Aortic insufficiency is a pathological change in the work of the heart, characterized by non-closure of the valve leaflets. This results in reverse blood flow from the aorta to the left ventricle. Pathology has serious consequences.

If you do not take up the treatment on time, then everything becomes complicated. The organs do not receive the required amount of oxygen. This leads to an increase in heart rate to fill the gap. If you do not intervene, the patient is doomed. After a certain time, the heart increases, then edema appears, due to pressure surges inside the organ, the left atrial valve may fail. It is important to consult a therapist, cardiologist or rheumatologist on time.

Aortic insufficiency is divided into 3 degrees. They differ in the divergence of the valve cusps. At first glance, it looks simple. It:

• Valsalva sinuses - These are located behind the aortic sinuses, just behind the valves, which are often called semilunar. The coronary arteries begin from this place.
• Anulus fibrosus - it has high strength and clearly separates the beginning of the aorta and the left atrium.
• The semilunar valves - there are three of them, they continue the endocardial layer of the heart.

The leaves are arranged in a circular line. When the valve is closed in a healthy person, the gap between the valves is completely absent. The degree and severity of aortic valve insufficiency depends on the size of the toe clearance.

First degree

The first degree is characterized by mild symptoms. The divergence of the valves is not more than 5 mm. Feels no different from the normal state.

Insufficiency of the aortic valve of the 1st degree is manifested by mild symptoms. With regurgitation, the blood volume is no more than 15%. Compensation occurs due to increased left ventricular impulses.

Patients may not even notice pathological manifestations. When the disease is in the stage of compensation, then therapy can be omitted, limited to preventive actions. Patients are prescribed observation by a cardiologist, as well as regular ultrasound checks.

Second degree

Insufficiency of the aortic valve, which belongs to the 2nd degree, has symptoms with a more pronounced manifestation, while the divergence of the leaflets is 5-10 mm. If this process occurs in a child, then the signs are subtle.

If, in the event of aortic insufficiency, the volume of blood returned back is 15-30%, then the pathology refers to a second-degree disease. Symptoms are not severe, but shortness of breath and palpitations may occur.

To compensate for the defect, the muscles and the valve of the left atrium are involved. In most cases, patients complain of shortness of breath when light loads, increased fatigue, strong beating hearts and pain.

During examinations with the use of modern equipment, an increase in the heartbeat is found, the apical impulse shifts slightly downward, the borders of the dullness of the heart expand (to the left by 10-20 mm). Using x-ray examination an increase in the left atrium downward is visible.

With the help of auscultation, you can clearly hear the murmurs along the sternum on the left side - these are signs of aortic diastolic murmur. Also, with the second degree of insufficiency, a systolic murmur appears. As for the pulse, it is increased and pronounced.

Third degree

The third degree of insufficiency, also called severe, has a discrepancy of more than 10 mm. Patients require serious treatment. More often, an operation is prescribed, followed by drug therapy.

When the pathology is at the 3rd degree, the aorta loses more than 50% of the blood. To compensate for the loss, the heart organ accelerates the rhythm.

Basically, patients often complain about:

• shortness of breath at rest or with minimal exertion;
• pain in the heart area;
• increased fatigue;
• constant weakness;
• tachycardia.

In studies, a strong increase in the size of the boundaries of dullness of the heart down and to the left is determined. Displacement also occurs in the right direction. As for the apical impulse, it is enhanced (spilled character).

In patients with a third degree of insufficiency, the epigastric region is pulsating. This indicates that the pathology has involved the right chambers of the heart in the process.

During the research, a pronounced systolic, diastolic murmur and Flint murmur appear. They can be heard in the area of \u200b\u200bthe second intercostal space on the right side. They have a pronounced character.

It is important at the first, even minor symptoms, to seek medical help from physicians and cardiologists.

Symptoms, Signs and Causes

When aortic valve insufficiency begins to develop, symptoms do not appear immediately. This period is characterized by the absence of serious complaints. The load is compensated by the left ventricular valve - it is able to withstand reverse flow for a long time, but then it stretches and deforms a little. Already at this time, pains, dizziness and frequent heartbeat occur.

The first symptoms of insufficiency:

• there is a certain sensation of pulsation of the cervical veins;
• strong tremors in the region of the heart;
• increased frequency of contraction of the heart muscle (minimizing the reverse blood flow);
• pressing and constricting pain in the chest area (with strong reverse blood flow);
• the onset of dizziness, frequent loss of consciousness (occurs with poor-quality oxygen supply to the brain);
• appearance general weakness and decreased physical activity.

During a chronic illness, the following symptoms appear:

• pain in the heart area even when calm, without stress;
• fatigue quickly appears during exercise;
• persistent tinnitus and sensation strong ripple in the veins;
• the occurrence of fainting during a sharp change in body position;
• the head hurts badly in the front part;
• arterial pulsation visible to the naked eye.

When the pathology is in a decompensated degree, the exchange in the lungs is impaired (often the appearance of asthma is observed).

Aortic insufficiency is accompanied by severe dizziness, fainting, as well as pain in the chest cavity or its upper parts, frequent shortness of breath and palpitations without rhythm.

The causes of the disease:

• congenital aortic valve disease.
• complications after rheumatic fever.
• endocarditis (the presence of a bacterial infection of the inner part of the heart).
• changes with age - this is due to wear of the aortic valve.
• an increase in the size of the aorta - a pathological process occurs with hypertension in the aortic region.
• hardening of the arteries (as a complication of atherosclerosis).
• aortic dissection, when the inner layers of the main artery are separated from the middle layers.
• violation of the functionality of the aortic valve after its replacement (prosthetics).

Less common reasons are:

• aortic valve injury;
• diseases of an autoimmune nature;
• the consequences of syphilis;
• ankylosing spondylitis;
• manifestations of diffuse-type diseases associated with connective tissues;
• complications after using radiation therapy.

It is important to consult a doctor at the first manifestations.

Features of the disease in children

Many children do not notice problems for a long time and do not complain of illness. In most cases, they feel good, but this does not last long. Many are still able to engage in sports training. But the first thing that torments them is shortness of breath and an increased heart rate. With these symptoms, it is important to see a specialist immediately.

At first, discomfort is noticed with moderate exertion. In the future, aortic valve failure occurs even in a calm state. Disturbed by shortness of breath, strong pulsation of the arteries located in the neck. At the same time, treatment should be of high quality and timely.

Symptoms of the disease can manifest as murmurs in the area of \u200b\u200bthe largest artery. As for physical development, in children it does not change with insufficiency, but there is a noticeable blanching of the skin of the face.

On examination of an echocardiogram, aortic valve insufficiency is expressed as a moderate increase in the lumen at the orifice of the artery. There are also noises in the left chest area, which indicates the progress of the discrepancy between the lunar flaps (more than 10 mm). Strong tremors are explained by the increased work of the left ventricle and atrium in the compensation mode.

Diagnostic methods

To correctly assess changes in the functionality of the heart and its systems, you need to undergo high-quality diagnostics:

1. dopplerography;
2. x-ray (effectively identifies pathological changes in the valves and tissues of the heart);
3. echocardiography;
4. phonocardiography (detects murmurs in the heart and aorta);

When examining, experts pay attention to:

• complexion (if it is pale, it means insufficient blood supply to small peripheral vessels);
• rhythmic dilation of the pupils or their constriction;
• the state of the language. Pulsations, change its shape (noticeable upon examination);
• head shaking (involuntary), which occurs in the rhythm of the heart (this is caused by strong tremors in the carotid arteries);
• visible pulsation of the cervical vessels;
• heart tremors and their strength on palpation.

The pulse is unstable, there are ups and downs. With the use of auscultation of the heart organ and its vessels, murmurs and other signs can be detected faster and more accurately.

Treatment

At the very beginning, aortic regurgitation may not require special treatment (first degree), only prevention methods are applicable. Later, therapeutic or cardiological treatment is prescribed. Patients should follow the recommendations of specialists regarding the way of organizing life.

It is important to limit physical activity, stop smoking or drinking alcohol and be systematically examined by ultrasound or ECG.

With drug treatment of the disease, doctors prescribe:

If the disease is in the last degree, then only surgical intervention will help.

Cases when a patient needs urgent consultation with a surgeon:

• when the state of health has deteriorated sharply, and the return ejection towards the left ventricle is 25%;
• with violations of the left ventricle;
• when 50% of the blood volume is returned;
• a sharp increase in the size of the ventricle (more than 5-6 cm).

Today there are two types of operations:

1. Surgical intervention associated with the implantation. It is performed with a reverse ejection of the aortic valve of more than 60% (it should be noted that today biological prostheses are almost never used).
2. Operation in the form of intra-aortic balloon counterpulsation. It is done with a slight deformation of the valve leaflets (at 30% blood ejection).

Aortic insufficiency may not occur if preventive actions are taken in a timely manner against rheumatic, syphilis and atherosclerotic pathologies.

Exactly surgical care helps to get rid of the problems under consideration. Timeliness and quality of measures taken can greatly increase the chance of a person returning to normal life.

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Patient 45 years old. Survey. ECHOKG data: the width of the lumen of the aortic root is 30.0 mm, the excursion of the aortic walls is not reduced. Systolic divergence of the aortic valve leaflets is 20.0 mm. the maximum diameter of the left atrium (DLP max.) \u003d 30.0 mm. mitral valve leaflets move in antiphase speed E F front sash 3.5 cm / sec; mitral-septal separation 6.0 mm. the maximum amplitude of the divergence of the mitral valve leaflets (MC RS) \u003d 29.0 mm. End diastolic size of the left ventricle (EDR LV) \u003d 50.0 mm; The end systolic dimension of the left ventricle (CSR LV) \u003d 32.0 mm. Left ventricular end-diastolic volume (LV EDV) \u003d 118.0 ml, left ventricular end-systolic volume (LV EDV) \u003d 41.0 ml. Stroke volume (SV) \u003d 77.0 ml ... ..

Questions:

1. Give an overall rating.
2. To estimate the indices of central hemodynamics and global contractility of the left ventricle.
3. The chambers of the heart are not dilated, the valve apparatus is intact, there are no signs of hypertrophy and local violations of the myocardial contractility of the left ventricle.
4. Indicators of global contractility of the left ventricle and central hemodynamics within normal limits.

A 40-year-old patient has a history of: - rheumatoid arthritis in childhood. ECHOKG data. The width of the lumen of the aortic root is 28.0 mm. Excursion of the aortic walls is moderately reduced. Increased echogenicity of the aortic valve cusps, decreased mobility. In the upper part of the lumen of the aortic root, there are multiple additional echo signals throughout the entire cardiac cycle. Systolic opening of the aortic valve cusps \u003d 8.0 mm. The maximum diameter of the left atrium (DLP max.) \u003d 42.0 mm. The leaflets of the mitral valve move in antiphase; the maximum amplitude of the divergence of the mitral valve leaflets (MC RS) \u003d 28.0 mm. End diastolic size of the left ventricle (EDD LV) \u003d 51.0 mm; The final systolic dimension of the left ventricle (CSR LV) \u003d 33.0 mm. End diastolic volume of the left ventricle (EDV LV) \u003d 124.0 ml, Ejection fraction (EF) \u003d 64.5%….

Questions:

1. Give an overall assessment and indicate pathology
2. What kind of syndrome are we talking about the severity of violations.

1. There is a change in the cusps of the aortic valve with a decrease from the systolic divergence. There is a noticeable hypertrophy of the left ventricular myocardium with initial disturbances in diastolic function, a decrease in the elasticity of the hypertrophied left ventricle. Increased systolic pressure gradient between the left ventricle and aorta.

2. This is a moderate aortic stenosis syndrome with preserved contractile function of the left ventricle.

Patient 36 years old. Childhood history of rheumatoid arthritis. ECHOKG data: the width of the lumen of the aortic root is 28.0 mm, the excursion of the aortic walls is not reduced. Systolic divergence of the aortic valve leaflets 18.0 mm; the maximum diameter of the left atrium (DLP max.) \u003d 50.0 mm. Mitral valve leaflets increased echogenicity have a unidirectional "P" - shaped movement. End diastolic size of the left ventricle (EDR LV) \u003d 49.0 mm; The end systolic dimension of the left ventricle (CSR LV) \u003d 34.0 mm. End diastolic volume of the left ventricle (EDV lv) \u003d 113.0 ml, end systolic volume of the left ventricle (ESV LV) \u003d 47.0 ml. Ejection fraction (EF) \u003d 58.4%; Anteroposterior shortening fraction ( D S) \u003d 30.6% .. The thickness of the interventricular septum at the end of diastole (TMZhP cd) \u003d 10.0 mm; excursion of the interventricular septum (E IVS) \u003d 7.0 mm; the thickness of the posterior wall of the left ventricle at the end of diastole (TZS cd) \u003d 9.2 mm. excursion of the posterior wall of the left ventricle (EZSLZH) \u003d 9.0 mm ...

Questions:

1. What syndrome are we talking about? The severity of the violations.

1. There is a marked dilation of the left atrium and right ventricle. Hypertrophy of the right ventricular myocardium. Increased echogenicity of the mitral valve leaflets, their deformation, decreased mobility. There is an increase in the linear velocity of the diastolic transmitral blood flow and its turbulent nature, the area of \u200b\u200bthe left atrioventricular opening is markedly reduced. Doppler echocardiography of the outflow tract of the right ventricle and the mouth of the pulmonary artery revealed signs of pulmonary arterial hypertension. Relative insufficiency of the pulmonary valve.

2. We are talking about the syndrome of stenosis of the left atrioventricular orifice (mitral stenosis), moderate severity. In this case, mitral stenosis is probably of rheumatic origin.

Patient 30 years old. Anamnesis: 2 years ago, an abortion complicated by a septic condition and the development of infective endocarditis. After a course of inpatient treatment, recurrence of infective endocarditis was not observed, it is constantly observed by a therapist and cardiologist.

ECHOKG data: the width of the lumen of the aortic root is 27.0 mm, the excursion of the aortic walls is normal. Systolic divergence of the aortic valve leaflets is 19.0 mm. the maximum diameter of the left atrium (DLP max.) \u003d 52.0 mm. the leaflets of the mitral valve move in antiphase, making an "M" -shaped movement, there is a slight increase in their echogenicity and thickening, mostly of the anterior leaflet, where there is a site of calcification closer to the base of the leaflet ...

Questions:

1. Give an overall assessment and indicate the pathology.

1.Dilatation of the left atrium and left ventricle takes place. Signs of volume loading on the left ventricle (increased excursion of its walls during cavity dilation). Signs of left ventricular myocardial hypertrophy. There are signs of organic changes in the aortic cusps of the aortic valve, without impairment of their mobility. Doppler echocardiography revealed signs of grade IV mitral regurgitation.

2. We are talking about the syndrome of mitral regurgitation (severe mitral regurgitation). The cause of mitral insufficiency was the transferred infectious endocarditis

Patient 40 years old. Complaints about the sensation of pulsation in the head and neck. Pain in the region of the heart (behind the breastbone) of a pressing character during physical exertion, passing after a few minutes at rest. The above complaints appeared 2 years ago. Previously, he considered himself practically healthy. The examination revealed a positive Wasserman reaction ( RW).

ECHOKG data: the width of the lumen of the aortic root is 45.0 mm, the excursion of the aortic walls is increased. Systolic divergence of the aortic valve leaflets is 22.0 mm., The aortic valve leaflets are mobile, their echogenicity is normal; there is a systolic non-closure of the aortic valve leaflets, the maximum left atrial diameter (DLP max.) \u003d 37.0 mm., the mitral valve leaflets move in antiphase, making an "M" -shaped movement, the systolic divergence of the mitral valve leaflets is 28.0 mm.

Questions:

1. Give a general description of the pathology.
2. What syndrome are we talking about?

1.There is an expansion of the lumen of the aortic root, with a relatively small change on the side of the aortic valve cusps, the mobility of which is not reduced, but there are signs of incomplete closure of them in diastole. There is a markedly pronounced dilatation of the left ventricle, hypertrophy of its myocardium, signs of volume loading on the left ventricle, diastolic tremor of the anterior mitral valve leaflet indicates a mechanical effect on the flow leaflet penetrating diastole from the aorta into the left ventricle. Doppler ECHO-KG study revealed pronounced signs of aortic regurgitation.

2. This is a syndrome of severe aortic valve insufficiency. The existing complaints, including attacks of angina pectoris, are associated with hemodynamic disturbances against the background of this syndrome. The cause of aortic insufficiency is presumably syphilitic meso-aortitis.

Patient 30 years old. Complaints of shortness of breath, palpitations during exercise, heaviness in the right hypochondrium, pasty legs. In the anamnesis, he was repeatedly treated for drug addiction in narcological hospitals; 2 years ago he had infective endocarditis. ECHOKG data: the width of the lumen of the aortic root is 35.0 mm, the excursion of the aortic walls is normal. Systolic divergence of the aortic valve leaflets is 19.0 mm. The leaflets of the aortic valve without visible changes; the maximum diameter of the left atrium (DLP max.) \u003d 35.0 mm. the leaflets of the mitral valve move in antiphase, making an "M" -shaped movement, speed E F front sash 3.6 cm / sec; the maximum amplitude of the divergence of the mitral valve leaflets (RS MK) \u003d 29.0 mm ...

Questions:

1. Give a general description of the pathological changes.
2. What syndrome are we talking about? The severity of the violations.

1. There are changes in the right heart. Dilation of the right ventricle and right atrium. Signs of volume loading on the right ventricle, hypertrophy of its myocardium. Signs of severe tricuspid regurgitation. Indirect signs of increased pressure in the right chambers of the heart and inferior vena cava. Signs of penetration of the regurgitant stream of the inferior vena cava and hepatic veins. Indirect signs of organic changes in the cusps of the tricuspid valve with the preservation of their mobility.

2. This is a syndrome of tricuspid valve insufficiency (severely expressed insufficiency). The cause of isolated tricuspid insufficiency in this case is probably a previous infectious endocarditis.

The patient is 28 years old. Complaints of stabbing-aching pain in the apex of the heart, long-term or short-term (less than 1 minute), without a clear connection with physical activity. Occasionally "interruptions" in the work of the heart, discomfort in the precordial region. Received for examination.

ECHOKG data: the width of the aortic root lumen is 27.0 mm, the excursion of the aortic walls is not reduced. Systolic divergence of the aortic valve leaflets is 21.0 mm. The leaflets of the aortic valve are of normal echogenicity. The maximum diameter of the left atrium (DLP max.) \u003d 32.0 mm. the leaflets of the mitral valve move in antiphase speed, making an "M" -shaped movement. Speed \u200b\u200bE F front sash 3.7 cm / sec; mitral-septal separation 5.0 mm. The maximum amplitude of the divergence of the leaflets of the mitral valve (RS MK) \u003d 29.0 mm ...

Questions:

1. Give an overall rating.
2. What syndrome are we talking about? The severity of the violations.

1.There is a change in the leaflets of the mitral valve with systolic sagging (deflection) of the anterior leaflet into the cavity of the left atrium. There are signs of organic changes in the leaflets of the mitral valve without disturbing their opening. The signs of mitral regurgitation were revealed. The rest of the heart chambers were not enlarged, no signs of functional impairment were revealed.

2. It is a syndrome of mitral valve prolapse (prolapse). In this case, stage II mitral valve prolapse with stage II mitral regurgitation and a sign of myxomatous degeneration of the leaflets.

The most common causes of organic aortic valve insufficiency are:

• Rheumatism (about 70% of cases);
• Infective endocarditis;
• More rare causes of this defect include atherosclerosis, syphilis, systemic lupus erythematosus (Liebman-Sachs lupus endocarditis), rheumatoid arthritis, etc.

In rheumatic endocarditis, thickening, deformation and wrinkling of the semilunar valve leaflets occur. As a result, their tight closure during diastole becomes impossible, and a valve defect is formed.

Infective endocarditis often affects previously altered valves (rheumatic lesions, atherosclerosis, congenital anomalies, etc.), causing deformation, erosion or perforation of the valves.

It should be borne in mind the possibility of the occurrence of relative insufficiency of the aortic valve as a result of a sharp expansion of the aorta and fibrous ring of the valve in the following diseases:

• arterial hypertension;
• aortic aneurysms of any genesis;
• ankylosing rheumatoid spondylitis.

In these cases, as a result of the expansion of the aorta, there is a divergence (separation) of the aortic valve cusps and they also do not close during diastole.

Finally, one should remember about the possibility of a congenital aortic valve defect, for example, the formation of a congenital bicuspid aortic valve or aortic enlargement in Marfan syndrome, etc.

Insufficiency of the aortic valve with congenital defects is rare and is more often combined with other congenital defects.

Insufficiency of the aortic valve leads to the return of a significant part of the blood (regurgitation) ejected into the aorta back into the left ventricle during diastole. The volume of blood returning to the left ventricle may exceed half of the total cardiac output.

Thus, with insufficiency of the aortic valve, during diastole, the left ventricle fills as a result of both the flow of blood from the left atrium and aortic reflux, which leads to an increase in the end diastolic volume and diastolic pressure in the left ventricular cavity.

As a result, the left ventricle is enlarged and significantly hypertrophied (the end diastolic volume of the left ventricle can reach 440 ml, with a norm of 60-130 ml).

Hemodynamic changes

Loose closure of the aortic valve leaflets leads to regurgitation of blood from the aorta to the LV during diastole. The reverse blood flow begins immediately after the closure of the semilunar valves, i.e. immediately after the II tone, and can continue throughout the diastole.

Its intensity is determined by the changing pressure gradient between the aorta and the LV cavity, as well as the size of the valve defect.

The mitralization of vice - the possibility of "mitralization" of aortic insufficiency, i.e. occurrence of relative mitral valve insufficiency with significant LV dilatation, dysfunction of the papillary muscles and expansion of the fibrous ring of the mitral valve.

In this case, the valve flaps are not changed, but do not completely close during ventricular systole. Usually, these changes develop in the late stages of the disease, with the onset of LV systolic dysfunction and pronounced myogenic dilatation of the ventricle.

"Mitralization" of the insufficiency of the aortic valve leads to regurgitation of blood from the LV to the LA, expansion of the latter and a significant aggravation of stagnation in the pulmonary circulation.

The main hemodynamic consequences of aortic valve insufficiency are:

• Compensatory eccentric LV hypertrophy (hypertrophy + dilatation), which occurs at the very beginning of the defect formation.
• Signs of left ventricular systolic failure, stagnation of blood in the pulmonary circulation and pulmonary hypertension, developing with decompensation of the defect.
• Some features of arterial blood filling vascular system a large circle of blood circulation:

Increased systolic blood pressure;

Lowered diastolic blood pressure;

Increased pulsation of the aorta, large arterial vessels, and in severe cases, muscle-type arteries (arterioles), caused by an increase in arterial filling during systole and a rapid decrease in filling in diastole;

Impaired perfusion of peripheral organs and tissues due to a relative decrease in effective cardiac output and a tendency to peripheral vasoconstriction.

• Relative insufficiency of coronary blood flow.

1. Eccentric left ventricular hypertrophy

An increase in LV diastolic blood filling leads to a volume overload of this part of the heart and an increase in the EDV of the ventricle.

As a result, pronounced eccentric LV hypertrophy (myocardial hypertrophy + dilatation of the ventricular cavity) develops - the main mechanism for compensating for this defect. For a long time, an increase in the force of LV contraction, which is due to an increased muscle mass ventricle and the inclusion of the Starling mechanism, ensures the expulsion of the increased blood volume.

Another peculiar compensatory mechanism is tachycardia characteristic of aortic insufficiency, leading to a shortening of diastole and some limitation of blood regurgitation from the aorta.

2. Cardiac decompensation

Over time, a decrease in LV systolic function occurs and, despite the continued growth of the EDV of the ventricle, its stroke volume no longer increases or even decreases. As a result, the EDV in the LV, the filling pressure and, accordingly, the pressure in the LA and the veins of the pulmonary circulation increase. Thus, stagnation of blood in the lungs in the event of LV systolic dysfunction (left ventricular failure) is the second hemodynamic consequence of aortic valve insufficiency.

In the future, with the progression of violations of LV contractility, persistent pulmonary hypertension and hypertrophy, and in rare cases, and pancreatic insufficiency. In this regard, it should be noted that with decompensation of aortic valve insufficiency, as well as with decompensation of aortic stenosis, clinical manifestations of left ventricular failure and blood stagnation in the pulmonary circulation always prevail, while signs of right ventricular failure are poorly expressed or (more often) absent altogether.

3.

The third hemodynamic consequence of aortic valve insufficiency is significant features of filling the arterial bed of the systemic circulation with blood, which are often detected even at the stage of defect compensation, i.e. even before the development of left ventricular failure. The most significant of them are:

Decrease in diastolic pressure in the aorta, which is explained by regurgitation of part of the blood (sometimes significant) in the LV

A pronounced increase in pulse pressure in the aorta, large arterial vessels, and with severe insufficiency of the aortic valve - even in the arteries of the muscle type (arterioles). This diagnostically important phenomenon arises as a result of a significant increase in LV SV (increased systolic blood pressure) and a rapid return of some blood to the LV (“emptying” of the arterial system), accompanied by a drop in diastolic blood pressure. It should be noted that an increase in the pulse oscillations of the aorta and large arteries and the appearance of pulsations of arterioles unusual for resistive vessels underlie numerous clinical symptoms detected in aortic valve insufficiency.

4. "Fixed" cardiac output

It was shown above that in case of aortic insufficiency at rest for a long time, the LV can provide the expulsion of an increased systolic blood volume into the aorta, which fully compensates for the excessive diastolic filling of the LV.

However, with physical exertion, i.e. in conditions of even greater intensification of blood circulation, the compensatory increased pumping function of the LV is not enough to "cope" with an even more increased volume overload of the ventricle, and a relative decrease in cardiac output occurs.

5. Impaired perfusion of peripheral organs and tissues

With the long-term existence of aortic valve insufficiency, a peculiar paradoxical situation arises: despite a sharp increase in cardiac output (more precisely, its absolute values), there is a decrease in perfusion of peripheral organs and tissues.

This is primarily due to the inability of the LV to further increase the stroke volume during physical and other types of exercise (fixed SV). With decompensation of the defect, a decrease in LV systolic function is also of great importance (both at rest and during exercise). Finally, activation of SAS, RAAS and tissue neurohormonal systems, including endothelial vasoconstrictor factors, also plays a role in disturbances in peripheral blood flow.

In case of severe aortic regurgitation, perfusion disorders of peripheral organs and tissues can also be caused by the described features of the blood filling of the arterial vascular system, namely: rapid outflow of blood from the arterial system or, at least, stopping or slowing down the movement of blood through peripheral vessels during diastole.

6. Insufficiency of coronary circulation

One more important consequence of aortic valve insufficiency should be especially explained - the occurrence of coronary circulation insufficiency, which is explained by two main reasons associated with the peculiarities of intracardiac hemodynamics in this defect:

Low diastolic pressure in the aorta.
As you know, filling of the coronary vascular bed of the LV occurs during diastole, when intramyocardial tension and diastolic pressure in the LV cavity decrease and, accordingly, the pressure gradient between the aorta (about 70-80 mm Hg) and the LV cavity (5– 10 mm Hg), which determines the coronary blood flow. It is understood that a decrease in diastolic pressure in the aorta leads to a decrease in the aortic-left ventricular gradient, and coronary blood flow drops significantly.

The second factor leading to the occurrence of relative coronary insufficiency is a high intramyocardial LV wall tension during ventricular systole, which, according to Laplace's law, depends on the level of intracavitary systolic pressure and LV radius. Expressed ventricular dilatation is naturally accompanied by an increase in intramyocardial tension of its wall. As a result, LV work and myocardial oxygen demand increase sharply, which is not fully provided by coronary vessels functioning in unfavorable conditions from a hemodynamic point of view.

Clinical manifestations

Formed aortic valve insufficiency for a long time (10-15 years) may not be accompanied by subjective clinical manifestations and may not attract the attention of the patient and the doctor. The exception is cases of acutely developed aortic valve insufficiency in patients with infective endocarditis, dissecting aortic aneurysm, etc.

One of the first clinical manifestations of the disease is unpleasant sensation of increased pulsation in the neck, in the head, as well as increased heartbeats (patients "feel their heart"), especially in the supine position. These symptoms are associated with the high cardiac output and arterial pulse pressure described above.

These feelings are often joined by heart palpitationsassociated with sinus tachycardia characteristic of aortic valve insufficiency.

With a significant defect of the aortic valve, the patient may develop dizziness, a sudden feeling of lightheadedness and even a tendency to faint, especially with exertion or a rapid change in body position. This indicates a failure of cerebral circulation caused by the inability of the left ventricle to adequately change cardiac output (fixed stroke volume) and impaired cerebral perfusion.

Heartache (angina pectoris) - can also occur in patients with severe aortic valve defect, and long before the onset of signs of LV decompensation. Pain is usually localized behind the sternum, but often differ in character from typical angina pectoris.

They are not as often associated with certain external provoking factors (for example, physical activity or emotional stress), as angina attacks in patients with coronary artery disease. The pain often occurs at rest and is of a pressing or constrictive character, usually lasts long enough and is not always well controlled by nitroglycerin. Attacks of nocturnal angina pectoris, accompanied by profuse sweating, are especially difficult for patients.

Typical anginal attacks in patients with aortic valve insufficiency, as a rule, indicate the presence of concomitant ischemic heart disease and atherosclerotic narrowing of the coronary vessels.

The period of decompensation is characterized by the appearance of signs of left ventricular failure.

Dyspnea first appears during exercise, and then at rest. With a progressive decline in LV systolic function, dyspnea becomes orthopnea.

Then it is joined by attacks of suffocation (cardiac asthma and pulmonary edema). Characterized by the appearance of rapid fatigability during exercise, general weakness. For obvious reasons, all symptoms associated with insufficiency of cerebral and coronary circulation are aggravated by the occurrence of left ventricular failure. Finally, in more rare cases, when it persists and progresses for a long time pulmonary hypertension, and patients do not die from left ventricular failure, individual signs of blood stagnation in the venous bed of the systemic circulation (edema, heaviness in the right hypochondrium, dyspeptic disorders) associated with a drop in systolic function of the hypertrophied pancreas may be detected.

However, more often this does not happen, and the symptoms described above predominate in the clinical picture, due to damage to the left heart, features of the blood filling of the arterial vascular system of the great circle and signs of blood stagnation in the veins of the pulmonary circulation.

Inspection

During a general examination of patients with aortic insufficiency, first of all, attention is drawn to the pallor of the skin, indicating insufficient perfusion of peripheral organs and tissues.

With a pronounced defect of the aortic valve, numerous external signs of systolic-diastolic pressure drops in the arterial system, as well as increased pulsation of large and smaller arteries, can be detected:

• increased pulsation of the carotid arteries ("Dance of carotids"), as well as visible pulsation in the area of \u200b\u200ball superficially located large arteries (brachial, radial, temporal, femoral, arteries of the rear of the foot, etc.);
• de Musset symptom - rhythmic shaking of the head back and forth in accordance with the phases of the cardiac cycle (in systole and diastole);
• quincke's symptom ("capillary pulse", "precapillary pulse") - alternating redness (in systole) and blanching (in diastole) of the nail bed at the base of the nail with sufficiently intense pressure on its top. In a healthy person, with such pressure, both in systole and in diastole, a pale coloration of the nail bed remains. A similar variant of Quincke's "precapillary pulse" is detected by pressing on the lips with a glass slide;
• landolfi symptom - pulsation of the pupils in the form of their constriction and expansion;
• muller's symptom - pulsation of the soft palate.

Palpation and percussion of the heart

The apical impulse is significantly enhanced due to LV hypertrophy, diffuse ("domed") and displaced to the left and downward (LV dilatation). With a pronounced defect of the aortic valve, the apical impulse can be determined in the VI intercostal space along the anterior axillary line.

Systolic tremors are often detected at the base of the heart - along the left and right edges of the sternum, in the jugular notch, and even on the carotid arteries. In most cases, it does not indicate concomitant aortic insufficiency, stenosis of the aortic opening, but is associated with the rapid expulsion of an increased blood volume through the aortic valve. In this case, the opening of the aortic valve becomes relatively "narrow" for the sharply increased volume of blood ejected into the aorta during the expulsion period. This contributes to the onset of turbulence in the aortic valve region, the clinical manifestation of which is low-frequency systolic tremors, detected by palpation, and functional systolic murmur at the base of the heart, determined by auscultation.

Diastolic tremor in the precordial region with aortic valve insufficiency is extremely rare.

Percussion in all patients with aortic insufficiency is determined by a sharp shift of the left border of the relative dullness of the heart to the left. The so-called aortic configuration with an accentuated "waist" of the heart is characteristic.

Only when LA dilatation occurs, due to the mitralization of the defect, can the waist of the heart be flattened.

Heart auscultation

Typical auscultatory signs of aortic insufficiency are diastolic murmur in the aorta and at Botkin's point, weakening of II and I heart sounds, as well as the so-called "accompanying" systolic murmur in the aorta of a functional nature.

I tone changes... Usually, I tone at the apex is weakened as a result of a sharp volume overload of the LV and a slowdown in isovolumic contraction of the ventricle. Sometimes I tone is split.

II tone changes... Depending on the etiology of defect II, the tone can either increase or weaken until it disappears. Deformation and shortening of the valve cusps due to rheumatism or infective endocarditis contributes to the weakening of the II tone on the aorta or its disappearance. Syphilitic lesion of the aorta is characterized by an intensified II tone with a metallic tinge (“ringing” II tone).

Pathological III tone is heard in aortic insufficiency quite often. The appearance of the III tone indicates a pronounced volume overload of the LV, as well as a decrease in its contractility and diastolic tone.

Diastolic murmur on the aorta is the most characteristic auscultatory sign of aortic insufficiency. The murmur is best heard in the II intercostal space to the right of the sternum and in the III – IV intercostal space at the left edge of the sternum and is carried out to the apex of the heart.

Diastolic murmur in aortic regurgitation begins in the protodiastolic period, i.e. immediately after the II tone, gradually weakening during the diastole. Depending on the degree of regurgitation, the frequency response of diastolic murmur changes: slight regurgitation is accompanied by soft blowing, mainly high-frequency murmur; with severe regurgitation, a mixed frequency composition of the noise is determined, severe regurgitation leads to the appearance of a coarser low and medium frequency noise. This nature of the noise is observed, for example, with syphilitic damage to the aorta.

It should be remembered that with the decompensation of the defect, tachycardia, as well as with combined aortic heart disease, the intensity of the diastolic murmur of aortic insufficiency decreases.

Functional noise

Flint's functional diastolic murmur - This is a presystolic murmur of relative (functional) stenosis of the left atrioventricular opening, which is occasionally heard in patients with organic insufficiency of the aortic valve.

It occurs as a result of the displacement of the anterior cusp of the mitral valve by a stream of blood regurgitating from the aorta, which creates an obstacle to diastolic blood flow from the LA to the LV, during active atrial systole.

In the genesis of this noise, the vibration of the leaflets and chords of the mitral valve is probably also important, resulting from the "collision" of turbulent blood flows entering the LV cavity from the aorta and LA.

At the same time, at the apex of the heart, in addition to the wired organic diastolic murmur of aortic insufficiency, a presystolic noise amplification is also heard - Flint's murmur.

Functional systolic murmur relative stenosis of the aortic opening is often heard in patients with organic insufficiency of the aortic valve.

The murmur arises due to a significant increase in the systolic blood volume ejected into the LV aorta during the expulsion period, for which the normal unchanged aortic valve opening becomes relatively narrow - a relative (functional) stenosis of the aortic orifice is formed with turbulent blood flow from the LV to the aorta.

At the same time, in the aorta and at Botkin's point, in addition to the organic diastolic murmur of aortic insufficiency, during the expulsion of blood, a functional systolic murmur is heard, which can be carried out to the entire region of the sternum, the apex of the heart and spread to the region of the jugular notch and along the carotid arteries.

When examining the vascular system in patients with aortic valve insufficiency, it is necessary to pay attention to the existence of two more vascular auscultatory phenomena:

1. Symptom Durozier (double noise Durozier)... This unusual auscultatory phenomenon is heard over the femoral artery in the groin, just below the pupar ligament.

With a simple application of a stethoscope in this area (without pressure), the tone of the femoral artery can be determined - a sound that is synchronous with the local arterial pulse. With gradual pressure by the head of the stethoscope in this area, an artificial occlusion of the femoral artery is created and at first a quiet and short, and then more intense systolic murmur begins to be heard.

Subsequent compression of the femoral artery sometimes leads to the appearance of a diastolic murmur. This second murmur is quieter and shorter than the systolic murmur. The phenomenon of double murmur of Durozier is usually explained by a higher than normal volumetric blood flow rate or retrograde (towards the heart) blood flow in large arteries.

2. Traube double tone - a rather rare sound phenomenon when two tones are heard on a large artery (for example, a femoral one) (without compression of the vessel). The second tone is usually associated with the reverse blood flow in the arterial system, due to pronounced regurgitation of blood from the aorta to the LV.

Arterial pressure

With aortic insufficiency, an increase in systolic and a decrease in diastolic blood pressure occurs, as a result, pulse blood pressure increases.

The decrease in diastolic pressure with aortic valve insufficiency requires comment. With direct invasive measurement BP in the aorta diastolic pressure never drops below 30 mm Hg. Art. However, when measuring blood pressure by the Korotkov method in patients with severe aortic valve insufficiency, diastolic pressure is often reduced to zero. This means that during the measurement of blood pressure, when the pressure in the cuff decreases below the true diastolic pressure in the aorta above the artery, Korotkoff tones are still heard.

The reason for this discrepancy between direct and indirect measurement of blood pressure lies in the mechanisms of the appearance of Korotkoff sounds when measuring blood pressure. One way or another, Korotkoff sounds are determined by auscultation as long as intermittent blood flow remains in a large artery. In a healthy person, such a “pulsating” blood flow is artificially created when the brachial artery is compressed by the cuff. When the pressure in the cuff reaches diastolic blood pressure, the difference between the blood flow velocity in the brachial artery in systole and diastole decreases, and Korotkoff's sounds sharply weaken (phase IV of Korotkoff sounds) and disappear altogether (phase V).

Severe aortic valve insufficiency is characterized by the constant existence of a large circle of "pulsating" blood flow in the arterial system. Therefore, if you listen to the area of \u200b\u200ba large artery (even without compressing it with a cuff), sometimes (with severe aortic insufficiency) you can hear sounds reminiscent of Korotkov's tones. It should be remembered that an "endless tone" on a large artery (or diastolic blood pressure \u003d 0) can also be determined with a pronounced decrease in the tone of the arterial wall, for example, in patients with neurocirculatory dystonia.

In most cases, the pulse on the radial artery has characteristic features: a rapid rise (increase) of the pulse wave and its equally sharp and rapid decline are determined.

The arterial pulse becomes fast, high, large and fast (pulsus celer, altus, magnus et frequens). Such a pulse, creating an alternation of rapid and strong tension in the walls of the arteries, can lead to the fact that tones begin to be determined on the arteries, where sounds are not normally heard. Moreover, the severity of pulsus celer et magnus can be reflected in the appearance of the so-called "palmar tone", determined on the inner surface of the patient's hand, applied to the doctor's ear.

Instrumental diagnostics

ECG

An electrocardiographic study reveals a turn of the electrical axis of the heart to the left, an increase in the R wave in the left chest leads, and, later, a downward shift of the ST segment and inversion of the T wave in the standard and left chest leads.

In case of insufficiency of the aortic valve, the ECG determines:

• With aortic valve insufficiency, in most cases, signs of pronounced LV hypertrophy without its systolic overload are revealed, i.e. without changing the terminal part of the ventricular complex.
• Depression of the RS – T segment and flattening or inversion of T are observed only during the period of defect decompensation and the development of heart failure.
• In case of "mitralization" of aortic insufficiency, in addition to signs of LV hypertrophy, signs of left atrial hypertrophy (P-mitrale) may appear on the ECG.

X-ray examination

In case of aortic valve insufficiency, as a rule, clear radiographic signs of LV enlargement are revealed. In direct projection already on the most early stages the development of the disease is determined by a significant lengthening of the lower arch of the left contour of the heart and displacement of the apex of the heart to the left and down.

In this case, the angle between the vascular bundle and the LV contour becomes less obtuse, and the “waist” of the heart becomes more accentuated (“aortic” configuration of the heart). In the left anterior oblique projection, a narrowing of the retrocardial space occurs.

In addition to the described radiological signs, in patients with aortic insufficiency, the expansion of the ascending part of the aorta is determined. Finally, the decompensation of the defect is accompanied by the appearance of signs of venous congestion in the lungs, described above.

Echocardiography

Echocardiographic examination reveals a number characteristic symptoms... The end diastolic dimension of the left ventricle is increased. Determined hyperkinesia of the posterior wall of the left ventricle and interventricular septum. High-frequency flutter (tremor) of the anterior cusp of the mitral valve, the interventricular septum, and sometimes the posterior cusp during diastole is recorded. The mitral valve closes prematurely, and during the period of its opening, the amplitude of the leaflet movement is reduced.

Cardiac catheterization

During cardiac catheterization and carrying out appropriate invasive studies in patients with aortic insufficiency, an increase in cardiac output, LV ED and the volume of regurgitation are determined. The latter indicator is calculated as a percentage in relation to the stroke volume. The volume of regurgitation rather well characterizes the degree of aortic valve insufficiency.

Diagnostics and differential diagnostics

Recognition of aortic valve insufficiency usually does not cause difficulties with diastolic murmur at Botkin's point or on the aorta, an increase in the left ventricle and certain peripheral symptoms of this defect (high pulse pressure, an increase in the pressure difference between the femoral and brachial arteries up to 60-100 mm Hg. ., characteristic changes in pulse).
However, diastolic murmur in the aorta and in the V point can also be functional, for example, with uremia. With concomitant heart defects and small aortic regurgitation, recognition of the defect may be difficult. In these cases, echocardiographic examination helps, especially in combination with Doppler cardiography.

The greatest difficulties arise in establishing the etiology of this defect. Other rare causes are possible: myxomatous valve lesion, mucopolysaccharidosis, osteogenesis imperfecta.

Rheumatic origin heart disease can be confirmed by anamnesis data: approximately half of these patients have indications of typical rheumatic arthritis. Convincing signs of mitral or aortic stenosis also support a rheumatic etiology of the defect. Identifying aortic stenosis can be difficult. Systolic murmur above the aorta, as mentioned above, is also heard in pure aortic insufficiency, and systolic tremor above the aorta occurs only with its sharp stenosis. In this regard, echocardiographic examination is of great importance.

The appearance of aortic insufficiency in a patient with rheumatic mitral heart disease is always suspicious of the development infective endocarditis, although, may be due to the recurrence of rheumatism. In this regard, in such cases, it is always necessary to conduct a thorough examination of the patient with repeated blood cultures. Insufficiency of the aortic valve of syphilitic origin in last years is much less common. Diagnosis is facilitated by identifying signs of late syphilis in other organs, such as lesions of the central nervous system. In this case, the diastolic murmur is better heard not at the Botkin-Erb point, but above the aorta - in the second intercostal space on the right and spreads widely downward, on both sides of the sternum. The ascending part of the aorta is enlarged. In a significant number of cases, positive serological reactions, the reaction of immobilization of pale treponema is of particular importance.

Aortic insufficiency may be due to atherosclerosis... With atheromatosis of the aortic arch, the valve ring expands with the occurrence of slight regurgitation, less often atheromatous lesion of the valves of the valve itself is noted. With rheumatoid arthritis (seropositive), aortic insufficiency is observed in approximately 2-3% of cases, and with a long course (25 years) of ankylosing spondylitis, even in 10% of patients. Cases of rheumatoid aortic insufficiency have been described long before the appearance of signs of damage to the spine or joints. Even less often, this defect is observed in systemic lupus erythematosus (according to V.S. Moiseev, I.E. Tareeva, 1980, in 0.5% of cases).

Prevalence marfan syndrome in pronounced form, according to various data, from 1 to 4 - 6 per 100,000 population.
Cardiovascular pathology, along with typical changes in the skeleton and eyes, is part of this syndrome, but it is found with difficulty in almost half of these patients only with the help of echocardiography. In addition to the typical lesion of the aorta with the development of its aneurysm and aortic insufficiency, damage to the aortic and mitral valves is possible. With an obvious familial predisposition and pronounced extracardiac signs of cardiovascular disease, the syndrome is detected in childhood. If the anomalies of the skeleton are not very pronounced, as in the patient described above, then heart damage can be found at any age, however, usually in the third, fourth and even sixth decades of life. Changes in the aorta concern primarily the muscle layer; necrosis with cysts are found in the wall, fibromyc-somatous changes in the valves are possible. Aortic regurgitation often progresses gradually, but it can appear or worsen suddenly.

Cystic necrosis, without other signs of Marfan syndrome, is referred to as erdheim syndrome... It is believed that similar changes can occur simultaneously or independently in the pulmonary arteries, causing them, the so-called congenital idiopathic expansion. An important differential diagnostic feature that allows to distinguish the lesion of the aorta in Marfan syndrome from syphilitic is the absence of its calcification. The defeat of the mitral valve and chords with their break occurs only in some patients, usually accompanies the defeat of the aorta and leads to prolapse of the mitral valve leaflets with mitral insufficiency.

A rare cause of aortic regurgitation can be takayasu's disease - nonspecific aortoarteritis, which occurs mainly in young women in the second - third decade of life and is associated with immune disorders. The disease usually begins with common symptoms: fever, weight loss, joint pain. In the future, the clinical picture is dominated by signs of damage to large arteries extending from the aorta, more often from its arch. Due to impaired patency through the arteries, the pulse often disappears, sometimes only on one arm. The defeat of the large arteries of the aortic arch can lead to cerebrovascular insufficiency and visual impairment. The defeat of the renal arteries is accompanied by the development of arterial hypertension. Insufficiency of valves, the aorta may be due to the expansion of the aortic arch in patients with gagant cell arteritis. This disease develops in the elderly, manifested by damage to the temporal arteries, which, in typical cases, are palpable in the form of a dense painful knotty cord. Possible damage to the intracardiac arteries.

Aortic insufficiency is often combined with a variety of extracardiac manifestations, a careful analysis of which makes it possible to establish the nature of the heart defect.

Forecast

The life expectancy of patients, even with severe aortic insufficiency, is usually more than 5 years from the moment of diagnosis, and in half - even more than 10 years.

The prognosis worsens with the addition of coronary insufficiency (angina attacks) and heart failure. Drug therapy in these cases is usually ineffective. The life expectancy of patients after the onset of heart failure is about 2 years. Timely surgery significantly improves the forecast.

The aortic valve is the area of \u200b\u200bthe heart that sits between the left ventricle and the aorta. It is needed to exclude the return of the released blood to the cell.

What is the aortic valve made of?

Passing heart 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, underlies the formation.
• Three semilunar valves along the edge of the annulus fibrosus - connecting, obscure the lumen of the artery. When the aortic crescents are closed, a contour is formed that resembles the brand name of a Mercedes car. They are normally the same, with a flat surface. AK valves are made of two types of tissues - connective and fine muscle.
• Valsalva sinuses - the 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-fold; unlike the latter, it is devoid of both tendon chords and papillary muscles. The mechanism of action is passive. The aortic valve is driven by blood flow and a pressure differential between the left heart ventricle and the attached artery.

Algorithm of the aortic valve

The work cycle looks like this:

1. Elastin fibers return the leaflets to their original position, take them to the walls of the aorta and open them for blood flow.
2. The aortic root narrows, tightening the crescent moon.
3. The pressure in the heart chamber rises, the mass of blood is pushed out, pressing the outgrowths against the inner walls of the aorta.
4. The left ventricle contracted, the current slowed down.
5. The sinus at the walls of the aorta creates vortices that deflect the leaflets, and the opening in the heart is closed by a valve. The process is accompanied by a loud bang, which is audible through a stethoscope.

When and why does aortic valve disease occur?

According to the time of occurrence, aortic valve defects are divided into congenital and acquired.

Congenital malformations of AK

Disorders are formed during embryonic development.

There are such types of anomalies:

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

The bicuspid structure of the aortic valve is a fairly common anomaly: up to 20 cases per 1,000 children. But usually 2 valves are enough to provide sufficient blood flow, no treatment is required.

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

In congenital malformations with stenosis of the aortic orifice, bicuspid AK is detected in 85% of sick children. In adults, about 50% of these cases.

One-leaf aortic valve - rare vice... The sash opens thanks to a single commissure. This disorder results in severe aortic stenosis.

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

Such CHD (congenital heart defects) in children are usually formed after infections that a woman has had during pregnancy, due to adverse 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 - AK tissues are damaged.

Acquired aortic heart is caused by various diseases. Of great importance in the formation of such defects are autoimmune diseases, rheumatism, which provokes 4 out of 5 disorders. In case of a disease, the valves of the AK are spliced \u200b\u200bin the part of the base and wrinkled, many thickenings appear, which is why deformation forms on the pockets.

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

The membrane inside the heart and the leaflet becomes inflamed. Then microbes will settle on tissues and create tubercle colonies. From above, those are covered with blood proteins and form a growth on the valve, resembling warts. These structures prevent the valve parts from closing.

There are other causes of AK anomalies:

• Hypertension;
• Enlarged aortic valve.

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

Acquired aortic valve abnormalities 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.

AC leaflet fibrosis

Often, when diagnosed, a cardiologist detects fibrosis of the aortic valve cusps. What it is? This is a disease in which the valves thicken, the number of blood vessels and tissue nutrition deteriorates, and some areas die off. And the more extensive the lesions, the more severe the patient's symptoms.

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

Fibrosis also occurs when the hormonal background changes, metabolic disorders, after myocardial infarction, excessive physical exertion, uncontrolled medication.

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

AK stenosis

This is an AK defect, in which the area of \u200b\u200bthe lumen decreases, which is why the blood does not leave during contraction. From this, the left ventricle increases, pains, high blood pressure appear.

Distinguish between congenital and acquired stenosis.

The following disorders contribute to the development of this pathology:

• Single or bivalve AK, while tricuspid is the norm;
• Membrane with a hole under the aortic valve;
• The muscular roller, which is located above the valve.

Streptococcal, staphylococcal infections lead to the development of stenosis, which penetrate into the heart with blood flow, causing the same endocarditis. Another reason is systemic diseases.

Not the least role in the origin of aortic valve stenosis is played by age-related disorders, calcification, atherosclerosis. 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 by the size of the lumen:

• Light - up to 2 cm (at a rate of 2.0–3.5 cm 2);
• Moderate - 1–2 cm 2;
• Heavy - up to 1 cm 2.

Stages of AK deficiency

Allocate the degree of insufficiency of the aortic valve:

• At 1 degree there are practically no symptoms of the disease. The walls of the heart on the left are slightly enlarged, the capacity of the left ventricle increases.
• At grade 2 (period of latent decompensation) there are no pronounced symptoms yet, but the morphological change in the structure is already more noticeable.
• At grade 3 coronary insufficiency is formed, the blood partially returns to the left ventricle.
• At 4 degrees Insufficiency of AK, the contraction of the left ventricle is weakened, resulting in stagnation in the vessels. Shortness of breath, a feeling of lack of air, pulmonary edema develops, and heart failure develops.
• At grade 5 disease salvation of the sick becomes an insoluble task. The heart contracts weakly, causing blood stasis. This is a near-death condition.

AK deficiency symptoms

The disease sometimes goes unnoticed. Aortic valve defect affects well-being if the reverse flow reaches 15-30% of the volume of the left ventricular capacity.

Then the following symptoms arise:

• Pain in the heart resembling angina pectoris;
• Headache, vertigo;
• Sudden loss of consciousness;
• Dyspnea;
• Vascular pulsation;
• Increased heartbeat.

With the aggravation of the disease, puffiness and heaviness in the hypochondrium on the right are added to these symptoms of aortic capan insufficiency due to stagnant processes in the liver.

If the cardiologist suspects AK defect, then he pays attention to the following visual signs:

• Pallor of the skin;
• Change in pupil size.

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

On examination and auscultation of the patient, the doctor notes a pronounced systolic murmur. Measurement of pressure shows that the upper indicator is growing and the lower one is decreasing.

Diagnosis of AK defects

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

In addition to the physical examination, if an aortic valve defect is suspected, general analysis urine and blood. This reveals other disorders, inflammation. Biochemical research determines the level of proteins, uric acid, glucose, cholesterol, reveals lesions of internal organs.

The value is represented by the information obtained using hardware diagnostic techniques:

• Electrocardiogram - indicates the frequency of contractions and the size of the heart;
• Echocardiography - determines the size of the aorta and lets you know if the valve anatomy is distorted;
• Transesophageal diagnosis - a special probe helps to calculate the area of \u200b\u200bthe aortic ring;
• Catheterization - measures the pressure in the chambers, shows the characteristics of the blood flow (used in patients over 50 years old);
• Doppler ultrasonography - gives an idea of \u200b\u200bthe return blood flow, the severity of prolapse, the compensatory reserve of the heart, the severity of the stenosis and determines whether surgery is required;
• Bicycle ergometry - is carried out for young patients with suspicion of AK defect in the absence of patient complaints.

Treatment of AK defects

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

Conservative techniques

In most cases, AK deficiency develops gradually. With the right medical care manages to stop the progression. For drug treatment use drugs that affect the symptoms, the strength of myocardial contractions, prevent arrhythmias.

These are the following groups of funds:

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

Only a doctor chooses medicines, determines the dosage and duration of treatment.

Who is the surgery indicated for?

You can't do without radical techniques if the heart stops performing functions.

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

Surgery is required for the following conditions:

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

The patient is denied a surgical operation 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 surgery that are prescribed for AK deficiency:

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

Upon reaching the AK, the structure swells and restores the tight closing of the valves.

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

This allows you to functionally restore the work of the heart apparatus. Replacement of the arterial valve is indicated when the reverse flow is 25-60%, there are numerous and significant manifestations of the disease, the size of the ventricle exceeds 6 cm.

The operation is well tolerated and allows you to get rid of arterial insufficiency... The surgeon dissects 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 childhoodthen the annulus fibrosus grows with the body. Instead of a removed pulmonary valve, a prosthesis is installed, which works longer in this place.

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

Predictions, complications of AK defects

How many live with similar pathologies? The prognosis depends on the stage at which treatment is started and the cause of the anomaly. Usually, the survival rate for a pronounced form, if there are no symptoms of decompensation, is 5-10 years. Otherwise, the lethal outcome occurs within 2-3 years.

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

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

Insufficiency of AK is a serious ailment that, without supervision by a cardiologist and treatment, leads to life-threatening complications. Against the background of the anomaly, myocardial infarction, arrhythmias, 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 CHD, including the abnormal structure of the valve - single-leaf, bicuspid. Prevention consists in healthy habits, regular walks in the area with green spaces, refusal of 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, cereals. It is also necessary to reduce psycho-emotional stress.

Video: Insufficiency of the aortic valve.

Aortic insufficiency is a pathology in which the aortic valve leaflets do not close completely, as a result of which the return of blood to the left ventricle of the heart from the aorta is impaired.

This disease causes many unpleasant symptoms - chest pains, dizziness, shortness of breath, irregular heartbeats, and more.

The aortic valve is a shutter in the aorta that has 3 cusps. Designed to separate the aorta and left ventricle. In a normal state, when blood flows from this ventricle into the aortic cavity, the valve closes tightly, pressure is created, due to which the flow of blood through the thin arteries to all organs of the body is ensured, without the possibility of reverse effusion.

If the structure of this valve has been damaged, it only partially overlaps, which leads to a reverse flow of blood into the left ventricle. Wherein organs stop receiving the required amount of blood for normal functioning, and the heart has to contract more intensively to compensate for the lack of blood.

As a result of these processes, aortic insufficiency is formed.

According to statistics, this aortic valve insufficiency occurs in about 15% of peoplehaving any kind of heart disease and often accompanies diseases such as the mitral valve. As an independent disease, this pathology occurs in 5% of patients with heart defects. Most often it affects males, as a result of exposure to internal or external factors.

Useful video on aortic valve insufficiency:

Causes and risk factors

Aortic regurgitation occurs when the aortic valve has been damaged. The reasons that lead to its damage can be the following:

Other causes of the disease, which are much less common, can be: connective tissue diseases, rheumatoid arthritis, ankylosing spondylitis, diseases immune system, long-term radiation therapy for the formation of tumors in the chest area.

Types and forms of the disease

Aortic insufficiency is divided into several types and forms. Depending on the period of formation of the pathology, the disease is:

• congenital- occurs due to poor genetics or the adverse effects of harmful factors on a pregnant woman;
• acquired- appears as a result of various diseases, tumors or injuries.

The acquired form, in turn, is divided into functional and organic.

• functional- is formed when the aorta or left ventricle expands;
• organic- occurs due to damage to the valve tissue.

1, 2, 3, 4 and 5 degrees

Depending on the clinical picture of the disease, aortic insufficiency is of several stages:

1. First stage... It is characterized by the absence of symptoms, a slight enlargement of the heart walls on the left side, with a moderate increase in the size of the left ventricular cavity.
2. Stage two... The period of latent decompensation, when pronounced symptoms are not yet observed, but the walls and cavity of the left ventricle are already greatly increased in size.
3. Stage Three. Formation of coronary insufficiency, when there is already a partial reflux of blood from the aorta back into the ventricle. It is characterized by frequent painful sensations in the region of the heart.
4. Stage four. The left ventricle contracts weakly, which leads to congestion in the blood vessels. Symptoms such as shortness of breath, shortness of breath, pulmonary edema, heart failure are observed.
5. Fifth stage... It is considered a dying stage, when it is almost impossible to save the patient's life. The heart contracts very weakly, as a result of which internal organs blood stagnation occurs.

Dangers and complications

If the treatment began untimely, or the disease proceeds in an acute form, pathology can lead to the development of the following complications:

• - a disease in which an inflammatory process forms in the valves of the heart as a result of exposure to damaged valve structures of pathogenic microorganisms;
• lungs;
• heart rhythm failures - ventricular or atrial premature beats, atrial fibrillation; ventricular fibrillation;
• thromboembolism - the formation of blood clots in the brain and other organs, which is fraught with the occurrence of strokes and heart attacks.

In the treatment of aortic insufficiency surgically, there is a risk of developing complications such as: destruction of the implant, endocarditis. Operated patients often have to take medications for life to prevent complications.

Symptoms

The symptoms of the disease depend on its stage. In the initial stages, the patient may not experience any discomfort., since only the left ventricle is exposed to the load - a fairly powerful part of the heart, which is able to withstand failures in the circulatory system for a very long time.

With the development of pathology, the following symptoms begin to appear:

• Throbbing sensations in the head, neck, increased heart rate, especially when lying down. These signs arise due to the fact that a larger volume of blood enters the aorta than usual - to normal quantity blood is added, which returned to the aorta through a loosely closed valve.
• Pain in the region of the heart... They can be compressive or squeezing, appear due to impaired blood flow through the arteries.
• Heart palpitations... It is formed as a result of a lack of blood in the organs, as a result of which the heart is forced to work at an accelerated rhythm in order to compensate for the required volume of blood.
• Dizziness, fainting, severe headaches, vision problems, buzzing in the ears... Typical for stages 3 and 4, when blood circulation in the brain is disturbed.
• Weakness in the body, increased fatigue, shortness of breath, abnormal heart rhythms, increased sweatinge. At the beginning of the disease, these symptoms occur only during physical exertion, later they begin to bother the patient and in a calm state. The appearance of these signs is associated with a violation of blood flow to the organs.

The acute form of the disease can lead to overloading of the left ventricle and the formation of pulmonary edema in conjunction with a sharp decrease in blood pressure. If during this period, surgical care is not provided, the patient may die.

When to see a doctor and which one

This pathology needs timely medical care... If you find the first signs - increased fatigue, throbbing in the neck or head, pressing pain in the sternum and shortness of breath - you should consult a doctor as soon as possible. This disease is treated therapist, cardiologist.

Diagnostics

To make a diagnosis, the doctor examines the patient's complaints, his lifestyle, anamnesis, then the following examinations are carried out:

• Physical examination... Allows to identify such signs of aortic insufficiency as: pulsation of the arteries, dilated pupils, expansion of the heart to the left, enlargement of the aorta in its initial section, low blood pressure.
• Analysis of urine and blood... With its help, you can determine the presence of concomitant violations and inflammatory processes in the body.
• Biochemical blood test... Shows the level of cholesterol, protein, sugar, uric acid. It is necessary in order to identify organ damage.
• ECGto determine the heart rate and size of the heart. Find out all about.
• Echocardiography... Allows you to determine the diameter of the aorta and pathology in the structure of the aortic valve.
• X-ray... Shows the location, shape and size of the heart.
• Phonocardiogramfor examining heart murmurs.
• CT, MRI, KKG - to study blood flow.

Treatment methods

In the initial stages, when the pathology is poorly expressed, patients are prescribed regular visits to a cardiologist, an ECG examination and an echocardiogram. Moderate aortic regurgitation is treated with medication, the goal of therapy is to reduce the likelihood of damage to the aortic valve and the walls of the left ventricle.

First of all, drugs are prescribed that eliminate the cause of the development of pathology. For example, if the cause is rheumatism, antibiotics may be indicated. As additional funds are prescribed:

• diuretics;
• aCE inhibitors - Lisinopril, Elanopril, Captopril;
• beta blockers - Anaprilin, Transikor, Atenolol;
• angiotensin receptor blockers - Naviten, Valsartan, Losartan;
• calcium blockers - Nifedipine, Corinfar;
• drugs to eliminate complications resulting from aortic insufficiency.

In severe forms, surgery may be prescribed... There are several types of surgery for aortic insufficiency:

• aortic valve plastic;
• aortic valve replacement;
• implantation;
• heart transplant - performed in case of severe heart damage.

If aortic valve implantation has been performed, patients are prescribed lifelong intake of anticoagulants - Aspirin, Warfarin... If the valve has been replaced with a prosthesis made of biological materials, anticoagulants will need to be taken in short courses (up to 3 months). Plastic surgery does not require taking these drugs.

To prevent relapse, antibiotic therapy, strengthening the immune system, and timely treatment of infectious diseases can be prescribed.

Forecasts and preventive measures

The prognosis for aortic insufficiency depends on the severity of the disease, as well as on what disease caused the development of the pathology. Survival of patients with pronounced form aortic insufficiency without symptoms of decompensation is approximately equal to 5-10 years.

The decompensation stage does not give such comforting predictions – drug therapy with it, most patients are ineffective, without timely surgical intervention, dies within the next 2-3 years.

Prevention measures for this disease are:

• prevention of diseases that cause damage to the aortic valve - rheumatism, endocarditis;
• hardening of the body;
• timely treatment of chronic inflammatory diseases.

Aortic valve insufficiency - an extremely serious illness that should not be left to chance... Folk remedies will not help matters here. Without proper drug treatment and constant monitoring by doctors, the disease can lead to serious complications, up to and including death.