15–20 minutes after the cessation of blood supply, pronounced microcirculatory disorders are detected in its wall: total tissue swelling, slowdown and cessation of blood movement in sharply saturated capillaries and venules, multiple hemorrhages.

After 30 minutes, leukocytes and lymphocytes appear in the edematous stroma of the intestinal mucosa, and a macrophage reaction develops.

Within 1–1.5 hours, the intestinal wall undergoes necrosis, which begins with ulceration of its mucous membrane. In the retina of the eye, the infarction has a white character, which, under conditions of venous stagnation, transforms into hemorrhagic. The area of ​​the affected tissue in the form of a cone faces the optic disc and is usually localized in the temporal segment. Microscopically, destruction of the inner layers of the retina, ganglion cells and nerve fibers is revealed against the background of impaired microcirculation, edema and hemorrhages.

Very rarely, infarctions are observed in the liver, muscles, and bones. The consequences of a heart attack are extremely significant for the body.

Thus, damage to >30% of LV tissue during MI is accompanied by the development of AHF with cardiac arrest.

Damage to the conduction system of the heart during the formation of necrosis leads to severe rhythm disturbances.

With an extensive transmural infarction, sometimes swelling of the necrotic area of ​​the heart wall occurs and its thinning - an acute cardiac aneurysm develops. In some cases, desynchronization of the processes of myomalacia, resorption of necrotic masses and organization of the infarction zone leads to rupture of the aneurysm, filling the pericardial cavity with blood with a fatal outcome.

As a result of MI, ruptures of the interventricular septum and separation of the papillary muscles can occur, which also leads to serious consequences.

In the longer term, an extensive scar zone, changing the geometry of heart contraction and intracardiac hemodynamics, contributes to the development of CHF and general venous hyperemia.

Cerebral infarction accompanied by swelling, microcirculation disorders and metabolic disorders both in the immediate vicinity of the lesion and in distant areas.

The outcome of a heart attack is determined by its size, location and rate of development of the pathological process.

The death of such patients can be caused both by the lesion in the brain itself and by causes not directly related to it.

Often, with the slow formation of a heart attack, patients die not from destructive changes affecting the vital centers of the brain, but due to heart failure, pneumonia and other associated pathologies that complicate the course of the heart attack.

A serious complication of cerebral infarction is hemorrhage into softened tissue.

Both cerebral edema and an increase in its volume due to restoration of blood flow through the vessels in the ischemic zone can cause dislocation and infringement of the brain stem.

With a favorable outcome, a scar or cyst is formed at the site of the infarction with more or less significant dysfunction of the central nervous system.

Intestinal infarction requires mandatory surgical intervention, since the final phase of its development is gangrene with perforation of the intestinal wall.

The entry of intestinal contents into the abdominal cavity leads to the development of peritonitis. Peritonitis can also be caused by splenic infarction, which usually ends in the formation of a rough scar that deforms the organ. A pulmonary infarction usually does not pose an immediate threat to the patient’s life.

However, its course can be complicated by post-infarction pneumonia, suppuration and spread of the inflammatory process to the pleura with the development of pneumothorax and gangrene of the lung. One of the most typical causes of infarction suppuration is the entry of a purulent embolus into the vessel.

This causes purulent melting of the lung tissue and the formation of an abscess at the site of the infarction.

With renal infarction , which usually heals through scarring of the corresponding area, life-threatening complications arise with suppuration or with extensive lesions, especially with symmetrical necrosis of the cortical layer, which can result in acute renal failure.

A.S. Gavrish "Blood circulation"

Heart attack (from Latin infarcire - to stuff, stuff)- a focus of necrosis that occurs as a result of cessation of blood supply, i.e. ischemia. Therefore, infarction is also called vascular or ischemic necrosis.
Essentially a heart attack- This is a consequence and extreme expression of ischemia. A heart attack can have a different shape, size, consistency, color, appearance.

The immediate cause of a heart attack is: prolonged spasm, thrombosis, arterial embolism, as well as functional tension of the organ in conditions of insufficient blood supply.
Of great importance for the occurrence of a heart attack is the insufficiency of anastomoses and collaterals, which depends on the degree of damage to the walls of the arteries and narrowing of their lumens (atherosclerosis, obliterating endarteritis), on the degree of circulatory disturbance (for example, venous stagnation) and on the level of exclusion of the artery by a thrombus or embolus.
Therefore, heart attacks usually occur in those diseases that are characterized by severe changes in the arteries and general circulatory disorders (rheumatism, heart defects, atherosclerosis, hypertension, prolonged septic endocarditis). The development of a heart attack due to functional burden of an organ, usually the heart, whose blood supply is impaired, should also be associated with acute insufficiency of collateral circulation.
Insufficiency of anastomoses and collaterals is associated with venous infarctions that occur during vein thrombosis in conditions of congestive plethora. For the occurrence of a heart attack, the state of tissue metabolism is also of great importance, i.e., the metabolic background against which an ischemic heart attack develops.

More often, infarctions are wedge-shaped, the base of the wedge faces the capsule, and the tip faces the hilum of the organ. Heart attacks of this form are formed in the spleen, kidneys, and lungs, which is determined by the nature of the angioarchitecture of these organs - the main type of branching of their arteries. Less commonly, heart attacks have an irregular shape.

Such infarctions occur in the heart, brain, intestines, i.e. in those organs where not the main, but the scattered or mixed type of branching of the arteries predominates. An infarction may involve most or all of an organ (subtotal or total infarction) or be detected only under a microscope (microinfarction).
If the infarction develops according to the type of coagulation necrosis, then the tissue in the area of ​​necrosis thickens and becomes dry (myocardial infarction, kidney, spleen), but if the infarction is formed according to the type of liquefaction necrosis, it softens and liquefies (infarction of the brain, intestines). Depending on whether the tissue in the area of ​​the infarction is saturated with blood, three types of infarction are distinguished: white, white with a hemorrhagic rim, and red.
1. White (ischemic) infarction is represented by a white-yellow area, well delimited from the surrounding tissue. It usually occurs in areas of insufficient collateral circulation, which prevents the flow of blood into the area of ​​necrosis. It occurs especially often in the spleen, less often in the kidneys.
2. The white infarction hemorrhagic rim is also represented by a white-yellow area, but this area is surrounded by a hemorrhage zone. It is formed as a result of the fact that vascular spasm along the periphery of the infarction is replaced by their paretic expansion and the development of diapedetic hemorrhages. Such an infarction is usually found in the kidneys and myocardium.
3. With a red (hemorrhagic) infarction, the area of ​​necrosis is saturated with blood, it is dark red and well demarcated. A favorable condition for such hemorrhagic impregnation is venous stagnation. The angioarchitecture of the organ is also of particular importance for the development of red infarction. Hemorrhagic infarction occurs, usually in the lungs, rarely in the intestine, spleen, and kidneys.

The outcome of a heart attack depends on the characteristics of the causative factor and the disease that complicates the heart attack, on the condition of the body and the organ in which it develops, and on the size of the heart attack. Small foci of ischemic necrosis can undergo autolytic melting, followed by complete regeneration. The most common favorable outcome of a heart attack developing as dry necrosis is its organization and scar formation.

The organization of a heart attack can result in its petrification or hemosiderosis, if we are talking about the organization of a hemorrhagic infarction. At the site of a heart attack that develops as a type of liquefaction necrosis, for example in the brain, a cyst forms.
Unfavorable outcome of heart attack- its purulent melting, which is usually associated with thrombobacterial embolism in sepsis. Therefore, such heart attacks are called septic. The significance of a heart attack for the body is extremely great, and primarily because a heart attack is ischemic necrosis. Everything that has been said about the meaning of necrosis also applies to infarction.

A focus of necrosis in a tissue or organ that occurs as a result of cessation or a significant decrease in arterial inflow, or less commonly, venous outflow.

A heart attack is vascular (dyscirculatory) necrosis.

The causes of a heart attack are thrombosis, embolism, prolonged arterial spasm or functional overstrain of an organ in conditions of insufficient blood supply (the latter is observed only during myocardial infarction).

The form of infarction depends on the structural features of the vascular system of a particular organ, the presence of anastomoses, and collateral blood supply (angioarchitectonics). Thus, in organs with a main arrangement of vessels, triangular (cone-shaped, wedge-shaped) infarctions occur, while with a scattered or mixed type of branching of vessels, an irregular shape of the infarction is observed. And in appearance, white and red heart attacks are distinguished.

White (ischemic, bloodless) infarction

occurs due to damage to the corresponding artery. Such infarctions occur in the spleen, brain, heart, kidneys and in most cases represent coagulation or, less commonly, colliquation (in the brain) necrosis. Approximately 24 hours after the onset of infarction, the necrosis zone becomes clearly visible, clearly contrasting its pale yellow or pale brown color with the zone of preserved tissue. Between them there is a demarcation zone, represented by inflammatory leukocyte and macrophage infiltration and hyperemic vessels with diapedesis of blood cells up to the formation of small hemorrhages. In the myocardium and kidneys, due to the large number of vascular collaterals and anastomoses, the demarcation zone occupies a significant area. In this regard, the infarction of these organs is called ischemic with hemorrhagic corolla.

Red (hemorrhagic) infarction

develops when arteries and (less commonly) veins are blocked and is usually found in the lungs, intestines, ovaries, and brain. Of great importance in the genesis of red infarction is the mixed type of blood supply, as well as the presence of venous stagnation. For example, obstruction of a branch of the pulmonary artery by a thromboembolus or thrombus causes blood to flow through the anastomoses into the zone of low pressure from the bronchial artery system, followed by rupture of the capillaries of the interalveolar septa. In very rare cases of blocking of these anastomoses (possibly in the presence of pneumonia of the same localization), a white infarction may develop in the lung. It is also extremely rare that with thrombosis of the splenic vein, not a white, but a red (venous) infarction of the spleen is formed. The necrosis area is saturated with blood, giving the affected tissues a dark red or black color. The demarcation zone in this infarction is not pronounced, as it occupies a small area.

Within several days, segmented neutrophils and macrophages partially resorb the necrotic tissue. On the 7th-10th day, ingrowth of granulation tissue from the demarcation zone is noted, gradually occupying the entire necrosis zone. Outcomes: A heart attack is organized and scarred. Another favorable outcome is also possible - the formation of a cyst (a cavity, sometimes filled with fluid) at the site of necrosis, which is often observed in the brain. With a small ischemic stroke (cerebral infarction), it is possible to replace it with glial tissue with the formation of a glial scar. Unfavorable outcomes of a heart attack include its suppuration.

Myocardial infarction is a form of coronary heart disease, which is necrosis of the heart muscle caused by a sudden cessation of coronary blood flow due to damage to the coronary arteries.

Heart and vascular diseases continue to be the leading cause of death worldwide. Every year, millions of people experience one or another manifestation of coronary heart disease - the most common form of myocardial damage, which has many types, invariably leading to disruption of the usual way of life, loss of ability to work and claiming the lives of a large number of patients. One of the most common manifestations of coronary artery disease is myocardial infarction (MI); at the same time, it is the most common cause of death in such patients, and developed countries are no exception.

According to statistics, in the United States alone, about a million new cases of heart attack are registered per year, approximately a third of patients die, and about half of the deaths occur within the first hour after the development of necrosis in the myocardium. Increasingly, among the sick there are able-bodied people of young and mature age, with several times more men than women, although by the age of 70 this difference disappears. With age, the number of patients is steadily growing, and more and more women are appearing among them.

However, one cannot fail to note the positive trends associated with a gradual decrease in mortality due to the emergence of new diagnostic methods, modern treatment methods, as well as increased attention to those risk factors for the development of the disease that we ourselves can prevent. Thus, the fight against smoking at the state level, the promotion of the basics of healthy behavior and lifestyle, the development of sports, and the formation of responsibility among the population regarding their health significantly contribute to the prevention of acute forms of coronary artery disease, including myocardial infarction.

Causes and risk factors of myocardial infarction

Myocardial infarction is necrosis (death) of a section of the heart muscle due to the complete cessation of blood flow through the coronary arteries. The reasons for its development are well known and described. The result of various studies of the problem of coronary heart disease has been the identification of many risk factors, some of which do not depend on us, and others that everyone can eliminate from their lives.

As is known, hereditary predisposition plays an important role in the development of many diseases. Coronary heart disease is no exception. Thus, the presence among blood relatives of patients with coronary artery disease or other manifestations of atherosclerosis significantly increases the risk of myocardial infarction. Arterial hypertension, various metabolic disorders, for example, diabetes mellitus, hypercholesterolemia, are also a very unfavorable background.

There are also so-called modifiable factors that contribute to acute coronary heart disease. In other words, these are those conditions that can either be completely eliminated or their influence significantly reduced. Currently, thanks to a deep understanding of the mechanisms of disease development, the emergence of modern methods of early diagnosis, as well as the development of new drugs, it has become possible to combat fat metabolism disorders, maintain normal blood pressure and blood sugar levels.

Do not forget that avoiding smoking, alcohol abuse, stress, as well as good physical fitness and maintaining adequate body weight significantly reduce the risk of cardiovascular pathology in general.

The causes of heart attack are conventionally divided into two groups:

1. Significant atherosclerotic changes in the coronary arteries;
2. Non-atherosclerotic changes in the coronary arteries of the heart.

The problem of atherosclerosis today is acquiring alarming proportions and is not only medical, but also social in nature. This is due to the variety of its forms, the manifestations of which can significantly complicate the life of such patients, and are also potentially fatal. Thus, coronary atherosclerosis causes the appearance of coronary heart disease, one of the most severe variants of which will be myocardial infarction. Most often, patients experience simultaneous damage to two or three arteries supplying blood to the heart muscle, with the amount of stenosis reaching 75% or more. In such cases, the development of an extensive heart attack, affecting several of its walls at once, is very likely.

Much more rarely, no more than 5-7% of cases, non-atherosclerotic changes in the vessels supplying it can act as the cause of myocardial infarction. For example, inflammation of the arterial wall (vasculitis), spasm, embolism, congenital abnormalities of vascular development, and a tendency to hypercoagulation (increased blood clotting) can also lead to impaired blood flow in the coronary arteries. Cocaine use, unfortunately, is quite common, including among young people, and can lead not only to severe tachycardia, but also to significant spasm of the arteries of the heart, which is inevitably accompanied by a malnutrition of the muscle with the appearance of foci of necrosis in it.

It is worth noting that only a heart attack resulting from atherosclerosis is an independent disease (nosology) and one of the forms of IHD. In other cases, when there is a non-atherosclerotic lesion, myocardial necrosis will only be a syndrome complicating other diseases (syphilis, rheumatoid arthritis, injuries of the mediastinal organs, etc.).

There are certain differences in the occurrence of myocardial infarction depending on gender. According to various data, in men aged 45-50 years, heart attacks are 4-5 times more common than among the female population. This is explained by the later onset of atherosclerosis in women due to the presence of estrogen hormones that have a protective effect. By the age of 65-70, this difference disappears, and about half of the patients are women.

Pathogenetic mechanisms of myocardial infarction development

In order to understand the essence of this insidious disease, it is necessary to recall the main features of the structure of the heart. Ever since school, each of us knows that it is a muscular organ, the main function of which is to pump blood into the systemic and pulmonary circulation. The human heart is four-chambered - has two atria and two ventricles. Its wall consists of three layers:

• Endocardium is the inner layer, similar to that in blood vessels;
• Myocardium is the muscle layer that bears the main load;
• Epicardium - covers the outside of the heart.

Around the heart there is a cavity called the pericardium (heart lining) - a limited space containing a small amount of fluid necessary for its movement during contractions.

During myocardial infarction, the middle, muscular layer is necessarily affected, and the endocardium and pericardium, although not always, are quite often also involved in the pathological process.

The blood supply to the heart is carried out by the right and left coronary arteries, which arise directly from the aorta. Closure of their lumen, and especially when collateral (bypass) blood flow paths are poorly developed, is accompanied by the appearance of foci (foci) of ischemia and necrosis in the heart.

It is known that the basis of the pathogenesis, or development mechanism, of acute myocardial infarction is atherosclerotic damage to the vascular wall and the resulting thrombosis and arterial spasm. The sequence of development of pathological changes is expressed by a triad:

1. Lipid plaque rupture;
2. Thrombosis;
3. Reflex vasospasm.

Against the background of atherosclerosis, in the walls of the arteries supplying blood to the heart, deposition of fat and protein masses occurs, which over time grow with connective tissue to form a fibrous plaque, which protrudes into the lumen of the vessel and significantly narrows it. In acute forms of IHD, the degree of narrowing reaches two-thirds of the vessel diameter and even more.

Increased blood pressure, smoking, and intense physical activity can provoke plaque rupture, damaging the integrity of the inner lining of the artery and the release of atheromatous masses into its lumen. A natural reaction to damage to the vascular wall in such a situation is thrombosis, which is, on the one hand, a protective mechanism designed to eliminate the defect, and on the other hand, it plays a major role in stopping blood flow through the vessel. Initially, a thrombus forms inside the damaged plaque, then spreads to the entire lumen of the vessel. Often, such blood clots reach 1 cm in length and completely close the affected artery, stopping blood flow in it.

When a blood clot forms, substances are released that cause vasospasm, which can be limited in nature or cover the entire coronary artery. At the stage of spasm development, an irreversible and complete closure of the lumen of the vessel and cessation of blood flow occurs - occlusive obstruction, leading to inevitable necrosis (necrosis) of a section of the heart muscle.

The latter pathogenetic mechanism of the appearance of necrosis in the heart during cocaine addiction is especially pronounced, when even in the absence of atherosclerotic lesions and thrombosis, a pronounced spasm can cause complete closure of the lumen of the artery. The likely role of cocaine must be remembered when cardiac infarction develops in young and previously healthy people who have not previously had any signs of atherosclerosis.

In addition to the described basic mechanisms for the development of myocardial infarction, various immunological changes, increased blood clotting activity, and an insufficient number of bypass (collateral) blood flow paths can have an adverse effect.

Video: myocardial infarction, medical animation

Structural changes in the focus of myocardial necrosis

The most common location of myocardial infarction is the wall of the left ventricle, which has the greatest thickness (0.8 - 1 cm). This is associated with a significant functional load, since blood is pushed out from here under high pressure into the aorta. If trouble arises - atherosclerotic damage to the wall of the coronary artery, a significant volume of the heart muscle remains without blood supply and undergoes necrosis. Most often, necrosis occurs in the anterior wall of the left ventricle, in the posterior wall, in the apex, and also in the interventricular septum. Heart attacks on the right side of the heart are extremely rare.

The zone of myocardial necrosis becomes noticeable to the naked eye within 24 hours from the beginning of its development: a reddish and sometimes gray-yellow area appears, surrounded by a dark red stripe. With a microscopic examination of the affected heart, a heart attack can be recognized by detecting destroyed muscle cells (cardiomyocytes) surrounded by an inflammatory “shaft”, hemorrhages and edema. Over time, the source of damage is replaced by connective tissue, which becomes denser and turns into a scar. In general, it takes about 6-8 weeks for such a scar to form.

Transmural myocardial infarction is spoken of when the entire thickness of the heart muscle undergoes necrosis; at the same time, it is very likely that the endocardium and pericardium are involved in the pathological process with the appearance of secondary (reactive) inflammation in them - endocarditis and pericarditis.

Damage and inflammation of the endocardium is fraught with the occurrence of blood clots and thromboembolic syndrome, and pericarditis over time will lead to the growth of connective tissue in the cavity of the cardiac sac. In this case, the pericardial cavity overgrows and the so-called “armored heart” is formed, and this process underlies the subsequent formation of chronic heart failure due to the restriction of its normal mobility.

With timely and adequate medical care, most patients who survive acute myocardial infarction remain alive, and a dense scar develops in their heart. However, no one is immune from repeated episodes of circulatory arrest in the arteries, even those patients in whom the patency of the heart vessels was restored surgically (stenting). In cases where, with an already formed scar, a new focus of necrosis occurs, they speak of a recurrent myocardial infarction.

As a rule, the second heart attack becomes fatal, but the exact number of them that the patient can endure has not been determined. In rare cases, there are three episodes of necrosis in the heart.

Sometimes you can encounter a so-called recurrent heart attack, which occurs during a period of time when scar tissue forms in the heart at the site of an acute attack. Since, as mentioned above, it takes an average of 6-8 weeks for a scar to “ripen,” it is during this period that a relapse can occur. This type of heart attack is very unfavorable and dangerous for the development of various fatal complications.

Sometimes a cerebral infarction occurs, the causes of which will be thromboembolic syndrome with extensive transmural necrosis involving the endocardium in the process. That is, blood clots formed in the cavity of the left ventricle when the inner lining of the heart is damaged, enter the aorta and its branches that carry blood to the brain. When the lumen of the cerebral vessels is blocked, brain death (infarction) occurs. In such cases, these necrosis is not called a stroke, since they are a complication and consequence of myocardial infarction.

Types of myocardial infarction

To date, there is no single generally accepted classification of heart attack. In the clinic, based on the amount of assistance needed, the prognosis of the disease and the characteristics of the course, the following types are distinguished:

• Large-focal myocardial infarction - can be transmural and non-transmural;
• Small focal – intramural (in the thickness of the myocardium), subendocardial (under the endocardium), subepicardial (in the area of ​​the heart muscle under the epicardium);
• Myocardial infarction of the left ventricle (anterior, apical, lateral, septal, etc.);
• Right ventricular infarction;
• Atrial myocardial infarction;
• Complicated and uncomplicated;
• Typical and atypical;
• Protracted, recurrent, repeated infarction.

In addition, periods of myocardial infarction are distinguished:

1. Pre-infarction;
2. Acute;
3. Spicy;
4. Subacute;
5. Post-infarction.

Manifestations of heart attack

The symptoms of myocardial infarction are quite characteristic and, as a rule, make it possible to suspect it with a high degree of probability even in the pre-infarction period of the disease. Thus, patients experience longer and more intense chest pain, which is less responsive to treatment with nitroglycerin, and sometimes does not go away at all. Shortness of breath, sweating, various arrhythmias and even nausea may occur. At the same time, patients are finding it increasingly difficult to endure even minor physical activity.

At the same time, characteristic electrocardiographic signs of impaired blood supply to the myocardium appear, and continuous monitoring for a day or more (Holter monitoring) is especially effective for identifying them.

The most characteristic signs of a heart attack appear in the acute period, when a zone of necrosis appears and expands in the heart. This period lasts from half an hour to two hours, and sometimes longer. There are factors that provoke the development of an acute period in predisposed individuals with atherosclerotic lesions of the coronary arteries:

• Excessive physical activity;
• Severe stress;
• Operations, injuries;
• Hypothermia or overheating.

The main clinical manifestation of necrosis in the heart is pain, which is very intense. Patients can characterize it as burning, squeezing, pressing, “dagger-like.” The pain has a retrosternal localization, can be felt to the right and left of the sternum, and sometimes covers the front of the chest. Characteristic is the spread (irradiation) of pain to the left arm, shoulder blade, neck, and lower jaw.

In most patients, the pain syndrome is very pronounced, which also causes certain emotional manifestations: a feeling of fear of dying, severe anxiety or apathy, and sometimes excitement is accompanied by hallucinations.

Unlike other types of coronary artery disease, a painful attack during a heart attack lasts at least 20-30 minutes, and the analgesic effect of nitroglycerin is absent.

Under favorable circumstances, at the site of the necrosis focus, so-called granulation tissue begins to form, rich in blood vessels and fibroblast cells that form collagen fibers. This period of a heart attack is called subacute, and it lasts up to 8 weeks. As a rule, it proceeds well, the condition begins to stabilize, the pain weakens and disappears, and the patient gradually gets used to the fact that he has suffered such a dangerous phenomenon.

Subsequently, a dense connective tissue scar forms in the heart muscle at the site of necrosis, the heart adapts to new working conditions, and post-infarction cardiosclerosis marks the onset of the next period of the disease, which continues for the rest of life after a heart attack. Those who have had a heart attack feel well, but there is a resumption of pain in the heart and angina attacks.

As long as the heart is able to compensate for its activity by hypertrophy (enlargement) of the remaining healthy cardiomyocytes, there are no signs of heart failure. Over time, the adaptive capabilities of the myocardium are depleted and heart failure develops.

It happens that the diagnosis of myocardial infarction is significantly complicated by its unusual course. This characterizes its atypical forms:

1. Abdominal (gastralgic) – characterized by pain in the epigastrium and even throughout the entire abdomen, nausea, vomiting. Sometimes it may be accompanied by gastrointestinal bleeding associated with the development of acute erosions and ulcers. This form of heart attack must be distinguished from peptic ulcer of the stomach and duodenum, cholecystitis, pancreatitis;
2. Asthmatic form - occurs with attacks of suffocation, coughing, cold sweat;
3. The edematous form is characteristic of massive necrosis with total heart failure, accompanied by edematous syndrome and shortness of breath;
4. Arrhythmic form, in which rhythm disturbances become the main clinical manifestation of MI;
5. Cerebral form - accompanied by symptoms of cerebral ischemia and is typical for patients with severe atherosclerosis of the vessels supplying blood to the brain;
6. Erased and asymptomatic forms;
7. Peripheral form with atypical localization of pain (mandibular, left-handed, etc.).

Video: non-standard signs of a heart attack

Diagnosis of myocardial infarction

Usually the diagnosis of a heart attack does not cause significant difficulties. First of all, it is necessary to carefully clarify the patient’s complaints, ask him about the nature of the pain, clarify the circumstances of the attack and the presence of the effect of nitroglycerin.

When examining the patient, pallor of the skin, signs of sweating are noticeable, and cyanosis (cyanosis) is possible.

A lot of information will be provided by such methods of objective research as palpation (feeling) and auscultation (listening). So, with palpation you can identify:

• Pulsation in the area of ​​the cardiac apex, precordial zone;
• Increased heart rate to 90 - 100 beats per minute;

When auscultating the heart, the following will be characteristic:

1. Muting the first tone;
2. Low systolic murmur at the apex of the heart;
3. A gallop rhythm is possible (the appearance of a third tone due to left ventricular dysfunction);
4. Sometimes a fourth sound is heard, which is associated with stretching of the muscle of the affected ventricle or with a disturbance in the conduction of impulses from the atria;
5. Systolic “cat purring” is possible due to the return of blood from the left ventricle to the atrium due to pathology of the papillary muscles or stretching of the ventricular cavity.

The overwhelming majority of people suffering from a large-focal form of myocardial infarction have a tendency to lower blood pressure, which, under favorable conditions, can normalize in the next 2-3 weeks.

A characteristic symptom of necrosis in the heart is also an increase in body temperature. As a rule, its values ​​​​do not exceed 38 ºС, and the fever lasts about a week. It is noteworthy that in younger patients and in patients with extensive myocardial infarction, the increase in body temperature is longer and more significant than in small foci of infarction and in elderly patients.

In addition to physical ones, laboratory methods for diagnosing myocardial infarction are of no small importance. So, the following changes are possible in the blood test:

• An increase in the level of leukocytes (leukocytosis) is associated with the appearance of reactive inflammation in the focus of myocardial necrosis, persists for about a week;
• An increase in erythrocyte sedimentation rate (ESR) is associated with an increase in the concentration in the blood of proteins such as fibrinogen, immunoglobulins, etc.; the maximum occurs 8-12 days from the onset of the disease, and ESR numbers return to normal after 3-4 weeks;
• The appearance of so-called “biochemical signs of inflammation” - an increase in the concentration of fibrinogen, C-reactive protein, seromucoid, etc.;
• The appearance of biochemical markers of necrosis (death) of cardiomyocytes - cellular components that enter the bloodstream during their destruction (AST, ALT, LDH, myoglobin protein, troponins and others).

It is difficult to overestimate the importance of electrocardiography (ECG) in the diagnosis of myocardial infarction. Perhaps this method remains one of the most important. An ECG is accessible, easy to perform, can be recorded even at home, and at the same time provides a large amount of information: indicates the location, depth, extent of the infarction, and the presence of complications (for example, arrhythmia). With the development of ischemia, it is advisable to record an ECG repeatedly with comparison and dynamic monitoring.

ECG signs of the acute phase of necrosis in the heart:

1. the presence of a pathological Q wave, which is the main sign of muscle tissue necrosis;
2. decrease in the size of the R wave due to a decrease in the contractile function of the ventricles and the conduction of impulses along nerve fibers;
3. dome-shaped shift of the ST interval upward from the isoline due to the spread of the infarction from the subendocardial zone to the subepicardial zone (transmural lesion);
4. formation of the T wave.

Based on typical changes in the cardiogram, one can determine the stage of development of necrosis in the heart and accurately determine its location. Of course, it is unlikely that you will be able to independently decipher the cardiogram data without a medical education, but ambulance doctors, cardiologists and therapists can easily establish not only the presence of a heart attack, but also other disorders of the heart muscle and conductivity.

In addition to the listed methods, echocardiography (allows you to determine the local contractility of the heart muscle), radioisotope scintigraphy, magnetic resonance and computed tomography (helps to assess the size of the heart and its cavities, and identify intracardiac blood clots) are used to diagnose myocardial infarction.

Video: lecture on the diagnosis and classification of heart attacks

Complications of myocardial infarction

Myocardial infarction both in itself poses a threat to life and through its complications. The majority of those who have undergone it remain with certain disturbances in the activity of the heart, associated primarily with changes in conduction and rhythm. Thus, in the first day after the onset of the disease, up to 95% of patients experience arrhythmias. Severe arrhythmias during massive infarctions can quickly lead to heart failure. The possibility of heart muscle rupture and thromboembolic syndrome also cause many problems for both doctors and their patients. Timely assistance in these situations will help the patient prevent them.

The most common and dangerous complications of myocardial infarction:

• Heart rhythm disturbances (extrasystole, ventricular fibrillation, atrioventricular block, tachycardia, etc.);
• Acute heart failure (with massive heart attacks, atrioventricular blockades) – the development of acute left ventricular failure with symptoms of cardiac asthma and alveolar pulmonary edema, which threaten the patient’s life, is possible;
• Cardiogenic shock is an extreme degree of heart failure with a sharp drop in blood pressure and impaired blood supply to all organs and tissues, including vital ones;
• Heart ruptures are a severe and fatal complication, accompanied by the release of blood into the pericardial cavity and an abrupt cessation of cardiac activity and hemodynamics;
• Cardiac aneurysm (protrusion of a section of the myocardium in the area of ​​necrosis);
• Pericarditis is inflammation of the outer layer of the heart wall during transmural, subepicardial infarctions, accompanied by constant pain in the heart area;
• Thromboembolic syndrome - in the presence of a blood clot in the infarction zone, in a left ventricular aneurysm, with prolonged bed rest, thrombophlebitis of the veins of the lower extremities.

Most life-threatening complications occur in the early post-infarction period, so careful and constant monitoring of the patient in a hospital setting is very important. The consequences of an extensive cardiac infarction include large-focal post-infarction cardiosclerosis (a massive scar that has replaced an area of ​​dead myocardium) and various arrhythmias.

Over time, when the heart's ability to maintain adequate blood flow to organs and tissues is depleted, congestive (chronic) heart failure appears. Such patients will suffer from edema, complain of weakness, shortness of breath, pain and interruptions in the functioning of the heart. Increasing chronic circulatory failure is accompanied by irreversible dysfunction of internal organs, accumulation of fluid in the abdominal, pleural and pericardial cavities. Such decompensation of cardiac activity will ultimately lead to the death of patients.

Principles of treatment of myocardial infarction

Emergency care for patients with myocardial infarction should be provided as soon as possible from the moment of its development, since delay can lead to the development of irreversible changes in hemodynamics and sudden death. It is important that there is someone nearby who can at least call an ambulance. If you are lucky and there is a doctor nearby, his qualified participation can help avoid serious complications.

The principles of helping patients with a heart attack come down to the step-by-step provision of therapeutic measures:

1. Pre-hospital stage – involves transporting the patient and providing the necessary measures by an ambulance team;
2. At the hospital stage, the maintenance of basic body functions, prevention and control of blood clots, cardiac arrhythmias and other complications in hospital intensive care units continue;
3. The stage of rehabilitation measures - in specialized sanatoriums for cardiac patients;
4. The stage of dispensary observation and outpatient treatment is carried out in clinics and cardiac centers.

First aid can be provided under time pressure and outside the hospital. It is good if it is possible to call a specialized cardiac ambulance team, which is equipped with the necessary equipment for such patients - medications, defibrillators, a pacemaker, and equipment for resuscitation measures. Otherwise, it is necessary to call a line ambulance team. Now almost all of them have portable ECG machines, which make it possible to quickly make a fairly accurate diagnosis and begin treatment.

The basic principles of care before arriving at the hospital are adequate pain relief and prevention of thrombosis. In this case the following is used:

• Nitroglycerin under the tongue;
• Administration of analgesics (promedol, morphine);
• Aspirin or heparin;
• Antiarrhythmic drugs if necessary.

Video: first aid for myocardial infarction

At the stage of inpatient treatment, measures taken to maintain the function of the cardiovascular system continue. Elimination of pain is the most important of them. Narcotic analgesics (morphine, promedol, omnopon) are used as analgesics; if necessary (severe agitation, fear), tranquilizers (Relanium) are also prescribed.

Thrombolytic therapy is of great importance. With its help, lysis (dissolution) of a blood clot is carried out in the coronary and small arteries of the myocardium with the restoration of blood flow. This also limits the size of the focus of necrosis, which means that the subsequent prognosis is improved and mortality is reduced. Of the drugs with thrombolytic activity, the most commonly used are fibrinolysin, streptokinase, alteplase, etc. An additional antithrombotic agent is heparin, which prevents subsequent thrombus formation and prevents thromboembolic complications.

It is important that thrombolytic therapy is started as early as possible, preferably in the first 6 hours after the onset of a heart attack, this significantly increases the likelihood of a favorable outcome by restoring coronary blood flow.

When arrhythmias develop, antiarrhythmic drugs are prescribed to limit the area of ​​necrosis, unload the heart, and also for cardioprotective purposes, β-blockers (propranolol, atenolol), nitrates (nitroglycerin intravenous drip), vitamins (vitamin E, xanthinol nicotinate) are prescribed.

Maintenance treatment after a heart attack can continue for the rest of your life, its directions:

1. Maintaining normal blood pressure levels;
2. Fighting arrhythmias;
3. Prevention of thrombosis.

It is important to remember that only timely and adequate treatment with medications can save the patient’s life, and therefore herbal treatment in no case will replace the possibilities of modern pharmacotherapy. At the rehabilitation stage, in combination with supportive treatment, it is quite possible to take various herbal decoctions as a supplement. Thus, in the post-infarction period, it is possible to use motherwort, hawthorn, aloe, and calendula, which have a general strengthening and calming effect.

Diet and rehabilitation

An important role is given to the nutrition of patients with myocardial infarction. Thus, in the intensive care unit in the acute period of the disease, it is necessary to provide food that will not be burdensome for the heart and blood vessels. Easily digestible, non-rough food is allowed, taken 5-6 times a day in small portions. Various cereals, kefir, juices, and dried fruits are recommended. As the patient's condition improves, the diet can be expanded, but it is worth remembering that fatty, fried and high-calorie foods, which contribute to the disruption of fat and carbohydrate metabolism with the development of atherosclerosis, are contraindicated.

The diet after a heart attack must include foods that promote bowel movements (prunes, dried apricots, beets).

Rehabilitation includes a gradual expansion of the patient’s activity, and, in accordance with modern concepts, the sooner it occurs, the more favorable the further prognosis. Early activity is the prevention of congestion in the lungs, muscle atrophy, osteoporosis and other complications. Physical rehabilitation after a heart attack is also important, which involves physical therapy and walking.

If the patient’s condition is satisfactory and there are no contraindications, further recovery is possible in cardiological sanatoriums.

The period of disability after a heart attack is determined individually depending on the severity of the course and the presence of complications. Disability is reaching significant numbers, and this is all the more sad because it is increasingly the young and able-bodied population that is suffering. Patients will be able to work if their work is not associated with strong physical or psycho-emotional stress, and their general condition is satisfactory.

Video: heart attack - from prevention to rehabilitation

To summarize, it is important to remember that you can avoid a heart attack by following a healthy lifestyle, good physical activity, avoiding bad habits and eating right. Taking care of our health is within the power of each of us. However, if such a misfortune does occur, you should not wait and waste precious time, you should immediately consult a doctor. Patients who have received adequate treatment and good rehabilitation live for more than one year after a heart attack.

What are the etiology and pathogenesis of hypertension

1. Classification of the disease - diagram

Arterial hypertension is a pathological increase in blood pressure, another name is hypertension. The pathogenesis of hypertension is not simple, and to date it has not been fully studied. It is generally accepted that the main cause of development lies in chronic stress.

Unlike hypertension, which is a symptom of more serious pathologies, arterial hypertension is an independent disease, which will be discussed in the article.

When a disturbance in peripheral vascular tone occurs, a favorable environment arises for the formation of hypertension. Deformed blood vessels cannot regulate metabolism. The medulla oblongata and hypothalamus cease to perform their functions correctly; as a result of the disrupted functioning of these organs, an increased amount of pressor substances is produced.

The chain continues in the arterioles; these small arteries stop responding to the minute ejection of blood from the heart. The pressure in the internal organs increases due to the fact that the arteries do not dilate.

When blood pressure in the kidneys increases, the organ begins to actively produce renin. The hormone enters the blood, where it begins to interact with the most powerful pressor substance - angiotensinogen.

There are scientific assumptions that the basis of the disease is hidden hereditary defects that manifest themselves under the influence of unfavorable factors, and it is they that provoke the mechanism for the development of hypertension.

The etiology and pathogenesis of hypertension include primary and secondary hypertension. Primary or essential hypertension is an independent disease, while secondary or symptomatic hypertension is a consequence of more serious pathological processes.

The exact causes of hypertension are difficult to determine, but it is possible to identify risk factors that provoke the development of hypertension:

• Constant physical or nervous tension - long-term stress not only gives rise to arterial hypertension, but also contributes to its active progression, in addition, it can cause such dangerous consequences as stroke and heart attack.
• Genetic predisposition - scientists have proven that the chances of developing hypertension directly depend on how many relatives have this disease.
• Excess weight - keep in mind that every ten kilograms of excess subcutaneous and, especially, visceral fat increases blood pressure by 2-4 mmHg. Art.
• Occupational factors - constant eye strain, exposure to noise or prolonged mental and emotional stress increase blood pressure and lead to the development of the disease.
• Excessively salty food - a person should consume no more than 5 grams of salt in one day; exceeding the dosage increases the risk of developing hypertension.
• Bad habits - frequent drinking of alcohol, smoking, as well as excessive coffee consumption increase blood pressure, in addition to hypertension, the risk of heart attack and stroke increases.
• Age-related changes - hypertension often appears in young men as a result of rapid growth, as well as in women in menopause, when hormonal imbalances occur.

Classification of the disease - diagram

Pathogenesis of hypertension - a diagram of the forms of pathology and the meanings during their development:

• In the mild form – systolic 140-180, diastolic – 90-105;
• In moderate form - systolic 180-210, diastolic - 105-120;
• In advanced forms, systolic is more than 210, diastolic is more than 120.

Stages of hypertension:

• The first stage - blood pressure rises for a short time, quickly returns to normal under favorable conditions;
• The second stage – high blood pressure is already stable, the patient needs constant medication;
• The third stage - complications of arterial hypertension develop, changes occur in the vessels and internal organs - the heart, brain, kidneys.

The onset of the disease can be recognized by the development of initial symptoms; against the background of overwork or stress, the patient may be bothered by:

• Head pain and dizziness, feeling of heaviness;
• Attacks of nausea;
• Frequent tachycardia;
• Feeling restless.

When the disease enters the second stage, symptoms appear more often, their appearance occurs in the form of hypertensive crises. Hypertensive crises are sudden and unexpected attacks of illness.

The pathology at the third stage differs from the first two in terms of damage to internal organs; they manifest themselves in the form of hemorrhages, visual impairment, and kidney diseases. To diagnose arterial hypertension, a conventional tonometer is sufficient.

Hypertension has a chronic course, as with any chronic disease, periods of improvement are followed by periods of exacerbation. The progression of the disease occurs at different rates; it was already mentioned above that two forms of hypertension are divided according to its progression. Slow development includes all three stages, the definition of each is primarily based on the presence or absence of changes in the internal organs - heart, kidneys, brain, retina.

Internal organs remain unchanged only at the first stage of pathology. The initial form of the disease is accompanied by increased secretion of adrenaline and norepinephrine, which is more likely for young men during the period of active growth and sexual development. What manifestations are characteristic of the initial form of hypertension?

Symptoms involve the heart muscle - pain in the heart and tachycardia, pain can radiate to the forearm. Other signs are redness of the face and the whites of the eyes, increased sweating, chills, a feeling of fear and internal tension.

There is no enlargement of the left ventricle of the heart, renal function is not changed, crises are rare. Diastolic pressure is 95-104 mmHg, systolic - 160-179 mmHg. Art. During the day, pressure readings can change; if a person rests, the pressure returns to normal. The second stage already involves changes in internal organs - one or more. First of all, the disorders affect the kidneys - fluid is retained in the body, resulting in swelling and puffiness of the face.

Patients' fingers go numb, frequent complaints include headaches, and blood flows from the nose. Studies such as ECG and radiography show an enlargement of the left ventricle, and changes also extend to the fundus of the eye. Renal blood flow is reduced, glomerular filtration is slowed down.

Renography shows a diffuse bilateral decrease in renal function. On the part of the central nervous system, manifestations of vascular insufficiency and transient ischemia are possible. At the second stage, diastolic pressure varies from 105 to 114 mmHg, and systolic pressure is 180-200 mmHg. Art.

At the last stage, pathological changes in the internal organs become pronounced, the pressure is constantly in the range of 200-230/115-129 mm Hg. Art. The condition is characterized by pressure surges and spontaneous decreases.

Hypertensive crises often occur, and along with them, cerebrovascular accidents, paralysis, and paresis occur. The changes affect the kidneys, the organ undergoes arteriolohyalinosis, arteriolosclerosis. Such conditions provoke a initially shriveled kidney, which becomes the first step to chronic renal failure.