Mitral regurgitation: causes, manifestations and treatment. Mitral valve insufficiency: causes, diagnosis and treatment of valve defect Causes of valvular pathology

Interferon status (IFN status) is a set of a number of indicators (parameters) characterizing the state of the main system of innate (nonspecific) immunity - the IFN system, its reactivity and functional activity, which provides the first line of defense of the body from various infectious (and non-infectious) agents recognized cells as an alarm signal.

Infection with various pathogens causes a protective response in cells with the synthesis of universal protective proteins - IFNs, which prevent and/or interrupt the spread of the infectious process, stimulate innate and adoptive immune responses and maintain the homeostasis of the body as a whole. The universal phenomenon of IFN formation is inherent in the cells of almost all vertebrates from fish to humans; viruses are natural inducers of IFN.

Recognition of viral and microbial structures, known as pathogen-associated molecular patterns (PAMPs), is carried out by the so-called pattern recognition receptors (PRR), which include the most studied Toll-like receptors (TLRs), which play a key role in the activation of the IFN system during viral or bacterial infections and in the associated induction of other parts of the innate immune response.

TLRs are sensitive to a wide range of viruses, bacteria, fungi and protozoa. The interaction of various pathogens with the corresponding TLRs activates signaling pathways for the expression of IFN genes, which mediate the induction of the innate immune response of the IFN system, promoting the production of other Th1 proinflammatory cytokines (TNF-α, IFN-γ), the development of the cellular immune response and adaptive immunity.

The variety of physiological functions of IFN discovered to date and the universal ability of different cells to produce different types of IFN indicate the existence in each cell of an IFN system, which is aimed at protecting against foreign genetic information and ensuring nucleic acid homeostasis of the body as a whole.

Implemented at the molecular and cellular levels, the IFN system forms a protective barrier against infectious agents much earlier than specific protective reactions of the immune system. The course and outcome of the disease depend on the speed and efficiency of switching on the IFN system in various forms of pathology. A timely, adequate response from the IFN system can ensure the elimination of pathogens from the body without the participation of a slower-responding adaptive immune system associated with the need to accumulate a clone of antigen-specific immune cells and antibodies. Delayed or reduced production of endogenous IFNs can lead to progression or chronicity of the disease, including death.

A reflection of the reactivity and functional activity of the IFN system is the IFN status, which includes the determination of 4 main indicators:

1. the level of production of IFN-α by blood leukocytes upon its induction in vitro by the standard IFN-α inducer - Newcastle disease virus (NDV). A load test that characterizes the IFN-α-producing ability of the patient’s blood leukocytes, in which the infection of his blood leukocytes with NDV is simulated in vitro and the amount of the protective protein produced by them, IFN-α, is determined;

2. the level of production of IFN-γ by blood leukocytes upon its induction in vitro by the standard IFN-γ inducer – phytohemagglutinin (PHA). A load test characterizing the IFN-γ producing ability of the patient's blood leukocytes, in which the interaction of blood leukocytes with the mitogen - PHA - is simulated in vitro and the amount of the protective protein produced by them - IFN-γ - is determined;

3. the level of spontaneous IFN production by blood leukocytes in vitro in the absence of any additional induction;

4. quantitative content of IFN circulating in the blood serum.

The combination of these indicators characterizes the state of the IFN system and the patient’s immunoreactivity in situ. Violations in various parts of the IFN system are determined by:

• acute and chronic viral and other intracellular infections;
• allergic, autoimmune, oncological diseases;
• recurrent acute respiratory viral infections and tonsillitis in frequently ill children;
• secondary immunodeficiencies associated with other forms of pathology.

All of the above diseases are indications for studying IFN status.

The study of IFN status indicators allows us to identify the following disorders in the IFN system of the studied patients:

• an increase in serum IFN titers associated with a decrease in the production of IFN-α and/or IFN-γ by blood leukocytes, indicating the acute stage of the disease;
• a decrease in the α- and γ-IFN producing ability of blood leukocytes in combination with the absence of serum IFN circulating in the blood, indicating a defective IFN system;
• a decrease in the α- and γ-IFN-producing ability of blood leukocytes in combination with the presence of spontaneous IFN production and the absence of IFN circulating in the blood, indicating a persistent viral or other intracellular infection.

Depending on the degree of decrease in the 2 most significant indicators of IFN status - the level of production of IFN-α and IFN-γ by blood leukocytes in vitro relative to the physiological norm, 4 degrees of insufficiency of the IFN system are distinguished according to the α- and/or γ-links of the IFN system, respectively :

• 1st degree – 2–4-fold decrease in the production of IFN-α and IFN-γ compared to the lower limit of the physiological norm;
• 2nd degree – 4–8 fold reduction;
• 3rd degree – 8–16 fold reduction;
• 4th degree – 16 or more fold reduction.

In case of insufficiency of the IFN system accompanying various forms of pathology in children and adults, it is necessary to carry out corrective IFN-stimulating therapy aimed at correcting the reduced production of α - and γ -IFN, modulating the functional activity of the IFN system and innate immunity, associated adaptive immunity and rehabilitation of the patient the body as a whole.

To select an adequate immunotropic drug and subsequent effective immunocorrective therapy, additional studies are required to determine the individual sensitivity of the patient's blood leukocytes to IFN drugs, IFN inducers or immunomodulators. Individual sensitivity studies are usually carried out in parallel with an in situ study of IFN status.

Individual sensitivity to drugs is studied based on the effectiveness of the corrective effect of the drug (correction coefficient) on the initially reduced production of IFN-γ by the patient’s blood leukocytes - the key cytokine that determines the direction, intensity and effectiveness of the body’s interferon and immune response to infectious agents (RF patent No. 2423705, 2009 .).

Depending on the values ​​of the correction factor, there are 5 options for individual sensitivity to immunoactive drugs:

• 2 – weak; an increase in the production of IFN-γ by the patient’s blood leukocytes in the presence of the drug relative to the original by 2 times;
• 4 – pronounced; an increase in the production of IFN-γ by the patient’s blood leukocytes in the presence of the drug relative to the original by 4 times;
• more than 4 – very pronounced; an increase in the production of IFN-γ by the patient’s blood leukocytes in the presence of the drug relative to the original by more than 4 times;
• 1 – lack of sensitivity; an increase in the production of IFN-γ by the patient’s blood leukocytes in the presence of the drug relative to the initial one is not tested;
• less than 1 – immunotoxicity; suppression of IFN-γ production by the patient’s blood leukocytes in the presence of the drug relative to the original.

The study of IFN status with determination of the individual sensitivity of the patient’s blood leukocytes to immunoactive drugs allows the attending physician to obtain advanced information about the effectiveness of subsequent immunocorrective therapy and make the correct scientifically based choice of a drug or combination of drugs that is adequate for this particular patient.

The use of IFN drugs, IFN inducers or immunomodulators combines well with antibiotics, antivirals and other drugs of basic therapy, increases the effectiveness and reduces the duration of treatment for the patient.

Born and acquired anomalies in the development of cardiac structures are considered to be common causes of early onset of disability among patients of all ages. Also a likely outcome is the death of the patient in the short term (3-5 years).

Recovery is unlikely, but the reasons for this do not lie in the potential incurability of the pathological processes. Everything is much simpler.

On the one hand, patients do not monitor their own health closely enough; this is the result of low medical culture and poor education.

On the other hand, most countries do not have an early screening program for heart problems. This is unusual, given that cardiac pathologies are practically in first place in the number of deaths.

Mitral regurgitation is a condition in which the valve is unable to close completely. Hence regurgitation or reverse flow of blood from the ventricles into the atria.

The working volumes of liquid connective tissue fall, not reaching adequate values. The weakness of the release causes insufficient functional activity of the structures.

Hemodynamics are disrupted, tissues do not receive enough oxygen and nutrients, hypoxia results in degenerative and dystrophic changes. This is a generalized process that disrupts all body systems.

Clinical typification of a pathogenic phenomenon is carried out for various reasons. Thus, depending on the origin, an ischemic form is distinguished, which is associated with hemodynamic disturbances. This is a classic variety.

The second is non-ischemic, that is, it is not associated with deviations in the provision of oxygen to tissues. It occurs less frequently, and only in the early stages.

Another way to classify the condition is based on the severity of the clinical picture.

• The acute type occurs as a result of rupture of the chordae tendineae of the valve and is determined by severe symptoms, as well as a high probability of complications and even death.
• Chronic and formed as a result of a long course of the main process, without treatment and goes through 3 stages. Recovery requires a lot of effort, more often it is prompt, which in itself can lead to fatal consequences (a relatively rare occurrence).

The main clinical classification is characterized by the severity of the pathological process:

• I. Full compensation phase. The organ is still able to realize its functions, the volume of returning blood is no more than 15-20% of the total amount (hemodynamically insignificant). This is a classic option, corresponding to the very beginning of the disease. At this moment, the patient does not yet feel the problem or the manifestations are so scarce that they do not provoke any suspicion. This is the best time for therapy.
• II. Partial compensation. The body can no longer cope. The amount of blood refluxing into the atrium is more than 30% of the total volume. Recovery is possible through surgical methods, dynamic monitoring is no longer carried out, the problem needs to be eliminated. The atria and ventricles are overloaded, the former are stretched, the latter are hypertrophied to compensate for the stretch. It is possible to stop the work of a muscle organ.
• III. Decompensation. Complete disruption of the activity of cardiac structures. Regurgitation is equivalent to grade 3 and is more than 50%; this leads to a pronounced clinical picture with shortness of breath, asphyxia, pulmonary edema, and acute arrhythmia. The prospects for a cure are vague; it is impossible to say exactly how likely a return to normal life is. Even with complex exposure, there is a high risk of permanent defect and disability.

Slightly less often, 5 clinical stages are distinguished, which is not of great importance. These are all the same variants of the 3rd phase of pathology, however, more differentiated in terms of prognosis and symptoms. Accordingly, they also talk about the dystrophic and terminal stages.
Classification is required to develop treatment pathways.

Features of hemodynamics

Mitral valve insufficiency of any degree is determined by impaired circulation (hemodynamics) in tissues and organs.

The process is generalized, therefore deviations in the functioning of all structures are likely, often leading to secondary processes and severe disability.

Clinical variants are renal failure, hepatic dysfunction, encephalopathy. Possible vascular dementia.

The essence of the process lies in the weakness of the mitral valve. Normally, its walls close tightly, preventing blood from the ventricles from returning to the atria.

Against the background of the phenomenon under consideration, regurgitation (backflow of blood from the ventricles into the atria) is a characteristic feature of the disease.

The volume of liquid connective tissue released is insufficient to adequately supply the organs. Depending on the stage, the working blood volume ranges from 75 to 30 percent or less. It turns out that the functional quantities are small.

In the early stages, the heart compensates for the insufficiency of the bicuspid valve by intensifying contractions and increasing the frequency of beats. But this doesn't last long.

On the other hand, the adaptive mechanisms themselves lead to defects of the cardiac structures: hypertrophy of the left ventricle, increased pressure in the pulmonary artery, stretching of the left atrium, and, as a result, the development of chronic heart failure.

Ultimately, a heart transplant may be required, which in most cases is a death sentence.

The clinical picture is most pronounced at stage 3 of the pathological process. The terminal phase is accompanied by total multiple organ failure.

The prospects for a cure are extremely disappointing. Hence the conclusion: if you have the first suspicion of heart problems, you need to contact a cardiologist.

Characteristic symptoms

As already noted, there are 3 phases of the pathological process. Slightly less common 5, this is a more accurate clinical option, but they are more of a scientific value than a practical one.

An approximate picture is this:

• Dyspnea. First, at the moment of intense mechanical load. In this case, it is difficult to understand where normal physiology ends and the disease begins. Because within the framework of poor body training, identical manifestations are possible. Later, in the subcompensated and completely uncontrolled stage, the symptom occurs at rest, even when the patient is lying down. This significantly reduces the quality of life and leads to pulmonary problems; compensatory mechanisms destroy the entire respiratory system and lead to increased pressure in the artery of the same name. This is a factor that worsens the underlying disease and worsens the prognosis.
• Arrhythmia. In different variations. From tachycardia to or. It is extremely rare that so-called non-dangerous forms of the pathological process occur within the framework of mitral insufficiency. Much more often these are threatening phenomena leading to cardiac arrest or heart attack. It is possible to determine interruptions yourself, but not always. The most accurate diagnostic method is electrocardiography.
• Fall in blood pressure. Sometimes to critical levels, especially during an acute process. Cardiogenic shock may develop. This is a lethal condition; in approximately 95% of situations it leads to the death of the patient, even with timely resuscitation and comprehensive treatment. Recovery is impossible, the prognosis is extremely unfavorable.
• Pulmonary edema.
• Also weakness, drowsiness, apathy. In the acute period, a panic attack occurs with inappropriate behavior and increased motor activity.
• Ascites. Or fluid accumulation in the abdominal cavity.
• Edema of the lower extremities. Diuretics are effective only at the first moment, then they do not bring the desired effect.

Stages of NMC

The stage of the pathological process, along with the degree, plays an important role in the clinical picture.

Highlight:

• Stage 1 of uric acid deficiency corresponds to the complete absence of manifestations. Or they are so insignificant that they do not attract attention.
• Stage 2 (moderate) is determined by a more pronounced clinical picture. The patient suffers from shortness of breath at rest and with minimal physical activity, chest pain of unknown origin, and problems with rhythm. But the quality of life is still acceptable, which is why many do not go to the doctor. Especially smokers who attribute their condition to the consequences of consuming tobacco products.
• Stage 3 (severe) is determined by severe symptoms and a significant decrease in important indicators.
• 4 terminal stage It almost always ends in death and recovery is impossible. Palliative care is provided to alleviate the condition and ensure a dignified death.

Mitral regurgitation of the 1st degree is the most favorable moment to begin treatment. Later, as the clinical picture becomes more complex, recovery is less likely.

Reasons for the development of pathology

The factors causing the problem are diverse. They always have a pathogenic origin.

Congenital and acquired heart defects

Paradoxically, the problem may arise as part of other cardiac changes and genetic abnormalities (more on this below).

Thus, against the background of aortic insufficiency, weakening of the muscles and tendon threads of the mitral valve is possible.

All pathological processes of this kind appear quite late. Some do not make themselves known at all until the result is fatal. Sometimes the diagnosis is made during the autopsy.

Valve prolapse

Clinical variant of organic changes in cardiac structure. It is characterized by retraction of the leaflets of the formation into the atria.

Cardiac ischemia

A typical age-related pathological process. Also occurs in patients who have had a myocardial infarction. It is accompanied by chronic malnutrition of cardiac structures, but there are no catastrophic phenomena yet.

The most likely consequence of a long-term condition is necrosis of cardiac formations. As a result of low trophism, dystrophy or weakening of the mitral valve occurs. Hence its inability to close tightly.

Even surgery is not a guarantee of recovery. We need to fight the root cause of the phenomenon.

Inflammatory pathologies of cardiac structures

Endocarditis as an option. Accompanied by severe damage to cardiomyocytes, usually of infectious origin (70% of cases), less often of autoimmune origin (the remaining 30%).

Both of these entail gradual destruction of anatomical structures. Treatment is combined with elimination of the inflammatory process and, as necessary, replacement of damaged atria.

The symptoms are pronounced, so it is almost impossible to miss the moment the process begins. Treatment is inpatient, under constant objective control.

Heart attack

Acute myocardial nutritional disorder. Accompanied by general necrosis of organ tissue. The extent depends on which vessel has undergone stenosis (narrowing) or occlusion (blockage).

In all cases, this is a common process, with the death of significant areas of cardiac structures. Even with timely and competent treatment in the hospital, the possibility of a full recovery is almost zero.

In any situation, a gross scar defect will remain, the so-called cardiosclerosis, when functional tissues are replaced by connective tissues that are incapable of contraction and excitation.

Genetic syndromes

Caused by burdened heredity, less often by other phenomena. Classic variants are Marfan disease, Ehlers-Danlos disease.

All processes, one way or another, are manifested by a group of symptoms, many have external signs. Disproportion of the limbs, deformations of the maxillofacial area, dysfunctional disorders of the liver, kidneys, and other organs.

The restoration is comprehensive. Usually the diagnosis can be made during infancy, the symptoms are pronounced, and many objective signs are present. Consultation with a geneticist is mandatory.

Autoimmune diseases

The classic process with cardiac abnormalities is systemic lupus erythematosus. Leads to the destruction of muscle and connective tissues of the body. Including heart ones. Mitral insufficiency develops relatively late, without treatment.

Rheumatism

Another variant of autoimmune disease. Accompanied by destruction of cadiomyocytes. It flows in waves, in fits and starts. Each episode worsens the condition of cardiac structures. Hence the need for ongoing treatment to prevent relapses and support heart function.

Subjective factors

Thus, according to clinical studies, the main contingent of cardiologist patients with suspected mitral regurgitation are people over 60.

Young people suffer less often and there are good pathological reasons for this. Older people experience natural aging and tissue degeneration. Smokers, alcoholics, people with chronic and especially chronic diseases are at greater risk.

Men get sick more often than women, the ratio is approximately two to one. What this is connected with is not known for certain. Assumed to have hard work and a penchant for bad habits.

Diagnostics

Cardiologists are involved in the management of patients with mitral regurgitation and suspected mitral regurgitation. Planning for radical treatment falls on the shoulders of specialized surgeons.

Approximate examination scheme:

• Oral survey. In the early stages there will be no complaints at all, but later the symptom complex is evident.
• Anamnesis collection. Family history, genetic factors, clarification of bad habits and lifestyle.
• Listening to heart sounds (auscultation), assessing the frequency of contractions. Allows you to detect arrhythmia at an early stage. Many deviations, however, are not detected by routine methods.
• 24-hour Holter monitoring. Blood pressure is detected over 24 hours at short intervals. It is better to conduct such events at home. This way the result will be more accurate.

• Electrocardiography. Study of rhythm using a special apparatus. Notices the slightest deviations in the functioning of the organ.
• Echocardiography. Ultrasound technique. Aimed at identifying changes in the myocardium. Classic findings are left ventricular hypertrophy and dilation of the atrial chambers.
• Angiography.
• If necessary - MRI or CT.

Activities are being carried out gradually. If an acute condition is observed, the minimum list must be followed.

Symptoms of mitral regurgitation may be nonspecific, therefore, in case of suspicious complaints, the patient should be hospitalized for at least a few days for an urgent assessment of the nature of the condition.

Treatment

The therapeutic effect is combined, using surgical techniques and conservative methods. Depending on the stage. One way or another prevails. The main characteristic of supervision is expediency.

Medication

Mitral regurgitation of the 1st degree is eliminated with medications, while the specific choice of drugs falls on the shoulders of the doctor.

Approximate diagram:

• Use of antihypertensive drugs. From ACP inhibitors to calcium antagonists and beta blockers. It is a classic treatment for hypertension and symptomatic increased arterial pressure.
• Antiplatelet agents. To normalize the rheological properties of blood. Fluidity is one of the main qualities of liquid connective tissue. Aspirin Cardio is prescribed.
• Statins. Against the background of cholesterolemia and atherosclerosis in this regard.

Other pathological processes, non-cardiac, but causing the failure itself, are eliminated accordingly.

For systemic lupus erythematosus, corticosteroids and immunosuppressants are prescribed; for recovery from liver failure, hepatoprotectors, etc.

Operational

Surgical methods are shown somewhat less frequently; this is a last resort. In fact, even stage 2 mitral valve insufficiency is not yet a reason for intervention.

Vital indicators are considered the basis for radical supervision, depending on the degree of their decline. Long-term follow-up and the use of medications as part of supportive care are possible.

When conservative recovery is not possible, cardiac surgery is no longer necessary.

Appointed:

• prosthetics (replacement) of the mitral valve with a biological or mechanical one;
• excision of adhesions for stenosis;
• stenting of coronary arteries, other methods.

Particularly severe cases require organ transplantation. This is akin to a death sentence, since the likelihood of finding a donor is extremely low even in developed countries, especially in backward countries.

Lifestyle changes are not effective. Unless you can give up smoking and alcohol. Folk remedies are strictly contraindicated. MK insufficiency is eliminated only by classical methods.

Prognosis and possible complications

Possible consequences:

• Myocardial infarction.
• Heart failure.
• Multiple organ failure.
• Stroke.
• Cardiogenic shock.
• Pulmonary edema.

These are potentially lethal phenomena. The prognosis for treatment is favorable only in the early stages. Survival rate 85%. With a long course of the pathological process, mortality reaches 60% in a five-year period. When connecting complications - 90%. The ischemic form of mitral regurgitation gives a worse prognosis.

Degenerative changes in the mitral valve, such as mitral valve regurgitation, are a common heart defect. The frequency is determined to be 15% of all congenital and acquired conditions.

Treatment is conservative at the initial stage or surgical at advanced stages, under the supervision of a cardiologist. The likelihood of complete relief from the pathology is low in the later stages. The process is difficult to detect at the initial moment, but this is the best time for therapy.

The mitral valve exists in every person and is located between the atrium and ventricle of the heart. The condition when there is a gap between the valve leaflets is called mitral valve insufficiency. This disease is dangerous due to its progression and interaction with other defects of the cardiac system.

The causes of this pathology can be both congenital heart disease and untreated infections. Almost always this disease is accompanied by other heart diseases.

Unfortunately, everyone is susceptible to mitral insufficiency, even small children. Let's take a closer look at what mitral valve insufficiency is, the etiology and pathogenesis of the disease, the main symptoms, methods of treatment and prevention.

Mitral valve insufficiency - description

Mitral regurgitation is a heart defect in which there is a reverse movement of blood from the left ventricle into the left atrium during contraction of the ventricles of the heart due to incomplete closure of its valves. Mitral regurgitation is the most common type of heart valve disorder.

It is detected in half of patients with heart defects, mainly in combination with mitral stenosis (narrowing of the right atrioventricular orifice) and with aortic defects - stenosis (narrowing of the aorta at the valve level) or aortic valve insufficiency (loose closure of the aortic valves at the time of relaxation of the ventricles ).

Mitral valve insufficiency rarely occurs in isolation (that is, without other heart defects) - only in every fiftieth patient with a heart defect.

The essence of this defect is a violation of the closing function of the valve due to fibrous deformation of the leaflets, subvalvular structures, dilatation of the fibrous ring or disruption of the integrity of the elements of the mitral valve, which causes the return of part of the blood from the left ventricle to the atrium.

These disturbances of intracardiac hemodynamics are accompanied by a decrease in minute volume of blood circulation and the development of pulmonary hypertension syndrome.

The main indicator of mitral valve insufficiency is how much blood there is regurgitation back into the left atrium. Accordingly, degrees of deficiency are distinguished.

1. I degree – regurgitation is mild. There is a slight flow of blood into the atrium, which is detected at the valve.

This leads to the fact that more blood accumulates in the atrium than it should (that which enters normally + abandoned). This blood enters the ventricle and causes it to contract with greater force than it should.

This leads to ventricular (left) hypertrophy. In this way, compensation for the defect occurs.

2. II degree - the flow of regurgitant blood reaches the middle of the atrium.

More blood is thrown back. Now the atrium is no longer able to push out all the blood without a significant fluctuation in pressure. There is an increase in pressure in the left atrium. Accordingly, the pressure in the pulmonary vessels increases.

3. III degree - the blood stream reaches the posterior wall of the atrium. Decompensation of the defect occurs.

The left atrium expands because the muscle is no longer able to push out all the blood. In particularly advanced cases, the right ventricle may also increase in size (it is difficult to pump blood to the lungs, where there is stagnation). However, this is quite rare.

All mitral valve insufficiency can be divided into three groups, depending on what is the root cause of the defect.

1. Organic failure. In these cases, the cause of insufficiency lies in the valve itself, which is affected by some factor.

In approximately 75% of people, the cause is rheumatism. There are a number of other causes of organic disorders:

• systemic lupus erythematosus - the valve contains a lot of connective tissue, which is affected in an autoimmune disease;
• scleroderma - this disease also refers to connective tissue diseases;
• myxomatous degeneration of the mitral valve - its leaflets are affected, losing the ability to tightly close the atrioventricular opening;
• infective endocarditis - quite often microorganisms affect the valve leaflets;
• mitral valve annulus calcification;
• It is also worth mentioning a number of conditions in which the valve leaflets or chords that give it its shape are torn off.

Mitral valve insufficiency is divided into four degrees according to severity. Stage 1 prolapse is the mildest form. In this case, the reverse blood flow is no more than 20% and the entire volume remains within the atrium. Very often this disease is diagnosed together with other heart problems.

Insufficiency of the 1st degree is difficult to diagnose, since it causes almost no visible symptoms, and also allows a person to lead a normal lifestyle. The disease does not prevent pregnancy. All causes that led to the appearance of stage 1 disease are divided into congenital and acquired.

In the first case, the heart defect may be hereditary and occur during fetal development. But most often the disease is acquired (in 99.4% of cases). The reasons that led to the development of stage 1 disease are:

1. Rheumatism. This damage is expressed as the inability of the immune system to fight certain types of streptococcus. At the same time, rheumatism of the joints and damage to other valves develops.
2. Cardiac ischemia. The chordae and papillary muscles responsible for closing the valve become weakened or torn.
3. Traumatic injuries. Most often lead to a more pronounced course of the disease.
4. Systemic lupus erythematosus. The patient develops damage to connective tissues. Mitral valve insufficiency can be congenital or acquired, including those that are part of the valves.


5. Infectious endocarditis. Damage to the mitral valve leaflets by pathogenic microorganisms.
6. Scleroderma. Another disease that affects connective tissue cells.
7. Myxomatous degeneration of the mitral valve. The valves separating the atrium lose the ability to close tightly, leaving a gap.
8. Relative deficiency. The valve is normal, but due to deformation of the left ventricle and stretching of the opening, it loses the ability to close it tightly.
9. Functional impairment. Pathologies associated with papillary muscles and myocardium.

The disease occurs in men and women, especially during pregnancy. The most common cause (75% of cases) is an infectious disease, pathogens. Timely treatment of diseases will be the best prevention of stage 1 deficiency.

Mitral valve insufficiency in children

This condition often occurs in young children and is congenital or acquired. The disease can begin to develop in the baby while still in the womb, which can happen for the following reasons:

• when the expectant mother receives a dose of radiation exposure;
• under the influence of x-ray radiation from the mother;
• in case the mother of the unborn baby carries various infections;
• heredity;
• genetic malformations of the baby in the womb, including those associated with connective tissue problems (Marfan and Ehlers-Danlos syndromes).

The registration of this disease in a child much later than his birth is associated with the influence of the following factors on his body:

• previously experienced heart surgery;
• endocarditis;
• valvulitis;
• heart injuries.

There are such child health problems in which the bicuspid valve undergoes functional failure, in particular:

• tumor formations;
• death or partial deformation of some areas of the heart located near the valve and responsible for its movement;
• rupture of the connective tissue through which the heart muscle contacts the papillary muscles;
• divergence of the valve leaflets due to an increase in the boundaries of the fibrous ring.

Other causes of illness in children may include:

• rheumatism;
• dilated cardiomyopathy;
• systemic lupus erythematosus;
• myocarditis;
• mitral valve prolapse;
• cardiac ischemia;
• arterial hypertension;
• aortic heart defects.

The congenital variant of the disease develops very rapidly and provokes heart failure in the child. Symptoms in general manifestations are characterized by:

• the child’s inability to engage in prolonged physical activity or exercise;
• weight loss, slow growth;
• appetite disorders;
• pain in the heart and chest;
• the appearance of shortness of breath;
• the presence of a dry cough;
• lethargy;
• tracing heart murmurs;
• formation of the heart hump.

The initial stage of mitral regurgitation in childhood can occur without visible manifestations, making itself felt only during the transition to a more severe form. Often this condition is accompanied by various heart problems - stenosis, prolapse, and so on.

The clinical picture of the disease varies according to its stage:

1. The first is that manifestations of insufficiency are minimal due to the double work of the left parts of the child’s heart.

Regurgitation (flow opposite to normal) accounts for up to 20% of the systolic blood volume (this is the name given to the amount of blood that the ventricles of the heart eject in one contraction).

2. The second is that the volume of blood flowing in the opposite direction is 20-40% of the systolic volume. Blood may begin to accumulate in the lungs, forming congestion.

As a result, the baby’s well-being deteriorates; he feels quickly tired, short of breath, and suffers from bouts of dry cough, sometimes with bloody spots in the sputum.

3. The third is a more severe form of the disease. About 40-60% of the blood moves in the wrong direction, which provokes the development of heart failure;
4. Fourth – regurgitation is more than 60%, the blood flow completely fills the entire left atrium, causing hemodynamic disturbances.

Diagnosis of the disease in childhood is carried out through non-invasive cardiac procedures:

• ultrasound examination;
• electrocardiograms;
• echocardiography;
• spiral computed tomography;
• magnetic resonance imaging;
• radiography.

In private situations, additional diagnostic procedures are required - coronary angiocardiography and catheterization of the cardiac cavities.

The doctor carefully examines the child, assesses his physical development, skin tone and elasticity, and measures his pulse and blood pressure. An important part of the examination is listening to heart rhythms, tones and noises, as well as looking for extraneous sounds when the lungs are working.

Percussion of the chest area allows you to clarify the size of the heart, its position and boundaries. Collection and analysis of anamnesis of illness and life involves clarifying complaints, symptoms of the disease, as well as the causative disease. In addition to this, urine and blood tests are prescribed.

Lack of treatment leads to irreversible complications and damage to the child’s internal organs, even death. Since the baby's body is constantly growing, the heart also increases in size, and therefore heart surgery has to be repeated several times. The child is under lifelong observation by a cardiologist and cardiac surgeon.

Since mitral regurgitation often acts as a complication of any causative disease, it is important to eliminate this disease to restore valve function.

The asymptomatic course of the chronic stage of this disease does not require special treatment measures. The remaining stages of the disease involve taking special medications, the tasks of which include:

• maintaining/stabilizing heart rhythms;
• prevention/treatment of circulatory failure.

Conservative therapy does not give the desired effect in the case of late stages of insufficiency, which explains the need for surgical operations (plastic or using a prosthesis).

The main reason for the development of mitral valve insufficiency is rheumatic in nature. In addition, organic mitral regurgitation can occur with infective endocarditis, Libman-Sachs warty endocarditis, and with systemic connective tissue diseases.

Functional (relative) mitral regurgitation can occur with sharp dilatation of the left ventricle due to aortic defects (“mitralization” of aortic defects, dilated cardiomyopathy, left ventricular aneurysm, prolapse of the mitral valve leaflets, calcification of the valve ring), disrupting the mechanism of its narrowing during ventricular systole.

The possibility of developing mitral insufficiency after mitral commissurotomy cannot be excluded. According to the flow, it is customary to distinguish between acute and chronic mitral insufficiency.

Acute mitral insufficiency:

• rupture of chordae tendineae as a result of infective endocarditis, myocardial infarction, trauma;
• damage to the papillary muscles;
• valve damage as a complication during cardiac surgery, perforation in infective endocarditis.

Chronic mitral insufficiency:

• rheumatic lesion;
• systemic diseases;
• congenital or hereditary diseases;
• hypertrophic cardiomyopathy;
• mitral valve calcification;
• tumors.

Incomplete closure of the mitral valve leaflets allows blood to flow back (regurgitation) from the ventricle into the atrium during systole. Excessive blood in the left atrium stretches its walls, while increased blood flow into the left ventricle causes it to dilate and then hypertrophy.

Subsequently, with the weakening of the left atrium and under the influence of regurgitant waves, the atrial myocardium loses its tone, the pressure in the cavity of the left atrium increases, which is retrogradely transmitted to the pulmonary veins - venous pulmonary hypertension occurs, which ends in progressive right ventricular decompensation.

Features of hemodynamics in mitral insufficiency:

• regurgitation up to 5 ml has no practical significance;
• clinical manifestations - with regurgitation in the left atrium of at least 10 ml;
• long-term compensation of the defect (provided by the hypertrophied left ventricle according to the Frank-Starling mechanism);
• rapid progression with decompensation.

An increase in stroke and cardiac output, a decrease in end-systolic volume and the absence of pulmonary hypertension are indicators of a compensated hemodynamic state.

This defect is quite successfully compensated by the internal reserves of the body (primarily the heart). Therefore, patients experience any discomfort for a long time and do not turn to doctors for help. However, a number of more or less specific symptoms can be noted.

1. A cough, initially dry, then with the addition of sputum streaked with blood, appears as the severity of blood stagnation in the vessels of the lungs increases.
2. Shortness of breath - occurs as a result of stagnation of blood in the vessels of the lungs.
3. Rapid heartbeat, a feeling of irregular heartbeat, cardiac arrest, upheavals in the left half of the chest - occurs with the development of arrhythmias (heart rhythm disturbances) due to damage to the heart muscle by the same process that caused mitral valve insufficiency (for example, heart injury or myocarditis - inflammation of the heart muscle ) and due to changes in the structure of the atrium.
4. General weakness and decreased performance are associated with impaired blood distribution in the body.

However, all these symptoms can also appear in other heart defects and diseases, so the clinical picture cannot be the basis for making a diagnosis; a number of studies are being carried out.

Clinically, in the stage of compensation of the defect, patients feel satisfactory, can perform significant physical activity, the pathology is detected by chance.

In the future, with a decrease in the contractile function of the left. ventricle and increased pressure in the pulmonary circulation, patients complain of shortness of breath during exercise and palpitations. Attacks of cardiac asthma and shortness of breath at rest may occur.

A cough may occur, and rarely, hemoptysis. Cardialgia is observed - stabbing, aching, pressing, without a clear connection with physical activity. Left ventricular failure may be joined by right ventricular failure (swelling, pain in the right hypochondrium due to liver enlargement and capsule stretching), and later - total decompensation.

During physical examination, attention is drawn to acrocyanosis and fades mitralis, sometimes “heart hump”. On palpation, an intensified diffuse apical impulse is found, caused by hypertrophy and dilatation of the left ventricle, localized in the fifth intercostal space outward from the midclavicular line or in the sixth intercostal space (more often in young patients).

The boundaries of relative cardiac dullness are expanded to the left, up and to the right. Auscultation of the heart: the first sound is weakened at the apex (up to its complete absence) - since there is no “period of valve closure,” vibrations caused by a wave of regurgitation can be layered.

An increased pathological third heart sound is often heard, caused by vibrations of the walls of the left ventricle. The tone has main differences: dull in timbre, audible in a limited area.

The decisive sign of the defect is a systolic murmur - soft, blowing, decreasing, ending before the second sound appears, spreading to the axillary region, auscultated as much as possible during a deep breath with the patient lying on his left side. The louder and longer the systolic murmur, the more severe the mitral regurgitation.

Above the pulmonary artery there is an accent of the second tone, moderately expressed and associated with the development of congestion in the pulmonary circle. Often a splitting of the second tone is heard, associated with a delay in the aortic component of the tone, since the period of expulsion of an increased amount of blood from the left ventricle becomes longer.

When examining the lungs, signs are found indicating congestion in the pulmonary circulation (weakening of breathing, shortening of percussion sound, crepitus or fine, silent, moist rales in the posterior lower parts of the lungs).

Subsequent weakening of the right ventricle leads to stagnation of blood in the systemic circulation, which is clinically manifested by an enlarged liver and edema of the lower extremities. In the later stages, congestive cirrhosis of the liver and ascites develop.

With a compensated defect, the pulse and blood pressure remain normal; with decompensation, the pulse increases and blood pressure may decrease slightly. In later stages, atrial fibrillation is often observed.

Already during a routine examination one can suspect a change in the mitral valve:

• the patient’s characteristic complaints allow us to assess the degree of heart failure;
• murmurs are detected on auscultation;
• upon percussion, the boundaries of cardiac dullness shift to the left side.

The main diagnostically significant method for mitral regurgitation is ultrasound of the heart, which can be supplemented with Doppler ultrasound, which allows a more visual assessment of the degree of regurgitation.

With ECHO-CG it is possible to determine the cause of the heart defect, as well as complications of this condition. Based on the measurements obtained, the degree of deficiency can be judged.

It should be noted that isolated mitral valve disease is quite rare and in most cases is caused by rheumatic changes.

Much more often, ultrasound of the heart reveals combined insufficiency of the mitral and tricuspid valves. Such changes quickly lead to decompensation of heart failure and require prompt medical intervention.

Auxiliary diagnostic methods are:

1. ECG, which changes only with secondary transformation of the heart muscle.
2. X-ray of the chest, in which one can suspect a general increase in size of the heart.
3. Transesophageal ECG helps diagnose atrial rhythm disturbances.
4. Daily monitoring is performed for paroxysmal arrhythmias.
5. Phonocardiography can detect murmur.
6. With ventriculography using special contrast, the degree of regurgitation can be more accurately determined.
7. Coronary angiography is performed as preoperative preparation or if the ischemic nature of the defect is suspected.
8. Analysis of the medical history and complaints - how long ago shortness of breath, palpitations, cough (initially dry, then with sputum mixed with blood) appeared, what the patient associates with their occurrence.
9. Life history analysis. It is found out what the patient and his close relatives were ill with, who the patient is by profession (whether he had contact with pathogens of infectious diseases), whether there were infectious diseases.

The history may include indications of a rheumatic process, inflammatory diseases, chest injuries, and tumors.

10. Physical examination. On examination, cyanosis (blueness) of the skin, “mitral blush” (bright red coloring of the patient’s cheeks due to impaired oxygenation of the blood), “heart hump” is noted - this is a pulsating protrusion to the left of the sternum (the central bone of the chest to which the ribs are attached) behind due to a significant increase in the left ventricle of the heart.

Percussion (tapping) reveals expansion of the heart to the left. Auscultation (listening) of the heart reveals a murmur during systole (the period of contraction of the ventricles of the heart) in the region of the apex of the heart.

11. Blood and urine analysis. It is carried out to identify the inflammatory process and concomitant diseases.
12. Blood chemistry. The level of cholesterol (a fat-like substance), sugar and total blood protein, creatinine (a protein breakdown product), uric acid (a breakdown product of purines - substances from the cell nucleus) is determined to identify concomitant organ damage.
13. Immunological blood test. The content of antibodies to various microorganisms and the heart muscle (special proteins produced by the body that can destroy foreign substances or cells of the body’s own) and the level of C-reactive protein (a protein whose level increases in the blood during any inflammation) will be determined.
14. Electrocardiographic study (ECG) - allows you to evaluate the rhythm of the heartbeat, the presence of heart rhythm disturbances (for example, premature heart contractions), the size of the heart parts and its overload.

Mitral valve insufficiency is most characterized by an ECG showing an enlargement of the left atrium and left ventricle.

15. A phonocardiogram (a method for analyzing heart sounds) with mitral valve insufficiency demonstrates the presence of systolic (that is, during contraction of the ventricles of the heart) noise in the projection of the bicuspid valve.
16. Echocardiography (EchoCG - ultrasound examination of the heart) is the main method for determining the condition of the mitral valve.

The area of ​​the left atrioventricular orifice is measured, the mitral valve leaflets are examined for changes in their shape (for example, wrinkling of the leaflets or the presence of ruptures in them), loose closure during contraction of the ventricles of the heart, and the presence of vegetations (additional structures on the valve leaflets).

EchoCG also evaluates the size of the heart cavities and the thickness of its walls, the condition of other heart valves, thickening of the endocardium (the inner lining of the heart), and the presence of fluid in the pericardium (the sac around the heart).

Doppler echocardiography (ultrasound examination of the movement of blood through the vessels and chambers of the heart) reveals the reverse flow of blood from the left ventricle into the left atrium during ventricular contraction, as well as an increase in pressure in the pulmonary arteries (vessels that bring blood to the lungs).

17. X-ray of the chest organs - evaluates the size and location of the heart, changes in the configuration of the heart (protrusion of the shadow of the heart in the projection of the left atrium and left ventricle), the appearance of blood stagnation in the vessels of the lungs.
18. Catheterization of the cardiac cavities is a diagnostic method based on inserting catheters (medical instruments in the form of a tube) into the cardiac cavities and measuring the pressure in the left atrium and left ventricle.

With mitral valve insufficiency, the pressure in the left atrium becomes almost the same as in the left ventricle.

19. Spiral computed tomography (SCT), a method based on taking a series of X-rays at different depths, and magnetic resonance imaging (MRI), a method based on building chains of water when strong magnets are applied to the human body, allow one to obtain an accurate image of the heart.
20. Coronary cardiography (CCG) is a method in which contrast (a dye) is injected into the own vessels of the heart and the heart cavity, which makes it possible to obtain an accurate image of them, as well as to evaluate the movement of blood flow.

It is carried out when planning surgical treatment of a defect or suspected concomitant coronary heart disease.

Treatment of mitral regurgitation

A mild degree of the disease, which is not accompanied by the appearance of symptoms, does not require special treatment.

Moderate mitral valve insufficiency is not an indication for surgery. In this case, treatment is carried out with the help of medications:

• ACE inhibitors prevent secondary transformation of the heart myocardium and reduce symptoms of heart failure;
• beta blockers reduce the frequency of contractions of the left ventricle, thereby increasing the ejection fraction;
• diuretics accelerate the removal of fluid from the body and eliminate symptoms of stagnation;
• Vasodilators reduce the load on the heart by depositing blood and fluid in the peripheral arteries;
• cardiac glycosides stimulate heart contractions and help fight arrhythmia;
• It makes sense to use anticoagulants for persistent atrial fibrillation;
• antibiotics are prescribed for infective endocarditis;
• Hormonal medications can affect the course of rheumatism.

In case of acute development of regurgitation, intra-aortic balloon counterpulsation can be used. During this procedure, a special oval inflating balloon is inserted into the patient's aorta, which opens in opposition to the contractions of the heart.

As a result, coronary blood flow increases and the ejection fraction also increases. This measure is temporary and is mainly suitable for ischemia of the papillary muscles, or as preoperative preparation.

1. It is necessary to treat the underlying disease - the cause of mitral valve insufficiency.
2. Drug treatment is indicated for complications of mitral regurgitation (for example, treatment of heart failure, cardiac arrhythmias, etc.)
3. Mild or moderate mitral valve insufficiency does not require special treatment.

   In case of severe and severe mitral insufficiency, surgical treatment is performed: plastic surgery or replacement of the mitral valve.

4. Surgical treatment of tricuspid valve insufficiency is carried out exclusively under artificial circulation (during the operation, blood throughout the body is pumped not by the heart, but by an electric pump).

Types of operations:

• Plastic surgery (that is, normalization of blood flow through the left atrioventricular orifice while preserving the native mitral valve) is performed in case of mitral valve insufficiency of 2-3 degrees and the absence of pronounced changes in its leaflets.

• Ring annuloplasty (valve surgery) by sewing in a support ring at the base of the mitral valve leaflets. The ring consists of a metal base covered with synthetic fabric;
• Shortening of the chordae (tendon strands that attach the papillary muscles to the heart muscle - the internal muscles of the heart that ensure the movement of the valves);
• Removal of part of the elongated posterior mitral valve leaflet.

• biological prostheses (made from the aorta (that is, the largest vessel) of animals) - used in children and women who are planning pregnancy;
• mechanical valves (made from special medical metal alloys) are used in all other cases.

• After implantation of a mechanical prosthesis, patients need to constantly take drugs from the group of indirect anticoagulants (drugs that reduce blood clotting by blocking the liver's synthesis of substances necessary for clotting).
• After implantation of a biological prosthesis, anticoagulant therapy is carried out for a short period of time (1-3 months).
• After valve repair, anticoagulant therapy is not performed.

Along with the treatment of the underlying disease at stages 1 and 2 of insufficiency, supportive and corrective symptomatic drug treatment is carried out:

1. The use of vasodilators to regulate systolic pressure in the aorta and the effect of ACE inhibitors in this case are considered the most studied;
2. Adrenergic blockers;
3. The use of anticoagulants to avoid thrombosis;
4. Diuretics and antioxidants;
5. Antibiotics as a preventative measure, especially for prolapse.

It should be noted that drug treatment is futile and the patient’s condition should not be allowed to deteriorate to such an extent that irreversible consequences in the heart will reduce the prognosis for successful surgery or make the operation impossible, since the more complex the operation, the higher the mortality rate.

With the help of medications, the patient’s condition can be stabilized, but even with medications, the disease often progresses.

Surgery for illness

It is impossible to completely cure mitral valve defects with medication, especially at the border of stages 2, 3 and 4.

If the disease progresses or acute failure occurs, and there is no compelling reason to cancel the operation, surgery is the only effective method of treatment.

During the operation, plastic surgery or prosthetics of the required areas is performed, and the patient is connected to the artificial circulation system during the operation.

Plastic surgery is used when there are no pronounced changes in the structure of the mitral valve leaflets. Depending on the pathology (prolapse, “threshing” valve, etc.) the following is carried out:

• Correction of valve leaflet size;
• Shortening of tendon threads (regulation of valve movement);
• The size of the mitral ring is corrected; a special ring is sewn in at the base of its valves (annuloplasty).

Commissurotomy (expansion of the lumen of the mitral valve) can be performed transthoracically, without connecting to a heart-lung machine. In case of calcification and low mobility of the valve, a full-fledged operation is performed with the connection of artificial circulation.

Commissurotomy can eliminate serious defects, but after such an operation stenosis may subsequently develop.
Valvuloplasty is aimed at restoring a narrowed valve.

Balloon valvuloplasty does not require disconnecting the heart from the circulatory system; the operation is performed through an incision in the artery or vein of the thigh. This is the safest operation with the minimum number of complications.

Valve-sparing reconstructive surgeries in children, such as leaflet decalcification and commissuroplasty, have a favorable prognosis. But in three out of ten cases, you have to do a second operation to replace the mitral valve.

To avoid this, in the preoperative period the degree of regurgitation is measured, the exact parameters of the mitral valve and mitral ring are determined, the indicators are compared with the parameters of the child’s body, and a tentative prognosis is calculated according to which it is either advisable to perform reconstructive surgery or immediately perform mitral valve replacement.

Mitral valve replacement is used in cases of severe changes in the valve or when repair has failed. For children, biological prostheses made from animal aorta are used, which, as a rule, take root well.

The operation allows you to eliminate almost any defects, does not subsequently cause the development of stenosis, and after a six-month postoperative period the child will be able to lead a full life.

To prevent the disease, annual examinations are carried out. If the disease is asymptomatic, then the only preventive measure is an annual cardiac ultrasound procedure. It is necessary in order to prevent and identify in advance any changes in the functioning of the heart.

Preventive measures are also prescribed in case of secondary occurrence of the defect. In this case, all measures are aimed at eliminating foci of chronic infection that led to failure. Additionally, signs of hypercholesterolemia are eliminated. The patient should undergo regular diagnostic testing and visit the doctor.

If you follow all the doctor’s recommendations, as well as if you adhere to a healthy lifestyle, then mitral valve problems may not manifest themselves throughout your life. This disease does not greatly affect a person’s performance and has no contraindications.

Mitral valve insufficiency of the 1st degree is a minor form of the disease. Difficult to diagnose. Does not require surgery.

Treatment of any heart failure is mandatory; without timely treatment, congestion in organs and irreversible complications of varying degrees develop, but even with restraining drug treatment, mortality remains high.

Naturally, any heart surgery is a risk; mortality after open heart surgery is 1–3% for children and increases with the number of concomitant diseases.

Valvuloplasty and camisurotomy are temporary measures; treatment of insufficiency with these methods is impossible and over time the procedures will have to be repeated periodically. After prosthetics, the patient receives postoperative treatment and is under the supervision of a doctor for life.

During the appointment, a mandatory auscultation of the child’s heart is performed; other studies are prescribed as needed.

Source » hospital-israel.ru; lookmedbook.ru; pirogov-center.ru; iserdce.ru; mirbodrosti.com; detstrana.ru; bone-surgery.ru; lecheniedetej.ru"

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Description of the disease

MVR (mitral valve insufficiency) is the most common cardiac anomaly. Of all the sick 70% suffer from an isolated form of cerebrovascular accident. Typically, rheumatic endocarditis is the main underlying cause of the disease. Often, a year after the first attack, the heart condition leads to chronic failure, the cure of which is quite difficult.

The highest risk group includes people with valvulitis.. This disease damages the valve leaflets, as a result of which they undergo processes of wrinkling, destruction, and gradually become shorter than their original length. If valvulitis is at an advanced stage, calcification develops.

Septic endocarditis leads to the destruction of many cardiac structures, so NMC has the most severe manifestations. The valve flaps do not fit together tightly enough. When they are not completely closed through the valve, too much blood coming out, which provokes its reboot and the formation of stagnant processes, an increase in pressure. All signs lead to increasing insufficiency of uric acid.

Causes and risk factors

NMC affects people with one or more of the following pathologies:

1. Congenital predisposition.
2. Connective tissue dysplasia syndrome.
3. Mitral valve prolapse, characterized by regurgitation of 2 and 3 degrees.
4. Destruction and breakage of the chords, rupture of the valves of the mitral valve due to injuries in the chest area.
5. Rupture of the valves and chords with the development of infectious endocarditis.
6. Destruction of the apparatus that unites the valves in endocarditis resulting from connective tissue diseases.
7. Infarction of part of the mitral valve with subsequent scar formation in the subvalvular region.
8. Changes in the shape of the valves and tissues located under the valves when rheumatism.
9. Enlargement of the mitral annulus during dilatation cardiomyopathy.
10. Insufficiency of valve function in the development of hypertrophic cardiomyopathy.
11. MK insufficiency due to surgery.

Mitral regurgitation is often accompanied by another defect - mitral valve stenosis.

Types, forms, stages

With NMC the total stroke volume of the left ventricle is estimated. Depending on its quantity, the disease is divided into 4 degrees of severity (the percentage indicates the part of the blood that is redistributed incorrectly):

• I (the softest) - up to 20%.
• II (moderate) - 20-40%.
• III (medium form) - 40-60%.
• IV (heaviest) - over 60%.

According to the forms of its course, the disease can be divided into acute and chronic:

When determining the features of movement of the mitral valves, there are 3 types of pathology classification:

• 1 - standard level of mobility of the leaflets (in this case, painful manifestations consist of dilatation of the fibrous ring, perforation of the leaflets).
• 2 - destruction of the valves (the chords take the greatest damage, as they are stretched or ruptured, and a violation of the integrity of the papillary muscles also occurs.
• 3 - decreased mobility of the valves (forced connection of commissures, reduction in the length of the chords, as well as their fusion).

Danger and complications

With the gradual progression of NMC, the following disorders appear:

1. The development of thromboembolism due to constant stagnation of a large part of the blood.
2. Valve thrombosis.
3. Stroke. Previously occurring valve thrombosis is of great importance in the risk factors for stroke.
4. Atrial fibrillation.
5. Symptoms of chronic heart failure.
6. Mitral regurgitation (partial failure of the mitral valve to perform functions).

Symptoms and signs

The severity and severity of MCT depends on the degree of its development in the body:

• Stage 1 the disease has no specific symptoms.
• Stage 2 does not allow patients to carry out physical activity in an accelerated mode, since shortness of breath, tachycardia, pain in the chest, loss of heart rhythm, and discomfort immediately appear. Auscultation with mitral insufficiency determines increased tone intensity and the presence of background noise.
• Stage 3 characterized by left ventricular failure and hemodynamic pathologies. Patients suffer from constant shortness of breath, orthopnea, increased heart rate, chest discomfort, and their skin is paler than in a healthy state.

Find out more about mitral regurgitation and hemodynamics with it from the video:

When to see a doctor and which one

When identifying symptoms characteristic of MCT, it is necessary contact a cardiologist immediately, to stop the disease in its early stages. In this case, you can avoid the need to consult with other doctors.

Sometimes there is suspicion of a rheumatoid etiology of the disease. Then you should visit a rheumatologist for diagnosis and proper treatment. If there is a need for surgical intervention, treatment and subsequent the problem is resolved by a cardiac surgeon.

Common methods for detecting NMC:

Learn more about symptoms and diagnosis from the video:

It is necessary to distinguish NMC from other heart pathologies:

1. Myocarditis in severe form.
2. Congenital and acquired heart defects of related etiology.
3. Cardiomyopathies.
4. MK prolapse.

Therapy methods

If symptoms of cervical urinary tract are severe, surgical intervention is indicated for the patient. The operation is performed urgently for the following reasons:

1. In the second and later stages, despite the fact that the volume of blood ejected is 40% of its total amount.
2. In the absence of effect from antibacterial therapy and worsening of infectious endocarditis.
3. Increased deformation, sclerosis of the valves and tissues located in the subvalvular space.
4. In the presence of signs of progressive left ventricular dysfunction together with general heart failure occurring at 3-4 degrees.
5. Heart failure in the early stages can also be a reason for surgery, however, to form an indication, thromboembolism of large vessels located in the systemic circulation must be detected.

The following operations are practiced:

• Valve-sparing reconstructive surgeries are necessary to correct cerebrovascular accidents in childhood.
• Commissuroplasty and decalcification of the leaflets are indicated for severe MV insufficiency.
• Chordoplasty is intended to normalize the mobility of the valves.
• Translocation of cords is indicated when they fall off.
• Fixation of parts of the papillary muscle is carried out using Teflon gaskets. This is necessary when separating the head of the muscle from the remaining components.
• Prosthetics of the chords is necessary when they are completely destroyed.
• Valvuloplasty avoids leaflet rigidity.
• Anuloplasty is intended to relieve the patient of regurgitation.
• Valve replacement is carried out when it is severely deformed or when fibrosclerosis develops irreparably and interferes with normal functioning. Mechanical and biological prostheses are used.

Learn about minimally invasive operations for this disease from the video:

What to expect and preventative measures

With the development of cerebrovascular accident, the prognosis determines the severity of the disease, that is, the level of regurgitation, the occurrence of complications and irreversible changes in cardiac structures. Survival rate 10 years after diagnosis is higher than for similar severe pathologies.

If valve insufficiency is mild or moderate, women have the ability to bear and give birth to children. When the disease becomes chronic, all patients should undergo an annual ultrasound and visit a cardiologist. If worsening occurs, you should visit the hospital more often.

Prevention of NMC consists in preventing or promptly treating diseases that cause this pathology. All diseases or manifestations of mitral valve insufficiency due to an abnormal or reduced valve must be quickly diagnosed and promptly treated.

NMC is a dangerous pathology that leads to severe destructive processes in the heart tissue, and therefore requires proper treatment. Patients, if they follow the doctor’s recommendations, may, some time after starting treatment,

Mitral regurgitation is the incomplete closure of the valve at the moment when systole occurs in the heart.

The result of this pathology is the return of part of the blood flow to the atrium, located on the left side.

At the same time, there is an increase in pressure and blood volume in the atrium. In the article we will explain in more detail what it is, what types of deficiency exist, how they are diagnosed and treated.

Classification by degree

It is necessary to explain in more detail what pathology leads to. After the pressure in the left ventricle increases, blood from it retreats into the left atrium, increasing blood volume and pressure there.

Insufficiency of uric acid leads to a general increase in pressure, which results in stagnation of blood in the pulmonary vessels. All this is accompanied by regurgitation - the movement of blood flow in the opposite direction.

Rarely does the disease occur in patients in its pure form. The number of such people is only 5% of the sick. In children, the pure form of deficiency is rare. The disease itself is most often accompanied by other types of heart defects.

Modern classification in medicine distinguishes three degrees of pathology. The diagnosis depends on how severe the patient's regurgitation is.

Symptoms

Symptomatically, mitral valve insufficiency is not expressed at first. The owner of the pathology does not feel bad, since the natural functionality of the heart compensates for the failure.

The diagnosis may not be made for many years due to the absence of obvious signs.

Usually, pathology is discovered by chance - by a therapist when a specialist hears characteristic noises during an appointment. These noises are clearly audible if blood begins to flow into the atrium due to incomplete closure of the mitral valve.

You can hear how intensely the left ventricle contracts, even if mitral regurgitation is relative, that is, the volume indicator will not exceed 25%.

Every heartbeat occurs under load. Even when lying on the left side, the patient will experience palpitations.

The job of the atrium is to accommodate all the excess blood that comes from the left ventricle. Therefore, its volumes are increasing.

Contractions occur too quickly and incorrectly from a physiological point of view.

MR is characterized by atrial fibrillation. The function of the heart muscle as a pump changes due to the fact that the organ beats in the wrong rhythm.

The reason for the subsequent development of heart failure is severe regurgitation. When blood flow is impaired, blood clots form, leading to worsening organ damage

Signs of mitral regurgitation appear at later stages of pathology development.

Among them, the most obvious are:

• Cardiopalmus;
• Swelling of the lower extremities;
• Incurable cough of a non-productive type;
• Shortness of breath in any condition.

The listed symptoms are not enough to accurately diagnose mitral valve insufficiency. Similar signs appear with NTK - tricuspid valve insufficiency, and with bicuspid valve insufficiency. For other heart defects, the symptoms are just as typical.

The degree of manifestation of mitral valve insufficiency directly depends on the clinical stage of the disease at the time of diagnosis.

There are several stages in total:

• Compensation stage;
• Subcompensation stage;
• Stage of decompensation.

The compensation stage can last up to several decades in the absence of severe symptoms.

Only some patients experience discomfort - weakness, cold extremities, excessive fatigue. At this stage, the threat to life and health is small.

The stage of subcompensation occurs as valvular mitral insufficiency in the valve leaflets progresses. If attacks of rheumatic origin occur, compensatory mechanisms cease to cope.

With significant physical exertion, the patient experiences rapid heartbeat and heart rhythm is disturbed.

The decompensation stage occurs when the symptoms become as severe as possible. They are observed both in the active and resting stages . Characteristic attacks of suffocation, accompanied by coughing. In advanced cases, the stage of decompensation becomes terminal.

Causes of cardiac cerebrovascular accident

Experts associate the pathogenesis of mitral valve insufficiency with pathologies in the following cardiac regions:

• Mitral valve;
• Myocardium;
• Papillary muscles.

Minor mitral regurgitation may appear and develop further, even if the valve is functioning normally. The reason is the inability of such a valve to completely close the hole. The stretching of the hole is the result of an increase in the volume of the left ventricle.

To date, researchers have identified the following causes of mitral valve insufficiency:

• Past infectious diseases (endocarditis);
• Rheumatic lesions;
• Lesions of the mitral ring with calcification;
• Traumatic lesions of the mitral valve leaflets;
• Some autoimmune pathologies;
• MVP (mitral valve prolapse);
• Myocardial infarction;
• Cardiosclerosis developing after a heart attack;
• Arterial hypertension;
• Cardiac ischemia;
• Myocarditis;
• Dilated cardiomyopathy.

How is pathology diagnosed?

To suspect mitral valve insufficiency, an experienced specialist usually only needs to conduct an initial examination and take a medical history.

During the examination, you can find blue discoloration of the limbs, nails, lips, and ears. In later stages, cyanosis touches the face. The limbs swell, a systolic murmur is clearly audible.

To confirm insufficiency, differential diagnosis will be required, since there are symptomatic similarities with other valve pathologies.

A number of additional research procedures will be required, which, in addition to examination, are the main diagnostic methods:

• Chest X-ray;
• Echo-KG.

An x-ray taken of the chest area shows how enlarged the left ventricle is. An ECG can give the same result, but its disadvantage is the likelihood of errors during testing, whereas the increase will be visualized on an X-ray. Echo-CG in this case provides the most informative result.

Here you can see not only mitral valve defects, but also determine to what extent the insufficiency has developed.

Therapy

A cardiologist prescribes treatment depending on the extent and severity of the lesion. An important factor when choosing therapy is the pathogenesis of the disease in the patient. Certain groups of drugs are prescribed to eliminate symptoms.

The purpose of the operation is to restore the valve. As a measure, an option such as valve plastic surgery is used. This means eliminating the pathology of the valves and rings. In some cases, the valves can be replaced.

Sometimes the valve is completely removed and an artificial one is installed in its place. This method does not always eliminate regurgitation, but can significantly reduce it.

The result is improved structure of the mitral valve mechanism and prevention of ventricular and atrium damage.

The preferred method is prosthetics. Modern medicine makes it possible to reduce the risk of blood clots after installation of a prosthesis to a minimum. But the danger still remains, so a patient with a mitral valve prosthesis takes anticoagulant drugs all his life.

Lifestyle with NMC

When making a diagnosis, the patient must necessarily lead a healthy lifestyle - in its broadest sense.

Bad habits and foods hazardous to health are completely eliminated. It is necessary to consume less liquid and salts. Long walks in the fresh air are recommended.

Pregnancy with sUA deficiency is contraindicated only in case of severe hemodynamic disturbances.

There is a danger of NMPK - a violation of the uteroplacental blood flow during pregnancy, as a consequence of excessive load on the heart, which can lead to the death of both the fetus and the patient.

In other cases, the woman should be observed by her doctor before giving birth. During the birth process, a caesarean section is usually used.

Video: Mitral regurgitation

Forecast

The prognosis will not be favorable even in the absence of severe symptoms. The disease is characterized by progression. Lack of treatment leads to irreversible changes and death of the patient.

Modern technologies, coupled with competent and timely treatment, reduce the risk for the patient to a minimum. Surgery and taking certain medications prolongs life and improves its quality.

Doctor of Medical Sciences prof. ON THE. Didkovsky, Ph.D. I.K. Malashenkova

Federal State Institution Research Institute of Physical and Chemical Medicine of Roszdrav, MMA named after. THEM. Sechenov Ministry of Health and Social Development of the Russian Federation

The end of the 20th and beginning of the 21st centuries were marked by the rapid development of immunology, which significantly expanded our understanding of the importance and role of the immune system in maintaining human life, and the degree of complexity of its organization. The latest methods of studying immunity at the molecular level are being introduced into the practice of clinical immunology, and fundamentally new immunotropic drugs are being created (recombinant interferons, interleukins, etc.). In this article we will focus on modern methods of immunotherapy (IT): replacement immunotherapy, immunocorrection and immunorehabilitation for the most common human pathology associated with immune deficiency - infectious and inflammatory diseases (IIDs).

It is known that aggressive environmental factors, poor lifestyle and hereditary predisposition contribute to the development of secondary immunodeficiency (SID), which underlies chronic, often recurrent and treatment-resistant forms of SID.

It should be noted that stable immunity does not normally develop to most of the most common pathogens of IID (bacterial, intracellular). The role of antibiotics in the treatment of IID is undoubtedly important, but antibiotic therapy does not work on all forms of pathogens, including mutant strains, L-forms and others that cause the disease. Only the immune system suppresses new foci of infection, removes destroyed microorganisms and their toxins and protects the body from reinfection, so it must be capable of effective functioning at the local and systemic levels. At the same time, with the development of VID, the processes of recognition, absorption and destruction of infectious agents may be disrupted, which makes the immune response ineffective.

In many cases, the cause or important component of IID are viruses (rhino-, adeno-, entero-, herpes viruses, etc.), which have a suppressive effect on local and general immunity factors and contribute to the activation of other infections (Table 1). It should be noted that the role and presence of viruses is often not taken into account in the treatment of IVD.

Table 1

Thus, IVZ, incl. Mixed infections (bacterial, viral, fungal) have a multifactorial damaging effect on the immune system and other body systems, maintaining and aggravating VID.

Pathological changes that occur during a long course of IID against the background of VID (prolonged intoxication, an increase in foci of infection, reactivation of latent viral infections, dysfunction of the cytokine network, etc.) can provoke endogenous depression and also cause chronic fatigue syndrome. In addition, such patients have a significantly increased risk of developing autoimmune diseases and cancer.

Summarizing the above, I would like to emphasize the undoubted importance of carrying out IT in frequently and/or seriously ill patients with IVD to increase the effectiveness of treatment, improve the prognosis of the disease and the patient’s quality of life.

Unfortunately, the practicing doctor is currently faced with a shortage of objective information about the real capabilities of IT, its duration and methods of implementation. Paradoxically, against the backdrop of an ever-increasing number of immunotropic drugs, a similar phenomenon is observed even among clinical immunologists. Information about immunotropic drugs is predominantly commercial in nature.

The etiological and pathogenetic factors in the development of VID are widely discussed in the scientific literature /4, 8/. Clinical and laboratory signs of VID are distinguished. To decide whether to conduct IT, it is first of all important to evaluate the clinical markers of VID. These markers include:

A protracted, chronic or often recurrent infectious-inflammatory process that develops with damage to the mucous membranes and skin;

Activation of opportunistic flora, mixed infection, change of infection in the dynamics of the disease (usually against the background of antibiotic therapy) in areas of the inflammatory process; involvement of other organs in the process;

Resistance to antibacterial, antiviral or antifungal therapy, rapid development of relapse after treatment, frequent development of complications and side effects, pseudo-allergic and allergic reactions;

Recurrent infections caused by respiratory viruses; frequent reactivation of herpes viruses (including lymphotropic ones - EBV, HHV6, HHV7, HHV8); latent or active infection caused by hepatitis B, C, G, F, D viruses, papillomaviruses, etc.; often recurrent fungal infection; dysbiosis of mucous membranes;

The history includes a tendency to colds, chronic tonsillitis, repeated childhood infections (often in adulthood), pathological reactions to vaccination.

Laboratory signs of VID (Table 2) can be detected in one or several levels of immunity. If the IID is functional in nature, then the quantitative indicators of the immune system practically do not differ from the norm or are at its lower limit (which, in the presence of antigenic stimulation in connection with IID, can no longer be considered as the norm). Changes in immunity in these cases are detected by tests reflecting cell functions (response to stimulation, presence of activation markers on the membrane, etc.). It should be noted that the VID can be temporary or permanent.

table 2

Main laboratory markers of various clinical manifestations of VID

In case of VID with “structural” and functional changes, immunity indicators are quantitatively different from the normal level, a significant imbalance of the main subpopulations of lymphocytes, a deficiency in the production of immunoglobulins, interferons and other cytokines is revealed /5, 10/. According to the degree of severity, types of mild, moderate and severe are distinguished.

Indications for IT for IVZ

When determining indications for IT, clinical manifestations take priority over laboratory ones /7/. This is due to the fact that the immune system, a complex multi-level and multi-component structure, is constantly changing. Many of its parameters undergo changes and fluctuations over several minutes, hours, days. In addition, genetically determined features of the immune response are extremely diverse both among healthy individuals and among patients with VID. Therefore, when deciding on the need for IT, clinical markers of immune deficiency are first taken into account, and then the results of an immunological examination. To avoid false conclusions, it is advisable to study immunity indicators over time.

Replacement IT and immunocorrection may be necessary in severe cases of acute IID or in their protracted course, as well as in exacerbation of chronic forms of IID. Another type of IT, immunorehabilitation, is indicated for frequently recurrent and chronic IVD in the stage of reverse development and in remission of the disease. IT for acute IH is used infrequently, as a rule, in conditions that threaten the patient’s life, requiring replacement IT. In other conditions, replacement IT is carried out taking into account immunogram data and the clinical picture.

Indications for replacement IT for IVZ are:
1. Acute IID in patients with VID or in patients with concomitant severe diseases (diabetes, etc.).
2. Acute IVD with a protracted course, refractory to therapy.
3. Acute IVD with a threat to the patient’s life (threat of sepsis, etc.).
4. Exacerbations of frequently recurrent IIDs.
5. Subacute course of IVD.
6. Chronic IVD with moderate-severe and severe VID.

Patients with frequently or continuously recurrent chronic infections mainly need treatment with immunotropic drugs.

Modern approaches to the selection of immunocorrectors

An important aspect of IT is the choice of the appropriate immunotropic agent (immunocorrector) /5/. At the moment, four levels of selection of immunocorrectors can be distinguished (Table 3).

Table 3

Levels of selection of immunocorrectors

As can be seen from Table 3, at the 1st level of selection of an immunocorrector, an immunological examination is not performed on the patient (acute clinical situation requiring replacement IT, lack of an appropriate laboratory in a given medical institution, etc.). The choice of drug is made taking into account the type of IID, which is to a certain extent associated with disorders in specific parts of the immune system. In these situations, the doctor’s personal experience with immunotropic drugs, and in some cases their availability, plays an important role. It should be noted that at this level of selection, in patients with a severe course of the disease or with a long history of chronic IID, in the presence of other clinical markers of IID, unwanted and side effects of IT are more likely to occur: an increase in immune dysfunction, a pronounced exacerbation of the infectious process, reactivation of a viral infection. Therefore, in this category of patients, the use of immunocorrectors with an activating effect is carried out only after examination, while lower doses are prescribed at the beginning of treatment.

At the 2nd level of selection, immunological examination more often reveals insufficiency of antibody production, often with hyporeactivity of phagocytes; T-cell deficiency, often with deficiency of interferonogenesis and/or phagocytic system; imbalance or deficiency of pro-inflammatory and other cytokines, deficiency of cytotoxic lymphocytes. Severe combined VID is less commonly detected. When choosing an immunocorrector, the results of the patient’s history of IT are also taken into account. At this level, especially with a protracted or chronic course of the disease, it is advisable to conduct research for the presence of latent viral and bacterial infections, dysbiosis of the mucous membranes (as a result of VID). For the detection of herpes viral and other intracellular infections, PCR diagnostics are optimal, because serodiagnosis (level of IgG and IgM class antibodies) in these cases is not informative enough. Serological studies are more important to carry out in the dynamics of treatment of identified infections.

At the 3rd level of selection of an immunocorrector, it is important to study its effect on the patient’s blood cells in vitro(impact on neutrophil functions, interferonogenesis, etc.). The 4th level of selection of an immunocorrector seems to be the most modern and preferable, especially in cases of combined VID. Selection of drugs in vitro carried out using several methods (with assessment of the reaction to drugs of different parts of the immune system). Also at this level, the effect of selected immunocorrectors is monitored (dose, duration, or taking into account data from previously conducted studies) in the dynamics of treatment and/or the effect is assessed during repeated studies /5/.

General principles of IT during IVZ

IT is carried out against the background of basic treatment of IVD /7/.

In acute infectious processes and the presence of indications for immunocorrection (severity of the disease, threat of complications, presence of concomitant diseases associated with the development of VID), only replacement IT and auxiliary treatments such as detoxification and antioxidant therapy are indicated. Replacement IT includes the use of immunoglobulin preparations and recombinant interferon alpha. Other cytokines (recombinant interleukins), as well as thymic preparations, are used less frequently and, as a rule, in severe cases /2, 9/.

In case of protracted course of IVD or exacerbation of chronic processes, therapy with immunotropic drugs is carried out according to the results of the examination. According to indications, replacement IT is used (immunoglobulins for intravenous administration, thymus preparations, recombinant interferon alpha or interleukins) and/or immunocorrection of identified disorders, preferably under the control of an immunogram. Auxiliary treatments for this category of patients, along with detoxification and antioxidant therapy, include systemic enzyme therapy. The volume and duration of auxiliary therapy is determined by the clinical picture, the presence and severity of endotoxicosis markers, as well as the degree of production of reactive oxygen species (according to the NBT test, neutrophil chemiluminescence, etc.).

During the period of remission of the disease, if necessary (if clinical and/or laboratory signs of VID remain), immunocorrection is continued, while vaccine therapy or so-called therapy is used according to indications. bacterial immunocorrection (repeated courses).

When a latent viral infection (replicative phase) is detected, severe dysbiosis of the mucous membranes of the oropharynx, intestines, and genitourinary tract with the presence of pathogenic or excessive content of opportunistic microflora requires appropriate treatment /6/.

Necessary conditions for successful IT implementation are:
- complete mutual understanding and trust on the part of the patient;
- giving up alcohol and smoking, normalizing nutrition and physical activity;
- treatment of clinical manifestations of VID;
- treatment of metabolic disorders/normalization of homeostasis;
- treatment of concomitant diseases;
- regular monitoring by the attending physician.

The duration of the course of use of immunocorrectors is set individually and ranges from several weeks to several months. It is advisable to discontinue immunotropic drugs, as well as antioxidants, gradually. Patients, as a rule, need repeated IT courses. The duration of immunorehabilitation is 1 year or more.

It is important to note that with adequate immunocorrection, exacerbations of IID may occur and new foci of latent infection may be identified. If an exacerbation occurs against the background of restoration of immune reactivity, normalization of previously changed immunity parameters, such an exacerbation can be considered a positive result of IT. Against the background of restoration of the immune response, it is possible to cope with the infection and accelerate the onset of remission of the disease.

Characteristics of individual groups of immunotropic drugs

Immunoglobulins when administered intravenously, they quickly block toxins, foreign antigens, activate macrophages and antibody-dependent cytotoxicity and often make it possible to reverse the difficult clinical situation with IVD towards recovery. Indications for the use of immunoglobulin preparations are:

Acute severe infections;
- threat or development of infectious-septic syndrome;
- the presence of severe background diseases: decompensated or subcompensated diabetes mellitus and its complications, heart and lung failure, etc.;
- decrease in IgG level to 900 mg% or lower in case of severe or protracted infectious process;
- violation of the ratio of the main subclasses of IgG and a decrease in the avidity or affinity of IgG;
- no increase in specific IgG during intracellular infections;
- torpidity of the infectious process, protracted course, rapid development of relapse, despite adequate basic therapy against the background of low or reduced IgG levels.

The main preparations of immunoglobulins, the active substance of which is IgG from donor blood, include: Normal human immunoglobulin for intravenous administration, Intraglobin, Immunovenin, Octagam, Cytotect, Pentaglobin.

Interferon preparations have become firmly established in the clinical practice of doctors of various specialties. The functions of interferons are diverse and one of the most important is antiviral (stimulation of the production of antiviral proteins). This property made it possible to conditionally distinguish them from the cytokine system into an independent group of antiviral agents with a pronounced immunoregulatory effect. Interferons are involved in antimicrobial and antitumor protection and have radioprotective properties. In clinical practice, the most widely used drugs are recombinant interferon alpha (Reaferon, Altevir, Realdiron, Roferon-A, PegIntron, Intron A, Viferon).

Indications for the use of alpha interferon drugs for IVD are:
- pronounced insufficiency of production and/or defectiveness of the produced endogenous interferon alpha;
- combined VID with suppression of the interferon system, insufficiency of phagocytosis, activity of natural killer cells and cytotoxic CD8+ lymphocytes;
- acute conditions, if there is a threat of septic complications (as a natural stimulator of the phagocytic link);
- mixed bacterial-viral etiology of IVZ;
- protracted and chronic IVZ with bacterial-viral etiology;
- active replication of herpetic or other viral infection (hepatitis B, C, etc.);
- respiratory infections caused by intracellular microorganisms ( Chlamydia pneumoniae, Mycoplasma pneumoniae and etc.).

Interleukins(IL) - secretory regulatory proteins from the cytokine system. They are synthesized by cells of the immune system and its associated systems and ensure the interaction of cells with each other and with other body systems. With the help of IL, certain subpopulations of lymphocytes are activated, their proliferation and differentiation, and the performance of necessary functions. Not only “switching on” is carried out, but also “switching off”, the completion of the immune response to a specific foreign agent. With a deficiency of certain ILs, activated cells of the immune system can undergo apoptosis. The ability to produce IL is an important characteristic of the functional state of cells of the immune system. In the treatment of VID, recombinant analogs of IL are used - Betaleukin (IL-1), Roncoleukin (IL-2).

IL-1 is a pro-inflammatory IL and is produced by activated phagocytes. IL-1 is the main mediator of the launch of inflammatory reactions, the immune response (stimulates the proliferation of T cells, their synthesis of other ILs, activates phagocytes and epithelial cells, fibroblasts). Another key cytokine of the immune response, IL-2, is produced by activated T cells, mainly (up to 90%) CD4+ lymphocytes (T-helper type 1). The amount of IL-2 synthesized determines the magnitude of the T-cell immune response. IL-2 is the main factor in the growth and proliferation of T cells, is necessary for the functioning of cytotoxicity systems, stimulates the synthesis of other ILs, activates B cells, etc. Due to the special biological properties of ILs, therapy with exogenous drugs does not lead to suppression of endogenous production, but, on the contrary , has a supporting and stimulating effect on the processes of their synthesis. The greatest clinical experience has been accumulated with recombinant IL-2.

Indications for the use of recombinant IL-2 are:

In acute processes:
- severe IVD and lack of effect from the therapy;
- threat or presence of septic complications;
- severe purulent processes, furunculosis;
- severe hyporeactivity or suppression of the T-link of immunity, which is not corrected by appropriate therapy with thymomimetics and other immunocorrectors;
- severe type, caused by concomitant pathology, for example, decompensated diabetes mellitus.

For chronic processes:
- prolonged course of the disease, mixed infections;
- chronic viral infections, reactivation of latent viral infection;
- preservation of clinical markers of VID (change of pathogen, refractoriness to antibiotic therapy, etc.);
- complex therapy of severe mycoses.

Recombinant IL-2 is currently considered as the drug of choice for many severe and advanced IIDs against the background of VID, as well as as a basic drug in program immunorehabilitation. Encouraging results have also been obtained with its extracorporeal use.

Recombinant IL-1 preparations are used less frequently. Indications for their use are:
- toxic leukopenia (not lower than 3.0·10 9 /l);
- severe VID after extensive surgical interventions;
- severe VID after suffering purulent-septic processes;
- chroniosepsis with symptoms of suppression (hypoor anergy of a number of links) of the immune system;
- reduction or absence of IL-1 production, suppression of the functional activity of phagocytes, lymphocytes, antibody formation;
- chronic infectious and inflammatory torpid processes of the upper respiratory tract and genitourinary tract (local application).

Adjuvant therapies

Detoxification is an important part of “preparing” the immune system for active influences. Under the influence of toxins, microbial suppressive proteins, prolonged exposure to foreign antigens, superantigens, oxidants, pro-inflammatory cytokines and other factors, the properties of the membranes of cells of the immune system and its associated systems change, and membrane receptors are blocked. In addition, with prolonged activation of certain cells, a phase of their suppression or hyporeactivity begins. Against this background, medicinal immunocorrective effects may be ineffective or even harmful. Detoxification, which allows you to remove or reduce “suppressive pressure”, is a necessary link in the implementation of IT for both acute and chronic IID. It includes enterosorption, plasmapheresis, hemosorption, parenteral administration of detoxifying solutions. In many cases, without this stage, the reaction to immunocorrectors may be inadequate or even paradoxical. In acute severe conditions, hemosorption and/or plasmapheresis is used with intravenous administration of immunoglobulins, which enhance the detoxifying effect.

Antioxidants They also play an important role in auxiliary treatment. Increased formation of ROS (provide bactericidal activity of neutrophils) under conditions of inflammation and intoxication leads to depletion of the antioxidant system (AOS) and the development of oxidative stress. Cascade-like damage to the membranes of the cells of the affected organ and cells of the immune system may occur. There are a number of drugs of different chemical nature that can suppress the formation of free forms of oxygen (radicals). Some drugs neutralize the formed radicals and remove them from the body, others help restore AOS /3/. To achieve an optimal therapeutic effect, combinations of different drugs with antioxidant effects are used: vitamins (ascorbic acid, vitamins P, E, A, etc.), microelements (selenium, zinc, manganese, etc.), lipoic acid, immunocorrectors with antioxidant activity ( Imunofan, Polyoxidonium, Galavit, Glutoxim, etc.), Mexidol, Emoxipin, Ceruloplasmin.

Oral medications are used as adjuncts in the treatment of chronic IIDs. systemic enzymes— Wobenzym, Phlogenzym, Wobe-Mugos E. These drugs give fewer side effects than enzymes for parenteral administration (trypsin, chymotrypsin, etc.) and can be used for a long time. Systemic enzymes improve microcirculation and tissue trophism, promote the removal of toxins from the body, have their own fibrinolytic activity, increase the concentration of antibiotics at the site of inflammation, affect the synthesis of IL, and have immunocorrective properties (stimulate the activity of natural killer cells, cytotoxic lymphocytes, reduce the degree of autoaggression).

Immunocorrection for various types of VID in patients with IVD

Immunocorrection for insufficiency of T-cell immunity It is usually carried out with the use of thymomimetics (Tactivin, Timalin, Timogen, Imunofan, Immunomax). Indications for their use are:

Persistent lymphopenia;
- decrease in the percentage and/or number of total CD3+ T-lymphocytes, CD4+ T-helper cells;
- the presence of a viral and/or fungal infection (which may indirectly indicate dysfunction of the T-link of immunity);
- increased content of T-null, double CD4+, CD8+ lymphocytes;
- a decrease in the content of activated lymphocytes or the absence of their increase in the presence of IVZ.

In the absence of the possibility of selecting an immunocorrector and history data on the effectiveness of thymomimetics in a patient in cases of T-cell failure in combination with hyporeactivity or suppression of phagocytes, Thymogen, Taktivin or Timostimulin are prescribed, which have a stimulating effect on both lymphocytes and phagocytes. In case of T-cell failure in combination with activation of neutrophils/phagocytes, the predominance of free radical processes and excessive production of pro-inflammatory cytokines (TNF-alpha, IL-1, etc.), the drug of choice is Imunofan (which also has antioxidant activity). It is also possible to combine thymomimetics with antioxidants (Glutoxim, Mexidol), but it is advisable to evaluate these drugs in tests in vitro.

Repeated courses of therapy with thymomimetics are prescribed after 1, 3, 6 months based on the results of the examination if T-cell failure persists or reoccurs (impaired ratio of lymphocyte subpopulations and/or change, decrease in their number, functional failure).

Immunocorrection for deficiency in lymphocyte antiviral defense factors - systems of natural and specific cytotoxicity - is carried out using thymus preparations (Tactivin), Immunomax, recombinant interferon alpha, and less often - interferon inducers; if they are ineffective, recombinant IL-2 drugs are prescribed. This form of VID is often refractory to therapy.

Immunocorrection for insufficiency of the phagocytic system and humoral deficiency (insufficient antibody formation). Phagocytes are the first line of defense of the body from everything foreign and from destroyed and abnormal “self”. The reaction of phagocytes to exo- and endogenous stimuli is almost instantaneous. The functions of phagocytes are diverse: the absorption and destruction of microorganisms, the presentation of antigens for the development of subsequent stages of the immune response, the production of pro-inflammatory ILs to trigger a cascade of immune reactions and the formation of an immune response, extracellular killing using “oxygen explosion” products, and much more. Phagocytes contain more than 50 different mediators and enzymes in the cytoplasm, which are released depending on the type of stimulus. Phagocytes participate in the processes of inflammation, repair, hematopoiesis, in the functioning of the endocrine and nervous systems, etc. In a resting state, phagocytes secrete immunosuppressive proteins necessary to complete the immune response and, possibly, to prevent autoaggression.

In VID, disruption of individual or many functions of phagocytes occurs quite often and causes an inadequate immune response and chronicity of infections. Suppression of phagocytes often reflects intoxication (endotoxicosis) and may be accompanied by paradoxical reactions. To prevent them, it is necessary to use detoxification methods. Drugs that are used to stimulate phagocytosis (Polyoxidonium, Myelopid, Lykopid, Methyluracil, Galavit, etc.) often activate antibody formation. Indications for the use of phagocytosis and antibody formation stimulators, according to an immunological examination, are:
- hyporeactivity of phagocytes, with insufficient bactericidal activity and impairment of other functions (IL synthesis, phagocytosis, digestion, chemotaxis);
- insufficiency of the B-link of immunity - production of antibodies (IgG) - with an IgG content in the blood serum of at least 800 mg%;
- leukopenia and neutropenia.

In addition to the above, the drugs Derinat, Gepon, Neupogen, Betaleukin, Cycloferon, etc. also have a stimulating effect on phagocytosis and antibody formation. These properties of the drugs are taken into account when choosing IR.

For immunocorrection and immunorehabilitation in case of insufficiency of the phagocytic system and antibody formation, immunocorrectors of bacterial origin are also used. Such immunocorrectors activate all the functions of phagocytes and help increase antibody formation. The use of bacterial immunocorrectors helps prevent exacerbations of IVI and accelerates the resolution of the process against the background of basic therapy. It induces short-term protective immunity and prolongs the remission of chronic IIDs. Drugs of this group (mainly systemic use) secondary activate other parts of the immune system. Bacterial immunocorrectors are most widely used for IH of the respiratory and genitourinary tract. These include: Ribomunil, Broncho-munal, Imudon, IRS-19, SolkoTrichovak, SolkoUrovak, etc.

Indications for the use of immunocorrectors of bacterial origin for IVD are the same as for the use of stimulators of phagocytosis and antibody formation. They are prescribed in the acute period and in case of prolonged exacerbation of IVD against the background of etiological therapy. Also, these drugs are used in the remission stage of IVZ to prevent exacerbations of the disease. To increase the effectiveness of therapy, bacterial immunocorrectors can be combined with Polyoxidonium, Methyluracil, Myelopid, interferon alpha, etc.

In the presence of concomitant autoimmune diseases and/or latent viral infection (herpes viruses, etc.), bacterial immunocorrectors, incl. oral, should be used with caution under the monitoring of indicators of autoaggression and reactivation of viral infection (according to serological studies and DNA diagnostics), because activation and proliferation of T-helper cells and B-lymphocytes under their influence can cause exacerbation of these diseases against the background of a still existing type. Reproduction of lymphotropic herpes viruses can occur in parallel with the proliferation of infected cells.

Immunocorrection for interferonogenesis deficiency depending on the stage of the disease and the severity of interferon deficiency, it is carried out using both replacement immunotherapy with recombinant interferon and interferon inducers. With preserved reserve abilities of the interferon system (determined by tests in vitro) the use of interferon inducers is successful, the production of their own interferons, which are not antigenic, is stimulated. Substances of different chemical nature have the ability to induce the synthesis of interferons, and each of them acts only on a certain group of cells that have the corresponding receptors. For example, Amiksin causes the production of alpha and beta interferons in T-lymphocytes. Indications for the use of interferon inducers for IVD are:

Insufficient production of interferons against the background of preserved reserve capacity of the IFN system (according to laboratory studies);
- mixed bacterial-viral nature of IID in acute non-severe conditions;
- protracted and chronic IVZ due to bacterial-viral infection;
- detection of replication of herpetic or other viral infection (in complex therapy);
- IVD caused by intracellular microorganisms such as Chlamydia, Mycoplasma etc., non-severe course;
- acute viral diseases.

The use of interferon inducers is possible only in short courses of 3-4 weeks, because further stimulation of producer cells can lead to hypo- and unresponsiveness of the interferon system. Repeated courses of treatment are carried out according to indications no earlier than 2-3 months after the end of the 1st course of therapy. Our studies have shown the effectiveness of using interferon synthesis inducers in many patients in lower doses than the average therapeutic dose. A good effect is observed when alternating interferon inducers and recombinant interferon alpha. The main drugs that induce interferon synthesis are the above-mentioned Amiksin, as well as Cycloferon, Neovir, Ridostin, Kagocel.

Immunocorrection for combined type begins with auxiliary treatment methods and replacement IT, taking into account the most altered indicators of immunity. Subsequently, under the control of immunograms, immunocorrection is carried out with the selection of level 3-4 drugs (see Table 3). Treatment of combined VID is usually long-term, step-by-step, complex, and immunorehabilitation is mandatory.

Conclusion

The principles of IT are based on the etiology and pathogenesis of VID and include diagnostics and the use of detoxification methods, replacement immunotherapy, immunocorrection and program immunorehabilitation according to indications under the control of immune parameters in dynamics. It is also important to treat complications of VID and associated diseases.

With permanent variants of VID, taking into account the multifactorial nature of their development, neither monotherapy with immunotropic drugs nor short courses of combination therapy can provide a long-term clinical effect and normalization or improvement of the immune and related systems. Carrying out immunocorrection and immunorehabilitation will require time and effort, incl. and from the patient himself. It may be necessary to change the work and rest schedule, restore normal sleep duration, in some cases - change work, place of residence, give up bad habits, psychological help, use of psychotropic drugs, restore the balance of proteins, vitamins, microelements, etc. A doctor, based on the principles of IT for IVD, can treat VID in this category of patients, perform immunocorrection under the control of immune status parameters, and also develop an individual immunorehabilitation program. The implementation of such programs can significantly reduce the number of exacerbations of ICH, improve the patient’s quality of life and, to a certain extent, will serve as the prevention of cancer and autoimmune diseases.

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