Principles of immunocorrective therapy for infectious and inflammatory diseases. Mitral valve insufficiency, what is it and what is the prognosis for life with cerebrovascular accident? Causes of valve pathology

October 12, 2016

Nonspecific resistance of the organism is characterized by the concept “ interferon status", serving as an integral criterion of the functional state of the IFN system.

The term “interferon status” was proposed by F.I. Ershov in 1986. At the same time, a methodology for determining IFN status was developed and scientific evidence of changes in various parts of the IFN system in various forms of pathology was presented. In subsequent years, this technique was widely used to determine the parameters of the IFN system in patients with viral hepatitis, influenza and acute respiratory viral infections, herpes, with autoimmune, oncological and allergic diseases and other forms of pathology and, as a result, the effect on IFN status of exogenous IFN- drugs was shown. a, -b, -g and IFN inducers. As it turned out, reduced interferonogenesis indicates chronicity of the disease and progression of the viral infection. IFN deficiency syndromes with complete or partial loss of various links of the IFN system (alpha or gamma IFN) are the cause or consequence of acute and chronically recurrent viral infections, congenital or acquired defects that accompany stressors, autoimmune, allergic, oncological diseases and AIDS. It should be noted that in 10 - 20% of cases, even in practically healthy people, various types of interferon formation disorders are determined. Generally, " interferon status", as an indicator of the functional activity of the interferon system, it allows one to judge the immunoreactivity of the organism in situ.

Currently, the method for determining “interferon status” is carried out using a micromethod using a technique in a virological box, observing sterile conditions. Whole heparinized blood of healthy and sick people is used for the study. IFN status should be determined on the day of blood sampling. The method for determining IFN status allows you to determine the following main quantitative parameters (U/ml):

circulating (serum) IFN in the blood;
the level of production of IFN-a by leukocytes upon stimulation with Newcastle disease virus (NDV), Kansas strain, and subsequent inactivation of the inducer virus in vitro;
the level of IFN-g production by leukocytes when inducing them with a mitogen - phytohemagglutinin (PHA R, Difco) at a dose of 10 μg/ml in vitro.
level of spontaneous IFN production in vitro.

Establishment of IFN status in more than 500 whole blood samples of practically healthy individuals made it possible to determine average quantitative values of the physiological norm of IFN status indicators. Thus, for the indicators of IFN-a fine for adults take values of 640 U/ml, IFN-g – 128 U/ml, serum IFN< 2-8 Ед/мл, спонтанно продуцируемого ИФН < 2 Ед/мл. При недостаточности интерфероногенеза 1, 2, 3, 4 степени продукция a-ИФН лейкоцитами соответственно составляла 320, 160-80, 40 и менее 40 Ед/мл, продукция g-ИФН лейкоцитами – 64, 32-16, 8, 4 и менее Ед/мл. За показатели ИФН-a в норме for children up to 14 years of age the values are 320 U/ml, IFN-g – 64 U/ml, serum IFN< 2-8 Ед/мл, спонтанно продуцируемого ИФН < 2 Ед/мл. При дефиците интерфероногенеза 1, 2, 3, 4 степени продукция a-ИФН лейкоцитами соответственно составляла 160, 80-40, 20 и менее 20 Ед/мл, продукция g-ИФН лейкоцитами – 32, 8-16, 4 и менее Ед/мл. Следует подчеркнуть, что у пожилых людей старше 60 лет в 70% случаев обнаруживается физиологическая недостаточность системы ИФН по 2 или 3 показателям, причём у каждого второго доминирует дефицит продукции g-ИФН (иммунного ИФН), что коррелирует со снижением у них показателей врожденного и адаптивного иммунитета.

It should be noted that the above physiological norms were determined almost 20 years ago. At present, the environmental situation is constantly deteriorating. For example, a persistent herpes viral infection is detected in almost every individual; socio-psychological tension and stressful situations are increasing in society, which gradually leads to the fact that the physiological norms of IFN status are decreasing.

An important addition to the definition of IFN status is the later developed identification of the individual sensitivity of a particular patient to drugs that induce IFN and immunomodulators, which is assessed by the increase in IFN-a and -g titers after exposure of peripheral blood leukocytes to these drugs in vitro. The sensitivity of leukocytes to drugs is assessed depending on the increase in titers:

At more than 4x magnification, it is very pronounced;
At 3-4x magnification - pronounced;
With a 2-fold increase in the titers of alpha-, gamma-IFN under the influence of the drug - weak sensitivity;
If the value of IFN-alpha, -gamma does not change under the influence of the drug, there is a lack of sensitivity.

A study of IFN status with determination of sensitivity to drugs should be prescribed before the start of therapy to identify the optimal sensitivity of blood leukocytes to specific drugs in a particular patient, which makes it possible to recommend the use of the most active drugs for therapy.

Assessment of the identified changes can serve as a guide in the diagnosis, treatment and prognosis of diseases of both viral and non-viral etiology. We note the following indications for which a study of IFN status is necessary:

viral infections: acute and chronic forms;
allergic and autoimmune diseases;
recurrent opportunistic infections;
frequently ill children, elderly people;
congenital and acquired defects of the IFN system;
clinical trials of IFN drugs, IFN inducers and immunomodulators;
clinical use of the above drugs and assessment of the effectiveness of therapy;
development of individual treatment regimens with IFN drugs, its inducers and other immunoactive drugs.

The following can be noted: stress, acute viral infections, allergic conditions are accompanied by an increase in the level of circulating interferon and a decrease in the level of induced production of a- and g-IFN by leukocytes. In bronchial asthma, allergic rhinitis, atopic dermatitis, and urticaria, the level of circulating interferon often correlates with the severity of the disease. Chronic viral infections (influenza, herpes, hepatitis) are accompanied by suppression of all indicators of interferon status. The same is typical for autoimmune diseases (systemic lupus erythematosus, rheumatoid arthritis, multiple sclerosis, ulcerative colitis, psoriasis). Acute lymphocytic leukemia and malignant formations are accompanied by a deficiency of inducible products, especially interferon gamma.

It should be noted that the results of the study of interferon status must be considered in conjunction with other laboratory and clinical anamnestic data. A decrease in the production of alpha and gamma interferon, which can be both a cause and a consequence of acute and chronic viral diseases, indicates a congenital or acquired deficiency of the interferon system and can be considered as an indication for interferon-stimulating therapy.

The study of interferon status parameters is used to select and evaluate the effectiveness of therapy when using exogenous interferon preparations, interferon inducers and immunomodulators.

During clinical trials of IFN drugs and their inducers and/or during their subsequent clinical use, there is a need to study monitoring of IFN status indicators as a criterion for the effectiveness of the proposed therapy.

Considering the pronounced antitumorigenic activity of g-IFN, its close direct and feedback relationship with the system of interleukins and natural killer cells, deficiency of g-IFN production in elderly people, in the absence of other causes, can be considered as a preclinical marker of oncogenic diseases. Frequently ill children and women of childbearing age may also be included in the risk group, especially in the presence of various gynecological diseases associated with papilloma, herpes, cytomegalovirus and chlamydial infections, given that, as a rule, these infections have a latent persistent nature.

All of the above indicates the advisability of periodic testing of the IFN system in humans. When identifying functional inferiority of the IFN system in various age groups at increased risk and in various pathological conditions, correction of the IFN system is necessary. Scientifically based tactics of preventive and therapeutic correction of defects in the IFN system using IFN drugs and its inducers, as well as immunomodulators, can increase the nonspecific resistance of the body in various pathological conditions and, as a rule, shows a correlation with clinical results. Normalization of interferon status indicators usually coincides in time with the recovery process.

As mentioned above, exogenous IFN (natural and especially its recombinant forms) has become widespread in medical practice. It should be noted that long-term use of interferon therapy in oncological diseases, hepatitis B and C, multiple sclerosis, papillomatosis, leads to the formation of antibodies that can partially neutralize the effect of the drug (NAT-neutralizing antibodies). Testing (detection and quantification) of NAT is an essential component of care for these patients because it provides information about one of the most important factors determining clinical response to IFN therapy.

The prospect of widespread clinical use of IFN inducers and immunomodulators as prevention and treatment requires determination of the sensitivity of their leukocytes to these drugs in healthy individuals and patients with various forms of pathology and scientifically based monitoring of the effectiveness of their action. Determination of IFN status indicators and their assessment make it possible to carry out such control, as well as the choice of adequate (preventive and therapeutic) regimens for the use of these and other biologically active drugs.

Evaluating information content of IFN status indicators, can be done conclusions:

indicators of IFN status in general make it possible to judge the immunoreactivity of the organism in situ;
an increase in serum IFN titers may indicate an acute stage of the disease;
there is a direct relationship between the levels of IFN types 1 and 2 and the severity of the disease and an inverse relationship with the amount of serum IFN;
a decrease in the production of IFN-a and IFN-g indicates a defect in the IFN system (congenital or acquired) and is an indication for IFN-stimulating therapy;
low production of IFN-g or its absence in people over 60 years of age in the absence of other reasons may be a preclinical marker of cancer;
restoration (normalization) of IFN status indicators usually coincides with recovery processes;
Determination of IFN status over time when using exogenous IFN drugs, IFN inducers or immunomodulators can serve as a criterion for the effectiveness of therapy in patients.

Significance indicators of IFN status are high, especially when assessing the clinical condition of both a healthy individual and a sick person. Based on the totality of IFN status indicators, one can assess one or another degree of system insufficiency based on the ability to produce IFN by blood leukocytes or interpret increased levels of circulating IFN in the blood and its spontaneously produced synthesis.

It is necessary to take into account the important fact that timely prescribed, individually selected treatment with a preliminary test to determine the sensitivity of a particular person’s leukocytes to drugs of IFN inducers and/or immunomodulators will subsequently lead to correction of the IFN status of this individual and faster clinical stabilization/recovery .

Considering the above, it should be noted that changes in IFN status in various forms of pathology with the necessary subsequent correction of these disorders are associated with the use of corrective drugs, which include IFN drugs, IFN inducers, and immunomodulators.

Literature

Grigoryan S.S., Mayorov I.A., Ivanova A.M., Ershov F.I. Assessment of human interferon status using whole blood samples. Questions of virology. 1988; 4: 433-436.
Grigoryan S.S., Ospelnikova T.P., Ershov F.I. Determination of individual sensitivity of people to interferon inducers and other drugs (based on the effect on interferon status). Guidelines. Moscow. 2000; 14s.
Ershov F.I. The interferon system is normal and pathological. M., Medicine. 1996, 239 p.

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.

Degree	How to express
First	Grade 1 NMC is characterized as moderate. The expression is that the flow of blood entering the left atrium will not be significant or dangerous. Regurgitation will be approximately 25% and concentrated only near the mitral valve itself. For grade 1, treatment and prognosis will be positive since the symptoms are minor.
First	Symptoms appear only in systolic murmurs. Another manifestation is a slight expansion of the cardiac border to the left side. The electrocardiogram does not reveal pathological changes.
Second	NMC stage 2 is the 2nd degree of mitral insufficiency. The blood flow is able to reach the very middle of the left atrium. Blood reflux can reach up to 50% of the total blood flow. Here, an increase in pressure cannot be avoided, since without this the atrium does not have the opportunity to push out blood. One of the symptoms is the formation of pulmonary hypertension.
Second	When hypertension already occurs, the patient experiences shortness of breath and cough. Heart rate increases even in a calm state. An electrocardiogram will show how much the functionality of the atrium has changed. A detailed examination demonstrates a systolic murmur. The cardiac boundaries usually expand two centimeters to the left side, and about half a centimeter to the right side and upward.
Third	When failure develops to degree 3, blood flow is able to penetrate into the atrium all the way to the posterior wall. Systolic volume can reach 90%. Decompensation begins.
	Another manifestation is hypertrophy of the left atrium, when it loses the ability to push out all the accumulated blood.
	Signs of grade 3 mitral regurgitation are detected on the ECG, which shows hypertrophy of the mitral wave and murmur during systole. Using a phonendoscope you can hear noises. The expansion of the cardiac boundaries becomes more obvious.

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%.

The left ventricle becomes more voluminous due to stretching, which is the result of constant pumping of excess blood

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 detect 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.

In cardiological practice, a heart defect such as mitral valve insufficiency is often encountered. The movement of blood in the cavity of the heart depends on the functioning of the valves. The bicuspid valve is located in the left parts of the organ. It is located in the area of the atrioventricular opening. When it closes incompletely, blood rushes back into the atrium, which leads to disruption of the organ.

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Valvular dysfunction

Mitral regurgitation is an acquired heart defect in which the valve leaflets do not close completely, which leads to the backflow (regurgitation) of blood into the atrium. This condition leads to the appearance of various clinical symptoms (shortness of breath, edema). The isolated form of this defect is diagnosed very rarely.

It accounts for no more than 5% of all cases of this pathology. Most often, mitral regurgitation is combined with a narrowing of the left orifice between the atrium and the ventricle, aortic valve defects, atrial septal defect and the septum between the ventricles. During preventive heart examinations, bicuspid valve dysfunction is detected in 5% of the population. In most cases the degree of deviation is insignificant. This defect is detected using ultrasound.

Disease severity

Mitral insufficiency comes in several types: ischemic, non-ischemic, acute and chronic, organic and functional. The ischemic form is caused by a lack of oxygen in the heart muscle. Organic pathology develops as a result of damage to the valve itself or tendon cords. In the functional form of this defect, disruption of blood flow is associated with an increase in the cavity of the left ventricle.

There are 4 degrees of this pathology: mild, moderate, severe and severe. This defect includes 3 stages. In the compensation stage, the backflow of blood into the atrium does not exceed 20-25% of the total blood volume during heart contraction. This condition does not pose a danger, since compensatory mechanisms are activated (increased work of the left atrium and left ventricle).

In the subcompensation stage, congestion is observed in the pulmonary circulation (lungs). The left parts of the heart are heavily overloaded. Blood regurgitation is 30-50%. Stage 3 inevitably leads to severe heart failure. From 50 to 90% of the blood returns back to the atrium. With this pathology, the valve begins to sag.

The degree of sagging varies (from 5 to 9 mm). When assessing the condition of the mitral valve, the size of the opening between the atrium and the ventricle is also taken into account. With a mild degree it is less than 0.2 cm², with a moderate degree it is 0.2-0.4 cm², and with a severe degree there is a hole larger than 0.4 cm². In the latter case, the left atrium is constantly filled with blood.

Etiological factors of the disease

The following reasons for the development of this acquired heart defect in children and adults are identified:

rheumatism;
endocarditis of infectious nature;
acute form of myocardial infarction;
deposition of calcium salts in the area of the valve leaflets;
bulging of the valves forward due to weakness of the connective tissue;
autoimmune diseases (lupus, scleroderma);
coronary heart disease due to atherosclerosis or thrombosis of the coronary arteries;
dilated cardiomyopathy;
myocarditis;
cardiosclerosis.

The ischemic form of the defect often develops against the background of myocardial sclerosis after a heart attack. Sometimes this pathology becomes a manifestation of Marfan and Ehlers-Danlos syndrome. The expansion of the fibrous ring and the ventricular cavity causes the development of relative insufficiency of the bicuspid heart valve. The bicuspid valve is a heart structure made of connective tissue. It is located in the fibrous ring.

In a healthy person, during contraction of the left stomach, blood rushes into the aorta. It moves in only one direction (from the left atrium to the left ventricle and aorta). If the valve is not completely closed, blood regurgitation occurs (reverse reflux). The condition of the valve leaflets largely depends on the health of the chordae tendineae. These are the structures that allow flexibility and movement of the valve. When inflammation or injury occurs, the chords are damaged, which leads to disruption of the tone of the valves. They don't close completely. A small hole is formed through which blood flows freely.

Clinical manifestations in the early stages

The signs of this pathology depend on the degree of regurgitation. In the first two stages, the following symptoms are possible:

rapid heartbeat;
heart rhythm disturbance;
fast fatiguability;
weakness;
malaise;
dyspnea;
chest pain;
cough;
slight swelling of the lower extremities.

With mitral valve insufficiency of the 1st degree, complaints may be absent. The body compensates for these violations. This stage can last several years. Most often, such patients complain of chilly legs and weakness. In the second stage (subcompensation), the first signs of heart failure appear (shortness of breath, tachycardia).

Shortness of breath occurs with physical exertion. Its appearance can be caused by long walking, heavy lifting, or climbing stairs. She doesn't bother her when she's alone. Shortness of breath is a feeling of lack of air. The heart of such patients begins to beat faster (80 or more beats per minute). The heart rhythm is often disturbed, such as atrial fibrillation.

With it, the atria are excited and contract randomly at a frequency of 300-600 beats per minute. Long-term arrhythmia can cause heart attack, ischemic stroke and vascular thrombosis. With mitral valve insufficiency of the 2nd degree, edema may appear on the feet and legs. Both limbs are affected symmetrically. Cardiac edema worsens in the evening. They are bluish in color, cold to the touch and grow gradually.

Late stage manifestations

Symptoms of stage 3 mitral valve insufficiency are most pronounced. Due to significant regurgitation, venous blood stagnates in the pulmonary circle, which leads to an attack of cardiac asthma. Most often, attacks occur at night. They are characterized by lack of air, shortness of breath, and dry cough. Symptoms are most pronounced when the person is lying down. Such people breathe through their mouths and have difficulty speaking.

At stage 3 of mitral insufficiency, complaints become constant. The symptoms are disturbing even at rest. Such people often develop pulmonary edema. Sometimes hemoptysis is observed. Edema syndrome is pronounced. Swelling appears not only on the limbs, but also on the face and other parts of the body.

Impaired blood flow leads to stagnation in the liver. This manifests itself as pain in the hypochondrium on the right. Depletion of the heart muscle leads to multiple organ failure. Against the background of mitral ventricular failure, the right side of the heart often suffers. Right ventricular failure develops. The following symptoms are observed:

increase in abdominal volume (ascites);
acrocyanosis;
bulging veins in the neck area.

The most serious complication of mitral disease is atrial fibrillation.

How are patients examined?

Treatment of patients begins after a final diagnosis is made. Diagnostics includes:

collection of anamnesis of life and illness;
identification of main complaints;
physical examination;
electrocardiography;
Ultrasound of the heart;
heart murmur analysis;
immunological blood test;
X-ray of the chest organs;
Dopplerography;
general blood and urine analysis.

If necessary, coronary angiography (examination of the coronary arteries using a dye) and spiral computed tomography are performed. In order to determine the pressure in the left side of the heart, catheterization is performed. Physical examination is very informative. With mitral insufficiency, the following changes are detected:

the presence of a heart hump;
increased apical impulse;
increase in the boundaries of cardiac dullness;
weakening or absence of 1 heart sound;
systolic murmur at the apex;
splitting or accent of 2 tones in the area of the pulmonary artery.

Cardiac ultrasound can determine the severity of mitral regurgitation. This is the main method for diagnosing this defect. During an ultrasound of the heart, the condition of the valves, the size of the atrioventricular orifice, the presence of pathological inclusions in the valve area, the size of the heart and its individual chambers, wall thickness and other parameters are assessed.

Conservative treatment tactics

Treatment of patients with this defect can be conservative or surgical. It is necessary to identify the main cause of this pathology. If bicuspid valve insufficiency has developed against the background of rheumatism, then treatment involves the use of glucocorticoids, NSAIDs and immunosuppressants. Additionally, antibiotics may be prescribed. Sanitation of all foci of chronic infection is required.

In the case of coronary heart disease against the background of atherosclerosis, lifestyle changes are required (giving up alcohol and tobacco products, following a diet, limiting exercise, eliminating stress), and using statins (Simvastatin, Lovastatin, Atorvastatin). If necessary, beta blockers and antiplatelet agents are prescribed.

Drug treatment for bicuspid valve insufficiency includes the use of the following medications:

reducing vascular resistance (ACE inhibitors);
antiarrhythmic drugs (Cordarone, Novocainamide);
beta blockers (Bisoprolol);
diuretics (Veroshpiron, Indapamide);
anticoagulants (Heparin, Warfarin);
antiplatelet agents (Thrombo ACC).

Diuretics reduce the volume of blood circulating in the vessels. Nitrates are necessary to reduce afterload on the heart. In case of developed heart failure, the use of glycosides is indicated. In case of mild severity of the defect and absence of symptoms, drug therapy is not required.

Therapeutic actions

For moderate to severe mitral regurgitation, surgical intervention is required.

In the terminal stage, surgery is not performed. The most common procedures are plastic surgery or prosthetics. This treatment is aimed at preserving the heart valves. Plastic surgery is indicated in the following situations:

with prolapse of the bicuspid valve;
when the structures of the valve apparatus rupture;
when the valve ring expands;
with relative insufficiency of the bicuspid valve.

Surgical treatment is also carried out if a woman plans to have children. Prosthetics are organized when plastic surgery is ineffective or when there are gross changes. After installation of prostheses, you need to take indirect anticoagulants. Possible complications after surgery include the development of atrioventricular block, thromboembolism, and secondary infective endocarditis.

If complications (pulmonary edema) develop in the later stages, then additional drug therapy is carried out. In case of swelling, oxygen supply is indicated. Diuretics and nitrates are used. For high blood pressure, antihypertensive drugs are prescribed. The prognosis for life and health is determined by the degree of regurgitation, the person’s age and the presence of concomitant pathology.

If all doctor's recommendations are followed, the five-year survival rate reaches 80%. 6 out of 10 people live 10 years or more. The worst prognosis is observed with the ischemic form of mitral regurgitation. With a defect of mild to moderate severity, sick women can carry a child and give birth. Thus, disruption of the bicuspid heart valve is a dangerous condition that causes heart failure and early death of patients.

Normally, in a healthy person, the mitral valve completely closes the opening between the left ventricle and the atrium to prevent backflow of blood. If the valve is defective, the hole does not close completely and leaves a gap. During the systole phase, blood flows back into the left atrium (the phenomenon of regurgitation), where its volume and pressure increase. After this, blood enters the left ventricle, and volume and pressure there also increase.

Description and causes of pathology

This pathology affects adults more than children. Often mitral regurgitation is accompanied by blood vessel defects and stenoses (compression of the lumen). It is extremely rare in its pure form.

This defect is less often congenital and more often acquired. Degenerative changes in some cases affect the tissues of the leaflets and valve and the structures underneath it. In others, the chords are affected and the valve ring is overextended.

Some of the causes of acute mitral valve insufficiency are acute myocardial infarction, severe blunt trauma to the heart, or endocarditis of infectious origin. With these diseases, the papillary muscles, chordae tendons are torn, and the valve leaflets are torn off.

Other causes of mitral insufficiency:

joint inflammation;
restrictive cardiomyopathy;
some autoimmune diseases.

With all these systemic diseases, chronic mitral valve insufficiency is observed. Genetic diseases with chromosomal mutations, accompanied by connective tissue defects of a systemic nature, lead to mitral valve insufficiency.

Ischemic valve dysfunction occurs in 10% of cases of post-infarction cardiac sclerosis. Prolapses, tears or shortening of the mitral valve with lengthening of the chordae tendons and papillary or papillary muscles also lead to mitral regurgitation.

Relative mitral valve regurgitation can occur without its structural changes as a result of dilation of the left ventricle and the fibrous ring. This can happen when:

dilated cardiomyopathy;
coronary heart disease;
cardiac aortic defects;
myocarditis.

Very rarely, mitral valve insufficiency is a consequence of calcification of the valve leaflets or hypertrophic myopathy.

Congenital mitral regurgitation is characterized by the presence of the following diseases:

parachute valve deformation;
splitting of the mitral valves;
artificial fenestration.

Symptoms of heart valve pathology

Symptoms of this pathological process increase as the deficiency develops. During a period of compensated mitral valve regurgitation, symptoms may not appear. This stage can last a long time (up to several years) without any symptoms.

Subcompensated degree of deficiency is accompanied by:

the patient develops shortness of breath;
rapid fatigue appears during physical and mental work;
weakness;
rapid heartbeat even at rest;
dry cough and hemoptysis.

In the process of development of stagnation in the venous circulation, cardiac asthma develops, manifested in the form of a night cough, the patient “does not have enough air.” Patients complain of pain behind the sternum in the region of the heart, radiating to the left shoulder, forearm, scapula and hand (anginal pain).

With the further course of the pathology, failure of the right ventricle of the heart develops. Symptoms such as:

acrocyanosis - blueness of the extremities;
swelling of the legs and arms;
the veins of the neck swell;
Ascites (accumulation of fluid in the abdominal cavity) develops.

On palpation, an enlarged liver is felt. The enlarged atrium and pulmonary trunk compress the laryngeal nerve, resulting in hoarseness - Ortner's syndrome.

In the decompensated stage, a greater number of patients are diagnosed with atrial fibrillation.

Types of mitral valve pathologies

Depending on the course of the pathological process, acute or chronic mitral insufficiency occurs.

For reasons of occurrence, there are ischemic and non-ischemic mitral valve insufficiency.

If pathology is observed on the part of the valve structure, then they speak of organic mitral regurgitation. In this case, the lesions affect either the valve itself or the threads of the tendons that fix it.

In diseases of the heart muscle, dilatation of the left ventricle may occur due to hemodynamic overstrain. As a result, relative or functional mitral valve insufficiency develops.

Degrees of the disease

Depending on the size of the lumen and the severity of regurgitation, the clinical degrees of manifestation of mitral regurgitation are determined:

Mitral valve insufficiency of the 1st degree - compensated - is characterized by insignificant blood flow (less than 25%) and disturbances only in the valve structure. The state of health does not change, there are no symptoms or complaints. ECG diagnostics does not reveal pathology to this extent. During auscultation, the cardiologist hears slight noises during systole when the valve leaflets close; the boundaries of the heart are slightly wider than normal.
Mitral regurgitation of the 2nd degree, subcompensated, is characterized by filling the atrium with blood to almost half (up to 25-50%). To empty the atrium of blood, pulmonary hypertension develops. A person at this moment suffers from shortness of breath, tachycardia even during rest, and a dry cough. ECG diagnoses changes in the atrium. During auscultation, murmurs are detected during systole, the boundaries of the heart increase, especially on the left (up to 2 cm).
Mitral valve insufficiency of the 3rd degree is accompanied by filling of the left atrium with blood up to 90%. Its walls increase in size. The decompensated stage begins, in which blood is not removed from the atrium. Symptoms such as swelling and an increase in the size of the liver upon palpation appear. There is an increase in venous pressure. ECG signs are diagnosed: enlargement of the left ventricle, mitral wave. On auscultation - increased murmurs in systole, expansion of the cardiac boundaries, especially the left one.
Grade 4 mitral insufficiency is called dystrophic. Pathological structural changes in the valve and blood stagnation in the pulmonary circulation occur. Symptoms of the third degree increase significantly. Surgical operations are very widely used at this stage and provide favorable resolution.
5th degree – terminal. Patients present with a clinical picture of the third stage of cardiovascular failure. The patient's condition is very serious and does not allow surgical interventions. The prognosis for the course of the pathology is extremely unfavorable, most often it is death due to complications.

Diagnosis of mitral valve pathology

Diagnosis of mitral regurgitation should be based on the following comprehensive measures:

conversation, examination, palpation and percussion, auscultation of the patient;
ECG (electrocardiogram) data;
chest x-ray data;
echocardiography data;
cardiac ultrasound data;
results of probing of the cardiac cavities;
Ventriculography data.

Competent history taking during a thorough questioning, examination, palpation and percussion of the patient can coordinate the doctor for further research for an accurate diagnosis. Percussion reveals the expanded borders of the heart, especially on the left side. During auscultation, depending on the degree of mitral insufficiency, systolic murmurs of varying intensity are detected.

According to X-ray and ECG data, dilation of the left ventricle and atrium is diagnosed.

The most informative diagnostic method is echocardiography, here you can evaluate the defect and the degree of damage to the valve itself. For a more specific diagnosis in the presence of atrial fibrillation, transnutritive echocardiography is used.

Treatment of cardiac pathology

In case of mitral valve insufficiency, treatment should only be prescribed by a cardiologist. You cannot self-medicate and resort to traditional methods!

Treatment should be aimed at eliminating the cause that caused mitral regurgitation, that is, at the disease preceding the pathological process.

Depending on the degree of mitral regurgitation and the severity of the condition, drug treatment may be carried out; in some cases, surgery is necessary.

Mild and moderate degrees require the use of medications, the action of which is aimed at reducing the heart rate, vasodilators (vasodilators). It is important to lead a healthy lifestyle, not drink or smoke, and avoid states of physiological fatigue and psychological stress. Outdoor walks are shown.

In case of mitral valve insufficiency of the 2nd degree, as well as in the third, lifelong anticoagulants are prescribed to prevent vascular thrombosis.

Surgical solution to the problem

Starting from the third degree, with obvious pathological changes, they resort to surgical restoration of the valve. This should be done as early as possible to prevent irreversible degenerative changes in the left ventricle.

The following indications for surgery exist:

the reverse outflow of blood accounts for more than 40% of the blood ejected by the heart;
there is no positive effect in the treatment of infectious endocarditis;
irreversible sclerotic changes in the mitral valve;
severe dilatation of the right ventricle, systole dysfunction;
vascular thromboembolism (one or many).

Reconstructive operations are performed on the valve leaflets and its ring. If such an operation is impossible, then the valve is reconstructed - removing the damaged one and replacing it with an artificial one.

Modern medicine uses the most high-tech xenopericardial and synthetic materials for mitral valve replacement. There are also mechanical prostheses that are made from special metal alloys. Biological prostheses involve the use of animal tissue.

In the postoperative period, the risk of thromboembolism increases, so appropriate medications are prescribed. In rare cases, damage to the prosthetic valve occurs, then another operation is performed and a second synthetic valve is installed to replace it.

Prognosis and prevention

A favorable prognosis for grade 1-2 mitral regurgitation is given in almost 100% of cases. The patient can maintain his ability to work for many years. It is important to be under the supervision of specialists, undergo consultations and diagnostic examinations. During such phases of the disease, even pregnancy and bearing a child are allowed. Permission to deliver in these cases is carried out by performing a Caesarean section.

More severe pathological changes with insufficiency lead to severe disorders of the circulatory system as a whole. Unfavorable prognosis is usually assumed when chronic heart failure is associated with the disease. Mortality rates for this category are quite high.

Mitral regurgitation is a serious defect, so its identification, diagnosis, and treatment should not be delayed.

The main preventative measures for this pathology are aimed at preventing the development of complications. First of all, this:

healthy lifestyle of the patient;
moderation in food;
refusal of fatty and spicy foods;
giving up alcohol and smoking.

Primary prevention begins in childhood and includes elements such as hardening, timely treatment of infectious diseases, including dental caries and inflammatory diseases of the tonsils.

Secondary prevention involves taking medications that dilate blood vessels (vasodilators), improve blood flow, and lower blood pressure.

Mitral regurgitation can recur even after surgery. Therefore, you need to take care of yourself, take all medications prescribed by the doctor, and follow his advice.

Return blood flow in the left chambers of the heart disrupts normal pumping function. Mitral valve insufficiency of the 1st degree is manifested by minimal symptoms that do not create difficulties for everyday life. As valvular insufficiency worsens, clinical manifestations increase, which requires a full range of therapeutic and diagnostic procedures. Treatment tactics and prognosis for life depend on the stage of the disease and the presence of cardiac complications.

Causes of valve pathology

Regurgitation is a state of blood circulation when, against the background of a malfunction of the valve apparatus, the possibility of non-physiological reflux of blood back into the atrium arises (we wrote more about regurgitation in the article:). The main reasons for the malfunction of the mitral valve are the following factors:

rheumatic disease;
cardiac defects of congenital origin;
infectious-septic endocarditis;
ischemia of the heart muscle (CHD);
systemic types of pathology (scleroderma, arthritis, lupus);
traumatic damage to smooth muscle tissue or chordae tendineae;
cardiovascular diseases contributing to left ventricular dilatation.

The most common cause of pathology is infection. Cicatricial post-inflammatory changes in the valve between the atrium and the ventricle form regurgitant blood flow and the main manifestations of the disease.

Causes of mitral insufficiency

Types of disease

Depending on the causative factors, there are 2 groups of mitral valve pathology:

rheumatic origin (direct damaging effect on the valve);
non-rheumatic pathology (pathological changes in the perivalvular structures - tendon cords, muscle tissue or valve ring).

It is important to distinguish the anatomical and functional type of cardiac pathology. In the first case, regurgitation occurs against the background of organic changes in the valve. The second option is relative insufficiency caused by overstretching (dilatation) of the valve ring due to myocarditis, or coronary artery disease.

Depending on the severity of symptoms, there are 3 successive stages of the disease:

Compensatory (1st degree) – minimal manifestations of the disease;
Mitral valve insufficiency of the 2nd degree (subcompensation) - problems arise during physical activity;
Decompensation (grade 3) – symptoms appear at rest.

Hemodynamic changes caused by the anatomical defect of the valve are of great importance for clinical manifestations. At the initial stage of the disease, when an increased amount of blood enters the left atrium (inflow from the veins and regurgitation), compensatory hypertrophy occurs, ensuring the absence of pronounced symptoms. Then the cardiac muscle of the left ventricle hypertrophies, which has to work hard to ensure adequate blood flow to the aorta.

Stage 3 decompensation or mitral valve insufficiency occurs when the heart is unable to provide systemic blood flow.

Symptoms of valve insufficiency

The long-term absence of manifestations of the disease is due to slow organic changes and compensatory capabilities of the heart muscle. Primary signs of mitral valve insufficiency occur against the background of a serious unexpected load and are manifested by the following complaints:

severe lack of air (shortness of breath);
severe weakness with rapid fatigue;

As the insufficiency of the mitral valve function increases, the symptoms intensify: swelling of the legs occurs, suffocation, coughing and shortness of breath in the absence of movement can be bothersome.

The prognosis for recovery depends on the timeliness of visiting a doctor - it is optimal to start therapy at the stage of a compensated type of pathology.

Diagnostic principles

Listening to heart sounds (auscultation) during the initial examination will allow the doctor to suggest the presence of pathology. Typical auscultatory signs include:

pansystolic murmur;
weakening or absence of the first tone;
third tone, the presence of which indicates severe regurgitation;
accent of the second tone over the pulmonary artery.

An experienced specialist, having assessed auscultatory signs, will make a preliminary diagnosis and refer for additional examination:

Electrocardiography, which can reveal signs;
X-ray of the chest area (detecting an enlarged heart, identifying signs of pulmonary hypertension and valve);
Echocardiography with Doppler (assessment of anatomical changes, detection of regurgitant blood flow);
Contrast angiocardiography (the optimal and most reliable method for diagnosing pathology).

Cardiac ultrasound can assess the severity of mitral regurgitation.

When compensated, the following ultrasound signs will be typical:

reverse cast no more than 30%;
the area of the valve defect is no more than 0.2 cm2;
regurgitant blood does not reach the middle of the atrium.

Against the background of subcompensation:

return blood flow reaches the middle of the atrium and is up to 50%;
the area of the unclosed hole is 0.2-0.4 cm2.

With decompensation, regurgitant reflux exceeds 50%, blood fills the entire atrium, and the valve defect is more than 0.4 cm 2.

An important factor for choosing treatment tactics is to identify the cause of valve pathology: Therapy for rheumatic lesions differs from functional disorders associated with myocarditis or the consequences of coronary artery disease.

Treatment tactics

The choice of therapy method is determined by the following criteria:

causative factor of valve pathology;
stage of the disease;
the presence of concomitant diseases (hypertension, ischemic heart disease, endocrine pathology, atherosclerosis).

In case of insufficiency of mitral valve function, treatment can be medicinal and surgical.

Conservative methods

The main goals of therapy are to reduce the load on the left chambers of the heart and prevent complications. The following methods are used for this:

antibiotic therapy;
antimicrobial prevention of endocarditis and relapses of rheumatism;
limiting physical activity;
diet therapy with salt restriction;
anticoagulants;
symptomatic drugs (hypotensive, diuretic, and cardiac glycosides).

It is necessary to regularly see a doctor even if there are no symptoms during the initial stage of mitral regurgitation.

Surgery

Against the background of decompensation with a pronounced degree of regurgitation, when drug therapy is ineffective, 2 surgical treatment options are used:

reconstructive valve surgery;
valve replacement.

The choice of method is individual - for each specific patient, a different version of the operation is selected. The prognosis largely depends on the timeliness of the surgical intervention performed. Possible postoperative complications include septic endocarditis, thromboembolism, and prosthetic malfunction.

Risk of dangerous complications

Against the background of effective therapy and in the long-term postoperative period, unpleasant consequences and illnesses are possible. Dangerous complications of the rheumatic variant of valvular insufficiency are the following pathologies:

left ventricular congestive heart failure;
septic endocarditis;
pulmonary heart with typical;
vascular thromboembolism with a high risk of sudden death.

After valve surgery, the prognosis is better and the risk of complications is lower than when using an artificial valve prosthesis.

The main factor in the occurrence of regurgitant blood flow in the left chambers of the heart is rheumatic damage to the valve apparatus.

At the beginning of the disease there are no symptoms, but as the disease progresses and the backflow of blood into the left atrium increases, the manifestations of cardiac pathology increase.

The basis of primary diagnosis is ECG and echocardiography. In difficult cases, the doctor will refer you for a contrast study (angiocardiography). Drug treatment will be effective if the disease is detected early. Against the background of decompensation, surgery will be required to restore the functions of the valve apparatus.