Aortic insufficiency. Aortic valve: structure, mechanism of operation

Any heart defect is associated with valve abnormalities. Aortic valve defects are especially dangerous, since the aorta is the largest and most important artery in the body. And when the operation of the apparatus that supplies oxygen to all parts of the body and the brain is disrupted, the person is practically incapacitated.

The aortic valve is sometimes formed in utero with defects. And sometimes heart defects are acquired with age. But whatever the reason for the dysfunction of this valve, medicine has already found a treatment in such cases - aortic valve replacement.

Anatomy of the left side of the heart. Functions of the aortic valve

The four chamber structure of the heart must work in perfect harmony to perform its main function- provide the body with nutrients and air carried by the blood. Our main organ consists of two atria and two ventricles.

The right and left parts are separated by the interventricular septum. There are also 4 valves in the heart that regulate blood flow. They open in one direction and close tightly to allow blood to flow in only one direction.

The heart muscle has three layers: endocardium, myocardium (thick muscle layer) and endocardium (external). What happens in the heart? The depleted blood, which has given up all its oxygen, returns to the right ventricle. Arterial blood passes through the left ventricle. We will consider in detail only the left ventricle and the work of its main valve, the aortic.

The left ventricle is cone-shaped. It is thinner and narrower than the right one. The ventricle is connected to the left atrium through the atrioventricular orifice. The mitral valve leaflets are attached directly to the edges of the hole. The mitral valve is bicuspid.

The aortic valve (valve aortae) consists of 3 leaflets. The three valves are called: right, left and posterior semilunar (valvulae semilunares dextra, sinistra, posterior). The leaflets are formed by a well-developed duplication of the endocardium.

The atrium muscles are isolated from the ventricular muscles by a plate of right and left fibrous rings. The left fibrous ring (anulus fibrosus sinister) surrounds the atrioventricular foramen, but not completely. The anterior sections of the ring are attached to the aortic root.

How does it work left side hearts? Blood enters, the mitral valve closes, and an impulse occurs - contraction. Contraction of the heart walls pushes blood through the aortic valve into the widest artery, the aorta.

With each contraction of the ventricle, the valves are pressed against the walls of the vessel, allowing a free flow of oxygenated blood. When the left ventricle relaxes for a split second to allow the cavity to fill with blood again, the aortic valve of the heart closes. This is one cardiac cycle.

Congenital and acquired aortic valve defects

If problems arise with the aortic valve during the baby’s intrauterine development, it is difficult to notice. Usually the defect is noticed after birth, since the baby’s blood bypasses the valve, directly into the aorta through the open ductus arteriosus. Deviations in heart development can be noticed only through echocardiography, and only from 6 months.

The most common valve abnormality is the development of 2 leaflets instead of 3. This heart defect is called a bicuspid aortic valve. The anomaly is not in any danger to the child. But 2 sashes wear out faster. And by adulthood, maintenance therapy or surgery is sometimes needed. Less commonly, a defect such as a single-leaf valve occurs. Then the valve wears out even faster.

Another anomaly is congenital aortic valve stenosis. The semilunar valves either fuse together, or the valvular fibrous ring itself, to which they are attached, is excessively narrow. Then the pressure between the aorta and the ventricle differs. Over time, the stenosis intensifies. And interruptions in the work of the heart prevent the child from fully developing; it is difficult for him to exercise even in the school gym. Severe disruption of blood flow through the aorta may at some point lead to sudden death of the child.

Acquired defects are a consequence of smoking, excessive eating, sedentary and stressful lifestyle. Since everything in the body is connected, after 45-50 years all minor ailments usually develop into diseases. The aortic valve of the heart gradually wears out in old age, as it works constantly. Exploitation of your body's resources and lack of sleep wear out these important parts of the heart faster.

Aortic stenosis

What is stenosis in medicine? Stenosis means narrowing of the lumen of a vessel. Aortic stenosis is a narrowing of the valve that separates the left ventricle of the heart from the aorta. There are minor, moderate and severe. This defect can affect the mitral and aortic valves.

With a minor valve defect, a person does not feel any pain or other warning symptoms, because the increased work of the left ventricle will be able to compensate for the poor functioning of the valve for some time. Then, when the compensatory capabilities of the left ventricle are gradually exhausted, weakness and poor health begin.

The aorta is the main blood vessel. If the valve is malfunctioning, all vital organs will suffer from lack of blood supply.

The causes of heart valve stenosis are:

1. Congenital valve defect: fibrous membrane, bicuspid valve, narrow ring.
2. A scar formed by the connective tissue just below the valve.
3. Infectious endocarditis. Bacteria that enter the heart tissue change the tissue. Due to the colony of bacteria, connective tissue grows on the tissue and on the valves.
4. Deforming osteitis.
5. Autoimmune problems: rheumatoid arthritis, lupus erythematosus. Due to these diseases, connective tissue grows in the place where the valve is attached. Growths form on which more calcium is deposited. Calcification occurs, which we will remember later.
6. Atherosclerosis.

Unfortunately, in most cases, aortic stenosis is fatal if valve replacement is not performed in time.

Stages and symptoms of stenosis

Doctors distinguish 4 stages of stenosis. At first, there is practically no pain or discomfort. Each stage has a corresponding set of symptoms. And the more serious the stage of development of stenosis, the sooner surgery is needed.

• The first stage is called the compensation stage. The heart is still coping with the load. A deviation is considered minor when the valve lumen is 1.2 cm 2 or more. And the pressure is 10-35 mm. rt. Art. There are no symptoms at this stage of the disease.
• Subcompensations. The first symptoms appear immediately after exercise (shortness of breath, weakness, palpitations).
• Decompensation. It is characterized by the fact that symptoms appear not only after exercise, but also in a calm state.
• The last stage is called terminal. This is the stage when strong changes have already occurred in anatomical structure hearts.

Symptoms of severe stenosis are:

• pulmonary edema;
• dyspnea;
• sometimes attacks of suffocation, especially at night;
• pleurisy;
• cardiac cough;
• pain in the chest area.

Upon examination, the cardiologist usually detects moist rales in the lungs during listening. Pulse is weak. Noises are heard in the heart, vibration created by the turbulence of blood flows is felt.

Stenosis becomes critical when the lumen is only 0.7 cm2. The pressure is more than 80 mm. rt. Art. At this time, the risk of death is high. And even an operation to eliminate the defect is unlikely to change the situation. Therefore, it is better to consult a doctor during the subcompensatory period.

Development of calcification

This defect develops due to a degenerative process in the tissue of the aortic valve. Calcification can lead to severe heart failure, stroke, and general atherosclerosis. Gradually, the aortic valve leaflets become covered with calcareous growth. And the valve calcifies. That is, the valve flaps no longer close completely, but also open weakly. When a bicuspid aortic valve is formed at birth, calcification quickly renders it inoperable.

And also calcinosis develops as a consequence of malfunction endocrine system. Calcium salts, when they do not dissolve in the blood, accumulate on the walls of blood vessels and on the heart valves. Or a kidney problem. Polycystic kidney disease or nephritis also leads to calcification.

The main symptoms will be:

• aortic insufficiency;
• dilatation of the left ventricle (hypertrophy);
• interruptions in heart function.

A person must monitor his health. Chest pain and increasingly frequent periodic attacks of angina should be a signal to undergo a cardiac examination. Without surgery for calcinosis, in most cases a person dies within 5-6 years.

Aortic regurgitation

During diastole, blood from the left ventricle flows into the aorta under pressure. This is how the large circle of blood circulation begins. But with regurgitation, the valve “releases” blood back into the ventricle.

Valve regurgitation, or aortic valve regurgitation, in other words, has the same stages as valve stenosis. The reasons for this condition of the valves are either an aneurysm, or syphilis, or the mentioned acute rheumatism.

Symptoms of deficiency are:

• low pressure;
• dizziness;
• frequent fainting;
• swelling of the legs;
• slow heart rate.

Severe failure leads to angina and ventricular enlargement, as with stenosis. And such a patient also needs valve replacement surgery in the near future.

Valve seal

Stenosis can form due to the fact that endogenous factors cause the appearance of various growths on the valve leaflets. The aortic valve becomes compacted, and problems begin in its operation. The causes of hardening of the aortic valve can be many untreated diseases. For example:

• Autoimmune diseases.
• Infectious lesions (brucellosis, tuberculosis, sepsis).
• Hypertension. Due to prolonged hypertension, tissues become thicker and coarser. Therefore, over time, the lumen narrows.
• Atherosclerosis is the clogging of tissues with lipid plaques.

Tissue compaction is also a common sign of aging. The consequence of compaction will inevitably be stenosis and regurgitation.

Diagnostics

Initially, the patient must provide all the necessary information to make a diagnosis to the doctor in the form of an accurate description of the ailments. Based on the patient's medical history, the cardiologist prescribes diagnostic procedures for additional medical information.

Must be assigned:

• X-ray. The shadow of the left ventricle increases. This can be seen in the arc of the heart's contour. Signs of pulmonary hypertension are also visible.
• ECG. The examination reveals ventricular enlargement and arrhythmia.
• Echocardiography. On it, the doctor notices whether or not there is sealing of the valve flaps and thickening of the walls of the ventricle.
• Probing cavities. The cardiologist must know the exact value: how much the pressure in the aortic cavity differs from the pressure on the other side of the valve.
• Phonocardiography. Heart murmurs (systolic and diastolic murmurs) are recorded.
• Ventriculography. Prescribed to detect mitral valve insufficiency.

With stenosis, an electrocardiogram shows disturbances in the rhythm and conduction of biocurrents. On the x-ray you can clearly see signs of darkening. This indicates congestion in the lungs. You can clearly see how dilated the aorta and left ventricle are. And coronary angiography shows that the amount of blood ejected from the aorta is less. This is also an indirect sign of stenosis. But angiography is only done for people over 35 years old.

The cardiologist also pays attention to symptoms that are visible even without instruments. Pale skin, Musset's sign, Müller's sign - such signs indicate that the patient most likely has aortic valve insufficiency. Moreover, the bicuspid aortic valve is more susceptible to insufficiency. The doctor must take into account congenital characteristics.

What other signs can suggest a diagnosis to a cardiologist? If, while measuring pressure, the doctor notices that the upper pressure is much higher than normal, and the lower (diastolic) is too low, this is a reason to refer the patient for echocardiography and an x-ray. Extra noise during diastole, heard through a stethoscope, also does not bode well. This is also a sign of deficiency.

Treatment with drugs

For the treatment of insufficiency initial stage The following classes of drugs may be prescribed:

• peripheral vasodilators, which include nitroglycerin and its analogues;
• diuretics are prescribed only for certain indications;
• calcium channel blockers, such as Diltiazem.

If the pressure is very low, nitroglycerin preparations are combined with Dopamine. But beta blockers are contraindicated in cases of aortic valve insufficiency.

Aortic valve replacement

Surgeries to replace the aortic valve are now being carried out quite successfully. And with minimal risk.

During the operation, the heart is connected to a heart-lung machine. The patient is also given complete anesthesia. How can a surgeon perform this minimally invasive surgery? There are 2 ways:

1. The catheter is inserted directly into femoral vein and rises to the aorta against the flow of blood. The valve is secured and the tube is removed.
2. The new valve is inserted through an incision in the left chest. An artificial valve is inserted, and it slides into place, passing through the apical part of the heart, and is easily removed from the body.

Minimally invasive surgery is suitable for those patients who have concomitant diseases and open chest it is forbidden. And after such an operation, a person immediately feels relief, since the defects are eliminated. And if there are no complaints about your health, you can be discharged within a day.

It should be noted that artificial valves require constant use of anticoagulants. Mechanical ones can cause blood clotting. Therefore, after the operation, Warfarin is immediately prescribed. But there are also valves made from biological materials that are more suitable for humans. If a valve is installed from porcine pericardium, the drug is prescribed only for a few weeks after the operation, and then discontinued, as the tissue takes root well.

Aortic balloon valvuloplasty

Aortic balloon valvuloplasty is sometimes prescribed. This is a painless operation the latest developments. The doctor monitors all ongoing actions through special X-ray equipment. A catheter with a balloon is passed to the mouth of the aorta, then the balloon is installed in place of the valve and expanded. This eliminates the problem of valve stenosis.

Who is the operation indicated for? First of all, such an operation is performed on children with a congenital defect, when a single or bicuspid aortic valve is formed instead of a tricuspid one. It is indicated for pregnant women and people before another heart valve transplant.

After this operation, the recovery period is only 2 days to 2 weeks. Moreover, it is very easily tolerated and is suitable for people with poor health, and even for children.

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Normally, the AC consists of three crescents. In 0.5% of the population, a congenital bicuspid valve is found, which is prone to degenerative changes with the development of combined aortic disease in the form of regurgitation and stenosis (Fig. 1). In addition, these people have an increased risk of aortic dissection. A bicuspid valve can be diagnosed during a routine echocardiogram. In elderly patients, as well as with long-term arterial hypertension Focal sclerotic changes in the AC without significant obstruction often occur. Minimal aortic regurgitation is also common, especially in old age.

Rice. 1. Typical view of a congenital bicuspid aortic valve (parasternal cross-section). The arrow indicates the round shape of the valve opening

Aortic stenosis is the most common severe valvular heart disease in the European population and is an indication for surgical treatment. The disease begins with focal sclerosis, which, spreading, leads to severe thickening, calcification and immobility of the aortic semilunar cusps. These changes are well recognized by echocardiography. The presence of even mild aortic stenosis, in which only a slight acceleration of blood flow is noted (maximum speed ‹2.5 m/s), leads to a clear deterioration in the cardiovascular prognosis. Severe aortic stenosis (aortic orifice area <1.0 cm2 or area index <0.6 cm2) requires careful assessment of clinical symptoms or signs of deterioration in LV function, the appearance of which becomes an indication for aortic valve replacement. The most important EchoCG indicators characterizing the severity of aortic stenosis are the average and maximum gradients on the aortic valve, as well as the area of ​​the aortic opening, which is usually calculated using the blood flow continuity equation:

SАО = SLVOT × VTILVOT / VTI,

where SАО is the area of ​​the aortic opening; SLVOT is the cross-sectional area of ​​the LV outflow tract, calculated through its diameter D, as π × D2/4; VTILVOT - time integral of linear velocity in the LV outflow tract (calculated in pulsed Doppler mode); VTI is the time integral of the linear velocity of blood flow through the AV (calculated in constant-wave Doppler mode; Fig. 2).

Rice. 2. A - the principle of the flow continuity equation. From the law of conservation of mass it follows that the product of the cross-sectional area and the average flow velocity or the integral of its velocity (v) is constant for each section of the pipe, which is reflected in the equation of blood flow continuity in the upper left corner of the figure. The aortic orifice area is calculated by solving the equation for CSA2.

B - an example of using the blood flow continuity equation in severe aortic stenosis.

I) Aortic stenosis (arrow) in parasternal longitudinal section; note concentric LV hypertrophy.

II) Enlarged image of the AC region with measurement of the diameter of the LV outflow tract (D) at a distance of 2 cm from the AC annulus.

III) Recording of blood flow in the LV outflow tract in pulsed Doppler mode with calculation of the velocity integral over time (VTILVOT).

IV) Recording of blood flow through the AV in continuous wave Doppler mode with calculation of the velocity time integral (VTIAS). From the blood flow continuity equation, the aortic orifice area (A) is calculated using the formula: A = π × (D2/4) × VTILVOT / VTIAS, which is 0.6 cm2 and corresponds to severe stenosis.

Sometimes, especially with transesophageal echocardiography, the area of ​​the narrowed aortic opening can be determined directly by the planimetric method. It must be remembered that the area of ​​the aortic opening does not depend on stroke volume, therefore, in case of impaired LV function, it remains the only reliable indicator for assessing the severity of aortic stenosis.

Sometimes, in cases of severe LV dysfunction and suspected severe aortic stenosis, stress echocardiography with dobutamine helps clarify valve function and prognosis.

Among all valve defects, aortic regurgitation is the most difficult for EchoCG assessment of its severity. The causes of aortic regurgitation may be dilation of the ascending aorta (for example, with Marfan syndrome), valve calcification, infective endocarditis, degenerative changes such as prolapse, rheumatic disease, etc. The semi-quantitative severity of aortic regurgitation can be assessed in the following ways (Fig. 3):

• assessment of valve morphology and degree of LV enlargement;
• determination of the ratio of the width of the base of the regurgitation jet to the diameter of the LV outflow tract in the parasternal longitudinal section (≥65% - a sign of severe regurgitation);
• calculation of the half-life of the pressure gradient between the aorta and the LV from the flow of aortic regurgitation recorded in continuous-wave Doppler mode (half-life of the pressure gradient ‹250 ms - characteristic feature severe regurgitation);
• recording of holodiastolic reverse blood flow in the descending aorta (from the supraclavicular approach) with an end-diastole velocity >16 cm/s indicates severe regurgitation.

Rice. 3. Aortic regurgitation.

A - parasternal longitudinal section: the regurgitant jet (in diastole) occupies the entire outflow tract of the LV.

B - enlarged transesophageal long-axis image of the aortic valve: prolapse of the non-coronary aortic crescent (arrow).

B - aortic regurgitation in continuous wave Doppler mode. The white line indicates the slope corresponding to the decrease in the diastolic velocity of aortic regurgitation, from which the half-life of the pressure gradient between the aorta and LV can be determined.

D - pulsed Doppler study of blood flow in the descending aorta from the supraclavicular approach: a clear holodiastolic reverse flow (the arrow indicates reverse blood flow that continues until the end of diastole). VoA is the ascending aorta.

An important part of the examination of patients with moderate and severe aortic regurgitation is the assessment of LV function (size and EF) and the diameter of the ascending aorta.

Signs of damage to the aortic valve in infective endocarditis are vegetation, newly emerging aortic regurgitation, structural defects of the semilunar valves and the transition of the process to perivalvular tissue with the formation of para-aortic abscesses and fistulas (for example, between the aortic root and left atrium). Such complications are especially well recognized during transesophageal examination.

Frank A. Flachskampf, Jens-Uwe Voigt and Werner G. Daniel

Front flap mitral valve without signs of pathology is recorded in the second standard position of the sensor in the form of the letter M.
For a more complete understanding and subsequent interpretation of parameters, reflecting the mechanism of the mitral valve, we consider it appropriate to provide a descriptive description of the movement according to the diagram.

General excursion of the mitral valve is determined in systole by the vertical displacement of the valves in the SD interval, diastolic discrepancy is determined horizontally in the interval of the SD segment. The speed of early diastolic opening and closing is calculated graphically using the method described above by constructing tangents to the corresponding sections of the mitral valve movement curve.

Semilunar valves. The aortic valves and the aorta itself are located in the IV standard position of the sensor. In diastole, the valves are recorded on the echocardiogram in the form of a “snake” in the center of the aortic lumen. The divergence of the aortic valves in systole resembles a “diamond-shaped figure.”

Systolic aortic valve divergence equal to the distance between their terminal sections facing the lumen of the aorta. The lumen of the aorta in systole and diastole is determined by the outlines of its inner surface in the corresponding phases cardiac cycle regarding ECG.

Left atrium, like the aorta, is recorded in the IV standard position of the sensor. The echocardiogram shows almost only the posterior wall of the left atrium. Its anterior wall in echocardiography is considered to coincide with the posterior surface of the aorta. According to these signs, the size of the cavity of the left atrium is determined.

Normal EchoCG (echocardioscopy)

Average echocardiographic parameters are normal(according to literature):
Left ventricle.
The thickness of the posterior wall of the left ventricle is 1 cm in diastole and 1.3 cm in systole.
The end-diastolic size of the left ventricular cavity is 5 cm.
The final systolic size of the left ventricular cavity is 3.71 cm.
The rate of contraction of the posterior wall of the left ventricle is 4.7 cm/s.
The relaxation rate of the posterior wall of the left ventricle is 10 cm/s.

Mitral valve.
The total excursion of the mitral valve is 25 mm.
Diastolic divergence of the mitral leaflets (at the level of point E) is 26.9 mm.
The opening speed of the transition flap (EG) is 276.19 mm/s.
The speed of early diastolic closure of the anterior wall is 141.52 mm/s.

The valve opening duration is 0.47±0.01 s.
The opening amplitude of the front leaf is 18.42±0.3& mm.
The lumen of the base of the aorta is 2.52±0.05 cm.
The size of the cavity of the left atrium is 2.7 cm.
End diastolic volume - 108 cm3.

The final systolic volume is 58 cm3.
Stroke volume - 60 cm3.
Exile faction - 61%.
The speed of circular contraction is 1.1 s.
The mass of the left ventricular myocardium is 100-130 g.

Definition: aortic valve insufficiency (aortic insufficiency) is a heart defect in which the semilunar cusps of the aortic valve do not completely close the aortic opening during diastole of the left ventricle. As a result, blood flows back from the aorta into the left ventricle (aortic regurgitation).

Etiology of aortic insufficiency:- against the background of a number of diseases, anatomical changes in the aortic valve occur, leading to its insufficiency. Against the background of rheumatic endocarditis, wrinkling and shortening of the semilunar valves occurs as a result of the inflammatory-sclerotic process. In infectious (septic) endocarditis (ulcerative endocarditis), partial disintegration occurs with the formation of defects, followed by scarring and shortening of the valve leaflets. For syphilis, atherosclerosis of some systemic diseases connective (rheumatoid arthritis, ankylosing spondylitis), the main role in the formation of aortic insufficiency is played mainly by damage to the aorta itself. As a result of the expansion of the aorta and its valve ring, the semilunar valves are retracted with their incomplete closure. It is extremely rare that aortic insufficiency occurs against the background of a closed chest injury with rupture or tear of the valve leaflets.

Due to the fact that the valve leaflets do not completely close the lumen of the aortic ostium, during diastole blood enters the left ventricle not only from the left atrium, but also from the aorta due to reverse blood flow (aortic regurgitation) during diastolic relaxation of the left ventricle, the pressure in it is lower than in the aorta. This leads to overfilling and greater distension of the left ventricle during diastole. During systole, the left ventricle contracts with greater force, throwing an increased volume of blood into the aorta. Volume load causes an increase in the work of the left ventricle, which leads to its hypertrophy. Thus, hypertrophy and then dilatation of the left ventricle occurs. Increased cardiac output in systole and aortic regurgitation in diastole, leading to a sharper than normal drop in pressure in the aorta and arterial system during the diastolic period. Increased systolic blood volume compared to normal causes an increase in systolic blood pressure, the return of part of the blood to the ventricle leads to a more rapid drop in diastolic pressure, the values ​​​​of which become lower than normal. A sharp fluctuation in pressure in the arterial system causes increased pulsation of the aorta and arterial vessels.

The defect is compensated by the increased work of the powerful left ventricle, so the health of patients can remain satisfactory for a long time. However, over time, complaints appear.

The main complaints may be: - pain in the heart area, similar to angina pectoris. They are caused by coronary insufficiency due to an increase in oxygen demand against the background of myocardial hypertrophy and increased work of the left ventricle, as well as a decrease in blood supply coronary arteries with low diastolic pressure in the aorta.

Dizziness: sensations of “noise” and “pulsation” in the head occur as a result of a malnutrition of the brain against the background of sharp fluctuations in blood pressure and low diastolic pressure. When the defect is decompensated, symptoms of heart failure appear: decreased tolerance to physical activity, inspiratory shortness of breath, palpitations. As heart failure progresses, the following may occur: - cardiac asthma, pulmonary edema.

Examination (a number of symptoms are revealed):

1. Paleness of the skin (low blood supply to the arterial system during diastole due to reduced diastolic blood pressure).

2. Pulsation of peripheral arteries (increased systolic blood pressure against the background of a larger than normal stroke volume of the left ventricle; and a rapid decrease in diastolic blood pressure against the background of aortic regurgitation).

Pulsation: carotid arteries (“carotid dance”); subclavian, brachial, temporal, etc.

Rhythmic shaking of the head, synchronous with the arterial pulse (Muse's symptom) - occurs in severe aortic insufficiency due to pronounced vascular pulsation due to mechanical transmission of vibrations.

A rhythmic change in the color of the nail bed when pressing on the end of the nail (Quincke's capillary pulse). A more accurate name is pseudocapillary Quincke's pulse, because It is not the capillaries that pulsate, but the smallest arteries and arterioles. It is noted in cases of severe aortic insufficiency.

Similar origin have: - pulsatory hyperemia soft palate, pulsation of the iris, rhythmic increase and decrease in the area of ​​redness of the skin after friction.

When examining the heart area, the apical impulse is often noticeable, enlarged in area and shifted downward and to the left (the result of increased work against the background of the volume load of the hypertrophied left ventricle).

Palpation

On palpation, a displacement of the apical impulse is determined in the sixth, sometimes in the seventh, intercostal space, outward from the midclavicular line. The apical impulse is strengthened, diffuse, lifting, dome-shaped, which indicates a large enlargement of the left ventricle and its hypertrophy.

Percussion

Percussion reveals a shift in the borders of cardiac dullness to the left. In this case, the configuration of cardiac dullness is determined by percussion, which has a pronounced cardiac waist (aortic configuration).

Auscultation

A characteristic auscultatory sign of aortic insufficiency is a diastolic murmur heard in the aorta (2nd intercostal space to the right of the sternum) and at the Botkin-Erb point. This noise is blowing in nature, protodiastolic. It weakens towards the end of diastole, as blood pressure in the aorta falls and blood flow slows down (therefore, the noise is of a decreasing nature, with a maximum severity at the beginning of diastole.)

Auscultation also reveals: weakening of the first sound at the apex (during systole of the left ventricle there is no period of closed valves, with incomplete closure of the aortic valve leaflets, which reduces the intensity of tension at the beginning of systole) (phase of isometric contraction, and leads to a weakening of the valve component of the first sound) . The second sound on the aorta is also weakened, and with significant damage to the mitral valve leaflets, the second sound may not be heard at all (a decrease in the contribution of the aortic valve leaflets to the formation of the valve component of the second sound). In some cases, with syphilitic and atherosclerotic lesions of the aorta, the II tone may remain quite loud, and even its accent may be noted.

With aortic insufficiency, murmurs of functional origin may be heard. This is a systolic murmur at the apex, caused by relative mitral valve insufficiency against the background of left ventricular dilatation and stretching of the fibrous mitral valve ring, which leads to its incomplete closure, although the mitral valve leaflets remain intact. Diastolic murmur (presystolic murmur - Flint murmur) may appear relatively less frequently at the apex. It is associated with the fact that functional stenosis of the left atrioventricular orifice occurs, due to the fact that the jet of aortic regurgitation lifts the anterior leaflet of the mitral valve, located closer to the outflow tract of the left ventricle, and causes the closure of the atrioventricular orifice, which creates an obstacle to transmitral diastolic blood flow.

Study of pulse and blood pressure.

The arterial pulse in aortic insufficiency, due to increased systolic output of the left ventricle and large fluctuations in blood pressure, becomes fast, high, large (pulsus celler, altus, magnus). Blood pressure changes as follows: systolic increases (increased stroke output), diastolic decreases (a more pronounced and rapid decrease in blood pressure in diastole due to the reverse flow of blood from the aorta into the left ventricle against the background of aortic regurgitation). Pulse blood pressure (the difference between systolic and diastolic) increases.

Sometimes, when measuring blood pressure, a so-called “infinite tone” may be noted (when the pressure in the manometer cuff reaches zero, Korotkoff sounds remain). This is explained by the sound of the first tone on the peripheral artery when an increased pulse wave passes through the section of the vessel compressed by the stethoscope.

When listening to arteries, the first sound above the arteries (carotid, subclavian) becomes louder due to the passage of a larger pulse wave (increases systolic output), while the first sound can be heard on arteries more distant from the heart (brachial, radial). As for the femoral artery, with severe aortic insufficiency, two tones are sometimes heard (double Traube sound), which is associated with vibrations of the vascular wall, both during systole and during diastole (reverse blood flow against the background of aortic regurgitation). In aortic insufficiency, femoral artery when it is compressed with a stethoscope, two noises can be heard (one in systole, the other in diastole) - a double Vinogradov-Durozier murmur. The first of these noises is stenotic noise, due to the passage of a pulse wave through a vessel narrowed by a stethoscope. The genesis of the second murmur is probably associated with the movement of blood towards the heart in diastole against the background of aortic regurgitation.

Data from additional research methods.

Physical examination data (palpation, percussion) indicate hypertrophy and dilatation of the left ventricle are confirmed by additional research methods.

On ECG there are signs of left ventricular hypertrophy (deviation electrical axis heart to the left, deep S waves in the right chest leads, high R waves in the left chest leads, increased internal deviation time in the left chest leads). Changes in the final part of the ventricular complex, as a result of hypertrophy and overload of the left ventricle (downward depression of the ST segment in combination with an asymmetric negative or biphasic T wave in I, AVL and left precordial leads).

During X-ray examination– enlargement of the left ventricle with an emphasized cardiac waist (aortic configuration), expansion of the aorta and increased pulsation.

During phonocardiographic study (PCG)– above the aorta, a decrease in the amplitude of sounds is detected, especially a second and decreasing diastolic murmur with a maximum at the beginning of diastole.

It should be noted that currently FCG is used relatively rarely and has an auxiliary value. This is due to the fact that the emergence of such a modern method as Doppler echocardiography (including color Doppler echocardiography) provides much more information (not only qualitative, indicating the presence of aortic insufficiency, but also quantitative, by which one can judge the magnitude of aortic regurgitation and the severity of the defect) .

Echocardiography, Doppler echocardiography.

An echocardiographic study reveals signs indicating intracardiac hemodynamic disturbances characteristic of this defect: an increase in the cavity of the left ventricle, hypertrophy of its myocardium, increased systolic excursion of its walls, indicating a volume load on the left ventricle. When examining in M ​​mode at the level of the mitral valve leaflets, an increase in the cavity of the left ventricle, hypertrophy of its myocardium, and increased systolic excursion of its walls may be noted, indicating a volume load on the left ventricle. When examining in M ​​mode at the level of the mitral valve leaflets, a peculiar sign may be noted during echolocation of the anterior leaflet, associated with its vibrations under the influence of the jet of aortic regurgitation (flutter - symptom).

Doppler echocardiographic examination makes it possible to directly confirm aortic insufficiency: - both the presence of the latter and the degree of its severity (see section “Echocardiography for heart defects”.

Thus, by evaluating the data obtained from physical and additional methods of examining the patient, it is possible, in accordance with the proposed algorithm, to analyze the results obtained in order to finally establish aortic insufficiency as a heart defect with its clinical characteristics.

The algorithm for assessing examination data provides for the identification of three groups of signs of this heart defect:

1. Valve signs that directly confirm an existing valve defect:

A. Physical: - on auscultation, diastolic (protodiastolic) noise and weakening of the second sound on the aorta and at the Botkin-Erb point.

B. Additional methods: on FCG - in the aorta there is a decrease in the amplitude of sounds, especially the second tone; diastolic, decreasing murmur.

Doppler echocardiography: signs of aortic regurgitation (mild, moderate, severe regurgitation)

2. Vascular signs:

“Carotid Dance”; Musset's symptom; changes in blood pressure (increased systolic, decreased diastolic, increased pulse pressure). Listening to the “infinite tone” when determining blood pressure using the Korotkoff method. Changes in arterial pulse (pulsus celler, altus, magnus). Double Traube tone, double Vinogradov-Durozier noise. Quincke's sign (pseudo-capillary pulse), pulsatory hyperemia of the soft palate, pulsation of the iris.

3. Left ventricular signs (signs of hypertrophy and

volume overload on the entire left ventricle.

A. Physical:

Shift down and to the left of the apical impulse. The apical impulse is strengthened, lifting, dome-shaped. Percussion shift of cardiac dullness to the left. Aortic configuration of cardiac dullness with a pronounced cardiac waist.

B. Additional methods:

X-ray examination - confirms the physical data (expanded shadows of the heart to the left, aortic configuration); expansion and pulsation of the aorta.

ECG - signs of hypertrophy and systolic overload of the left ventricle.

ECHO-CG – signs of left ventricular dilatation (increased end-diastolic volume); increased systolic excursion of the walls of the left ventricle, hypertrophy of its myocardium.

The above three groups of signs are mandatory for aortic insufficiency as a heart defect.

As for vascular signs, characteristic changes in pulse and blood pressure are sufficient to establish aortic insufficiency as a heart defect. Such signs as Muset's symptom, Quincke's symptom; the double murmur of Vinogradov-Durozier et al. does not always occur and is usually found in severe aortic insufficiency.

After a diagnosis of heart disease has been established, clinical and anamnestic data suggest its etiology.

If there are signs of heart failure, indicate the symptoms indicating its presence, and also in the formulation of the clinical diagnosis indicate the stage of congestive heart failure according to N.D.’s classification. Strazhesko, V.Kh. Vasilenko and her NYHA functional class.

Aortic stenosis (stenosis of the aortic mouth).

Definition: Aortic stenosis is a heart defect in which there is an obstacle to the expulsion of blood into the aorta during contraction of the left ventricle as a result of a decrease in the area of ​​the aortic ostium. Aortic stenosis occurs when the cusps of the aortic valve fusion, or appears as a result of cicatricial narrowing of the aortic opening.

Etiology: there are three main causes of aortic stenosis: rheumatic endocarditis, the most common reason, degenerative aortic stenosis (against the background of the atherosclerotic process, sclerosis, calcification occurs), valve rings and aortic valve leaflets), congenital aortic stenosis (including with a bicuspid aortic valve).

With rheumatic etiology of aortic valve stenosis, there is usually concomitant aortic insufficiency, often plus mitral valve disease.

The mechanism of hemodynamic disorders.

Normally, the area of ​​the aortic orifice is 2-3 cm. Clinical manifestations occur when the aortic mouth is narrowed by 3-4 times - less than 0.75 cm, and when the area of ​​the aortic opening is 0.5 cm, aortic stenosis is considered critical. If the degree of narrowing of the aortic opening is small, then no significant circulatory disturbance occurs. If there is an obstacle to the expulsion of blood into systole, the left ventricle has to contract with great tension, resulting in a systolic pressure gradient between the left ventricle and the aorta. The increased pressure gradient provides the desired value of the stroke volume of the left ventricle when blood is expelled through the narrowed orifice during the allotted time interval (the ejection period). That is, there is a resistance load during the expulsion of blood, which significantly increases the mechanical work of the left ventricle and causes its pronounced hypertrophy. Hemodynamic disorders are caused by the organic capabilities of the left ventricle and cause its pronounced hypertrophy. Hemodynamic disorders are caused by a limitation in the ability of the left ventricle to adequately increase cardiac output when it comes to intense physical activity. If the degree of stenosis is small, then incomplete systolic emptying of the left ventricle may occur. This leads to the fact that during diastole, a normal amount of blood from the left atrium enters the incompletely emptied left ventricle (increased atrial systole for adequate filling of the hypertrophied left ventricle with increased diastolic pressure). Hyperfunction of the left atrium can lead to its dilatation. Changes in the left atrium may be the cause atrial fibrillation, which in turn can sharply worsen intracardiac hemodynamics in aortic stenosis. Over time, with the development of cardiac decompensation and impaired emptying of the left chambers of the heart, the increased pressure in them is retrogradely transmitted to the pulmonary veins and to the venous knee of the pulmonary circulation. Subsequently, venous stagnation of blood occurs in the pulmonary circulation, as well as an increase in pressure in the pulmonary artery system as a result of the Kitaev reflex. This in turn leads to a load on the right ventricle with subsequent decompensation and dilatation, increased pressure in the right atrium and the development of congestion in the right atrium. big circle blood circulation

Clinical picture.

Aortic stenosis can be a compensated heart defect for many years and does not cause any complaints even with heavy physical exertion. This is explained by the large compensatory capabilities of the powerful left ventricle. However, with pronounced narrowing of the aortic mouth, characteristic clinical symptoms appear. In patients with severe aortic stenosis, a classic triad of symptoms is observed: - angina pectoris; fainting during physical exertion; development of heart failure (which initially occurs of the left ventricular type). The occurrence of angina pectoris even with absolutely normal coronary arteries in aortic stenosis is associated with relative coronary insufficiency of the hypertrophied left ventricle (discrepancy between the increased myocardial oxygen consumption and the degree of its vascularization).

A certain role may be played by the Venturi effect, which consists in the suction effect of a blood stream when passing through a stenotic valve at the level of the ostia of the coronary arteries. A certain role may be played by the absence of an increase in cardiac output adequate to physical activity (“fixed stroke volume”), which is reflected in an adequate increase in coronary blood flow for an intensively working hypertrophied left ventricle. Fainting during physical activity occurs due to dilation of blood vessels in working muscles and redistribution of blood flow to the muscles with a simultaneous decrease in blood supply to the brain. As for the signs of left ventricular failure, they are first a consequence of impaired diastolic relaxation of the left ventricle; in the later stages, systolic dysfunction also develops.

The appearance of the above clinical symptoms indicates both the presence of significant stenosis and the onset of decompensation. After the appearance of the above clinical symptoms, the life expectancy of patients with aortic stenosis rarely exceeds 5 years (after the onset of angina 5 years, after the appearance of fainting 3 years, after the appearance of signs of heart failure - 1.5 - 2 years). Therefore, the occurrence of any of these symptoms is absolute indication to surgical treatment.

The general purpose of the lesson: - to train students based on physical and additional examination data: to identify the presence of aortic heart disease (aortic stenosis), to give a general clinical description of this defect, indicating its possible etiology and prognosis.

1. Complaints. Identification of complaints characteristic of aortic stenosis (see above - clinical picture).

2. Inspection. Pallor of the skin is typical for patients with aortic stenosis, which is associated with low blood supply to the arterial system.

3. Palpation. The apical impulse, due to powerful hypertrophy of the left ventricular myocardium, is shifted to the left, less often downward, high, resistant, lifting “dome-shaped”. When palpating the heart area, in some cases, systolic trembling (“cat’s purring”) is detected in the second intercostal space to the right of the sternum and above the manubrium of the sternum. This phenomenon is due to the fact that the high-speed turbulent blood flow passing through the narrowed opening of the aortic valve ring causes its vibration, which is mechanically transmitted to the surrounding tissues. The systolic nature of the tremor is confirmed by the fact that it begins immediately after the first sound and coincides with the arterial pulse.

4. Percussion. Reveals a shift of the boundaries of relative cardiac dullness to the left. At the same time, the severity of the cardiac waist is emphasized and the contours of cardiac dullness acquire a characteristic aortic configuration, which is associated with an increase in the significantly hypertrophied left ventricle.

5. Auscultation. Above the aorta (2nd intercostal space to the right of the sternum), the second tone is weakened. The reason is severe deformation, thickened leaflets of the aortic valve, leading to decreased mobility and “slamming speed.” In the case of immobility of the fused aortic valve leaflets, the second sound may not be heard at all. With aortic stenosis of atherosclerotic origin, if it is not clearly expressed, the second sound above the aorta, on the contrary, can be enhanced (the dense walls of the aorta better reflect the sound when the valve leaflets slam shut). Aortic stenosis is characterized by a systolic murmur in the aorta (second intercostal space to the right of the sternum), which is associated with blood flow through the narrowed opening of the aortic ostium. This noise in the direction of blood flow is well carried out on the carotid arteries, and in some cases, is heard in the interscapular space. Systolic murmur with aortic stenosis has all the distinctive features of “organic” noise - loud, persistent, long-lasting, rough timbre. In some cases, the noise is so loud that it can be heard from all points of auscultation, but the epicenter of this noise will be located above the places where the aortic valve is heard (the second intercostal space to the right of the sternum and the Botkin-Erb point, i.e. the 2nd and 5th auscultation point), with the noise volume decreasing as it moves away from the specified auscultation points.

At the apex (1st point of auscultation), a weakening of the first tone may be noted, which is associated with excessive hypertrophy of the left ventricle and, as a consequence, slow contraction during systole (systole lengthens).

After the onset of heart failure, there is usually a decrease in the volume and duration of the systolic murmur (a decrease in the linear and volumetric velocity of blood flow against the background of decreased contractility of the left ventricle).

6. Study of pulse and blood pressure. An obstacle to the expulsion of blood from the left ventricle leads to a decrease in the speed of volumetric blood flow in systole, blood passes into the aorta slowly and in smaller quantities. This leads to the fact that with aortic stenosis the arterial pulse is small, slow, rare (pulsus parvus, tardus et rarus).

Systolic blood pressure usually decreases, diastolic blood pressure does not change or increases, so pulse pressure will be reduced.

II. ECG data. Signs of noticeably pronounced hypertrophy of the left ventricle are recorded (deviation of the electrical axis of the heart to the left, deep S waves in the right chest leads, high R waves in the left chest leads. A change in part of the ventricular complex is noted as a consequence of hypertrophy and overload of the left ventricle (sloping depression of the ST segment in combination with an asymmetric negative or biphasic T wave in I, aVL and left chest leads.

X-ray examination.

The heart, due to the increase in the fourth arc of the left contour, acquires a peculiar shape - a “boot” or “duck”. There is an expansion of the aorta in the ascending section (poststenotic expansion). Signs of defoliation of the aortic valve leaflets are often found.

Phonocardiography (PCG). As a method, FCG currently has only an auxiliary value and is used relatively rarely, since its diagnostic capabilities are inferior to such modern methods such as echocardiography and Doppler echocardiography.

On FCG, changes in heart sounds characteristic of this defect are noted: - a decrease in the amplitude of the first sound recorded at the apex of the heart and a decrease in the second sound above the aorta. Especially typical for aortic stenosis is a systolic murmur with a characteristic diamond-shaped shape (increasing-decreasing systolic murmur).

Sphygmography (recording vibrations of the artery wall). The sphygmogram of the carotid artery shows a slower rise and fall of the pulse wave (slow pulse), a low amplitude of the pulse waves and a characteristic jaggedness of their peaks (a curve resembling a “cockscomb” due to the reflection of fluctuations associated with the conduction of systolic noise to the vessels of the neck).

How diagnostic method, sphygmography is currently used very rarely, since there are modern highly informative research methods, which were mentioned above.

Ultrasound research methods (echocardiography, Doppler echocardiography).

These methods are the most informative of all additional research methods. Thanks to them, it is possible to obtain reliably not only a qualitative characteristic (the presence of a heart defect), but also to provide fairly complete information about the severity of the defect, the compensatory capabilities of the heart, prognosis, etc. etc.

Echocardiography (ECHO CG)

With ECHO CG in two-dimensional mode (B-mode) and one-dimensional (M-Mode) thickenings, deformations of the aortic valve leaflets, a decrease in their mobility during systolic opening, and often signs of calcification in the area of ​​the aortic valve ring and valve leaflets are noted.

Doppler echocardiography (Doppler – ECHO – KG).

Doppler ECHO-CG reveals high-speed turbulent systolic aortic flow through a narrowed aortic ostium. Despite the reduced volumetric velocity of systolic transaortic blood flow, the linear velocity (m/sec) increases due to the narrowing.

With the help of Doppler ECHO CG, it is possible to determine the main indicators characterizing the severity of the defect.

Maximum velocity of systolic blood flow through the aortic valve ring (normal £ 1.7 m/sec).

Pressure gradient between the left ventricle and the aorta (taking into account the speed of blood flow according to Bernoulli’s formula - see section echocardiography).

The severity of aortic stenosis is indicated by:

Aortic valve ostial area (AVA)

In addition to changes in the aortic valve, echocardiography provides information about left ventricular hypertrophy, which occurs with this heart defect.

Aortic stenosis is characterized by pronounced hypertrophy of the left ventricular myocardium in the absence of significant dilatation of its cavity, and therefore the end-diastolic and end-systolic volume (EDV and ESV) of the ventricle for a long time differs little from the norm. The thickness of the interventricular septum (IVS) and the posterior wall of the left ventricle (PLW) are markedly increased.

In addition, against the background of pronounced hypertrophy of the left ventricle, in the absence of dilatation of the latter, an increase in the cavity of the left atrium may be noted (a decrease in the elasticity of the hypertrophied left ventricle and impaired filling during the period of diastolic relaxation creates an additional load on the atrium during its systole and makes emptying difficult).

In advanced cases of aortic stenosis, when myogenic dilatation of the left ventricle and its decompensation develop, the echocardiogram shows an increase in the cavity of the left ventricle, in some cases with the development of relative mitral regurgitation, which, together with an enlarged left atrium, resembles the changes that occur with mitral regurgitation ( mitral insufficiency). In this case, they talk about “mitralization” of the aortic defect.

With aortic stenosis, changes in the aorta can also be detected on the echocardiogram - poststenotic dilatation of the aorta (caused by an increase in the linear velocity of blood flow through the narrowed aortic opening).

Since aortic stenosis is “the most surgical heart defect” and surgery is the only promising one, then the presence of severe aortic stenosis (according to the pressure gradient and the degree of narrowing of the aortic valve opening) is an indication for consultation with a cardiac surgeon.

III. General assessment of symptoms identified during physical and additional examination in accordance with the general plan of the diagnostic algorithm.

Diagnostic algorithm: provides for the identification of the following signs of aortic stenosis:

1. Valvular signs: direct valvular signs of aortic stenosis are: rough systolic murmur and systolic tremor in the 2nd intercostal space to the right of the sternum, weakening of the second tone. The noise radiates to the vessels of the neck, and can radiate to all points of auscultation (austed over the entire region of the heart).

Confirmation of valve signs additional methods examinations: - on FCG above the aortic valve – rhomboid systolic murmur; with echocardiography - the aortic valve leaflets are compacted, their systolic opening is reduced, high-speed turbulent flow through the aortic mouth, an increase in the systolic pressure gradient between the left ventricle and the aorta.

2. Vascular signs (due to a characteristic hemodynamic disorder): small, slow, rare pulse; decrease in systolic and pulse blood pressure. Against this background, there may be signs of insufficient blood supply to the brain and heart (headaches, dizziness, fainting, attacks of angina). The sphygmogram of the carotid artery shows a slow rise of anacrota, a “cock’s crest” at the apex, a slow descent of catacrota, and a weak expression of incisura.

3. Left ventricular signs: (pronounced hypertrophy of the left ventricular myocardium: - shifted to the left, strengthened, high, resistant apical impulse, aortic configuration of the heart. Data: ECG (signs of hypertrophy and systolic overload of the left ventricle), echocardiography (thickening of the walls of the left ventricle, increase in its mass myocardium).

IV. The diagnosis is formulated with a presumable indication of the etiology of the defect. The severity of the defect and prognosis are indicated. If cardiac decompensation is present, indicate the stage of heart failure.

Tricuspid valve insufficiency.

Insufficiency of the tricuspid (three-leaf) valve (tricuspid insufficiency) can be either organic or relative.

Organic tricuspid insufficiency is based on damage to the tricuspid valve leaflets (rheumatic endocarditis), and very rarely, rupture of the capillary muscles of the tricuspid valve (as a result of trauma).

In the case of rheumatic etiology of tricuspid insufficiency, the latter is usually combined with damage to other heart valves, and is never isolated. As an isolated defect, tricuspid valve insufficiency is possible only with infective endocarditis (comparatively less common than other valve lesions in this disease).

Relative insufficiency of the tricuspid valve is more common and appears when the right atrioventricular orifice is stretched against the background of dilatation of the right ventricle of any origin, while the valve leaflets remain intact.

The mechanism of hemodynamic disorders.

During right ventricular systole, due to incomplete closure of the valve leaflets, some of the blood returns back to the right atrium (tricuspid regurgitation). Since the usual amount of blood from the vena cava enters the atrium at the same time, the latter stretches against the background of an increase in blood volume. During diastole, an increased volume of blood also enters the right ventricle from the right atrium, since that part of the blood that returned to the atrium during systole is added to the normal amount. The right ventricle increases in volume, the load on it increases.

When working under conditions of volume loading of the right ventricle and right atrium, hypertrophy of their myocardium occurs. Thus, with tricuspid insufficiency, compensation is supported by increased work of the right parts of the heart.

Clinical picture.

Given the relatively small mass of the right ventricle compared to the left and its lower compensatory potential, signs of right ventricular failure appear relatively quickly with stagnation in the systemic circulation (edema). lower limbs, enlarged liver; in severe cases, anasarca, hydrothorax, hydropericardium, ascites, cardiac cirrhosis).

The indicative basis of action (BAA) of a student at the patient’s bedside implies:

General plan for independent work: students work in a room with

The aortic valve is the part of the heart that is located between the left ventricle and the aorta. It is needed to prevent the return of released blood into the chamber.

What does the aortic valve consist of?

Permissive cardiac nodes are formed due to outgrowths of the inner layer of the heart.

AK consists of the following elements:

• Fibrous ring- formed from connective tissue, lies at the basis of formation.
• Three semilunar valves along the edge of the annulus fibrosus- when connecting, they obscure the lumen of the artery. When the aortic crescents close, a contour is formed that resembles the logo of a Mercedes car. Normally they are the same, with a smooth surface. AK valves are made of two types of tissues - connective and thin muscular.
• Sinuses of Valsalva- sinuses in the aorta, behind the semilunar valves, two are connected to the coronary arteries.

The aortic valve is different from the mitral valve. So, it is tricuspid, and not 2-cuspid, unlike the latter, it is devoid of both chordae tendons and papillary muscles. The mechanism of action is passive. The aortic valve is driven by blood flow and the pressure difference that occurs between the left heart ventricle and the associated artery.

Algorithm of the aortic valve

The work cycle looks like this:

1. Elastin fibers return the valves to their original position, move them to the walls of the aorta and open them to blood flow.
2. The aortic root narrows, tightening the crescent.
3. The pressure in the heart chamber increases, a mass of blood is pushed out, pressing the outgrowths against the inner walls of the aorta.
4. The left ventricle contracted and the flow slowed.
5. The sinus at the walls of the aorta creates vortices that deflect the valves, and the hole in the heart closes with a valve. The process is accompanied by a loud bang, which can be heard through a stethoscope.

When and why do aortic valve defects occur?

Aortic valve defects are divided into congenital and acquired according to the time of occurrence.

Congenital malformations of AK

Disorders are formed during embryonic development.

The following types of anomalies occur:

• Quadricuspid AC is a rare anomaly, occurring in 0.008% of cases;
• The valve is large, stretched and sagging, or less developed than others;
• Holes in the crescents.

The bicuspid structure of the aortic valve is a fairly common anomaly: there are up to 20 cases per 1 thousand children. But usually 2 leaflets are enough to ensure sufficient blood flow; no treatment is required.

If there is no crescent in the aortic valve, the person most often does not experience any discomfort. This condition is not considered a contraindication for pregnancy in female patients.

In case of congenital defects with stenosis of the aortic mouth, bicuspid aortic valve is detected in 85% of sick children. In adults, about 50% of such cases.

Unicuspid aortic valve is a rare defect. The valve opens thanks to a single commissure. This disorder leads to a severe form of aortic stenosis.

If such a patient gets sick with age infectious diseases, the valves wear out faster, and fibrosis or calcification may develop.

Such congenital heart defects (CHDs) in children usually form after infections that a woman had during pregnancy, due to unfavorable factors, exposure to x-rays.

Acquired anomalies

AK defects that arise with age are of two types:

• Functional - the aorta or left ventricle expands;
• Organic - AC tissue is damaged.

Acquired aortic heart disease is called various diseases. Of great importance in the formation of such defects are autoimmune diseases, rheumatism, which provokes 4 out of 5 disorders. When the disease occurs, the valves of the valves fuse together at the base and become wrinkled, many thickenings appear, causing deformation to form on the pockets.

Acquired AV defect is caused by endocarditis, which, in turn, is provoked by infections - syphilis, pneumonia, tonsillitis and others.

The membrane inside the heart and valve becomes inflamed. Then the microbes settle on the tissues and create colony tubercles. On top they become covered with blood proteins and form a growth on the valve, reminiscent of warts. These structures prevent the valve parts from closing.

There are other reasons for AK anomalies:

• Hypertension;
• Enlarged aortic valve.

As a result, the shape and structure of the base of the aorta may change, and tissue rupture occurs. Then the patient suddenly experiences characteristic symptoms.

Acquired anomalies in the structure of the aortic valve are sometimes the result of trauma.

There is a two-valve disorder - mitral-aortic, aortic-tricuspid. In the most severe cases, three valves are affected at once - aortic, mitral, tricuspid.

Fibrosis of the valve leaflets

Often during diagnosis, a cardiologist identifies fibrosis of the aortic valve leaflets. What it is? This is a disease in which the valves thicken, the number blood vessels and tissue nutrition deteriorates, some areas die. And the more extensive the lesions, the more severe the patient’s symptoms.

The most common cause of fibrosis of the valve leaflets is aging. Age-related changes cause atherosclerosis and the appearance of plaques on the valve, which also affects the arterial blood vessel.

Fibrosis also occurs when there is a change hormonal levels, metabolic disorders, after myocardial infarction, excessive physical activity, uncontrolled use of medications.

There are three types of fibrosis of the aortic valve leaflets:

AC stenosis

This is a defect of the arterial valve, in which the lumen area decreases, which is why the blood does not escape during contraction. This causes the left ventricle to enlarge, causing pain and increased blood pressure.

There are congenital and acquired stenosis.

The development of this pathology is facilitated by the following disorders:

• Single-leaf or double-leaf AK, while three-leaf is the norm;
• A membrane with a hole under the aortic valve;
• A muscle cushion that is located above the valve.

Streptococcal and staphylococcal infections lead to the development of stenosis, which penetrate the heart through the bloodstream, causing the same endocarditis. Another reason is systemic diseases.

Age-related disorders, calcification, and atherosclerosis also play an important role in the origin of aortic valve stenosis. Calcium and fatty plaques settle on the edges of the valves. Therefore, when the doors are open, the lumen itself is narrowed.

There are three degrees of aortic valve stenosis based on the size of the lumen:

• Light - up to 2 cm (with the norm being 2.0–3.5 cm2);
• Moderate - 1–2 cm2;
• Heavy - up to 1 cm 2.

Stages of AA deficiency

There are degrees of aortic valve insufficiency:

• At 1st degree There are practically no symptoms of the disease. The walls of the heart on the left become slightly larger, and the capacity of the left ventricle increases.
• At 2nd degree(period of latent decompensation) there are no pronounced symptoms yet, but the morphological change in the structure is already more noticeable.
• At 3 degrees Coronary insufficiency develops and blood partially returns to the left ventricle.
• At 4 degrees AV insufficiency weakens the contraction of the left ventricle, resulting in vascular congestion. Shortness of breath, a feeling of lack of air, swelling of the lungs develops, and the development of heart failure is observed.
• At grade 5 disease, saving the patient becomes an impossible task. The heart contracts weakly, causing blood to stagnate. This is a dying state.

Symptoms of AA deficiency

The disease sometimes goes unnoticed. Aortic valve disease affects health if the reverse flow reaches 15–30% of the left ventricular capacity.

Then the following symptoms arise:

• Heart pain resembling angina pectoris;
• Headache, vertigo;
• Sudden loss of consciousness;
• Dyspnea;
• Vascular pulsation;
• Increased heartbeat.

As the disease worsens, these symptoms of aortic valve insufficiency are supplemented by swelling and heaviness in the right hypochondrium due to congestive processes in the liver.

If a cardiologist suspects an AC defect, he pays attention to the following visual signs:

• Pale skin;
• Changing pupil size.

In children and adolescents, the chest area bulges due to excessive heartbeat.

When examining and auscultating the patient, the doctor notes a pronounced systolic murmur. Measuring pressure shows that the upper reading increases and the lower reading decreases.

Diagnosis of AC defects

The cardiologist analyzes the patient’s complaints, learns about lifestyle, diseases that were diagnosed in relatives, and whether they had such anomalies.

In addition to a physical examination, if aortic valve disease is suspected, a general analysis urine and blood. This reveals other disorders, inflammations. Biochemical research determines the level of proteins, uric acid, glucose, cholesterol, and identifies damage to internal organs.

The information obtained using hardware diagnostic techniques is valuable:

• Electrocardiogram- indicates the frequency of contractions and size of the heart;
• echocardiography- determines the size of the aorta and lets you know whether the valve anatomy is distorted;
• Transesophageal diagnostics- a special probe helps to calculate the area of ​​the aortic ring;
• Catheterization- measures the pressure in the chambers, shows the characteristics of blood flow (used in patients over 50 years old);
• Dopplerography- gives an idea of ​​the return flow of blood, the severity of prolapse, the compensatory reserve of the heart, the severity of stenosis and determines whether surgery is required;
• Bicycle ergometry- carried out by young patients if there is a suspicion of an AC defect in the absence of patient complaints.

Treatment of AC defects

In mild stages of failure - for example, with marginal fibrosis - observation by a cardiologist is prescribed. If, for more severe lesions of AK, treatment is prescribed - medicinal or surgical. The doctor here takes into account the condition of the aortic valve, the severity of the pathology, and the degree of tissue damage.

Conservative techniques

In most cases, AA deficiency develops gradually. With proper medical care, it is possible to stop the progression. For drug treatment they use drugs that affect symptoms, the strength of myocardial contractions, and prevent arrhythmias.

These are the following groups of funds:

• Calcium antagonists- do not allow mineral ions to enter cells and regulate the load on the heart;
• Vasodilation agents- reduce the load on the left ventricle, relieve spasms, reduce pressure;
• Diuretics- eliminate excess moisture from the body;
• β-blockers- prescribed if the aortic root is dilated, heart rhythm is disturbed, blood pressure is increased;
• Antibiotics- for the prevention of endocarditis during exacerbation of an infectious disease.

Only the doctor selects medications, determines the dosage and duration of treatment.

Who is suitable for surgery?

You cannot do without radical methods if the heart stops performing functions.

At congenital defect AK with minor abnormalities, surgery is recommended after 30 years. But this rule can be violated if the disease rapidly progresses. If the defect is acquired, the age limit rises to 55–70 years, however, even here the degree of changes in the aortic valve is taken into account.

Surgery is required for the following conditions:

• The left ventricle is partially or completely incompetent, the chamber size is 6 cm or more;
• Return of more than a quarter of the expelled blood volume, which is accompanied by painful symptoms;
• The volume of returned blood is above 50%, even in the absence of complaints.

The patient is denied surgery due to the following contraindications:

• Age from 70 years (there are exceptions);
• The proportion of blood flowing into the left ventricle from the aorta exceeds 60%;
• Chronic diseases.

There are several types of heart surgeries that are prescribed for AV failure:

Intra-aortic balloon counterpulsation. The operation is indicated for early AV failure. A balloon with a hose through which helium is supplied is placed into the femoral artery.

When the AC is reached, the structure inflates and restores the tight closure of the valves.

The most common operation consists of replacing damaged tissue with a silicone and metal structure.

This allows you to functionally restore the functioning of the heart apparatus. Arterial valve replacement is indicated when reflux is 25–60%, there are multiple and significant manifestations of disease, and the ventricular dimensions exceed 6 cm.

The operation is well tolerated and allows you to get rid of arterial insufficiency. The surgeon dissects the chest, which subsequently requires long-term rehabilitation.

Operation Ross. In this case, the aortic valve is replaced with a pulmonary valve. The advantage of this method of treatment is the absence of risks associated with rejection and destruction.

If the operation is performed in childhood, then the fibrous ring grows with the body. Instead of the removed pulmonary valve, a prosthesis is installed, which works longer in this place.

If the AC is formed by two valves, tissue plastic surgery is performed, in which the structures are preserved as much as possible.

Prognosis, complications for AC defects

How many people live with similar pathologies? The prognosis depends on the stage at which treatment is started and the cause of the anomaly. Typically, survival in severe forms, if there are no signs of decompensation, is 5–10 years. Otherwise, death occurs within 2–3 years.

To avoid the development of such a heart defect, doctors recommend following simple rules:

• Prevent diseases that can disrupt the structure of the valve;
• Carry out hardening procedures;
• At chronic diseases undergo timely treatment prescribed by the doctor.

AV insufficiency is a serious illness that, without observation by a cardiologist and treatment, leads to life-threatening complications. Against the background of the anomaly, myocardial infarction, arrhythmias, and pulmonary edema occur. The risk of thromboembolism - the formation of blood clots in organs - increases.

Compliance with preventive measures by a pregnant woman will help avoid congenital heart disease, including abnormal valve structure - unicuspid, bicuspid. Prevention consists of healthy habits, regular walks in areas with green spaces, avoiding food that is harmful to the body, heart and blood vessels - fast food, fatty, smoked, sweet, salty, refined foods.

You should get rid of bad habits - smoking, alcohol abuse. Instead, the daily menu includes vegetables and fruits - fresh, boiled, steamed or baked, low-fat fish, and cereals. It is also necessary to reduce psycho-emotional stress.

Video: Aortic valve insufficiency.