Atherosclerotic cardiosclerosis: clinical picture, classification, symptoms and treatment. Atherosclerotic heart disease Disease as a cause of death

A fairly severe pathology, which is the replacement of myocardial cells with connective structures, as a consequence of myocardial infarction - post-infarction cardiosclerosis. This pathological process significantly disrupts the functioning of the heart itself and, as a consequence, the entire body as a whole.

ICD-10 code

This disease has its own ICD code (in the International Classification of Diseases). This is I25.1 - called “Atherosclerotic heart disease. Coronary (arteries): atheroma, atherosclerosis, disease, sclerosis.”

ICD-10 code

I25.1 Atherosclerotic heart disease

Causes of post-infarction cardiosclerosis

As mentioned above, the pathology is caused by the replacement of necrotic myocardial structures with connective tissue cells, which cannot but lead to a deterioration in cardiac activity. There are several reasons that can trigger such a process, but the main one is the consequences of a myocardial infarction suffered by the patient.

Cardiologists classify these pathological changes in the body as a separate disease belonging to the group of coronary heart diseases. Typically, the diagnosis in question appears on the card of a person who has had a heart attack two to four months after the attack. During this time, the process of myocardial scarring is predominantly completed.

After all, a heart attack is a focal death of cells, which must be replenished by the body. Due to the current circumstances, replacement occurs not with analogues of cardiac muscle cells, but with scar-connective tissue. It is this transformation that leads to the disease discussed in this article.

Depending on the location and scale of the focal lesion, the degree of cardiac activity is also determined. After all, “new” tissues do not have the ability to contract and are not able to transmit electrical impulses.

As a result of the resulting pathology, stretching and deformation of the heart chambers are observed. Depending on the location of the lesions, tissue degeneration may affect the heart valves.

Another cause of the pathology in question may be myocardial dystrophy. A change in the heart muscle that appears as a result of a deviation from the metabolic norm in it, which leads to impaired blood circulation as a result of a decrease in the contractility of the heart muscle.

Trauma can also lead to a similar illness. But the last two cases, as catalysts for the problem, are much less common.

Symptoms of post-infarction cardiosclerosis

The clinical form of manifestation of this disease directly depends on the location of formation of necrotic foci and, accordingly, scars. That is, the larger the scarring, the more severe the symptomatic manifestations.

The symptoms are quite varied, but the main one is heart failure. The patient can also feel similar discomfort:

• Arrhythmia is a failure of the rhythmic functioning of an organ.
• Progressive shortness of breath.
• Decreased resistance to physical stress.
• Tachycardia – increased rhythm.
• Orthopnea is breathing problems when lying down.
• Nocturnal attacks of cardiac asthma may occur. Wait 5-20 minutes after the patient changes his body position to a vertical one (standing, sitting), breathing is restored and the person comes to his senses. If this is not done, then against the background of arterial hypertension, which is a concomitant element of the pathology, ontogenesis - pulmonary edema - can quite reasonably occur. Or as it is also called acute left ventricular failure.
• Attacks of spontaneous angina, and pain may not accompany this attack. This fact may manifest itself against the background of coronary circulatory disorders.
• If the right ventricle is affected, swelling of the lower extremities may occur.
• An increase in venous tracts in the neck area can be seen.
• Hydrothorax is an accumulation of transudate (fluid of non-inflammatory origin) in the pleural cavity.
• Acrocyanosis is a bluish discoloration of the skin associated with insufficient blood supply to small capillaries.
• Hydropericardium - dropsy of the cardiac membrane.
• Hepatomegaly is stagnation of blood in the vessels of the liver.

Large-focal post-infarction cardiosclerosis

The large-focal type of pathology is the most severe form of the disease, leading to serious disruptions in the functioning of the affected organ, and the entire organism as a whole.

In this case, myocardial cells are partially or completely replaced by connective tissues. Large areas of replaced tissue significantly reduce the performance of the human pump, including these changes that can affect the valve system, which only aggravates the current situation. With such a clinical picture, a timely, fairly in-depth examination of the patient is necessary, who will subsequently have to be very attentive to his health.

The main symptoms of macrofocal pathology include:

• The appearance of respiratory discomfort.
• Disruptions in the normal rhythm of contractions.
• Manifestation of pain symptoms in the retrosternal region.
• Increased fatigue.
• Quite noticeable swelling of the lower and upper extremities, and in rare cases, of the entire body, is possible.

It is quite difficult to identify the causes of this particular type of illness, especially if the source is a disease suffered relatively long ago. Doctors indicate only a few:

• Diseases of an infectious and/or viral nature.
• Acute allergic reactions of the body to any external irritant.

Atherosclerotic post-infarction cardiosclerosis

This type of pathology under consideration is caused by the progression of coronary heart disease by replacing myocardial cells with connective cells, due to atherosclerotic damage to the coronary arteries.

To put it simply, against the background of a prolonged lack of oxygen and nutrients experienced by the heart, the division of connective cells between cardiomyocytes (muscle cells of the heart) is activated, which leads to the development and progression of the atherosclerotic process.

The lack of oxygen occurs due to the accumulation of cholesterol plaques on the walls of blood vessels, which leads to a decrease or complete blockage of the blood flow.

Even if complete blockage of the lumen does not occur, the amount of blood entering the organ decreases, and, consequently, the cells do not receive oxygen. This shortage is especially felt by the heart muscles, even with a slight load.

In people who receive great physical activity, but have atherosclerotic problems with blood vessels, post-infarction cardiosclerosis manifests itself and progresses much more actively.

In turn, a decrease in the lumen of the coronary vessels can lead to:

• Failure in lipid metabolism leads to an increase in plasma cholesterol levels, which accelerates the development of sclerotic processes.
• Chronically high blood pressure. Hypertension increases the speed of blood flow, which provokes blood microvortices. This fact creates additional conditions for the sedimentation of cholesterol plaques.
• Addiction to nicotine. When it enters the body, it provokes spasm of the capillaries, which temporarily impairs blood flow and, consequently, the supply of oxygen to systems and organs. At the same time, chronic smokers have increased cholesterol levels in the blood.
• Genetic predisposition.
• Excess kilograms add stress, which increases the likelihood of developing ischemia.
• Constant stress activates the adrenal glands, which leads to an increase in the level of hormones in the blood.

In this situation, the process of development of the disease in question proceeds smoothly at a low speed. The left ventricle is primarily affected, since it bears the greatest load, and during oxygen starvation it is the one that suffers the most.

For some time the pathology does not manifest itself. A person begins to feel discomfort when almost all muscle tissue is interspersed with connective tissue cells.

Analyzing the mechanism of development of the disease, we can conclude that it is diagnosed in people whose age has exceeded the forty-year mark.

Lower post-infarction cardiosclerosis

Due to its anatomical structure, the right ventricle is located in the lower region of the heart. It is “served” by the pulmonary circulation. It received this name due to the fact that circulating blood captures only the lung tissue and the heart itself, without nourishing other human organs.

Only venous blood flows in the small circle. Thanks to all these factors, this area of ​​the human motor is least susceptible to negative factors, which lead to the disease discussed in this article.

Complications of post-infarction cardiosclerosis

As a consequence of developing post-infarction cardiosclerosis, other ailments may develop in the future:

• Atrial fibrillation.
• Development of a left ventricular aneurysm that has become chronic.
• Various blockades: atrial - ventricular.
• The likelihood of various thromboses and thromboembolic manifestations increases.
• Paroxysmal ventricular tachycardia.
• Ventricular extrasystole.
• Complete atrioventricular block.
• Sick sinus syndrome.
• Tamponade of the pericardial cavity.
• In especially severe cases, the aneurysm may rupture and, as a result, the death of the patient.

This reduces the patient’s quality of life:

• Shortness of breath increases.
• Performance and load tolerance decreases.
• Violations of heart contractions are visible.
• Rhythm disruptions appear.
• Ventricular and atrial fibrillation can usually be observed.

In the event of the development of an atherosclerotic disease, side symptoms can also affect non-cardiac areas of the victim’s body.

• Loss of sensation in the limbs. The feet and phalanges of the fingers are especially affected.
• Cold extremity syndrome.
• Atrophy can develop.
• Pathological disorders can affect the vascular system of the brain, eyes and other areas.

Sudden death in post-infarction cardiosclerosis

As sad as it sounds, a person suffering from the disease in question has a high risk of asystole (cessation of bioelectrical activity, leading to cardiac arrest), and as a consequence, the onset of sudden clinical death. Therefore, the relatives of this patient should be prepared for such an outcome, especially if the process is quite advanced.

Another reason that entails sudden death and is a consequence of post-infarction cardiosclerosis is the exacerbation of the pathology and the development of cardiogenic shock. It is he who, if assistance is not provided in a timely manner (and in some cases even with it), becomes the starting point of death.

Fibrillation of the ventricles of the heart, that is, scattered and multidirectional contraction of individual bundles of myocardial fibers, can also provoke mortality.

Based on the above, it should be understood that a person who has been given the diagnosis in question needs to especially carefully monitor his health, regularly monitoring his blood pressure, heart rate and rhythm, and regularly visiting his attending physician - a cardiologist. This is the only way to reduce the risk of sudden death.

Diagnosis of post-infarction cardiosclerosis

• If a heart disease is suspected, including the one discussed in this article, the cardiologist prescribes a number of tests to the patient:
• Analysis of the patient's medical history.
• Physical examination by a doctor.
• Tries to determine whether the patient has arrhythmia and how stable it is.
• Carrying out electrocardiography. This method is quite informative and can “tell” a qualified specialist quite a lot.
• Ultrasound examination of the heart.
• The purpose of rhythmocardiography is an additional non-invasive electrophysiological study of the heart, with the help of which the doctor receives a record of the rhythm variability of the blood-pumping organ.
• Positron emission tomography (PET) of the heart is a radionuclide tomographic study that allows you to localize hypoperfusion foci.
• Coronary angiography is a radiopaque method for studying the coronary artery of the heart to diagnose coronary heart disease using X-rays and contrast fluid.
• An echocardiogram is one of the ultrasound research techniques aimed at studying the morphological and functional changes of the heart and its valve apparatus.
• Establishing the frequency of manifestations of heart failure.
• Radiography allows one to determine changes in the dimensional parameters of the biological mechanism being studied. Basically, this fact is revealed due to the left half.
• To diagnose or exclude transient ischemia, in some cases a person has to undergo stress tests.
• A cardiologist, if the medical institution has such equipment, can prescribe Holter monitoring, which allows daily monitoring of the patient’s heart.
• Carrying out ventriculography. This is a more focused examination, an x-ray method for assessing the chambers of the heart, in which a contrast agent is injected. In this case, the image of the contrasted ventricle is recorded on a special film or other recording device.

Post-infarction cardiosclerosis on ECG

ECG or as it stands for - electrocardiography. This medical examination technique is aimed at analyzing the bioelectrical activity of myocardial fibers. An electrical impulse, having arisen in the sinus node, passes, thanks to a certain level of conductivity, through the fibers. In parallel with the passage of the pulse signal, a contraction of cardiomyocytes is observed.

When conducting electrocardiography, thanks to special sensitive electrodes and a recording device, the direction of the moving pulse is recorded. Thanks to this, the specialist can obtain a clinical picture of the functioning of individual structures of the cardiac complex.

An experienced cardiologist, having an ECG of the patient, is able to obtain an assessment of the main operating parameters:

• Automatic level. The ability of various parts of the human pump to independently produce an impulse of the required frequency, which has an exciting effect on the myocardial fibers. Extrasystole is assessed.
• The degree of conductivity is the ability of cardiac fibers to conduct the signal from the place of its origin to the contracting myocardium - cardiomyocytes. It becomes possible to see whether there is a lag in the contractile activity of a particular valve or muscle group. Usually, a mismatch in their operation occurs precisely when conductivity is disrupted.
• Assessment of the level of excitability under the influence of a created bioelectric impulse. In a healthy state, under the influence of this irritation, a certain muscle group contracts.

The procedure itself is painless and takes little time. Taking into account all the preparation, this will take 10 – 15 minutes. In this case, the cardiologist receives a quick, fairly informative result. It should also be noted that the procedure itself is not expensive, which makes it accessible to the general public, including low-income people.

Preparatory activities include:

• The patient needs to expose his torso, wrists, arms and legs.
• These areas are moistened with water (or soap solution) by the medical worker performing the procedure. After this, the passage of the impulse and, accordingly, the level of its perception by the electrical device improves.
• Pinches and suction cups are placed on the ankle, wrists and chest, which will catch the necessary signals.

At the same time, there are accepted requirements, the implementation of which must be strictly monitored:

• A yellow electrode is attached to the left wrist.
• On the right - red.
• A green electrode is placed on the left ankle.
• On the right - black.
• A special suction cup is placed on the chest in the area of ​​the heart. In most cases there should be six.

After receiving the charts, the cardiologist evaluates:

• The height of the voltage of the teeth of the QRS indicator (failure of ventricular contractility).
• The level of shift of the S – T criterion. The probability of their reduction below the norm isoline.
• Assessment of T peaks: the degree of decrease from the norm, including the transition to negative values, is analyzed.
• Varieties of tachycardia of different frequencies are considered. Atrial flutter or fibrillation is assessed.
• Presence of blockades. Assessment of failures in the conductive capacity of the conductive bundle of cardiac tissues.

The electrocardiogram must be deciphered by a qualified specialist who, based on various types of deviations from the norm, is able to put together the entire clinical picture of the disease, localizing the focus of the pathology and making the correct diagnosis.

Treatment of post-infarction cardiosclerosis

Considering that this pathology is a rather complex manifestation and due to the important function that this organ performs for the body, therapy for relieving this problem must necessarily be comprehensive.

These are non-drug and medicinal methods, if necessary, surgical treatment. Only timely and full-scale treatment can achieve a positive resolution of the problem with coronary disease.

If the pathology is not yet very advanced, then through drug correction it is possible to eliminate the source of the deviation, restoring normal functioning. By directly influencing the pathogenesis links, for example, the source of atherosclerotic cardiosclerosis (forming cholesterol plaques, blockage of blood vessels, arterial hypertension, and so on), it is quite possible to cure the disease (if it is in its infancy) or significantly support normal metabolism and functioning.

It should also be noted that self-medication with this clinical picture is absolutely unacceptable. Medications can be prescribed only with a confirmed diagnosis. Otherwise, you can cause even more harm to the patient, aggravating the situation. In this case, it is possible to obtain irreversible processes. Therefore, even the attending physician, a cardiologist, must be absolutely sure of the correctness of the diagnosis before prescribing therapy.

For the atherosclerotic form of the disease in question, a group of medications is used to combat heart failure. These are pharmacological agents such as:

• Metabolites: rikavit, midolate, mildronate, apilac, ribonosine, glycine, milife, biotredin, antisten, riboxin, cardinate, succinic acid, cardiomagnyl and others.
• Fibrates: normolip, gemfibrozil, gevilon, ciprofibrate, fenofibrate, ipolipid, bezafibrate, regulip and others.
• Statins: Recol, Mevacor, Cardiostatin, Pitavastatin, Lovasterol, Atorvastatin, Rovacor, Pravastatin, Apexstatin, Simvastatin, Lovacor, Rosuvastatin, Fluvastatin, Medostatin, Lovastatin, Choletar, Cerivastatin and others.

Metabolic agent glycine It is accepted quite well by the body. The only contraindication to its use is hypersensitivity to one or more components of the drug.

The drug is administered in two ways - under the tongue (sublingual) or placed between the upper lip and gum (buccal) until completely absorbed.

The drug is prescribed in dosage depending on the age of the patient:

Children who have not yet turned three years old - half a tablet (50 ml) two to three times throughout the day. This regimen is practiced for one to two weeks. Then, for seven to ten days, take half a tablet once a day.

Children who are already three years old and adult patients are prescribed a whole tablet two to three times a day. This regimen is practiced for one to two weeks. If there is a therapeutic need, the treatment course is extended to a month, then a month-long break and a second course of treatment.

Lipid-lowering drug gemfibrozil prescribed by the attending physician orally half an hour before meals. The recommended dosage is 0.6 g twice a day (in the morning and evening) or 0.9 g once a day (in the evening). You should not bite the tablet. The maximum permissible dosage is 1.5 g. The duration of treatment is one and a half months, and more if necessary.

Contraindications for this medication include: primary biliary cirrhosis of the liver, increased intolerance to the patient’s body of the components of gemfibrozil, as well as pregnancy and lactation.

The lipid-lowering drug fluvastatin is administered regardless of food intake, whole, without chewing, together with a small amount of water. It is recommended to use in the evening or just before bed.

The starting dosage is selected individually - from 40 to 80 mg daily and adjusted depending on the effect achieved. At a mild stage of the disorder, a reduction to 20 mg per day is allowed.

Contraindications for this medicine include: acute illnesses affecting the liver, the general serious condition of the patient, individual intolerance to the components of the drug, pregnancy, lactation (in women) and childhood, since the absolute safety of the drug has not been proven.

Used the same way angiotensin-converting enzyme inhibitors(APF blockers): olivine, normapress, invoril, captopril, minipril, lerin, enalapril, renipril, calpiren, corandil, enalacor, miopril and others.

ACE blocker enalapril taken regardless of food. For monotherapy, the starting dose is a single dose of 5 mg daily. If a therapeutic effect is not observed, after a week or two it can be increased to 10 mg. The drug should be taken under constant monitoring by a specialist.

With normal tolerance, and if necessary, the dosage can be increased to 40 mg daily, divided into one or two doses throughout the day.

The maximum permissible daily amount is 40 mg.

When prescribed together with a diuretic, the second one must be stopped a couple of days before enalapril is administered.

The drug is contraindicated in case of hypersensitivity to its components, during pregnancy and lactation.

Complex therapy includes diuretics: furosemide, Kinex, Indap, Lasix and others.

Furosemide in tablet form is taken on an empty stomach without chewing. The maximum permissible daily amount for adult patients is 1.5 g. The starting dosage is determined at the rate of 1 – 2 mg per kilogram of the patient’s weight (in some cases, up to 6 mg per kilogram is allowed). The next dose of the drug is not allowed earlier than six hours after the initial administration.

Edema indicators in chronic heart failure are controlled with a dosage of 20 to 80 mg daily, divided into two to three doses (for an adult patient).

Contraindications to use may be the following diseases: acute renal and/or hepatic dysfunction, comatose or precomatous state, impaired water and electrolyte metabolism, severe glomerulonephritis, decompensated mitral or aortic stenosis, children (up to 3 years), pregnancy and lactation.

To activate and normalize heart contractions, drugs such as Lanoxin, Dilanacin, Strophanthin, Dilacor, Lanicor or Digoxin are often taken.

Cardiotonic drug cardiac glycoside, digoxin is prescribed as a starting amount of up to 250 mcg daily (for patients whose weight does not exceed 85 kg) and up to 375 mcg daily (for patients whose weight exceeds 85 kg).

For elderly patients, this amount is reduced to 6.25 - 12.5 mg (a quarter or half a tablet).

It is not recommended to administer digoxin if a person has a history of diseases such as glycoside intoxication, second-degree AV block or complete block, in the case of Wolff-Parkinson-White syndrome, as well as with hypersensitivity to the drug.

If a combination of drug and non-drug therapy does not bring the expected effect, the consultation prescribes surgical treatment. The range of operations performed is quite wide:

• Expansion of narrowed coronary vessels, allowing to normalize the volume of passing blood.
• Shunting is the creation of an additional path bypassing the affected area of ​​a vessel using a system of shunts. The operation is performed on an open heart.
• Stenting is a minimally invasive intervention aimed at restoring the normal lumen of the affected arteries by implanting a metal structure into the vessel cavity.
• Balloon angioplasty is an intravascular bloodless surgical method used to eliminate stenoses (narrowings).

Basic methods of physiotherapy have not found their application in the treatment protocol for the disease in question. Only electrophoresis can be used. It is applied topically to the cardiac area. In this case, drugs from the group of statins are used, which, thanks to this therapy, are delivered directly to the sore spot.

Spa therapy with mountain air has proven itself well. As an additional method, specialized physical therapy is also used, which will increase the overall tone of the body and normalize blood pressure.

Psychotherapy with a diagnosis of post-infarction cardiosclerosis

Psychotherapeutic therapy is a system of therapeutic effects on the psyche and through the psyche on the human body. It will not interfere with the relief of the disease discussed in this article. After all, how correctly a person is configured in terms of treatment largely depends on his attitude in therapy, the correctness of following all the doctor’s instructions. And as a result – a higher degree of results obtained.

It should only be noted that this therapy (psychotherapeutic treatment) should only be carried out by an experienced specialist. After all, the human psyche is a delicate organ, damage to which can lead to an unpredictable ending.

Nursing care for post-infarction cardiosclerosis

The responsibilities of nursing staff in caring for patients diagnosed with post-infarction cardiosclerosis include:

• General care for such a patient:
  • Replacement of bedding and underwear.
  • Sanitation of the premises with ultraviolet rays.
  • Ventilation of the room.
  • Compliance with the attending doctor's instructions.
  • Carrying out preparatory measures before diagnostic studies or surgery.
  • Teaching the patient and his relatives the correct administration of nitroglycerin during a painful attack.
  • Training the same category of people to keep an observation diary, which will subsequently allow the treating doctor to trace the dynamics of the disease.
• It is the responsibility of nursing staff to conduct conversations on the topic of caring for one’s health and the consequences of ignoring problems. The need for timely intake of medications, control of daily routine and nutrition. Mandatory daily monitoring of the patient's condition.
• Help in finding motivation to change lifestyle, which would reduce risk factors for pathology and its progression.
• Conducting advisory training on disease prevention issues.

Clinical observation for post-infarction cardiosclerosis

Clinical examination is a set of active measures that ensure systematic monitoring of the patient who has been diagnosed with the diagnosis discussed in this article.

The following symptoms become indications for medical examination:

• The occurrence of angina pectoris.
• Progression of angina pectoris.
• When heart pain and shortness of breath occur at rest.
• Vasospastic, that is, spontaneous pain symptoms and other symptoms of angina pectoris.

All patients with these manifestations are subject to mandatory hospitalization in specialized cardiology departments. Clinical observation for post-infarction cardiosclerosis includes:

• 24-hour monitoring of the patient and identification of his medical history.
• Diverse research and consultation with other specialists.
• Patient care.
• Establishing the correct diagnosis, the source of pathology and prescribing a treatment protocol.
• Monitoring the patient’s susceptibility to a particular pharmacological drug.
], [
• Nutrition should be complete and balanced, rich in vitamins (especially magnesium and potassium) and microelements. Portions should be small, but it is advisable to eat five to six times a day without overeating.
• Watch your weight.
• Heavy daily physical activity should not be allowed.
• Adequate sleep and rest.
• Stressful situations must be avoided. The person's condition must be emotionally stable.
• Timely and adequate treatment of myocardial infarction.
• A special therapeutic and physical training complex is recommended. Therapeutic walking.
• Balneotherapy - treatment with mineral waters.
• Regular dispensary monitoring.
• Spa treatment.
• Walking before bed and staying in a ventilated area.
• Positive attitude. If necessary, psychotherapy, communication with nature and animals, watching positive programs.
• Preventive massages.

It’s worth going into more detail about nutrition. Coffee and alcoholic beverages, as well as foods that have a stimulating effect on the cells of the nervous and cardiovascular systems, should disappear from the diet of such a patient:

• Cocoa and strong tea.
• Minimize salt intake.
• Limited – onions and garlic.
• Fatty fish and meats.

It is necessary to remove from the diet foods that provoke increased gas production in the human intestines:

• All legumes.
• Radish and radish.
• Milk.
• Cabbage, especially sour cabbage.
• By-products that provoke the deposition of “bad” cholesterol in blood vessels should disappear from the diet: internal organs of animals, liver, lungs, kidneys, brains.
• Smoked and spicy foods are not allowed.
• Eliminate from your diet supermarket products with a large amount of “E-shek”: stabilizers, emulsifiers, various dyes and chemical taste enhancers.

Prognosis of post-infarction cardiosclerosis

The prognosis of post-infarction cardiosclerosis directly depends on the location of pathological changes in the myocardium, as well as the level of severity of the disease.

If the left ventricle, which provides blood flow to the systemic circulation, is damaged, and the blood flow itself decreases by more than 20% of normal, then the quality of life of such patients undergoes a significant deterioration. With such a clinical picture, drug treatment acts as maintenance therapy, but cannot completely cure the disease. Without an organ transplant, the survival rate of such patients does not exceed five years.

The pathology under consideration is directly related to the formation of scar tissue, replacing healthy cells that have undergone ischemia and necrosis. This replacement leads to the fact that the area of ​​focal lesions completely “falls out” of the work process; the remaining healthy cells try to pull a greater load against the background of which heart failure develops. The more affected areas, the more severe the degree of pathology, the more difficult it is to eliminate symptoms and the source of pathology, leading the tissue to recovery. After diagnosis, treatment therapy is aimed at eliminating the problem as much as possible and preventing recurrence of a heart attack.

The heart is a human engine that requires some care and attention. Only if all preventive measures are taken can one expect long-term normal operation from it. But if something goes wrong and a diagnosis of post-infarction cardiosclerosis is made, then treatment should not be delayed in order to prevent the development of more serious complications. In such a situation, you should not rely on solving the problem yourself. Only with a timely diagnosis and the adoption of adequate measures under the constant supervision of a qualified specialist can one speak of a highly effective result. This approach to the problem will improve the patient’s quality of life, and even save his life!

It is important to know!

An increase in the activity of total creatine kinase and MB fraction is detected after operations or diagnostic procedures on the heart. Radiation therapy to the chest area may also cause mild hyperenzymemia. Tachyarrhythmia or heart failure rarely causes an increase in the activity of creatine kinase and CK-MB.

– a single name for the pathology of blood vessels, caused by the formation of cholesterol deposits inside large and medium-sized arteries. As fatty plaques accumulate in the intima (the inner walls of the arteries), the lumen of the bloodstream narrows and hemodynamics worsen.

The main consequence of a functional disease is a complication of the blood supply to vital organs. As a consequence - cardiosclerosis, angina pectoris, myocardial infarction, stroke.

Representatives of the stronger sex over the age of forty-five are considered a high-risk group, in whom, according to statistics, atherosclerosis is detected four times more often than in the fairer sex.

According to the tenth International Classification of Diseases (ICD-10), there is no code for atherosclerotic cardiosclerosis.

In medicine, the encoding I 25.1 is used, and it denotes atherosclerotic disease. Sometimes the code for cardiomyopathy is 125.5 or coronary heart disease (CHD) I20-I25.

Causes and risk factors

Every person, regardless of age and gender, should be aware of the causes of the development of atherosclerotic cardiosclerosis. The exact cause of the disease has not yet been established. But still, there are a number of factors that influence the formation of cholesterol plaques.

Consequences and complications

There are three stages of the disease:

1. The appearance of plaques. This pathology is caused by narrowing of the coronary vessels. Atherosclerosis of the heart valves and an increase in the volume of atherosclerotic plaque occurs.
2. Ischemic heart disease. Occurs due to arterial stenosis and oxygen starvation.
3. Development of atherosclerotic cardiosclerosis.

Myocardial infarction can also be a consequence of cardiosclerosis. According to the ICD-10 classification, it includes angina pectoris, primary, repeated and old heart attack, sudden death and heart failure. Coronary heart disease according to ICD-10 has code 125 and is noted in the medical history.

Symptoms

The heart is one of the most sensitive organs. Symptoms of atherosclerotic cardiosclerosis of the heart appear at the initial stage and are manifested by angina pectoris syndrome. Signs occur periodically and include:

The frequency of symptoms depends on the degree of the disease and the general health of the body.

Diagnostics

To determine the stage of the disease, clinical studies are prescribed. Blood biochemistry changes greatly in cardiosclerosis. In addition, it is necessary to take a general blood test. It will help determine the amount of blood cells. In this case, the important indicators will be:

1. Amount of cholesterol and triglycerides.
2. Atherogenicity, in which the indicator does not exceed the number three.
3. C-reactive protein and creatinine levels.

After passing the necessary tests, an ultrasound and Doppler are performed to determine the speed of blood flow. Additionally, MRI and angiography may be prescribed.

Treatment of atherosclerotic cardiosclerosis

The most effective treatment for the disease will be immediately after detection of the disease, namely at the initial stage. Treatment is carried out using the recommendations listed below.

Medication

Non-drug therapy

This type of treatment includes working to eliminate the factors leading to the disease:

1. Weight reduction.
2. Getting rid of bad habits.
3. High-quality diet.
4. Increased physical activity.
5. Physiotherapeutic procedures.

Surgical intervention

It is used if the above methods did not bring any results. The operation is performed to bypass the coronary aorta. It helps remove ischemia and restore blood circulation in blocked areas of blood vessels.

Laser and endovascular surgery

These are new methods of therapy that are performed under local anesthesia. They help restore blood flow in the arteries.

Disease as a cause of death

Prevention should include the following measures:

Atherosclerosis of the heart arteries can cause sudden cardiac arrest. Death may be unexpected, but often coronary disease and arterial hypertension present in a person indicate that the doctor’s advice must be followed. However, therapy and prevention of coronary artery disease are not carried out and ignored, which leads to dire consequences.

Atherosclerotic cardiosclerosis is a pathology in which connective tissue grows in the heart due to atherosclerosis of the coronary arteries. Atherosclerotic cardiosclerosis ICD 10 code – I25.1.

Atherosclerosis-cardiosclerosis is one of the manifestations of IHD. Atherosclerotic cardiosclerosis is manifested clinically by heart failure, conduction and heart rhythm disturbances, and angina pectoris. Diagnosis of the disease includes a number of laboratory and instrumental studies.

Treatment of this form of cardiosclerosis is conservative. Therapy is aimed at relieving heart pain, reducing cholesterol, normalizing conduction and heart rate, and improving blood circulation.

The main cause of the disease is the formation of atherosclerotic plaques at the site of damaged blood vessel tissue. They form gradually as cholesterol accumulates. Over time, the plaques increase in size, and the lumen of the vessel, accordingly, narrows. The result of this process is circulatory disorders, vessel curvature, high blood pressure, and insufficient oxygen supply to the body tissues.

Hypoxia of the heart occurs, which ultimately leads to the development of ischemic heart disease. With ischemic disease, myocardial function is disrupted, muscle tissue is replaced with connective tissue, which does not have the necessary elasticity. As a result, pain appears in the heart and the heart rhythm is disturbed.

Atherosclerotic plaques are formed as a result of the following reasons:

• unhealthy diet – excess fat in the food consumed leads to the development of obesity and the deposition of cholesterol in blood vessels;
• smoking – nicotine increases cholesterol levels in the body and promotes platelet agglutination, which has a bad effect on blood vessels;
• diabetes;
• hypodynamia - low physical activity leads to the fact that the myocardium is poorly supplied with oxygen, as a result of which stagnant processes occur in it and the proliferation of connective tissue begins.

Kinds

There are the following forms of atherosclerotic cardiosclerosis (AC):

• diffuse small focal;
• diffuse macrofocal.

By type of AK it can be:

• post-infarction – formed at the site of death of myocardial tissue;
• ischemic – develops due to heart failure, progresses slowly;
• transitional (mixed) - as the name implies, combines the characteristics of the two types of AK listed above.

Symptoms

The main danger of atherosclerotic cardiosclerosis is that in the initial stages of development this disease is asymptomatic.

Since AK is a form of ischemic heart disease, doctors usually focus on the clinical signs of this particular disease. However, there are a number of symptoms that can be used to diagnose atherosclerotic cardiosclerosis.

First of all, such symptoms include pain in the heart, which can be aching or sharp. Pain can be observed not only in the heart area, but also radiate to the left arm or shoulder blade. In addition, with AK, the patient experiences a feeling of constant fatigue, tinnitus, and headaches.

Another characteristic sign of the disease is shortness of breath. It occurs gradually, first after severe physical strain, then during normal walking or even at rest.

With AK, cardiac asthma worsens, and tachycardia develops (heart rate reaches 150 or more beats per minute at rest). One of the most striking symptoms of atherosclerotic cardiosclerosis is swelling of the limbs, which occurs due to problems with the liver.

Diagnostics

In order to make an accurate diagnosis, the doctor interviews the patient and studies his medical history. The specialist is interested in a history of atherosclerosis, arrhythmias, ischemic heart disease and other pathological conditions. During the interview, the doctor finds out what the patient is complaining about and identifies the symptoms of the disease.

After this, to make an accurate diagnosis, a number of laboratory and instrumental studies are prescribed, the most common of which are:

• ECG - performed to detect myocardial hypertrophy, detect scar tissue on it, detect heart rhythm disturbances and vascular insufficiency;
• blood test (biochemical and general) - shows high levels of cholesterol and other lipids;
• bicycle ergometry - helps to identify the degree of cardiac dysfunction and determine the functional reserves of the myocardium;
• echocardiography - allows you to determine the violation of the contractile function of the heart muscle.

Treatment

It is impossible to completely get rid of such a pathology as ischemic heart disease (CAD) and atherosclerotic cardiosclerosis. Treatment of this pathology consists of preventing exacerbations and relieving symptoms.

First of all, medications are prescribed that lower blood cholesterol levels. Most often these are drugs from the statin group. The duration of the course of treatment and dose of drugs is determined by the doctor. As a rule, treatment is long-term and sometimes lifelong.

In addition to statins, the prescription of vasodilators or agents that strengthen the walls of blood vessels is indicated.

If the course of atherosclerotic cardiosclerosis is accompanied by angina pectoris or there is a threat of developing a heart attack, then surgical intervention is possible, during which the largest vascular plaques are removed.

In parallel with the main therapy, the doctor may prescribe tranquilizers or antidepressants.

It should be remembered that self-medication is unacceptable! The attending physician must prescribe certain medications, determine their dosage and duration of treatment. Otherwise, a number of serious complications and even the death of the patient may develop.

Forecast

In severe cases, the possible outcome of the disease atherosclerotic cardiosclerosis is death.

The prognosis is influenced by the degree of myocardial damage, the presence of concomitant diseases, and arrhythmias. In severe cases, signs of ascites and pleurisy are observed, and heart failure develops. In case of aneurysm rupture, atherosclerotic cardiosclerosis is the cause of death of the patient.

Prevention

It is known that it is easier to prevent any disease than to deal with it for a long time and painfully. This statement also applies to atherosclerotic cardiosclerosis. To prevent the development of this disease, as well as its complications, it is necessary, first of all, to eat right.

Atherosclerotic cardiosclerosis – diet:

• limit or completely eliminate salt from the diet;
• do not eat after six o'clock in the evening;
• exclude substances that excite the cardiovascular system and central nervous system (cocoa, tea, coffee, alcohol);
• limit consumption of cholesterol-containing foods (animal entrails, eggs, brains);
• exclude some vegetables from the diet (radishes, radishes, onions, garlic);
• exclude foods that cause gas formation (cabbage, milk, legumes);
• food must be steamed, without salt; baked and boiled food, fruits and vegetables are also allowed (except for those listed above).

In addition to diet, it is necessary to lead a healthy lifestyle and be sure to exercise (swimming, walking, etc.) to strengthen the heart muscle.

It is necessary to undergo preventive examinations at the clinic at least once a year. This makes it possible to identify most cardiovascular diseases at an early stage, which significantly facilitates treatment and makes the prognosis more favorable. If you have the first signs of the disease, you should immediately seek help from a specialist.

PROFILE COMMISSION FOR THE SPECIALTY “PATHOLOGICAL ANATOMY” OF THE MINISTRY OF HEALTH OF THE RUSSIAN FEDERATION

RUSSIAN SOCIETY OF PATHOLOGISTS

FSBI "RESEARCH INSTITUTE OF HUMAN MORPHOLOGY"

GBOU DPO "RUSSIAN MEDICAL ACADEMY OF POSTGRADUATE EDUCATION" MINISTRY OF HEALTH OF THE RUSSIA

GBOU HPE "MOSCOW STATE MEDICAL AND DENTAL UNIVERSITY NAMED AFTER A.I. EVDOKIMOV" MINISTRY OF HEALTH OF THE RUSSIA

State Budgetary Educational Institution of Higher Professional Education "Russian National Research Medical University named after N.I. Pirogov" MINISTRY OF HEALTH OF THE RUSSIA

GBOU HPE "FIRST ST. PETERSBURG STATE MEDICAL UNIVERSITY NAMED AFTER ACADEMICIAN I.P. PAVLOVA" MINISTRY OF HEALTH OF THE RUSSIA

Formulation
pathological diagnosis
for coronary heart disease
(class IX “diseases of the circulatory system” ICD-10)

Moscow - 2015

Compiled by:

Frank G.A., Academician of the Russian Academy of Sciences, Doctor of Medical Sciences, Professor, Head of the Department of Pathological Anatomy of the State Budgetary Educational Institution of Further Professional Education of the Russian Medical Academy of Postgraduate Education of the Ministry of Health of Russia, Chief Freelance Pathologist of the Ministry of Health of Russia, First Vice-President of the Russian Society of Pathologists;

Zairatyants O.V., Doctor of Medical Sciences, Professor, Head of the Department of Pathological Anatomy, State Budgetary Educational Institution of Higher Professional Education, Moscow State Medical University named after. A.I. Evdokimova, Ministry of Health of Russia, Vice-President of the Russian and Chairman of the Moscow Society of Pathologists;

Shpector A.V., Doctor of Medical Sciences, Professor, Head of the Department of Cardiology, Faculty of Physical Education, State Budgetary Educational Institution of Higher Professional Education, Moscow State Medical University named after. A.I. Evdokimova, Ministry of Health of Russia, chief freelance cardiologist of the Moscow Department of Health;

Kaktursky L.V., Corresponding Member of the Russian Academy of Sciences, Doctor of Medical Sciences, Professor, Head of the Central Clinical Laboratory of the Federal State Budgetary Scientific Institution Research Institute of Human Morphology, Chief Freelance Pathologist of Roszdravnadzor, President of the Russian Society of Pathologists;

Mishnev O.D., Doctor of Medical Sciences, Professor, Head of the Department of Pathological Anatomy and Clinical Pathological Anatomy, State Budgetary Educational Institution of Higher Professional Education, Russian National Research Medical University named after. N.I. Pirogova, Ministry of Health of Russia, Vice-President of the Russian Society of Pathologists;

Rybakova M.G., Doctor of Medical Sciences, Professor, Head of the Department of Pathological Anatomy, First St. Petersburg State Medical University named after. acad. I.P. Pavlova of the Ministry of Health of Russia, chief freelance pathologist of the Health Committee of St. Petersburg;

Chernyaev A.L., Doctor of Medical Sciences, Professor, Head of the Department of Pathology, Federal State Budgetary Institution Research Institute of Pulmonology, Federal Medical and Biological Agency of Russia;

Orekhov O.O., Candidate of Medical Sciences, Head of the Pathoanatomical Department of City Clinical Hospital No. 67, Chief Freelance Pathologist of the Moscow Department of Health;

Losev A.V., Candidate of Medical Sciences, Head of the Pathoanatomical Department of the Regional Clinical Hospital of the Ministry of Health of the Tula Region, chief freelance pathologist of the Ministry of Health of the Tula Region and the Ministry of Health of Russia in the Central Federal District of the Russian Federation.

Abbreviations

• CABG – coronary artery bypass grafting
• IHD – coronary heart disease
• MI – myocardial infarction
• ICD-10 – International Statistical Classification of Diseases and Related Health Problems, Tenth Revision
• IDN - International Nomenclature of Diseases
• ACS – acute coronary syndrome
• CVD – cardiovascular diseases
• PCI – percutaneous coronary intervention

Methodology

Methods used to collect/select evidence:

Search in electronic databases.

Description of methods used to collect/select evidence:

Methods used to assess the quality and strength of evidence:

• - expert consensus
• - development of ICD-10
• - study of MNS.

Methods used to formulate recommendations:

Expert Consensus

Consultations and expert assessment:

The preliminary version was discussed at a meeting of the specialized commission in the specialty “pathological anatomy” of the Ministry of Health of Russia on 02/19/2015, at a meeting of the Moscow Society of Pathologists on 04/21/2015, after which it was posted on the website of the Russian Society of Pathologists (www.patolog.ru) for wide discussion, so that specialists who did not take part in the relevant commission and preparation of recommendations had the opportunity to familiarize themselves with them and discuss them. The final approval of the recommendations was carried out at the VIII Plenum of the Russian Society of Pathologists (May 22-23, 2015, Petrozavodsk).

Working group:

For the final revision and quality control of the recommendations, they were re-analyzed by members of the working group, who came to the conclusion that all the comments and comments of the experts were taken into account, and the risk of systematic errors in the development of recommendations was minimized.

Method formula:

The rules for formulating the final clinical, pathoanatomical and forensic medical diagnoses, filling out a statistical accounting document - a medical death certificate for coronary heart disease in accordance with the requirements of the current legislation of the Russian Federation and ICD-10 are given. The adaptation of domestic rules for the formulation of diagnosis and diagnostic terminology to the requirements and codes of ICD-10 was carried out.

Indications for use:

Unified rules for formulating the final clinical, pathological and forensic diagnosis, issuing a medical certificate of death for coronary heart disease in accordance with the requirements of the current legislation of the Russian Federation and ICD-10 throughout the country are necessary to ensure interregional and international comparability of statistical data on morbidity and causes death of the population.

Logistics:

International Statistical Classification of Diseases and Related Health Problems, Tenth Revision (ICD-10) with amendments for 1996-2015.

"" - approved by order of the Ministry of Health of the Russian Federation No. 241 of 08/07/1998.

annotation

Clinical recommendations are intended for pathologists, forensic experts, cardiologists and doctors of other specialties, as well as for teachers of clinical departments, graduate students, residents and senior students of medical universities.

The recommendations are the result of a consensus between clinicians, pathologists and forensic experts and are aimed at improving the quality of diagnosis of nosological units included in the group concept of “coronary heart disease” (CHD), and their statistical recording among the causes of mortality in the population. The purpose of the recommendations is to introduce into practice unified rules for formulating a pathological diagnosis and issuing medical death certificates for ischemic heart disease in accordance with the provisions of the Federal Law of November 21, 2011 No. 323-FZ “On the fundamentals of protecting the health of citizens in the Russian Federation” and the requirements of the International Statistical Classification diseases and health problems 10th revision (ICD-10). The rules apply to final clinical and forensic diagnoses in connection with the underlying general requirements for formulation and the need to compare them when conducting clinical expert work. Examples of constructing (formulating) pathological diagnoses and issuing medical death certificates are given.

Clinical recommendations are compiled based on a synthesis of literature data and the authors’ own experience. The authors are aware that the construction and formulation of diagnoses may change in the future as new scientific knowledge accumulates. Therefore, despite the need to unify the formulation of the pathological diagnosis, some proposals may serve as a basis for discussion. In this regard, any other opinions, comments and wishes of specialists will be received with gratitude by the authors.

Introduction

Diagnosis is one of the most important objects of standardization in healthcare, the basis for quality management of medical services, and documentary evidence of a doctor’s professional qualifications. The reliability of data provided by health authorities on morbidity and mortality of the population depends on the unification and strict adherence to the rules for formulating diagnoses and issuing medical death certificates. The responsibility assigned to pathologists and forensic experts is especially high.

The recommendations are the result of a consensus between clinicians, pathologists and forensic experts and are aimed at improving the quality of diagnosis of nosological units included in the group concept of “coronary heart disease” (CHD), and their statistical recording among the causes of mortality in the population.

Their need is due to:

• - statistical data on multiple and disproportionate excess of mortality rates from cardiovascular diseases (CVD), IHD and myocardial infarction (MI) in Russia compared to the EU countries and the USA, which may indicate different approaches to their diagnosis and recording. Thus, diseases of the ischemic heart disease group in Russia are chosen as the initial cause of death 3 times more often than in Europe. As a result of overdiagnosis of chronic forms of IHD, variants of cardiosclerosis make up the vast majority (up to 20%) among all nosological units - the initial causes of death. Their share among deaths in the IHD group reaches 90%, many times higher than the mortality rates from these diseases in the EU countries and the USA. The mortality rate is artificially increased both from IHD in general, reaching 30%, and from CVD, exceeding 60% among all causes of death, which is 3 times higher than in the EU countries and the USA.
• - the introduction in recent years of new definitions and classifications of acute coronary syndrome (ACS) and MI into international clinical practice.
• - WHO experts have introduced more than 160 changes and updates to ICD-10 over the past decades.
• - publication by the Central Research Institute for Organization and Informatization of Health Care of the Ministry of Health of the Russian Federation and the Ministry of Health of the Russian Federation of new recommendations for coding according to ICD-10 diseases of class IX “Diseases of the circulatory system”.

Cardiac ischemia

IHD (or coronary heart disease) - a group (generic) concept that includes pathological processes (nosological forms) arising as a result of acute or chronic myocardial ischemia (discrepancy between the level of supply of oxygenated blood and the level of need for it in the heart muscle), caused by spasm, narrowing or obstruction of the coronary arteries due to their atherosclerosis.

IHD in ICD-10 is included in class IX “Diseases of the circulatory system”, which combines a large number of group (generic) concepts and nosological units, identified both on the basis of their etiology and pathogenesis, and based on medical and social criteria (many pathogenetically represent are complications of atherosclerosis, arterial hypertension, diabetes mellitus). In particular, such IHD is a group concept. It includes a number of nosological forms, namely, types of angina pectoris, MI, cardiosclerosis, etc. In ICD-10, even such nosological units as acute and repeated MI are divided according to the localization of the pathological process and some other criteria into separate forms, which is necessary take into account when coding them.

Hypertension and secondary arterial hypertension with the diseases that caused them cannot be identified as independent nosological forms in the diagnosis if nosological units from the group of coronary artery disease (as well as from the groups of cerebrovascular diseases, ischemic lesions of the intestines, limbs and other main arteries) are diagnosed.

Class IX includes a number of terms, such as “hypertensive disease”, “atherosclerotic heart disease”, “past myocardial infarction”, etc. For them there are domestic analogues: “hypertensive disease” or “arterial hypertension”, “atherosclerotic cardiosclerosis” or “diffuse small-focal cardiosclerosis”, “post-infarction cardiosclerosis” or “large-focal cardiosclerosis”. When formulating a diagnosis, it is permissible to use terms adopted in domestic classifications, and to issue a medical death certificate, their analogues from ICD-10 with the corresponding codes.

Not used in diagnoses, since they represent group and/or unspecified pathological conditions in coronary artery disease (given in ICD-10 not for their use in a detailed diagnosis): acute ischemic heart disease, unspecified (I24.9), atherosclerotic cardiovascular disease, as described (I25 .0), chronic ischemic heart disease, unspecified (I25.9).

Cannot appear as an underlying disease pathological processes that are complications or manifestations of coronary artery disease and some other nosological forms (syndromes, symptoms): current complications of acute myocardial infarction (I23.0-I23.8), heart failure (I50), variants of arrhythmias (I44-I49), in addition to congenital rhythm and conduction disorders leading to fatal asystole, most of the pathological processes from the group “complications and ill-defined heart diseases” (I51), acute (but not chronic) cardiac aneurysm, pulmonary embolism (pulmonary embolism, except for obstetric practice for which in ICD-10 has a special class XV “Pregnancy, childbirth and the postpartum period” and corresponding codes), cor pulmonale (acute or chronic), pulmonary hypertension (except for primary, idiopathic, which is a nosological form), phlebothrombosis (but not thrombophlebitis) and etc. .

They are not used as a nosological unit - the main disease in deaths (the initial cause of death). the following pathological processes present in the group of coronary artery disease in class IX ICD-10: coronary thrombosis, not leading to myocardial infarction (I24.0), circulatory system disorders after medical procedures, not classified in other headings (I97).

Any mention of atherosclerosis of the coronary arteries in the clinical diagnosis sections is advisable (if appropriate vascular studies have been carried out, for example, angiography), and in pathoanatomical or forensic diagnoses, it is necessary to indicate:

• - localization and degree of maximum stenosis of specific arteries (in%)
• - localization and features (complication option) of unstable (“easy to break”) atherosclerotic plaques.

Additionally, it is also advisable to indicate the stage of atherosclerosis and its degree (area of ​​damage). There are 4 stages of atherosclerosis: I - lipid spots, II - lipid spots and fibrous plaques, III - lipid spots, fibrous plaques and “complicated lesions” (hemorrhages in fibrous plaques, atheromatosis, their ulcerations, thrombotic complications), IV - the presence of atherocalcinosis along with with previous changes. There are 3 degrees of severity of atherosclerosis of the aorta and arteries: moderate, damage to 25% of the intimal area, severe, damage to the area from 25% to 50%, severe, damage to the area of ​​more than 50%.

It is unacceptable to replace the term “atherosclerosis” with the terms “calcification” or “sclerosis” of the artery, since such lesions can be caused not only by atherosclerosis, but also by vasculitis or hereditary diseases.

Nosological units from the IHD group are excluded if the detected myocardial damage (angina pectoris syndrome, MI, cardiosclerosis) is caused not by atherosclerosis of the coronary arteries, but by other causes (coronarogenic and non-coronarogenic necrosis and their outcomes). In such cases, myocardial damage is indicated in the diagnosis under the heading “Complications of the underlying disease,” or, when the logic of constructing the diagnosis dictates this, as part of the manifestations of the underlying disease.

When formulating a diagnosis, you should choose one of the nosological forms included in IHD. It is unacceptable to simultaneously indicate several such units in different diagnostic headings, for example, MI in the “Main Disease” heading, and post-infarction cardiosclerosis – “Concomitant Disease”, or post-infarction and atherosclerotic cardiosclerosis even in one heading.

The modern clinical classification of IHD does not fully correspond to the morphological and ICD-10:

1. Acute forms of IHD:

1.1.Acute (sudden) coronary death;

1.2. Acute coronary syndrome:

1.2.1.. Unstable angina;

1.2.2. MI without ST segment elevation (non-ST-elevation myocardial infarction - NSTEMI);

1.2.3. MI with ST segment elevation (ST-elevation myocardial infarction - STEMI).

2. Chronic forms of IHD:

2.1. Angina (except unstable),

2.2. Atherosclerotic (diffuse small-focal) cardiosclerosis;

2.3. Ischemic cardiomyopathy;

2.4. Large-focal (post-infarction) cardiosclerosis;

2.5. Chronic cardiac aneurysm.

2.6. Other rare forms (painless myocardial ischemia, etc.).

The term “focal myocardial dystrophy” has been excluded from use and is not included in the classifications and ICD-10.(“acute focal ischemic dystrophy of the myocardium”), proposed by A.L. Myasnikov (1965). In the diagnosis, instead of this term, MI should be indicated (as its ischemic stage), and not always as part of coronary artery disease.

Angina pectoris is a group of distinguished clinical nosological units included in ICD‑10 (I20.0-I20.9). Its morphological substrate can be a variety of acute and chronic changes in the myocardium. It is not used in final clinical, pathological and forensic diagnoses.

Ischemic cardiomyopathy(code I25.5) is an extreme manifestation of long-term chronic myocardial ischemia with its diffuse damage (severe diffuse atherosclerotic cardiosclerosis, similar to dilated cardiomyopathy). The diagnosis of ischemic cardiomyopathy is established when there is severe dilatation of the left ventricular cavity with impaired systolic function (ejection fraction 35% or lower). The use of this diagnosis is advisable only in specialized cardiological medical institutions.

Diagnosis "chronic cardiac aneurysm"(in ICD-10 - "heart aneurysm" with code I25.3) does not require additional indication of the presence of post-infarction cardiosclerosis if it is limited to the walls of the aneurysm. Diagnosis “post-infarction (large-focal) cardiosclerosis does not require additional indication of the presence of atherosclerotic (diffuse small-focal) cardiosclerosis.

Silent myocardial ischemia(asymptomatic ischemia, code I25.6) is diagnosed in a patient when episodes of myocardial ischemia are detected on the ECG, but in the absence of angina attacks. Like angina, silent myocardial ischemia is not may appear in the final clinical, pathological or forensic diagnosis.

Syndrome X in a clinical diagnosis, it is established for a patient in whom, in the presence of angina attacks, coronary artery damage is not detected (angiographically, etc.), there are no signs of vasospasm, and other causes of angina syndrome that are not included in the group of coronary artery disease are excluded. “Stunned” myocardium- dysfunction of the left ventricle of the heart after episodes of acute ischemia without myocardial necrosis (including after myocardial revascularization). “Hibernating”, “asleep” (hibernating) myocardium- the result of a long-term decrease in coronary perfusion while maintaining myocardial viability (but with severe dysfunction). In the diagnosis, the terms “syndrome X”, “stunned” and “hibernating” myocardium are not used; there are no ICD-10 codes for them.

In foreign literature, instead of terms “atherosclerotic cardiosclerosis” and “diffuse small-focal cardiosclerosis” use essentially similar concepts: “diffuse or small focal atrophy of cardiomyocytes with interstitial myocardial fibrosis” or "atherosclerotic heart disease". Last term included in ICD-10 (code I25.1) .

Unjustified overdiagnosis of atherosclerotic (diffuse small-focal) or post-infarction (large-focal) cardiosclerosis as the main or competing, or combined disease should be avoided. Thus, this diagnosis is often erroneously established due to an insufficiently professional autopsy and superficial analysis of thanatogenesis, especially in observations of acute death, when the true initial cause of death is acute (sudden) coronary death. It is also important to differentiate between brown myocardial atrophy (with pronounced perivascular sclerosis and myofibrosis) in various severe diseases and in elderly deceased patients, and diffuse small-focal cardiosclerosis as a form of coronary artery disease. Often, nosological units from the group of chronic ischemic heart disease, which do not play a significant role in thanatogenesis, are incorrectly recorded as competing or combined diseases. They should be indicated in the heading “Concomitant diseases” (examples 1 - 5).

• Main disease: Bilateral focal confluent pneumonia in the VI-X segments of the lungs with abscess formation (bacteriologically - S. pneumoniae, date) J13.
• Background disease: Chronic alcohol intoxication with multiple organ lesions: .... (F10.1)
• Complications of the underlying disease: Acute general venous congestion. Brain swelling.
• Accompanying illnesses: Diffuse small-focal cardiosclerosis. Stenosing atherosclerosis of the coronary arteries of the heart (grade 2, stage II, stenosis of predominantly the branches of the left artery up to 50%). Atherosclerosis of the aorta (grade 3, stage IV).

Medical death certificate

I. a) Cerebral edema.

b) Pneumococcal bilateral pneumonia (J 13)

II. Chronic alcohol intoxication (F10.1).

• Main disease: Atherosclerotic (dyscirculatory) encephalopathy. Stenosing atherosclerosis of the cerebral arteries (grade 2, stage II, stenosis of predominantly internal carotid arteries up to 50%) (I67.8).
• Background disease: Hypertension: arteriolosclerotic nephrosclerosis (I10).
• Cachexia: brown myocardial atrophy, liver, skeletal muscles.
• Accompanying illnesses: Atherosclerosis of the aorta (grade 3, stage IV).

Medical death certificate

I. a) Cachexia

b) Atherosclerotic (dyscirculatory) encephalopathy (I67.8).

• Main disease: Intracerebral non-traumatic hematoma in the region of the subcortical nuclei of the right hemisphere of the brain (hematoma volume). Atherosclerosis of the cerebral arteries (grade 2, stage II, stenosis of predominantly the left middle cerebral artery up to 30%) (I61.0).
• Background disease: Hypertension: concentric myocardial hypertrophy (heart weight 430 g, wall thickness of the left ventricle 1.8 cm, right - 0.3 cm), arteriolosclerotic nephrosclerosis (I10).
• Complications of the underlying disease: A breakthrough of blood in the cavity of the right lateral and third ventricles of the brain. Swelling of the brain with dislocation of its trunk.
• Accompanying illnesses: Large focal cardiosclerosis posterior wall of the left ventricle. Stenosing atherosclerosis of the coronary arteries of the heart (grade 2, stage II, stenosis of predominantly the branches of the left artery up to 50%). Atherosclerosis of the aorta (grade 3, stage IV).

Medical death certificate

b) Blood breakthrough into the ventricles of the brain.

c) Intracerebral hematoma (I61.0).

II. Hypertension (I10).

• Main disease: Ischemic cerebral infarction (atherothrombotic) in the frontal, parietal lobes and subcortical nuclei of the left hemisphere (size of necrosis). Stenosing atherosclerosis of the cerebral arteries (grade 3, stage III, stenosis of predominantly the anterior and middle left cerebral artery up to 30%, red obstructive thrombus 2 cm long and unstable atherosclerotic plaque of the left middle cerebral artery) (I63.3).
• Complications of the underlying disease: Swelling of the brain with dislocation of its trunk.
• Accompanying illnesses: Diffuse small-focal cardiosclerosis. Stenosing atherosclerosis of the coronary arteries of the heart (grade 2, stage II, stenosis of predominantly the right artery up to 50%). Atherosclerosis of the aorta (grade 3, stage IV).

Medical death certificate

I. a) Brain edema with dislocation of its trunk.

• Main disease: Residual effects after intracerebral hemorrhage (date - according to the medical history): brown cyst in the region of the subcortical nuclei of the right hemisphere of the brain. Stenosing atherosclerosis of the cerebral arteries (grade 2, stage II, stenosis of predominantly the right posterior, middle and basilar cerebral arteries up to 30%) (I69.1).
• Background disease: Hypertension: concentric myocardial hypertrophy (heart weight 390 g, wall thickness of the left ventricle 1.7 cm, right 0.2 cm), arteriolosclerotic nephrosclerosis (I10).
• Complications of the underlying disease: Bilateral total focal confluent pneumonia (etiology).
• Accompanying illnesses: Large focal cardiosclerosis posterior wall of the left ventricle. Stenosing atherosclerosis of the coronary arteries of the heart (grade 2, stage II, stenosis of predominantly the left circumflex artery up to 50%). Atherosclerosis of the aorta (grade 3, stage IV).

Medical death certificate

I. a) Focal confluent pneumonia.

b) Residual effects after intracerebral hemorrhage (I69.1).

II. Hypertension (I10).

Acute coronary syndrome

The term “acute coronary syndrome” (ACS) was proposed by V. Fuster et al. (1985), but its definition has undergone a number of changes in recent years. Currently ACS is a group clinical concept within coronary artery disease, which unites various manifestations of acute myocardial ischemia caused bycomplicated by unstable atherosclerotic plaque of the coronary artery of the heart. The introduction of the concept of ACS into practice led to the exclusion from use of the term “acute coronary insufficiency”, which still appears in ICD-10 in the group “other acute forms of coronary artery disease” with the general code I24.8. Terms such as “pre-infarction condition” and “acute coronary insufficiency” are not used in the diagnosis.

ACS includes the following nosological forms:

Unstable angina;

MI without ST segment elevation (non-ST-elevation myocardial infarction - NSTEMI);

MI with ST segment elevation (ST-elevation myocardial infarction - STEMI).

They can result in acute (sudden) coronary (cardiac) death, which in some classifications is included in ACS. It should, however, be borne in mind that acute coronary, and even more so, cardiac death is not limited to ACS, just like MI. The previously used clinical sign in the form of the appearance of a pathological Q wave on the ECG is no longer a criterion for the diagnosis and classification of ACS. ACS, as a group concept, which is absent in ICD-10, cannot appear in the diagnosis. This is a preliminary diagnosis, a “logistical” concept, indicating the need for certain emergency treatment and diagnostic measures. In case of death, unstable angina cannot be indicated in the diagnosis. In the final clinical, pathological or forensic diagnoses, depending on the specific situation, either acute (sudden) coronary death (ICD-10 code - I24.8) or MI (ICD-10 codes - I21.-) should be recorded. and I22.-). In pathoanatomical and forensic diagnoses, changes in the ST segment during MI are indicated only if appropriate data are available in the final clinical diagnosis, with reference “according to the inpatient or outpatient card”, “according to the medical history”).

The cause of the development of ACS is acutely developed partial (with unstable angina and non-ST segment elevation MI) or complete occlusion (with ST segment elevation MI) of the coronary artery of the heart by a thrombus complicated by an unstable atherosclerotic plaque. Complications of unstable atherosclerotic plaque include hemorrhage into the plaque, erosion or rupture, dissection of its covering, thrombus, thromboembolism or atheroembolism of the distal parts of the same artery. Clinical criteria for diagnosing the causes of ACS in terms of damage to the coronary arteries of the heart are limited to the concepts of “complicated unstable atherosclerotic plaque” or “atherothrombosis,” which are often used interchangeably. However, it should be clarified that endothelial damage with the development of coronary artery thrombosis can also be observed in atherosclerotic plaques that do not meet the morphological criteria for their instability. In this regard, from a general pathological point of view, it is more correct to speak of a “complicated atherosclerotic plaque.”

Complicated (usually unstable) atherosclerotic plaque of the coronary artery of the heart is a mandatory morphological criterion for diagnosing nosological forms included in ACS. It is important to note that stenosis of the coronary arteries by atherosclerotic plaques before the development of their complications in 50% of patients is insignificant and amounts to less than 40%. Due to autothrombolysis or thrombolytic therapy, thrombi in the coronary arteries of the heart that were diagnosed during life (angiographically, etc.) may no longer be detected at autopsy. Even without thrombolytic therapy, after 24 hours, blood clots persist in only 30% of patients. Therefore, at autopsy, the detection of a complicated unstable atherosclerotic plaque, even without coronary artery thrombosis, is of fundamental importance.

Definitions of the concepts of ACS and type 1 MI (see below) dictate the requirements for examining the coronary arteries of the heart at autopsy: it is imperative to cut the coronary arteries longitudinally, limiting them to transverse sections only is unacceptable. It is advisable to use the method of opening the heart according to G.G. Avtandilov. In pathoanatomical and forensic medical diagnoses, it is mandatory to indicate the location, type (stable, unstable) and nature of complications of atherosclerotic plaques, the degree of stenosis of specific arteries, and a description of the stage and extent (area) of atherosclerotic arterial lesions is optional.

So, for example, the entry: “Acute myocardial infarction (localization, duration, size) is unacceptable.” Atherosclerosis of the coronary arteries of the heart (grade 2, stage II, stenosis up to 30%, thrombosis of the left coronary artery).” An example of a recommended entry could be the following wording: “Acute myocardial infarction (localization, duration, size). Stenosing atherosclerosis of the coronary arteries of the heart (complicated unstable atherosclerotic plaque with a rupture of the tire, a red obstructive thrombus 1 cm long in the left coronary artery at a distance of 1.5 cm from its mouth; atherosclerotic plaques that stenose the lumen of predominantly the left circumflex artery up to 40%).”

For pathoanatomical diagnosis of nosological forms as part of ACS, morphological verification of focal myocardial ischemia is necessary. Although irreversible necrotic changes in cardiomyocytes develop after 20-40 minutes of ischemia, the rate of development of necrosis is influenced by the state of collaterals and microvasculature, as well as the cardiomyocytes themselves and individual sensitivity to hypoxia. In addition, macro- and microscopic morphological signs of necrosis, which do not require the use of special diagnostic methods, appear no earlier than after 4-6 hours (up to 12 hours).

If myocardial ischemia of any origin is suspected, a macroscopic test is required, for example, with nitro blue tetrazolium or potassium tellurite. Histological diagnosis of myocardial ischemia is less specific and more labor-intensive, depending on the correct selection of the myocardial area suspicious for ischemia and research methods. Polarization microscopy is more reliable and can, to a certain extent, replace a macroscopic sample.

It should be borne in mind that positive results of macroscopic tests or relatively specific histological changes appear approximately 30 minutes after the onset of acute myocardial ischemia. They are also not a criterion for qualifying a focus of ischemia or necrosis as a nosological form of myocardial damage from the group of coronary artery disease.

Acute (sudden) coronary death

Under the term "acute (sudden) coronary death"in the clinic they mean sudden death within one hour (according to other definitions - from 6 to 12 hours) from the moment of the onset of the first symptoms (signs) of myocardial ischemia in coronary artery disease. In ICD-10, it is included in the group “other acute forms of ischemic heart disease” (code I24.8). A pathological or forensic diagnosis of acute (sudden) coronary death is established by excluding other causes of death based on clinical and morphological analysis. It is necessary to exclude focal myocardial ischemia. In cases where there is clinical and laboratory data on ACS or MI, and an autopsy reveals a complicated atherosclerotic plaque of the coronary arteries and focal myocardial ischemia, type I MI and its ischemic stage are diagnosed. If an autopsy reveals coronarogenic or non-coronarogenic focal myocardial ischemia not associated with coronary artery disease, the diseases that caused it are diagnosed, which become the main disease.

Concept"acute (sudden) cardiac death" is defined as sudden “cardiac” death (primary circulatory arrest), unexpected in nature and time of occurrence, even in the case of previously established heart disease, the first manifestation of which is loss of consciousness within one hour (according to other definitions - from 6 to 12 hours) from the moment the first symptoms appear. More often it is caused by lethal arrhythmias (ventricular tachycardia turning into ventricular fibrillation, primary ventricular fibrillation, bradyarrhythmias with asystole). In the clinic, the terms “acute cardiac death” and “acute coronary death” are often used as synonyms, with acute (sudden) cardiac death as a broader concept, a clinical syndrome for any lesions of the heart. However in ICD-10, the term “acute (sudden) cardiac death” excludes acute coronary death and the presence of ischemic heart disease . The diagnosis of “acute (sudden) cardiac death” (ICD-10 code - I46.1) is a “diagnosis of exclusion”, allowed after the absolute exclusion of the violent nature of death, acute coronary death, any heart disease and other nosological forms, when the nature of the pathological process and the corresponding morphological substrate underlying the heart damage cannot be established (examples 6, 7).

• Main disease: Acute coronary death(let’s use the term “Sudden coronary death”). Foci of uneven blood supply to the myocardium in the interventricular septum. Stenosing atherosclerosis of the coronary arteries of the heart (grade 3, stage II, stenosis of up to 50% of the branches of the left and right arteries) (I24.8).
• Complications of the underlying disease: Ventricular fibrillation (according to clinical data). Acute general venous congestion. Liquid blood in the cavities of the heart and the lumen of the aorta. Edema of the lungs and brain. Pinpoint hemorrhages under the epicardium and pleura.
• Accompanying illnesses: Chronic calculous cholecystitis, stage of remission.

Medical death certificate

I. a) Acute coronary death (let’s use the term “sudden coronary death”) (I24.8).

• Main disease: Sudden cardiac death. Ventricular fibrillation (according to clinical data) (I46.1).
• Complications of the underlying disease: Acute general venous congestion. Liquid blood in the cavities of the heart and great vessels. Edema of the lungs and brain.
• Accompanying illnesses: Chronical bronchitis

Medical death certificate

I. a) Sudden cardiac death (I46.1).

Myocardial infarction

Myocardial infarction is a coronarogenic (ischemic) necrosis of the myocardium, which can be either a nosological form as part of coronary artery disease or a manifestation or complication of various diseases or injuries accompanied by impaired coronary perfusion (coronaritis, thrombosis and thromboembolism of the coronary arteries, their developmental anomalies, etc. .) .

Modern definition, criteria for clinical diagnosis and classification of MI, called "Third Universal Definition of Myocardial Infarction" were the result of the 3rd international consensus reached in 2012 between the European Society of Cardiology, the American College of Cardiology Foundation, the American Heart Association and the World Heart Federation (Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction). They are based on refined provisions first set out in the materials of the 2nd international consensus in 2007 (Joint ESC/ACCF/AHA/WHF Task for the Redefinition of Myocardial Infarction, 2007). Some definitions presented in ICD-10 have been retained.

MI is considered acute 28 days old. and less.

Recurrent MI should be called when an ischemic attack recurs more than 3 days later. and in less than 28 days. after the previous one.

Repeated MI recognized when it develops after 28 days. after the primary. Both recurrent and repeated MI in ICD-10 have a common code (I22), the fourth character of which depends on the location of the necrosis focus.

In accordance with the “Third Universal Definition”, “the term acute MI should be used when there are proven signs of myocardial necrosis that has developed as a result of prolonged acute ischemia.” The classification of MI includes 5 types. It is advisable to indicate the types of MI in the diagnosis, although they do not have special codes in ICD-10 .

Spontaneous MI (MI type 1) is caused by rupture, ulceration or dissection of an unstable atherosclerotic plaque with the development of intracoronary thrombosis in one or more coronary arteries, leading to a decrease in myocardial perfusion with subsequent necrosis of cardiomyocytes. As already mentioned in the section “acute coronary syndrome”, due to thrombolysis (spontaneous or induced) an intracoronary thrombus may not be detected at autopsy. On the other hand, coronary artery thrombosis can also develop when a stable atherosclerotic plaque is damaged. In addition, type 1 MI can develop with atherocalcinosis of the coronary arteries of the heart, due to plasmorrhagia and cracking of petrification, leading to a rapid increase in the degree of arterial stenosis and/or thrombosis.

Type 1 MI is included in the group concept of ACS and is always a nosological form as part of IHD, therefore the diagnosis indicates either a competing or combined disease in the “Main disease” section (examples 8 - 11).

• Main disease: Acute transmural myocardial infarction (type 1) anterolateral wall and apex of the left ventricle (about 4 days old, size of the necrosis focus). Stenosing atherosclerosis of the coronary arteries of the heart (stenosis up to 50% of the left and unstable, with hemorrhage, atherosclerotic plaque of the left descending artery) (I21.0).
• Background disease: Renal arterial hypertension: eccentric myocardial hypertrophy (heart weight 390 g, wall thickness of the left ventricle 2.0 cm, right - 0.3 cm). Chronic bilateral pyelonephritis in remission, pyelonephritic nephrosclerosis (weight of both kidneys - ... g) (I15.1).
• We also allow the following option: 2. Background disease: Chronic bilateral pyelonephritis in remission, pyelonephritic nephrosclerosis (weight of both kidneys - ... g). Renal arterial hypertension: eccentric myocardial hypertrophy (heart weight 390 g, wall thickness of the left ventricle 2.0 cm, right - 0.3 cm).
• Complications of the underlying disease: Myomalacia and rupture of the anterior wall of the left ventricle of the heart. Pericardial hemotamponade (volume of escaping blood, ml). Acute general venous congestion. Edema of the lungs and brain.
• Accompanying illnesses: Gastric ulcer, remission stage: chronic callous epithelialized ulcer (diameter of the ulcerative defect) of the body of the stomach in the area of ​​its lesser curvature. Chronic indurative pancreatitis in remission.

Medical death certificate

I. a) Hemotamponade of the pericardium.

b) Rupture of the anterior wall of the left ventricle of the heart.

c) Acute anterior apical myocardial infarction (I21.0).

II. Renal arterial hypertension (I15.1).

• Main disease: Repeated macrofocal myocardial infarction (type 1) posterolateral wall of the left ventricle with transition to the posterior wall of the right ventricle (about 3 days old, size of the necrosis focus), large-focal cardiosclerosis of the lateral wall of the left ventricle (scar size). Eccentric myocardial hypertrophy (heart weight 360 g, wall thickness of the left ventricle 1.7 cm, right ventricle - 0.3 cm). Stenosing atherosclerosis of the coronary arteries of the heart (grade 3, stage II, unstable atherosclerotic plaque of the descending branch of the left artery with hemorrhage, stenosis of up to 60% of the mouth of the left artery) (I21.2).
• Background disease: Diabetes mellitus type 2, in the stage of decompensation (blood glucose - ..., date). Diabetic macro- and microangiopathy: atherosclerosis of the aorta (3rd degree, stage III), cerebral arteries (3rd degree, stage II, stenosis of the arteries of the base of the brain up to 25%), diabetic retinopathy (according to the medical history), diabetic nephrosclerosis (arterial hypertension - clinically) (E11.7).
• Complications of the underlying disease: Acute general venous congestion. Pulmonary edema.

Medical death certificate

I. a) Pulmonary edema.

b) Repeated myocardial infarction, posterolateral with transition to the right ventricle (I21.2).

• Main disease: Recurrent myocardial infarction (type 1): fresh (about 3 days old - or “from ... date”) and organizing foci of necrosis (about 25 days old) in the area of ​​the posterior wall and posterior papillary muscle of the left ventricle and the interventricular septum (size of foci of necrosis). Stenosing atherosclerosis of the coronary arteries of the heart (grade 2, stage II, unstable atherosclerotic plaque of the left circumflex artery with hemorrhage, stenosis of the branches of the left artery up to 60%) (I22.1).
• Background disease: Renovascular arterial hypertension: eccentric myocardial hypertrophy (heart weight 360 g, wall thickness of the left ventricle 1.9 cm, right - 0.2 cm). Stenosing atherosclerosis of the renal arteries (grade 3, stage III, obstructing organized thrombus of the left and stenosis of up to 25% of the right arteries). Primary shriveled left kidney (weight 25 g), atheroarteriolosclerotic nephrosclerosis of the right kidney (I15.0).
• We also allow the following option: 2. Background disease: Stenosing atherosclerosis of the renal arteries (grade 3, stage III, occlusive organized thrombus of the left and stenosis of up to 25% of the right arteries). Primary wrinkled left kidney (weight 25 g), atheroarteriolosclerotic nephrosclerosis of the right kidney. Renovascular arterial hypertension: eccentric myocardial hypertrophy (heart weight 360 g, wall thickness of the left ventricle 1.9 cm, right - 0.2 cm).
• Complications of the underlying disease: Avulsion of the posterior papillary muscle of the left ventricle. Cardiogenic shock (clinically), liquid dark blood in the cavities of the heart and the lumen of large vessels. Pinpoint hemorrhages under the pleura and epicardium. Acute general venous congestion. Respiratory distress syndrome.
• Accompanying illnesses: Atherosclerotic dementia (type, another characteristic - clinically), stenotic atherosclerosis of the cerebral arteries (2nd degree, stage II, stenosis of predominantly the left middle cerebral artery up to 50%), moderate atrophy of the cerebral hemispheres and internal hydrocephalus. Atherosclerosis of the aorta (grade 3, stage IV).

Medical death certificate

I. a) Cardiogenic shock.

b) Separation of the posterior papillary muscle of the left ventricle of the heart

c) Recurrent myocardial infarction of the posterior wall and interventricular septum (I22.1).

II. Renovascular arterial hypertension (I15.0).

• Main disease: Ischemic cerebral infarction (atherothrombotic) in the region of the subcortical nuclei of the right hemisphere of the brain (dimensions of the necrosis focus). Stenosing atherosclerosis of the cerebral arteries (grade 3, stage III, stenosis of predominantly the anterior and middle left cerebral arteries up to 30%, red occlusive thrombus and unstable, with hemorrhage, atherosclerotic plaque of the left middle cerebral artery) (I63.3).
• Competing disease:Acute subendocardial myocardial infarction (type 1) posterior wall of the left ventricle (about 15 days old, size of the necrosis focus). Stenosing atherosclerosis of the coronary arteries of the heart (grade 2, stage II, stenosis up to 50% and unstable, with hemorrhages, atherosclerotic plaques of the circumflex branch of the left coronary artery) (I21.4).
• Background disease: Hypertension: eccentric myocardial hypertrophy (heart weight 430 g, wall thickness of the left ventricle 1.8 cm, right - 0.3 cm), arteriolosclerotic nephrosclerosis (I10).
• Complications of the underlying disease: Bilateral focal pneumonia in the middle and lower lobes of the right lung (etiology). Acute general venous congestion. Edema of the lungs and brain.

Medical death certificate

I. a) Focal pneumonia.

b) Ischemic cerebral infarction (I63.3).

II. Acute subendocardial myocardial infarction (I21.4). Hypertension (I10).

MI secondary to ischemic imbalance (MI type 2) develops when a condition other than ischemic heart disease leads to an imbalance between oxygen demand and/or oxygen delivery (endothelial dysfunction, coronary spasm, embolism, tachycardia/bradyarrhythmias, anemia, respiratory failure, hypotension or hypertension with or without myocardial hypertrophy). Complicated unstable atherosclerotic plaques or atherothrombosis were absent at autopsy.

Type 2 MI in most cases is not a nosological form of IHD and should be indicated in the diagnosis under the heading “Complications of the underlying disease.” Of leading importance in its pathogenesis (and diagnosis) is comorbidity: the presence, in addition to atherosclerosis of the coronary arteries and ischemic heart disease, of concomitant diseases and/or their complications that contribute to the development of ischemic imbalance of the myocardium. Such concomitant diseases can be lung diseases, cancer, etc. Even with severe syndrome of chronic cardiovascular failure in a deceased person with atherosclerotic or post-infarction cardiosclerosis due to coronary artery disease, foci of ischemia or necrosis of the myocardium (in post-infarction cardiosclerosis, usually along the periphery of scars) should be regarded as a complication of the underlying disease, and not a recurrent myocardial infarction as part of coronary artery disease. Recurrent MI is diagnosed when signs of type 1 MI are detected.

The formulation of the diagnosis is based on the results of clinical and morphological analysis. There are no specific criteria that would allow morphological differentiation of small-sized MI in coronary artery disease from large-focal myocardial necrosis of hypoxic and mixed origin, which can develop in patients, for example, with severe anemia and the presence of atherosclerosis (but not atherothrombosis, as in type 1 MI). coronary arteries of the heart. In such observations, in the pathoanatomical diagnosis under the heading “Complications of the underlying disease,” it is more appropriate to use the term type 2 MI rather than “myocardial necrosis,” although the non-coronarogenic hypoxic factor plays a large role in its pathogenesis (examples 12, 13).

• Main disease: COPD: chronic obstructive purulent bronchitis in the acute stage. Focal pneumonia in segments III-IX of both lungs (etiology). Diffuse reticular pneumosclerosis, chronic obstructive pulmonary emphysema. Secondary pulmonary hypertension. Pulmonary heart (thickness of the walls of the right ventricle of the heart - 0.5 cm, GI - 0.8) (J44.0).
• Associated disease: Large-focal cardiosclerosis of the posterior wall of the left ventricle. Stenosing atherosclerosis of the coronary arteries of the heart (grade 2, stage II, stenosis of predominantly the left circumflex artery up to 40%) (I25.8).
• Background disease: Hypertension: eccentric myocardial hypertrophy (heart weight 390 g, left ventricular wall thickness 1.7 cm), arteriolosclerotic nephrosclerosis (I10).
• Complications of the underlying disease: Acute general venous congestion. Type 2 myocardial infarction in the region of the posterior wall of the left ventricle and the apex of the heart. Brown induration of the lungs, nutmeg liver, cyanotic induration of the kidneys, spleen. Edema of the lungs and brain.

Medical death certificate

b) COPD in the acute stage with bronchopneumonia (J44.0).

II. Large focal cardiosclerosis (I25.8)

Hypertension (I10).

• Main disease: Large focal cardiosclerosis of the posterior wall of the left ventricle. Stenosing atherosclerosis of the coronary arteries of the heart (grade 2, stage II, stenosis of predominantly the left circumflex artery up to 40%) (I25.8).
• Background disease:
• Complications of the underlying disease: Chronic general venous congestion: brown induration of the lungs, nutmeg liver, cyanotic induration of the kidneys, spleen. Subendocardial foci of myocardial necrosis (myocardial infarction type 2) in the region of the posterior wall of the left ventricle. Edema of the lungs and brain.

Medical death certificate

I. a) Chronic cardiovascular failure

b) Large focal cardiosclerosis (I25.8)

II. Hypertension (I10).

In rare cases, type 2 MI can be qualified as a form of coronary artery disease and listed in the “Major disease” section in the absence of any diseases and their complications causing hypoxic or metabolic damage to the myocardium (lack of comorbidity) and the presence of atherosclerosis of the coronary arteries of the heart with stenosis lumen by more than 50%. Such an example is a circular subendocardial MI, which developed with atherosclerotic lesions of 2 or 3 coronary arteries of the heart without a complicated plaque or atherothrombosis (Example 14).

• Main disease: Acute myocardial infarction (type 2) posterolateral wall of the left ventricle with transition to the posterior wall of the right ventricle (about 2 days old, the size of the necrosis focus), Stenosing atherosclerosis of the coronary arteries of the heart (3rd degree, stage III, stenosis of predominantly the left circumflex artery up to 70%) (I21. 2).
• Background disease: Hypertension: eccentric myocardial hypertrophy (heart weight 390 g, wall thickness of the left ventricle 1.7 cm, right 0.2 cm), arteriolosclerotic nephrosclerosis (I10).
• Complications of the underlying disease: Acute general venous congestion. Edema of the lungs and brain.

Medical death certificate

I. a) Acute cardiovascular failure

b) Acute myocardial infarction, posterolateral with transition to the right ventricle (I21.2).

II. Hypertension (I10).

Type 3 MI (MI leading to death when cardiac-specific biomarkers are not available) is a cardiac death with symptoms suggestive of myocardial ischemia and presumably new ischemic changes on the ECG or new left bundle branch block, if death occurs before blood samples are collected, or before cardiac-specific biomarkers are expected to rise, or in those rare situations where they have not been explored.

Type 3 MI is a clinical concept. An autopsy can diagnose acute coronary death, MI types 1 or 2, as well as other coronarogenic or non-coronarogenic myocardial necrosis of various pathogenesis. Depending on this, this type of myocardial necrosis may appear in various diagnostic categories.

Type 4 MI a is MI associated with percutaneous coronary intervention (PCI), or PCI-associated MI.

Type 4 b MI is a MI associated with coronary artery stent thrombosis..

Type 5 MI is a MI associated with coronary artery bypass graft surgery (CABG), or CABG-associated MI.

MI types 4 a, 4 b and 5 are nosological forms as part of coronary artery disease, developing as a complication of various types of percutaneous coronary interventions or CABG surgery performed for atherosclerotic lesions of the coronary arteries of the heart in patients with coronary artery disease. In the diagnosis, these types of MI are indicated as the underlying disease, and changes in the coronary arteries of the heart and the type of intervention are indicated as its manifestation, if there is no reason to formulate the diagnosis as for iatrogenic pathology.

Thus, in the final clinical, pathological or forensic diagnosis, MI can be presented as the main disease (or as a competing or combined disease), only if it is qualified as a nosological form from the group of IHD. All other types of myocardial necrosis (including, apparently, the majority of type 2 MI) are a manifestation or complication of various diseases, injuries or pathological conditions.

Myocardial necrosis is a group of focal irreversible myocardial damage that is heterogeneous in etiology, pathogenesis and morphogenesis, as well as in the volume of damage, clinical manifestations and prognosis. From the standpoint of general pathology, myocardial necrosis is usually divided into coronarogenic (ischemic, or MI [the term “MI” is not equivalent to its nosological form as part of coronary artery disease]) and non-coronarogenic (hypoxic, metabolic, etc.). According to clinical criteria, in accordance with the “Third International Consensus”, myocardial damage (mainly non-coronary) and MI are distinguished. In connection with the introduction into clinical practice of highly sensitive tests for determining the level of cardiac-specific biomarkers in the blood (especially cardiac troponin I or T), it is necessary to take into account that they can increase with minimal coronary and non-coronary myocardial damage (Table 1).

Table 1

Myocardial damage accompanied by increased cardiac troponin levels

Damage caused by primary myocardial ischemia

Rupture of unstable atherosclerotic plaque of the coronary artery of the heart

Intracoronary thrombosis

Damage secondary to ischemic imbalance in the myocardium

Tachy/bradyarrhythmias

Dissecting aneurysm, ruptured aortic aneurysm, or severe aortic valve disease

Hypertrophic cardiomyopathy

Cardiogenic, hypovolemic, or septic shock

Severe respiratory failure

Severe anemia

Arterial hypertension with or without myocardial hypertrophy

Spasm of the coronary arteries

Thromboembolism of the coronary arteries of the heart or coronaryitis

Endothelial dysfunction with damage to the coronary arteries of the heart without hemodynamically significant stenosis

Lesions not associated with myocardial ischemia

Myocardial contusion, cardiac surgery, radiofrequency ablation, pacing and defibrillation

Rhabdomyolysis with myocardial involvement

Myocarditis

Effect of cardiotoxic drugs (eg, anthracyclines, Herceptin)

Multifactorial or unknown myocardial damage

Heart failure

Stress cardiomyopathy (takotsubo)

Massive pulmonary embolism or severe pulmonary hypertension

Sepsis and terminal condition of the patient

Kidney failure

Severe neurological pathology (stroke, subarachnoid hemorrhage)

Infiltrative diseases (eg, amyloidosis, sarcoidosis)

Physical overexertion

The pathogenesis of myocardial necrosis is often mixed, so the identification of coronarogenic and non-coronarogenic types is often quite arbitrary. For example, the pathogenesis of myocardial necrosis in diabetes mellitus is associated with both ischemic and microcirculatory disorders, metabolic, hypoxic and neurogenic factors.

Coronarogenic (ischemic) necrosis of the myocardium develop as a result of impaired blood supply to the myocardium associated with damage to the coronary arteries of the heart. The main causes of the development of ischemic necrosis that are not included in the group of ischemic heart disease are the following:

• - (thrombo)vasculitis (coronaritis) and sclerosis of the coronary arteries (rheumatic diseases, systemic vasculitis, infectious and allergic diseases, etc.);
• - vasculopathy - thickening of the intima and media of the coronary arteries with metabolic disorders, proliferation of their intima (homocysteinuria, Hurler syndrome, Fabry disease, amyloidosis, juvenile arterial calcification, etc.);
• - myocarditis of various etiologies;
• - thromboembolism of the coronary arteries (with endocarditis, blood clots of the left side of the heart, paradoxical thromboembolism);
• - traumatic damage to the heart and its vessels;
• - primary cardiac tumor or metastases of other tumors to the myocardium (tissue embolism);
• - congenital anomalies of the heart and coronary arteries of the heart, non-atherosclerotic aneurysms with thrombosis or rupture;
• - systemic diseases with the development of narrowing of the coronary arteries of various origins, but not of an atherosclerotic nature;
• - disproportions between the myocardial need for oxygen and its supply (aortic stenosis, aortic insufficiency, thyrotoxicosis, etc.);
• - congenital and acquired coagulopathies with hypercoagulation (thrombosis and thromboembolism: DIC syndrome, paraneoplastic syndrome, antiphospholipid syndrome, erythremia, thrombocytosis, blood thickening, etc.);
• - disturbance of the structural geometry of the heart with a local pronounced decrease in coronary blood flow in cardiomyopathies, myocardial hypertrophy of any origin,
• - drug use (for example, cocaine-associated MI, etc.).

In particular, congenital aneurysm of the coronary artery of the heart with rupture (code Q24.5 according to ICD-10) and the development of hemotamponade of the heart should not be classified as a disease from the ischemic heart disease group. In the diagnosis, both the use of the term “MI” is allowed, which is more consistent with their general pathological essence, and “myocardial necrosis” (examples 15, 16).

• Main disease: Ulcerated subtotal gastric cancer with extensive tumor disintegration (biopsy – moderately differentiated adenocarcinoma, no., date). Cancer metastases to perigastric lymph nodes, liver, lungs (T4N1M1). C16.8
• Complications of the underlying disease: Paraneoplastic syndrome (hypercoagulation syndrome...). Obstructive red thrombus... coronary artery. Myocardial infarction anterior wall of the left ventricle.
• Accompanying illnesses: Chronic calculous cholecystitis, remission stage

Medical death certificate

I. a) Myocardial infarction

b) Paraneoplastic syndrome

c) Subtotal gastric cancer (adenocarcinoma) with metastases, T4N1M1 (C16.8)

• Main disease: Polyarteritis nodosa (periarteritis) with predominant damage to the coronary arteries of the heart, mesenteric arteries, .... (M.30.0)
• Complications of the underlying disease: Myocardial infarction in the region of the posterior and lateral walls of the left ventricle, ....

Medical death certificate

I. a) Myocardial infarction

b) Polyarteritis nodosa (M30.0)

Non-coronarogenic necrosis develop while maintaining coronary blood flow due to:

• - hypoxia (absolute or relative, with increased myocardial oxygen demand), characteristic of many diseases and their complications,
• - exposure to cardiotropic toxic substances, both exogenous, including drugs (cardiac glycosides, tricyclic antidepressants, antibiotics, cytostatics, glycocorticoids, chemotherapy drugs, etc.), and endogenous,
• - various metabolic and electrolyte disorders (with metabolic pathologies, organ failure, etc.),
• - dyshormonal disorders (diabetes mellitus, hypo- and hyperthyroidism, hyperparathyroidism, acromegaly),
• - neurogenic disorders, for example, in cerebrocardiac syndrome in patients with severe brain lesions (ischemic infarctions, traumatic and non-traumatic hematomas), which are also characterized by impaired blood supply to the myocardium (coronarogenic, ischemic component),
• - infectious-inflammatory and immune (autoimmune, immune complex) lesions of the myocardium and often the vessels of the heart, i.e. with a coronarogenic, ischemic component (infectious diseases, sepsis, rheumatic and autoimmune diseases, myocarditis).

Relative hypoxia occurs in various arrhythmias, myocardial hypertrophy, arterial hypo- and hypertension, pulmonary hypertension, heart defects, as well as many other conditions, including surgical interventions and injuries. Non-coronarogenic myocardial necrosis can be observed in cardiomyopathies, severe diseases with cardiac, renal, hepatic, pulmonary or multiple organ failure, severe anemia, sepsis and shock of any origin, as well as in the postoperative period, terminal condition and resuscitation illness (examples 17-23).

• Main disease: Alcoholic subtotal mixed pancreatic necrosis. Operation of laparotomy, sanitation and drainage of the omental bursa and abdominal cavity (date) (K85).
• Background disease: Chronic alcohol intoxication with multiple organ manifestations: alcoholic cardiomyopathy, alcoholic encephalopathy, polyneuropathy, fatty hepatosis (F10.2).
• Complications of the underlying disease: Pancreatogenic (enzymatic) shock. Myocardial necrosis in the area of ​​the anterior and lateral walls of the left ventricle. Respiratory distress syndrome. Necrotic nephrosis. Brain swelling.
• Accompanying illnesses: Large focal cardiosclerosis of the posterior wall of the left ventricle. Stenosing atherosclerosis of the coronary arteries of the heart (grade 2, stage II, stenosis of predominantly the left circumflex artery up to 40%).

Medical death certificate

I. a) Pancreatogenic shock

b) Alcoholic pancreatic necrosis (K85)

II. Chronic alcohol intoxication (F10.2)

Operation of laparatomy, sanitation and drainage of the omental bursa and abdominal cavity (date).

• Main disease: Nodular-branched cancer of the upper lobe bronchus of the left lung with massive tumor disintegration (... - histologically). Multiple cancer metastases to ... lymph nodes, bones (...), liver, ... (T4N1M1) (C34.1).
• Background disease: COPD in the acute stage: (c) Chronic obstructive purulent bronchitis. Diffuse reticular and peribronchial pneumosclerosis. Chronic obstructive pulmonary emphysema. Focal pneumonia in ... segments of both lungs (etiology). Foci of dysplasia and metaplasia of the bronchial epithelium (histologically) (J44.0).
• Complications of the underlying disease: Secondary pulmonary hypertension, cor pulmonale (heart weight - ... g, right ventricular wall thickness - ... see, ventricular index - ...). Acute general venous congestion. Empyema of the pleura on the left. Foci of myocardial necrosis in the area of ​​the apex of the heart and the posterior wall of the left ventricle. Pulmonary edema. Brain swelling.
• Accompanying illnesses:

Medical death certificate

I. a) Foci of myocardial necrosis

b) Pleural empyema

c) Cancer of the left upper lobe bronchus with widespread metastases (T4N1M1) (C34.1).

II. COPD in the acute stage with bronchopneumonia (J44.0).

• Main disease: Cancer of the left breast (… – histologically). Metastases to... lymph nodes, lungs, liver. Radiation and chemotherapy (….) (T4N1M1) (C50.8).
• Combined disease: Chronic bilateral pyelonephritis in the acute stage…. (N10).
• Background disease: Diabetes mellitus type 2, decompensated (blood biochemistry - ..., date). Atrophy and lipomatosis of the pancreas. Diabetic macro- and microangiopathy (...).
• Complications of the underlying disease: Acute general venous congestion. Focal confluent pneumonia in ... segments of the left lung (etiology). Foci of myocardial necrosis in the area of ​​the apex of the heart. Pulmonary edema.
• Accompanying illnesses: Large focal cardiosclerosis of the posterior wall of the left ventricle. Stenosing atherosclerosis of the coronary arteries of the heart (grade 2, stage II, stenosis of predominantly the left circumflex artery up to 50%).

Medical death certificate

I. a) Foci of myocardial necrosis

b) Focal pneumonia

c) Cancer of the left breast with widespread metastases (T4N1M1) (C50.8).

II. Chronic bilateral pyelonephritis in the acute stage (N10)

• Main disease: Hypertension with predominant damage to the heart and kidneys. Eccentric myocardial hypertrophy (heart weight 510 g, wall thickness of the left ventricle 2.2 cm, right - 0.4 cm) with pronounced dilatation of the cavities of the heart. Non-stenotic atherosclerosis of the coronary arteries of the heart (grade 1, stage II). Arteriolosclerotic nephrosclerosis with outcome in primary shriveled kidneys (weight of both kidneys 160 g) (I13.1).
• Complications of the underlying disease: CRF, uremia (blood biochemistry -..., date): uremic erosive-ulcerative pangastritis, fibrinous enterocolitis, fibrinous pericarditis, fatty liver. Chronic general venous congestion. Foci of myocardial necrosis in the anterior and posterior walls of the left ventricle (dimensions). Edema of the lungs and brain.
• Accompanying illnesses: Atherosclerosis of the aorta, cerebral arteries (2nd degree, stage II).

Medical death certificate

I. a) Uremia.

b) Hypertension with damage to the heart and kidneys (I13.1).

• Main disease: Cancer of the floor of the mouth (… - histologically). Cancer metastases to the cervical and submandibular lymph nodes on both sides (T4N1M0) (C04.8).
• Complications of the underlying disease: Necrosis of metastasis in the left submandibular lymph node with arrosion ... of the artery. Massive arrosive bleeding. Operation to stop bleeding (date). Hemorrhagic shock (...). Acute posthemorrhagic anemia (clinical test data). Acute general anemia of internal organs. Foci of myocardial necrosis in the posterior wall of the left ventricle. Respiratory distress syndrome. Necrotic nephrosis.
• Accompanying illnesses: Diffuse small-focal cardiosclerosis. Stenosing atherosclerosis of the coronary arteries of the heart (grade 2, stage II, stenosis of predominantly the branches of the left artery up to 50%). Atherosclerosis of the aorta (grade 3, stage IV).

Medical death certificate

I. a) Hemorrhagic shock

b) Necrosis of metastasis in the lymph node with arrosion of the artery and

bleeding.

c) Cancer of the floor of the mouth with metastases (T4N1M0) (C04.8).

• Main disease: Phlegmon of the upper and middle third of the thigh (L03.1).
• Background disease: Diabetes mellitus type 2, stage of decompensation (blood biochemistry - ..., date). Atrophy, sclerosis and lipomatosis of the pancreas. Diabetic macro- and microangiopathy, retinopathy, polyneuropathy, diabetic nephrosclerosis. E11.7
• Complications of the underlying disease: Sepsis (bacteriologically - ..., date), septicemia, septic shock: systemic inflammatory response syndrome (indicators ...). Hyperplasia of the spleen (mass...). Multiple organ failure syndrome (indicators...). Respiratory distress syndrome. Necrotic nephrosis. DIC syndrome. Myocardial necrosis posterior and lateral walls of the left ventricle.

Medical death certificate

I. a) Sepsis, septic shock

b) Phlegmon of the upper and middle third of the thigh (L03.1)

II. Diabetes mellitus type 2 (E11.7)

• Main disease: Acute phlegmonous perforated calculous cholecystitis. Operation of laparotomy, cholecystectomy, sanitation and drainage of the abdominal cavity (date) (K80.0).
• Complications of the underlying disease: Hepatic-renal failure, electrolyte disturbances (indicators - according to clinical data). Foci of myocardial necrosis in the region of the posterior and lateral walls of the left ventricle.
• Accompanying illnesses: Large focal cardiosclerosis of the posterior wall of the left ventricle. Stenosing atherosclerosis of the coronary arteries of the heart (grade 2, stage II, stenosis of predominantly the left circumflex artery up to 40%). Hypertension: concentric myocardial hypertrophy (heart weight 390 g, wall thickness of the left ventricle 1.7 cm, right 0.2 cm), arteriolosclerotic nephrosclerosis (I10). Atherosclerosis of the aorta (grade 3, stage IV).

Medical death certificate

I. a) Foci of myocardial necrosis

b) Hepatic-renal failure

c) Acute phlegmonous perforated calculous cholecystitis (K80.0)

II. Operation of laparotomy, cholecystectomy, sanitation and drainage of the abdominal cavity (date)

If myocardial necrosis develops in the first 4 weeks after surgery and there are no complicated unstable atherosclerotic plaques in the coronary arteries of the heart (atherothrombosis), they should be regarded as a complication and indicated in the heading “Complications of the underlying disease.” The exception is the detection of morphological signs of type 1 MI.

Thus, the only specific morphological diagnostic criterion for MI as a nosological form as part of coronary artery disease is a complicated, predominantly unstable atherosclerotic plaque of the coronary artery of the heart. In other cases, the classification of myocardial necrosis should be the result of clinical and morphological analysis.

In the differential diagnosis of coronarogenic and non-coronarogenic necrosis with MI as a nosological form as part of coronary artery disease, the following clinical and morphological criteria must be taken into account :

• - anamnestic and clinical laboratory data (if available, and a history of ischemic heart disease and/or a slight increase in the level of cardiac troponin cannot be criteria for diagnosing myocardial infarction from the ischemic heart disease group);
• - the presence of diseases and their complications that may cause the development of certain types of myocardial necrosis (comorbidity is more typical for type 2 MI);
• - changes in the coronary and intramural arteries of the heart (but the presence of stenosing atherosclerosis without a complicated atherosclerotic plaque or atherothrombosis cannot be a criterion for diagnosing MI from the ischemic heart disease group);
• - morphological (macro- and microscopic) features of the heart and its valve apparatus (changes in the structural geometry of the heart, damage to the valves, etc.);
• - number, size, localization and histological features of foci of necrosis (non-coronarogenic myocardial necrosis is usually multiple, small in size, located simultaneously in the blood supply basins of different arteries, sometimes with specific changes characteristic of the underlying disease or not corresponding in morphology to the timing of necrosis);
• - morphological features of the myocardium outside the necrosis zone (changes in cardiomyocytes - fatty degeneration, etc., stroma - inflammatory infiltration, etc., vessels - vasculitis, vasculopathy, etc., often characteristic of the underlying disease).

Literature

1. Oganov R.G. Cardiovascular diseases at the beginning of the 21st century: medical, social, demographic aspects and ways of prevention. http://federalbook.ru/files/FSZ/soderghanie/Tom.2013/IV/. pdf.
2. Samorodskaya I.V. Cardiovascular diseases: principles of statistical accounting in different countries. Healthcare. 2009; 7: 49-55. www.zdrav.ru.
3. Thygesen K. et al. Joint ESC/ACCF/AHAIWHF Task for the Redefinition of Myocardial Infarction. Eur. Heart J 2007;28:2525-2538 (JACC. 2007;50:2173-2195; Circulation. 2007;116:2634-2653).
4. Thygesen K., et al. The Writing Group on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction. Nat. Rev. Cardiol. Advance online publication. 25 August 2012; doi:10.1038/nrcardio.2012.122.
5. International Statistical Classification of Diseases and Related Health Problems; 10th revision: Updates 1998-2012. http://www.who.int/classifications/icd/icd10updates/en/index.html.
6. Weissman D.Sh. Guide to the use of the International Classification of Diseases in medical practice: in 2 volumes, volume 1. M.: RIO TsNIIOIZ, 2013.
7. On the peculiarities of coding some diseases from class IX ICD-10 / Letter of the Ministry of Health of the Russian Federation dated April 26, 2011 No. 14-9/10/2-4150.
8. The procedure for issuing “Medical death certificates” in cases of death from certain diseases of the circulatory system / Methodological recommendations. – M.: TsNIIOIZ, 2013. – 16 p.
9. Zairatyants O. V., Kaktursky L. V. Formulation and comparison of clinical and pathological diagnoses: Handbook. 2nd ed., revised. and additional – M.: MIA, 2011.
10. National manual of pathological anatomy. Ed. M.A. Paltsev, L.V. Kaktursky, O.V. Zayratiants. - M.: GEOTAR-Media, 2011.
11. International Statistical Classification of Diseases and Related Health Problems; 10th revision: In 3 volumes / WHO. – Geneva, 1995.
12. Collection of normative and methodological documents and standards for pathological services. System of voluntary certification of processes for performing pathological examinations and pathological services in healthcare. Federal Service for Supervision of Healthcare and Social Development of the Russian Federation. – M., Roszdravnadzor, 2007.
13. Industry standard “Terms and definitions of the standardization system in healthcare”, OST TO No. 91500.01.0005-2001, put into effect by order of the Ministry of Health of the Russian Federation dated January 22, 2001 No. 12.
14. Order of the USSR Ministry of Health No. 4 of 01/03/1952, Appendix 7.
15. Order of the USSR Ministry of Health dated April 4, 1983 No. 375 “On further improvement of the pathological service in the country.”
16. Methodological recommendations of the USSR Ministry of Health “Rules for the preparation of medical documentation of PJSC” (sectional section of work). D.S.Sarkisov, A.V.Smolyannikov, A.M.Wichert, N.K.Permyakov, V.V.Serov, G.G.Avtandilov et al., 1987
17. Federal State Statistics Service (Rosstat). www.gks.ru.
18. WHO/Europe, European mortality database (MDB), April, 2014. http://data.euro.who.int/hfamdb.
19. Shevchenko O.P., Mishnev O.D., Shevchenko A.O., Trusov O.A., Slastnikova I.D. Cardiac ischemia. – M.: Reafarm, 2005.
20. Kakorina E.P., Aleksandrova G.A., Frank G.A., Malkov P.G., Zairatyants O.V., Vaisman D.Sh. The procedure for coding causes of death in certain diseases of the circulatory system - Pathology Archive. - 2014. - T.76. - No. 4. - P.45-52.
21. Zairatyants O.V., Mishnev O.D., Kaktursky L.V. Myocardial infarction and acute coronary syndrome: definitions, classification and diagnostic criteria. - Archive of pathology. - 2014. – T.76. - No. 6. – P. 3-11.
22. Scottish Intercollegiate Guideline Network (2007). Acute Coronary Syndromes. SIGN; Edinburgh. http://www.sign.ac.uk/pdf/sign96.pdf. October 2009.
23. Kumar V., Abbas A.K., Astor J.C. Robbins Basic Pathology. 9th Ed. Philadelphia, London, Toronto, Montreal, Sydney, Tokyo: Elsevier Inc., 2013.
24. Avtandilov G.G. Fundamentals of pathological practice. Manual: 2nd ed. M.: RMAPO, 1998.
25. British Heart Foundation. Factfile: Non-atherosclerotic causes of myocardial infarction (2010). http://bhf.org.uk/factfiles
26. Egred, M., Viswanathan G., Davis G. Myocardial infarction in young adults. Postgraduate med. J. 2005; 81(962):741-755.
27. Kardasz I., De Caterina R., Myocardial infarction with normal coronary arteries: a conundrum with multiple aetiologies and variable prognosis: an update. J. intern. Med. 2007; 261(4):330-348.

Cardiosclerosis is a disease accompanied by pathological changes in the structure of the myocardium. Its muscle fibers are replaced by epithelial tissue that does not have contractility.

Accordingly, the heart can no longer fully perform its previous functions, the patient notes a deterioration in his health, and is at risk of developing complications, in particular, myocardial infarction. The most common disease today is atherosclerotic cardiosclerosis.

In order to understand what the disease is, it is necessary not only to familiarize yourself with the definition of atherosclerotic cardiosclerosis in Wikipedia, but also to carefully consider the sequence of its development.

Initially, vascular atherosclerosis appears. This is a violation of the elasticity of their walls, as well as a deterioration in transport capacity, provoked by the accumulation of fatty plaques on the walls, narrowing the lumen, and, accordingly, reducing the amount of blood transported through the vessels. As a result, the heart ceases to receive the proper amount of nutrients, and oxygen starvation occurs. These factors provoke the launch of pathological processes in the myocardium, one of them is tissue scarring, replacement of muscle fibers with connective tissue. So the heart ceases to cope with its functions fully, and the risk of complications increases.

Important! In ICD 10, atherosclerotic cardiosclerosis has code I25.1. But often doctors can assign other codings to it, depending on the characteristics of the manifestation.

Reasons for the development of the disease

Considering the fact that atherosclerotic cardiosclerosis causes ischemic heart disease, which, in turn, provokes atherosclerosis, the main root causes of the disease should be considered in order to be able to avoid at least some of them, minimizing the risks of developing the disease:

• arterial hypertension - a very often considered cardiac pathology develops against the background of arterial hypertension;
• unbalanced diet rich in animal fats;
• diabetes;
• smoking, which increases cholesterol levels and provokes vasospasm;
• being overweight;
• sedentary lifestyle.

Knowing the main reasons that can trigger the development of atherosclerosis, you can avoid its development at an early stage. And if the disease does appear, then you can understand what measures should be taken, in addition to drug treatment, in order to stop its development and aggravation by complications.

Features of symptoms

As for those that make it possible to identify the disease at an early stage, the clinical picture of atherosclerotic cardiosclerosis can be quite varied. In some cases, a person does not observe any fundamental changes in his own health, so he does not see a doctor for a long time. But, over time, the first manifestations of the disease will begin to develop, which are as follows:

• pain behind the sternum, which can radiate to the left shoulder blade;
• shortness of breath, developing even in a state of physical rest;
• swelling of the lung tissue, causing a dry cough;
• increased fatigue, decreased performance;
• myocardial infarctions that occur repeatedly.

As soon as such symptoms of atherosclerotic type cardiosclerosis begin to appear, it is necessary to urgently consult a cardiologist. The doctor will prescribe a full examination, after which he will be able to make the correct diagnosis and give recommendations regarding further treatment.

How is diagnosis done?

Usually, in the absence of additional indications, a person will have to undergo a standard set of diagnostic procedures and studies. These will be:

1. detailed blood tests that provide information about cholesterol levels, as well as the presence of concomitant diseases, if any;
2. ECG is performed as a one-time procedure, as well as using Holter monitoring. Allows you to track the characteristics of the heart rhythm and disruptions in it, identify signs of scarring of myocardial tissue and hypertrophy;
3. echocardiography – allows you to track disturbances in myocardial contractility, as well as determine the localization of its pathological foci;
4. bicycle ergometry – makes it possible to obtain information about the functional reserves of the heart, as well as the degree of dysfunction of the organ’s muscles.

After the data and results of the examination are received, the doctor can talk about prescribing effective treatment.

Features of therapy

Treatment of atherosclerotic cardiosclerosis is carried out comprehensively, which eliminates all its symptoms and stops progression. The patient will be prescribed:

• blood thinners such as aspirin;
• diuretics to lower blood pressure;
• means for dilating blood vessels and improving blood flow through them;
• medications to reduce the heart's oxygen demand;
• means for normalizing metabolism in tissues;
• antiarrhythmic drugs - they are used in the treatment of atherosclerotic cardiosclerosis with cardiac arrhythmia.

In addition to conservative treatment, a person will have to follow a special diet that will help avoid complications. Its main rule is less cholesterol and salt. That is why you need to exclude fatty, fried and smoked foods, and replace meat with sea fish if possible. You should eat as many fruits and vegetables as possible, as well as grains. Doctors will also recommend limiting the volume of liquid to 1.5 liters per day, and salt to 3-5 g per day. Each patient will be provided with individual recommendations. Do not forget about moderate physical activity, which will help strengthen blood vessels and stabilize the functioning of the heart.

The prognosis for survival for the cardiac pathology in question will be quite encouraging if you follow all the recommendations listed above. From them it is clear that the success of treatment depends to a large extent on the patient himself.

In contact with