Mitral heart defects and pulmonary hypertension in the practice of a rheumatologist and therapist (Lecture No. 2. Mitral regurgitation. Modern issues of diagnosis and treatment)

Aortic regurgitation is mistakenly taken to be the name of the disease. Some are even trying to find an analogue in the ICD due to lesions of the aortic valves of various natures. Regurgitation is a physical phenomenon caused by the return of fluid flow. When applied to the aorta, it is the reverse flow of blood into the left ventricle. This is the meaning given to the term in functional diagnostics.

If previously experienced doctors could indicate this process only from a subjective point of view (as a result of auscultation and determination of the characteristic noise on the aorta), then with the introduction of ultrasound examination of the heart into practice, it became possible to see the movement of blood in the opposite direction. And the Doppler ultrasound method made it possible to assess the degree of return and connect this diagnostic sign to solving the problem of choosing a treatment method.

Prevalence

Patients with aortic regurgitation are recorded only in functional diagnostic rooms. Therefore, prevalence can be judged in relation to the number of Doppler-examined patients rather than in relation to the total population.

Various degrees and signs of reverse blood flow through the aortic opening are found in 8.5% of examined women and 13% of men. Among all heart defects in adults, chronic aortic regurgitation is detected in every tenth patient. Most often in old age in men.

List of sources

• L.A. Boqueria, O.L. Bockeria, E.R. Jobava review article “Functional mitral regurgitation in atrial fibrillation”, 2015
• Mashina T.V., Golukhova E.Z. Left ventricular diastolic dysfunction in patients with atrial fibrillation: pathogenetic mechanisms and modern ultrasound assessment methods (analytical review). Creative cardiology. 2014
• Karpova N.Yu., Rashid M.A., Kazakova T.V. , Shostak N.A. Aortic regurgitation, Regular issues of “RMZh” No. 12 from 06/02/2014

What anatomical structures are involved in the formation of regurgitation?

The structure of the four chambers of the heart ensures normal filling of the ventricles (blood flows from the atria) and active ejection into the aorta from the left ventricle, and into the pulmonary artery from the right. The valve system between the cavities and main vessels forms a natural barrier to the return flow.

View of an unclosed aortic opening when the heart is stopped, when valve replacement is required

The physiology of valves, their structure, and muscle bundles for tension react to blood pressure and obey nerve impulses that control the functions of the heart. Any violations of the structure and structure contribute to incomplete closure of the valves. The blood, having passed through the hole, is directed back.

The heart has 4 types of valves between:

• atria and ventricles on the left and right;
• left ventricle and aorta;
• right ventricle and pulmonary artery.

Accordingly, depending on the location of the lesion, mitral regurgitation, return through the tricuspid valve, and incompetence of the valves in the pulmonary artery are possible.

Aortic regurgitation seems to be a special case of dysfunction of the valve apparatus.

Pathogenesis

The heart is a muscular, hollow organ consisting of 4 chambers: 2 atria and 2 ventricles. The right and left parts of the heart are separated by a septum. Blood enters the ventricles from the atria, and is then pushed out through the vessels: from the right sections - into the pulmonary artery and pulmonary circulation, from the left sections - into the aorta and systemic circulation.

The structure of the heart includes 4 valves that determine the flow of blood. The tricuspid valve is located in the right half of the heart between the ventricle and the atrium the mitral is located in the left half . The pulmonary valve and are located on the vessels leaving the ventricles .

Normally, the valve flaps regulate the direction of blood flow, close and prevent reverse flow. When the shape of the valves, their structure, elasticity, and mobility change, the complete closure of the valve ring is disrupted, and some of the blood is thrown back and regurgitates.

Mitral regurgitation

Mitral regurgitation occurs as a result of functional valve insufficiency. When the ventricle contracts, part of the blood flows back into the left atrium. At the same time, blood flows there through the pulmonary veins. All this leads to overfilling of the atrium and stretching of its walls. During the subsequent contraction, the ventricle ejects a larger volume of blood and thereby overloads the remaining cavities of the heart. Initially, the muscular organ reacts to overload with hypertrophy , and then with atrophy and stretching - dilatation . To compensate for the loss of pressure, the vessels are forced to narrow, thereby increasing peripheral resistance to blood flow. But this mechanism only aggravates the situation, because regurgitation intensifies and right ventricular failure . At the initial stages, the patient may not make any complaints and not feel any changes in his body due to the compensatory mechanism, namely, a change in the configuration of the heart, its shape.

Mitral valve regurgitation can develop due to calcium and cholesterol on the coronary arteries, due to dysfunction of the valves, heart disease, autoimmune processes, changes in metabolism , and ischemia of certain areas of the body. Mitral regurgitation manifests itself differently depending on the degree. Minimal mitral regurgitation may not manifest itself clinically.

What is grade 1 mitral regurgitation? The diagnosis is established if the backflow of blood into the left atrium extends to 2 cm. Stage 2 is said if the pathological flow of blood in the opposite direction reaches almost half of the left atrium. Grade 3 is characterized by reflux beyond half of the left atrium. At grade 4, the flow of reverse blood reaches the left atrial appendage and can even enter the pulmonary vein.

Aortic regurgitation

When the aortic valves fail, part of the blood returns during diastole back to the left ventricle. The large circulation suffers from this , since a smaller volume of blood enters it. The first compensatory mechanism is hypertrophy, the walls of the ventricle thicken.

Muscle mass, which has increased in volume, requires more nutrition and oxygen flow. The coronary arteries cannot cope with this task and the tissues begin to starve, hypoxia . Gradually, the muscle layer is replaced by connective tissue, which is unable to perform all the functions of the muscular organ. Cardiosclerosis develops , heart failure progresses.

As the aortic annulus expands, the valve also enlarges, which ultimately leads to the fact that the aortic valve leaflets cannot fully close and close the valve. There is a reverse flow of blood into the ventricle, when it is refilled, the walls stretch and a lot of blood begins to flow into the cavity, and little into the aorta. Compensatoryly, the heart begins to contract more often, all this leads to oxygen starvation and hypoxia , stagnation of blood in large-caliber vessels.

Aortic regurgitation is classified by degree:

• 1st degree: reverse blood flow does not extend beyond the boundaries of the outflow tract of the left ventricle;
• 2 degrees: the blood stream reaches the anterior leaflet of the mitral valve;
• 3 degrees: the jet reaches the boundaries of the papillary muscles;
• 4 degrees: reaches the wall of the left ventricle.

Tricuspid regurgitation

Tricuspid valve insufficiency is most often secondary in nature and is associated with pathological changes in the left parts of the heart. The mechanism of development is associated with an increase in pressure in the pulmonary circulation, which creates an obstacle to sufficient release of blood into the pulmonary artery from the right ventricle. Regurgitation may develop due to primary tricuspid valve incompetence. Occurs when pressure in the pulmonary circulation increases.

Tricuspid regurgitation can lead to emptying of the right side of the heart and congestion in the venous system of the systemic circulation. Externally it manifests itself as swelling of the neck veins and bluish discoloration of the skin. Atrial fibrillation may develop , and the liver may increase in size. Also classified by degree:

• Tricuspid valve regurgitation grade 1. Tricuspid regurgitation of the 1st degree is a minor reflux of blood that does not manifest itself clinically and does not affect the general well-being of the patient.
• Tricuspid valve regurgitation of the 2nd degree is characterized by the reflux of blood at a distance of 2 cm or less from the valve itself.
• Grade 3 is characterized by throwing more than 2 cm from the tricuspid valve.
• At grade 4, the reflux of blood spreads over a long distance.

Pulmonary regurgitation

If the pulmonary valves do not close properly during diastole, the blood partially returns to the right ventricle. At first, only the ventricle is overloaded due to excessive blood flow, then the load increases on the right atrium. Signs of heart failure gradually increase, and venous congestion .

Pulmonary artery regurgitation or pulmonary regurgitation is observed with endocarditis , atherosclerosis , syphilis , and maybe congenital. Most often, diseases of the pulmonary system are simultaneously recorded. Blood reflux occurs due to incomplete closure of the valve in the artery of the pulmonary circulation.

Pulmonary regurgitation is classified by degree:

• Pulmonary regurgitation grade 1. It does not manifest itself clinically; upon examination, a slight backflow of blood is detected. Grade 1 regurgitation does not require specific treatment.
• Pulmonary regurgitation of the 2nd degree is characterized by the reflux of blood up to 2 cm from the valve.
• Grade 3 is characterized by a throw of 2 cm or more.
• At grade 4, there is a significant reflux of blood.

The mechanism of regurgitation in normal and pathological conditions

Cardiologists identify minor physiological regurgitation, which is possible under normal conditions. For example, 70% of tall adults have incomplete closure of the tricuspid valve, which the person is not aware of. Ultrasound reveals slight swirling flows when the valves are completely closed. This does not affect general blood circulation.

Pathology occurs during inflammatory processes:

• rheumatism,
• infective endocarditis.

Most typical for mitral localization, the formation of heart disease. It should not be confused with prolapse (stretching and bending of the valves into the atrium). It is with prolapse that physiological regurgitation often occurs and is found in growing children and adolescents. It is taken into account as a possible cause of extrasystole. The child must be observed by a cardiologist and re-examined. No special treatment is required.

The formation of scars after an acute heart attack, against the background of cardiosclerosis, in the area approaching the valve leaflets and threads, leads to breakdown of the necessary tension mechanism and changes the shape of the leaflets. Therefore, they do not completely close.

In a pathological process, an equally significant role is played by the diameter of the outlet, which must be blocked. Significant enlargement due to left ventricular dilatation or hypertrophy prevents the tight junction of the aortic valve leaflets.

Main valvular causes of aortic regurgitation

The causes of damage to the aortic valves, the diameter of the hole between the left ventricle and the initial part of the aorta, are:

• rheumatic inflammation localized along the line of valve closure - tissue infiltration at the initial stage leads to wrinkling of the valves, forming a hole in the center for the passage of blood during systole into the cavity of the left ventricle;
• bacterial sepsis with damage to the endocardium and aortic arch;
• warty and ulcerative endocarditis in severe forms of infection (typhoid fever, influenza, measles, scarlet fever), pneumonia, cancer intoxication (myxoma) - the valves are completely destroyed;
• congenital defects (formation of two leaflets instead of three) involving the aorta, large ventricular septal defect;
• specific autoimmune processes in the ascending aorta in chronic syphilis, ankylosing spondylitis, rheumatoid polyarthritis;
• hypertension, atherosclerosis - the process of compaction of the valves with the deposition of calcium salts, expansion of the ring due to dilatation of the aorta;
• consequences of myocardial infarction;
• cardiomyopathy;
• chest injuries with rupture of the muscles that contract the valves.

Bicuspid aortic valve is considered a type of congenital defect and increases the risk of regurgitation

The reasons include complications of treatment of heart diseases using catheter radiofrequency ablation, as well as cases of destruction of the biological valve prosthesis.

Causes associated with aortic damage

The portion of the aortic arch closest to the heart is called the aortic root. It is its structure that influences the “health of the valves” and the width of the gate ring from the left ventricle. Root lesions include:

• age-related or degenerative changes causing dilatation;
• cystic necrosis of the middle layer of the aorta in Marfan syndrome;
• dissection of the aneurysm wall;
• inflammation (aortitis) with syphilis, psoriatic arthritis, ankylosing spondylitis, ulcerative colitis;
• giant cell arteritis;
• malignant hypertension.

Among the reasons, a negative effect of drugs used to reduce appetite in obesity was found.

Consequences of aortic regurgitation

The return of blood to the left ventricle inevitably leads to its expansion and increase in volume. Possible expansion of the mitral annulus and further enlargement of the left atrium.

At the point of contact of the blood flow, “pockets” are formed on the endocardium. The greater the degree of regurgitation, the faster the left ventricular overload develops.

Studies have shown the meaning of heart rate:

• bradycardia increases the volume of return flow and promotes decompensation;
• tachycardia reduces regurgitation and causes greater adaptation.

conclusions

Regurgitation in the bicuspid valve occurs due to the inability of its leaflets to close tightly during systole. The danger of reverse blood flow is the expansion of the cavities of the heart and their excessive filling with blood. To support the pumping function, the myocardium hypertrophies compensatoryly. The heart muscle is not adapted for long-term stress of this degree, so decompensation occurs, expressed in characteristic clinical symptoms, the earliest of which is shortness of breath.

The gold standard for diagnosing regurgitation is Doppler ultrasound of the heart. Stages 3 and 4 of mitral regurgitation are subject to surgical treatment.

Forms of aortic regurgitation

It is customary to distinguish between acute and chronic aortic regurgitation.

Features of the acute form

Typical causes of acute aortic regurgitation are:

• injuries;
• dissecting aneurysm;
• infective endocarditis.

The volume of blood entering the left ventricle during diastole increases suddenly. Adaptation mechanisms do not have time to develop. The load on the left side of the heart and myocardial weakness increases sharply. Insufficient blood volume is released into the aorta to support general circulation.

Patients develop signs of pulmonary edema and cardiogenic shock. Symptoms are very severe when hypertension and aortic aneurysm dissection are combined.

Features of chronic aortic regurgitation

A distinctive feature of the chronic form is sufficient time for the full activation of compensatory mechanisms and adaptation of the left ventricle. This causes a period of compensation for circulatory disorders. Myocardial hypertrophy helps compensate for the reduced output.

When reserve energy reserves are depleted, a stage of decompensation occurs with severe heart failure.

3. Symptoms of the disease

Chronic mitral regurgitation is characterized by the absence of symptoms for many years. As a rule, patients do not know about heart disease for a long time, the symptoms of which appear gradually. The acute form of regurgitation is much more serious and is accompanied by the same symptoms as cardiogenic shock and acute heart failure.

We list the main symptoms of mitral valve regurgitation:

• constant shortness of breath;
• weakness and increased fatigue;
• dizziness;
• pain in the chest;
• confusion;
• swelling of the lower extremities.

If you notice at least two of the above symptoms, be sure to contact a good cardiologist. You may need immediate treatment.

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Clinical manifestations

In the acute form of aortic regurgitation, the patient suddenly exhibits signs of cardiogenic shock:

• severe weakness;
• pale skin;
• severe hypotension;
• dyspnea.

For pulmonary edema:

• the patient is suffocating;
• breathing is noisy and hoarse;
• when coughing, foamy sputum mixed with blood is released;
• face, lips, limbs are cyanotic;
• heart sounds are sharply muffled;
• A lot of moist rales are heard in the lungs.

With chronic aortic regurgitation, a long asymptomatic period is possible. Symptoms appear only with the development of myocardial ischemia and severe cardiac decompensation. The patient notes:

• shortness of breath on exertion;
• strong heartbeats;
• extrasystoles;
• angina attacks at night;
• a “cardiac asthma” clinic is possible.

During the examination, the doctor notes:

• shaking the head in rhythm with the pulsation of the heart;
• a typical pulse on the radial artery is a sharp shock wave and an immediate fall;
• trembling when palpating the chest at the base of the heart;
• expansion of the left cardiac border;
• pulsating carotid arteries;
• diastolic murmur on the aorta, along the left edge of the sternum in the third and fourth intercostal spaces, is better heard in a sitting position with a slight bend forward, the first sound is clapping.

Diagnostic methods

Indirect signs of aortic regurgitation are noted in:

1. chest x-ray - the left contour of the cardiac shadow is expanded to the side and down, the expansion of the aortic arch is similar to an aneurysm, there are clear signs of enlargement of the left atrium, calcifications may be detected in the aortic arch;
2. electrocardiogram - overload of the left chambers of the heart is revealed.

Deviation of the electrical axis to the left, a characteristic change in the shape of the ventricular complexes in leads I, AVL, V3-V6, negative T waves

Echocardiographic method

In the diagnosis of regurgitation, echocardiography serves as the main objective method; it allows one to determine the cause, the degree of regurgitation, the sufficiency of compensatory reserves, and circulatory disorders even in the asymptomatic stage of the disease with minimal disturbances. It is recommended for patients in the initial stage annually, and twice a year when clinical symptoms appear.

The calculations take into account the surface area of ​​the patient's body, due to the lack of pronounced expansion of the ventricular chamber in short people.

The most commonly used mode is color Doppler scanning. The sensors are installed in such a way as to measure the area of ​​blood flow at the aortic valves, in the initial part of the aorta, and compare it with the width of the passage. In severe cases, it exceeds 60% of the ring diameter.

The device allows you to record the time interval of the wave and establish the expansion of the left ventricle

In the practice of cardiologists, a division of the return jet into 4 degrees is used in relation to its length to the size and internal formations of the left ventricle:

• 1 - does not extend beyond half the length of the anterior leaflet at the mitral valve;
• 2 - reaches or crosses the gate;
• 3 - the flow value approaches half the length of the ventricle;
• 4 - the jet touches the top.

The definition of regurgitation depends on the area (width) of the jet, its location, the level of loss of blood ejection from the left ventricle, and the volume per contraction. Based on quantitative indicators, they are conventionally divided into mild, moderate and severe forms.

If information from Doppler sonography is not enough, the following is carried out:

• magnetic resonance imaging;
• radionuclide angiography;
• cardiac catheterization.

4. Diagnosis and treatment of mitral valve regurgitation

Diagnosis of mitral valve regurgitation may include:

• medical examination;
• echocardiogram - a procedure based on the use of sound waves to determine the shape, size and structure of heart tissue;
• chest x-ray;
• electrocardiogram of the heart, which allows to detect irregularities in the heart rhythm;
• cardiac catheterization - examination of the cavities of the heart, as well as nearby blood vessels, using a hollow flexible tube.

These tests not only detect mitral regurgitation, but also determine the degree of mitral regurgitation. The information obtained during the study is the basis on which further treatment is based.

The choice of treatment for mitral valve regurgitation depends primarily on the form of the disease, as well as the degree of its progression.

For example, in chronic cases, doctors most often prescribe constant monitoring of the patient’s heart condition and the use of special medications to eliminate the symptoms of the disease. These drugs include:

• vasodilators – a group of vasodilating drugs;
• diuretics and diuretics;
• anticoagulants - drugs that prevent the formation of blood clots.

If necessary, your doctor may recommend surgery to repair or replace the mitral valve. Patients with mitral regurgitation need to radically change their lifestyle in order to reduce the load on the heart. Doctors recommend avoiding intense physical activity and emotional stress, leading a healthy lifestyle and eating right.

Who is indicated for surgical treatment?

The only form of surgery is aortic valve replacement. The operation is indicated for:

• severe form of regurgitation with impaired left ventricular function;
• if the course is asymptomatic, with preserved ventricular function, but pronounced expansion (dilatation).

Aortic valve replacement surgery is often combined with coronary artery bypass grafting.

Forecast

The prognosis for the patient’s life depends on the underlying disease, the degree of regurgitation, and the form. An early mortality rate is typical for the acute development of pathology. In the chronic form, 75% of patients live more than 5 years, and half live 10 years or longer.

In the absence of timely surgical intervention, the development of heart failure is noted in the next 2 years.

Treatment of moderate clinical symptoms is accompanied by positive results in 90% of patients. This reinforces the importance of evaluating and monitoring patients with aortic regurgitation.

Procedures and operations

In cases of acute regurgitation, patients undergo emergency valve replacement. The modified valve is removed and an artificial one is installed in its place. In some cases, valve repair is sufficient. During the rehabilitation period, patients are prescribed medications that support normal cardiac activity: vasodilators and nootropics. In case of a chronic process, surgical interventions to replace the valve are also performed routinely as negative dynamics progress. In the absence of negative symptoms and stable EchoCG indicators, symptomatic therapy is prescribed.