Mitral valve prolapse: signs, degrees, manifestations, therapy, contraindications. Mitral valve prolapse in newborns What examination should be done

In order for the blood circulation of the pumping system of the heart to always occur in the right direction, there is a valve apparatus inside the atria and aorta that regulates blood flow. The valves open and close in such a way that the blood flow is directed only in one direction, avoiding the reverse flow. As soon as the atria pass blood to the aorta, they close, not allowing current into the original cavity. Mitral valve prolapse of the 1st degree provokes circulatory disorders.

To understand the cause of the appearance of such a pathology, it is necessary to know what the mitral valve is. This is part of the access device, which consists of flaps. If they begin to sag or bend towards the atrium, then the pathology is called mitral valve prolapse, abbreviated as MVP.

As a result of the deflection of the valves during the period of cardiac contraction, the blood leaving the atria partially returns back into their cavity. This problem is not dangerous or fatal, but due to impaired blood circulation, infectious pathogens can quickly land on the valve apparatus, causing serious inflammatory processes. Also, MV prolapse contributes to arrhythmic disorders.

If a person has retrograde blood flow, it is called regurgitation. As a rule, the sagging of the valve leaflets by less than 3 mm does not allow the blood to return back into the cavity of the left atrium.

There are two types of MV prolapse:

1. Primary or congenital;
2. Acquired.

If the pathology develops against the background of previous heart diseases (myocarditis, endocarditis, heart attack, defects), then it is referred to as a secondary type. The congenital type of prolapse occurs in 30-40% of people who do not feel any disorders in the cardiovascular system at all. In most cases, congenital pathologies cause virtually no heart problems.

Mitral valve prolapse with 1st degree regurgitation: how to determine?

Retrograde blood flow allows the classification of MVP. To determine the degree of sagging of the valve flaps, the amount of blood that fills the left ventricle is assessed. Most often, patients experience mitral valve prolapse with grade 1 regurgitation. That is, the valves sag towards the atria by 3-6 mm, but no more. In this case, reverse circulation does not cause significant disturbances in blood flow and patients do not experience unpleasant symptoms of the disease.

It is generally accepted that with grade 1 prolapse of the mitral valve, a person’s health condition is normal. Usually the problem is detected during random diagnostic procedures. No treatment is prescribed for the pathology, but regular visits to a cardiologist are mandatory.

Many patients are interested in whether it is possible to play sports when mitral valve prolapse with weak retrograde flow is detected. Doctors say that moderate physical activity is not contraindicated, but rather necessary. Recommended sports activities include:

But even with 1st degree of MVP, it is strictly forbidden to engage in weightlifting and use strength training equipment.

As for more serious pathologies, prolapse, which causes the valves to bend up to 9 mm into the atria, is classified as the second degree of pathology. In this case, drug treatment is used, and physical activity should be selected by a cardiologist.

Grade 3 MVP is characterized by sagging of more than 9 mm. This pathology leads to the development of serious changes in the structure of the heart muscle. Often, third-degree prolapse causes mitral valve insufficiency and severe arrhythmias. To eliminate the problem, it is necessary to perform an operation - suturing the valves or prosthetic valve apparatus. After surgery, the doctor can select therapeutic exercises.

Diagnosis of 1st degree mitral valve prolapse: how to recognize?

Basically, MVP can be diagnosed based on the first complaints that the patient describes. But, since the first two degrees are practically asymptomatic, the pathology is detected by chance. With more serious sagging of the valve leaflets, people experience the following symptoms:

The diagnosis of mitral valve prolapse of the 1st degree is established after passing such studies as listening to the heartbeat with a stethoscope. But if the regurgitation is mild, the doctor will not be able to detect a heart murmur. In such cases, the patient is referred for ECHO-cardiography with Doppler examination. The diagnostic procedure allows you to see the condition of the valves and the return flow of blood into the atrium. There is no point in undergoing an ECG, because it does not reveal any changes.

MVP of the 1st degree in a child: main signs and causes of development

Symptoms of the disease at a young age can vary. Some babies do not experience heart failure at all. In other cases, the pathology has a pronounced course.

Grade 1 MVP in a child may be accompanied by the following manifestations:

• Pain in the chest;
• Increased heart rate;
• Fast fatiguability;
• Changes in mood;
• Short-term fainting states.

Pain in the chest is observed in approximately 30% of adolescent patients. Usually such phenomena are associated with strained chords, physical / emotional overstrain, oxygen starvation.

Rapid fatigue occurs in adolescents who do little physical activity. As a rule, this symptom is characteristic of those children who sit at the monitor for a long time or prefer mental activity. During physical education lessons they experience shortness of breath due to poor preparation.

It is not uncommon for children with MVP to suffer from neuropsychological signs. They complain of nervous breakdowns, mood swings, nervousness, irritability, tearfulness, aggression. If a child experiences emotional stress, he may faint.

MV prolapse often develops as a result of magnesium deficiency. This problem contributes to the disruption of collagen production. Also, magnesium deficiency is bad for the work of all body tissues and blood supply. Children experience electrolyte imbalance. It is important to note that a child with MVP is characterized by low weight, inappropriate for his height. Many children are diagnosed with scoliosis, anorexia, flat feet, muscle underdevelopment, myopathy, etc.

Prolapse of the anterior leaflet of the mitral valve: treatment in children and adults

If MVP is accompanied by severe symptoms, then they can be eliminated with the help of selected therapy. In some cases, it is possible to remove the signs of pathology, in others - to reduce their severity. Treatment is prescribed individually, taking into account the characteristics of the body, age, gender, genetic factors.

The choice of drugs depends on the severity of the clinical course of the disease. Typically, patients of different ages are prescribed the following groups of medications:

• Sedatives - if the symptoms are affected by a disorder of the functions of the autonomic nervous system;
• Beta blockers – helping to restore heart rhythm;
• Nutritious – to improve myocardial function;
• Anticoagulants – preventing the formation of blood clots in the atria.

But the main importance is adjusting the patient’s lifestyle. First of all, the degree of mental stress is normalized, which must be combined with physical exercise. To accurately adjust sports activities, you need to go to physical therapy, where an experienced specialist will select the best gymnastics complex for an individual. It's good to go to the pool for swimming.

In childhood, it is important to ensure that the child does not overexert himself nervously and mentally, as this will aggravate the pathology and cause chronic fatigue. To do this, parents need to adjust their study, work and rest schedules. From time to time, children are sent to sanatoriums, where they will receive specialized massages, mud treatment, acupuncture, etc.

For some patients, it is advisable to use herbal medicine. Doctors may recommend sedative herbal remedies - motherwort, St. John's wort, sage. Horsetail and ginseng are also used.

Medicines that may be prescribed include:

Also, for metabolic disorders, various physiotherapeutic procedures are used, which are selected on an individual basis. Surgical intervention is indicated only for the last degree of MVP.

In childhood, patients with mitral valve prolapse should be registered with a cardiologist. They should see a specialist every six months in order to promptly detect worsening pathology and promptly begin effective treatment. Physical exercises can be performed by almost all children, but with grades 2 and 3 of the disease they must be reduced, and in severe cases they must be limited.

Mitral valve prolapse occurs due to a disorder in the structure of connective tissue. MVP of the first and second degrees usually does not threaten the life and health of the child and is considered as a normal variant. Treatment may be needed if the disease progresses.

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Sveta asks:

Good afternoon. My granddaughter is diagnosed with stage 1 MVP. I know that regular physical exercise can be done, but she now has scoliosis, grade 2 S-shaped scoliosis. And she definitely needs to go in for sports. She started going to rowing and she likes it there. It’s only when she’s training that hiccups start. Can she do this sport?

Answers Bugaev Mikhail Valentinovich:

Hello. Her hiccups have nothing to do with the findings on the ultrasound of the heart. These findings do not require treatment. It is better to consult with orthopedists regarding the correct treatment of scoliosis.

Anton asks:

Hello! I am 18 years old. Three years ago I was diagnosed with stage 1 MVP. And exactly a year ago, while undergoing an examination, my diagnosis was clarified: grade 1 MVP (up to 4.7 mm), b/r. SCS syndrome (Holter). Moderate sinus bradycardia. I have been playing football since childhood. I started playing and training at a more professional level 4 years ago. Please tell me, is it possible for me to play sports with this diagnosis?

Answers Polishchuk Tatyana Viktorovna:

Dear Anton. A patient with mitral valve prolapse and carotid sinus syndrome should change their lifestyle, work and rest schedule; exclude overwork, excessive psycho-emotional and physical stress, intoxication at home and at work. Moderate systematic physical activity and proper rest (daily, weekly, monthly, annual) are recommended; visiting climatic and balneological resorts with a mild climate; water procedures, acupuncture, spinal massage. Much attention should be paid to the treatment of chronic foci of infection; if indicated, tonsillectomy (removal of the tonsils) is performed. Since the possibility of syncope and progression of changes in the mitral valve with age cannot be excluded, and there is also a possibility of severe complications, patients with mitral valve prolapse require dynamic monitoring by a cardiologist at least 1-2 times a year. In case of increasing changes and severe flexion of the valve leaflets (with regurgitation of III-IV degrees), surgery may be required. Football is not your sport.

Natalia asks:

Hello! They were diagnosed with stage 1-2 mitral valve insufficiency. The child was very active physically and was on a very strict diet. If you moderate the loads and return to normal nutrition, vitamins and follow all medical prescriptions, is there an option to outgrow and resume ballet classes? Thank you.

Answers Fesyuk Galina Nikolaevna:

Hello, Natalia! The cause of valve insufficiency is important. Sometimes this is a sign of rheumatism, then treatment with antibiotics, non-steroidal anti-inflammatory drugs for several years and in most cases complete recovery. If a sign of acute myocarditis, similar drugs, 1 month and full recovery. Myocardiosclerosis, slightly different treatment and also recovery. It is advisable to identify and treat. Only heavy loads without any reason could hardly have caused this. More likely, she was working out with a cold. I think active sports and a very strict diet are not entirely compatible. With proper treatment and adherence to the regimen, complete recovery is most likely. It is advisable to constantly monitor the situation. A rare variant of the disease is caused by a special congenital structure of the connective tissue. Then limiting the load and complete recovery is not possible. Treat and Monitor If valve insufficiency resolves, active training can be resumed. But in the most ideal scenario, 30% for it, and not earlier than 1-2 months after echocardiography control. Health.

Vlad asks:

Tell me what it means "prolapse of the 2nd degree" for the sickness of the heart of a child of 10 years.

Answers:

Hello, Vlada! Prolapse is a sagging of one of the heart valves (most often the mitral valve, which covers the opening from the left atrium to the left ventricle). The degree of prolapse is determined by the amount of valve sagging and the severity of intracardiac circulatory disorders associated with the presence of prolapse. Mitral valve prolapse of 1-2 degrees in the absence of clinical symptoms can be considered as a normal variant that requires observation by a cardiologist and does not require special treatment. Children with detected prolapse of one of the heart valves should be consulted in person with a pediatric cardiologist. Detailed information about prolapse and other congenital heart defects is contained in the popular science article Congenital heart defects - what is behind the diagnosis on our medical portal. Take care of your health!

Asks Nigaev Airat:

My daughter is 7 years old, studying in 1st grade, she has mitral valve prolapse, can she go to a dance club?

Answers Medical consultant of the portal “health-ua.org”:

Good afternoon. Mitral valve prolapse is a heart disease in which there is sagging of the mitral valve leaflets. As a result of incomplete closure of the valves, a reverse flow of blood into the left atrium is possible. There are several degrees of prolapse, on which the clinical manifestations of the defect depend. In some children, clinical manifestations are minimal, in which case physical activity is not limited. In some children, the clinical manifestations of the defect are quite pronounced, up to heart failure, in such cases, physical activity should be limited. To determine whether a girl can dance, a face-to-face consultation with a pediatric cardiologist is necessary. More information about congenital heart defects can be found on our portal:. All the best.

Galina asks:

Please tell me, is it possible to pass the test for a pilot with prolapse up to 6 mm and MR 1 degree. And does prolapse go away with age?

Answers Medical consultant of the portal “health-ua.org”:

Good afternoon. First of all, it is necessary to establish the cause of mitral valve prolapse. It may be congenital or acquired. It is also worth considering the clinical manifestations of this malformation. Some of them are absent, and the defect is detected during a random examination, and some have abnormalities in the work of the heart. Only a cardiologist can give recommendations on physical activity and career guidance, after an examination and a comprehensive examination. Prolapse will decrease or increase, depending on the cause that caused it, adequate treatment, prevention of complications, as well as on the individual characteristics of the organism. You can learn more about mitral valve prolapse on our portal: All the best.

Irina asks:

Hello, I did an ultrasound, the doctor diagnosed aortic insufficiency (1-2 degrees) or aortic regurgitation. The aortic valve has 3 leaflets, there have never been complaints about the heart, I go in for sports (unprofessionally) and prescribed to drink kudisan for 2 months. Tell me how dangerous this diagnosis is, what the prognosis is and how long they live with it

Answers Prophet Sergey Yurievich:

Good afternoon. Insufficiency of the 2nd degree is an indication for the appointment of minimal doses of drugs that reduce pressure to reduce the load on the valve (for example, Enap). Kudisan is unfortunately absolutely useless. Sports are contraindicated, maximum exercise. Ultrasound monitoring is recommended every 6-12 months to assess the dynamics of insufficiency. With adequate and timely treatment, they live long and happily into old age. But before you get upset about sports, do a repeat ultrasound examination in a specialized clinic. Only after assessing the degree of insufficiency by a highly specialized specialist and confirming the degree of regurgitation as moderate (grade 1-2) should one resort to the recommendations described above. with Minimal or slight deficiency, live as you lived.

Lena asks:

Good afternoon
My son is 10 years old, he has been seriously involved in sports for 3 years, training every day for 3-4 hours. There are no complaints.
Absolutely by chance!!! During a general examination (ultrasound), a bicuspid aortic valve was detected, stage 1 MVP. They sent me for a Doppler examination. Conclusion of the UPS: Bicuspid AC. Aortic insufficiency is minimal. Dysplastic cardiopathy. MVP stage 1, regurgitation 1/2 +. There is no evidence for aortic stenosis.
Tell me what to do.
Thank you in advance.

Answers Bugaev Mikhail Valentinovich:

Good afternoon. If I were you, I would double-check the EchoCG data again and again, preferably in different institutions, preferably where heart surgery is performed. If, in fact, there is a 2-leaf aortic valve, then I would recommend that you think about limiting heavy physical activity for your child, this will allow him to delay his meeting with a heart surgeon as much as possible. If aortic valve incompetence (more often insufficiency) appears with age, then this becomes an exclusively surgical problem requiring serious surgery, most often aortic valve replacement. At the moment, the child does not require any treatment. It is necessary to avoid infections and colds - these are measures to prevent infective endocarditis, a dangerous complication of any heart defect.

Anna asks:

Hello, I would like to ask the other day, I had my children undergo an ultrasound of the heart and they told me that the youngest has an additional chord of the left ventricle; my daughter, who is 8 years old, has grade 1 PMC and an additional chord of the left ventricle; my son is 12 years old and has an additional chord of the left ventricle. Please tell me what is it and how dangerous is it?

Answers Medical consultant of the portal “health-ua.org”:

Hello Anna! You will find detailed information about mitral valve prolapse in the article on our medical portal. Additional chord of the left ventricle is a minor cardiac anomaly and does not require any treatment. Patent foramen ovale (PFO) is a common anomaly that, when the window is large, can become hemodynamically significant and require treatment. If the LLC is small, only supervision is necessary. Thus, of your children, only your 12-year-old son needs an in-person consultation with a pediatric cardiologist. Take care of your health!

Asks Nepeina Irina Anatolevna:

In April 2011, the child's biochemistry ASL-O was 300. They treated him with summed (1 capsule 2 times a day - 3 days). A month after treatment, ASL-O was 800. An injection of retorpen was prescribed. Subsequent ASL-O analysis was normal. In April 2012, an ultrasound of the heart was performed. Thickening of the mitral valve leaflets was discovered. In April, ASL-O was 180, in May - 295. ECG - normal, Holter - normal. Doctors believe that the cause of thickening of the valves is a streptococcal infection and therefore suggest injecting Bicillin 1.5 million for six months. intramuscularly once every 3 weeks. Is treatment possible without an antibiotic?
I'm attaching an ultrasound. Now ASL-O is 170
"4th City Children's Clinical Hospital" Department of Ultrasound Diagnostics
June 11, 2012 18:2
Patient: Nezhina Svetlana Igorevna Date of birth: 02/19/2000 i
Department: Rheumatology No. ist. diseases: 4637 Name of the study: Ultrasound of the heart.
| Description:
!Weight40kg
PPT, 1.54m2
Heart rate, 103-90vmin.
Ultrasound window is good
AORTA (AO): 25 mm normal Echogenicity of the walls: normal AORTIC VALVE (AoV): Leaflets: normal

The amplitude of leaflet opening in systole is 15 mm

LEFT ATRIUM (LA): 25mm normal

LEFT VENTRICLE (LV): norm CDR 43mm CDR 23mm
KDO 80ml KSO 12ml

INTERVENTRICULAR SEPTUM (IVS): 7\9 (diastole/systole, mm)
normokinesis Defect: none.
POSTERIOR WALL OF THE LEFT VENTRICLE (PLV):7\9 (diastole/systole, mm)

INTERATRIAL SEPTUM (AS) Defect: no
RIGHT VENTRICLE (RV):
13mm norm
PW CW CFM
AORTIC VALVE(AoK)
Flow V: 1.1 m/s non-accelerated laminar
V Gradient 5 mm Hg Regurgitation st
V flow in the descending aorta: 1.3 m/s unaccelerated Gradient 7 mmHg

MITRAL VALVE (MK)
Swing: thickened
Prolapse PSMK 4.2mm
Sash movement:
in antiphase
Ve m/s Va m/s Ve >Va

Regurgitation stage 1

TRICUSPIDAL VALVE(TK)
Sashes: norm
Flow V: non-accelerated Gradient mm Hg

Regurgitation 0-1st degree gsd15mm Hg.

PULMONARY ARTERY VALVE (CL) Leaflets: normal

TRUNK OF THE PULMONARY ARTERY (PAL): Flow rate: 0.9 m/s non-accelerated
Gradient 3.8mm Hg
Regurgitation on KLA 0-1 tbsp.

ABDOMINAL AORTA (BAo) Main flow

LV SYSTOLIC FUNCTION:
Indices of LV contractile function: SV 68 ml MO 6.8 l/min
FV73% FU42%
Vcf 1.0v/s SI 4.4l/(min*m2)
J Contractility of the LV myocardium: normal COMMENTS:

Conclusion: MVP grade 1 4.2mm with 1st degree regurgitation. Additional chords in the apical part of the left ventricle.
Recommendations: Echocardiography monitoring after 1 year

Kozachenko Irina Vasilievna

Valentina asks:

Conclusion based on the results of an echocardiographic study: abnormal left ventricular trabeculae, arrhythmia, tricuspid aortic valve, non-coronary cusp prolapse, minimal regurgitation. Mitral valve prolapse 2 mm, minimal regurgitation. Tricuspid valve prolapse, minimal regurgitation. Pulmonary valve insufficiency 2(+). The dimensions of the cavities are within the age norm. ECG results: sinus rhythm, tachycardia (the child was afraid to go to the ECG). They were allowed to attend physical education classes without any restrictions. Both doctors said that everything is OK and within normal limits (for age) and that it often goes away, but I am at a loss. Whether it is necessary to change the cardiologist??? How can this be all around prolapses and everything is OK?

Answers Polishchuk Tatyana Viktorovna:

Dear Valentina. Despite the significant spread of this pathology in the pediatric population, many issues of diagnosis, differential diagnosis, prognosis and management tactics for children remain undeveloped. The same tactics for the management of children with MVP, regardless of its characteristics, leads, on the one hand, to underestimation of dangerous complications in this syndrome (infective endocarditis, life-threatening arrhythmias, etc.). In our opinion, the changes identified in your son may be due to various reasons , including connective tissue diseases (Marfan syndrome, Ehlers-Danlos syndrome, elastic pseudoxanthoma, etc.), therefore we consider the examination incomplete, and we recommend that you listen to the opinion of an independent specialist.

BALNUR asks:

I’m 21 years old, I was diagnosed with PROLAPS 1st stage with regurthi 1st stage tricuspid they say that it’s not scary, it’s normal but there’s nothing normal, nothing visible, my heart is beating hard with pain at the same time, it’s hard for me to breathe when it’s beating so hard... it’s tolerable, but I’m tired mentally and physically

Answers Medical consultant of the portal “health-ua.org”:

Good afternoon. Heart valve prolapse is the protrusion of the valve leaflets when the heart contracts. Depending on the size of the protrusion, they are distinguished from the degree. To 1 degree include prolapses less than 5 mm. Such prolapses are usually asymptomatic and are detected during a random examination. Tricuspid valve prolapse often does not manifest itself in any way and therefore does not require treatment. If you have unpleasant sensations, then you need to see a cardiologist and be thoroughly examined, you will need an ECG, ultrasound of the heart, Holter monitoring. Additional consultation with a neurologist is also necessary, since such symptoms can occur not only with heart disease, but also with disorders of the nervous system. All the best.

Mitral valve prolapse occurs quite often, according to various sources, in 2-16% of children. As a rule, it does not manifest itself for the time being, so it is usually detected at the age of 7-15 years. It happens that prolapse is discovered by chance during an ultrasound examination of the heart (echocardiography).

What is mitral valve prolapse?

There are four chambers in the human heart: the left atrium and ventricle, the right atrium and ventricle. Blood flows from the atria to the ventricles. The right and left parts of the heart do not normally communicate, and the atria and ventricles are connected through openings covered by valves. The mitral valve is provided between the left atrium and the left ventricle. It consists of two leaflets and is like doors that open and allow blood to flow into the left ventricle when the left atrium contracts. The incoming blood fills the cavity of the ventricle and automatically slams the “doors”. And then the ventricle contracts, the valve flaps are closed, tightly in contact with each other and do not release blood back into the atrium. This ensures blood flow in one direction.

Mitral valve prolapse- bending of its valves into the cavity of the left atrium during contraction of the ventricles of the heart. The valve flaps are so flexible and elastic that they inflate like sails.

The doctor can detect mitral valve prolapse by listening to the heart using a phonendoscope and confirm it using ultrasound of the heart (ECHO).

Causes of mitral valve prolapse

The mitral valve leaflets become overly elastic due to disruption of the structure of the connective tissue that makes up the framework of the mitral valve. This change, called connective tissue dysplasia, occurs in the patient not only in the mitral valve, but also in other organs where there is a lot of connective tissue. The cause of connective tissue can be a congenital defect in the structure of connective tissue and (or) an acquired metabolic disorder or microelements (deficiency of magnesium, potassium, selenium, silicon).

The cause of prolapse mitral valve there may be various disorders of the autonomic nervous system, leading to a disorder of the regulatory influence on the valve. Mitral valve prolapse often accompanies panic and other psycho-emotional disorders.

The occurrence of mitral valve prolapse may be associated with a genetic pathology of connective tissue (Marfan syndrome, Ehlers-Danlos syndrome, etc.) and be inherited. , endocrine disorders (increased thyroid function) can also cause prolapse. In these cases, prolapse is a consequence (one of the symptoms) of some disease, and it is called secondary.

There are a number of other factors contributing to the development of prolapse:

• Complicated course of pregnancy in the mother in the first 3 months (toxicosis, threat of miscarriage, ARVI) and childbirth (quick, rapid labor, vacuum extraction, cesarean section during childbirth), birth trauma.
• Predisposition to colds, early onset of angina,.

Mitral valve prolapse symptoms

In children with prolapse, as a rule, the structure of the entire connective tissue is changed, and not just the valve. Therefore, they have a number of features and signs of connective tissue dysplasia: myopia, flat feet, increased extension of small joints, poor posture (small or “straight back” syndrome), very elastic skin. Typically, in appearance, children with prolapse have an asthenic physique, thin and thin, with weak muscles, and often tall. The history of children with dysplasia includes congenital dislocations and subluxations of the hip joints, and hernias.

Attacks of “heart pain” are short-lived (lasting for 5-20 minutes), children feel them in the left half of the chest and describe them as “stabbing”, “pressing”, “aching”. There may be a feeling of "interruptions" in the work of the heart, "fading". Typically, such complaints arise in connection with emotional stress and are accompanied by various vegetative reactions (unstable mood, anxiety and fear, cold extremities, “chilliness”, palpitations, sweating, decreased or increased pressure, headaches, etc.), disappear spontaneously or after taking tincture of valerian, valocordin.

Why is mitral valve prolapse dangerous?

In most cases, mitral valve prolapse proceeds favorably and only in 2-4% leads to serious complications.

The main complications of mitral valve prolapse are:

Heart failure. Deflection of the mitral valve leaflets can lead to their incomplete closure and the occurrence of reverse blood flow (regurgitation) from the ventricle into the atrium. With mild regurgitation, treatment is not required and this does not affect the child’s well-being. If the reverse flow of blood is strong, overload of the heart and the development of heart failure (weakness, shortness of breath, swelling, palpitations, interruptions in heart function) are possible. The situation can even lead to surgery - replacing the mitral valve with an artificial valve.

Bacterial endocarditis. Bacteria settle on the flaps of the altered valve, multiply there, spoil and corrode it. A very unpleasant disease, difficult to treat.

Life-threatening arrhythmias. Quite often, children with prolapse have heart rhythm disturbances that are recorded on the ECG: sinus tachycardia, extrasystoles, paroxysmal tachycardia, sinus bradycardia, atrial fibrillation, etc. (see “Arrhythmias”).

Sudden death. Of course, it is very rare, but such cases have been described.

Tactics of observation and treatment of children with mitral valve prolapse

Treatment varies depending on the severity of prolapse (sagging of the valves) and the nature of the accompanying autonomic and cardiovascular changes (presence of arrhythmia, heart failure). As a rule, the course of prolapse does not cause serious concerns for the patient’s health and requires only observation, as well as the implementation of simple routine and restorative measures (daily routine, adequate sleep, some restrictions in sports) and preventive courses of vitamins, minerals and other drugs that support the work hearts.

Most children (in the absence of prolapse complications) tolerate physical activity well. If they have medical supervision, they can lead an active lifestyle without any restrictions on physical activity. Children can be recommended sports where the load is distributed evenly: swimming, skiing, skating, cycling, running at a slow pace, walking. Sports activities associated with jerky movements or sudden force loads are not recommended: jumping, wrestling, karate, barbell, etc.

Based on the fact that mitral valve prolapse is a particular manifestation of a disorder of the autonomic nervous system, treatment should be aimed at correcting autonomic dystonia. The treatment is long-term and complex and, mainly, non-drug, includes psychotherapy, auto-training, physiotherapy (electrophoresis with magnesium, bromine in the upper cervical spine), water procedures, acupuncture, spinal massage. The selection of treatment is made by the doctor individually, taking into account the characteristics of the patient.

To maintain the functioning of the myocardium when its metabolism is disrupted, courses of treatment with the following drugs are carried out:

• Potassium and magnesium preparations (panangin, asparkam magnerot, magne B6).
• Riboxin.
• Carnitine (elcar, carnitene).
• Coenzyme Q10.
• Dietary supplement "Lecithin".
• Horsetail. Helps replenish silicon deficiency. Used in the form of a decoction (10 g of horsetail herb per 200 ml of water), take 1 tbsp. l. 3 times a day, in courses.
• Triovit. A vitamin-mineral complex that replenishes the deficiency of vitamins C, E, beta-carotene (provitamin A) and selenium, which support heart function.
• Polyunsaturated fatty acids omega-3 and omega-6 (linseed oil, fish oil, Omega-3 dietary supplement, etc.).

Small anomalies of the development of the heart

Children with connective tissue dysplasia often exhibit minor anomalies in heart development. The most common lesions are left ventricular false chord and patent foramen ovale. They can occur alone or in combination, together with other manifestations of connective tissue dysplasia. Since the patient, as a rule, does not make any complaints, minor developmental anomalies can be an accidental finding. During the examination, the doctor hears a heart murmur and sends the child for an ultrasound examination of the heart - echocardiography, where the presence of a particular anomaly is confirmed.

False chord of the left ventricle is an additional formation in the ventricular cavity in the form of a thin stretched string. It may cause a fairly strong heart murmur.

Patent foramen ovale is a small opening (window) between the right and left atria. Its role is great when the child is in the womb. After birth there is no need for it and it closes. True, not all children, and sometimes not immediately after birth, but by the age of 5-6. If the window is small, 1-2 mm in diameter, it does not in any way disturb the general condition of the child.

There is nothing wrong with the presence of minor anomalies in the development of the heart; it is simply an individual feature of the structure of the child’s heart. They do not require special treatment, only observation of the patient. It is believed that minor anomalies in the development of the heart, although rare, but, like prolapse, can provoke cardiac arrhythmias and cause disturbances in myocardial metabolism. Therefore, the consequences of minor anomalies (disorders of myocardial rhythm and metabolism), if any, are subject to drug correction. In this case, the medications used are the same as for prolapse.

Clinical examination

Patients with mitral valve prolapse and minor cardiac anomalies should be re-examined by a pediatrician, cardiologist and undergo control studies (ECG, ECHO-CG) at least 2 times a year. If necessary, consultation with an otolaryngologist, psychoneurologist, or geneticist is carried out.

Title of training topic: Mitral valve prolapse in children.

The purpose of studying the educational topic: Teach diagnostics, methods of examining patients with mitral valve prolapse, evaluation of instrumental and laboratory tests. Teach students to treat mitral valve prolapse and conduct clinical monitoring.

Key terms:

Mitral valve prolapse;

Connective tissue dysplasia;

Mitral valve insufficiency;

echocardiography;

Vegetovascular dystonia;

Stigmas of dysembryogenesis.

Topic study plan:

The concept of mitral valve prolapse;

Epidemiology of MVP;

Etiology and pathogenesis of MVP;

Clinical manifestations of primary MVP;

Methods of instrumental diagnostics of PMK;

Criteria for the diagnosis of MVP;

Treatment methods;

Options for secondary PMC.

Presentation of educational material:

Mitral valve prolapse

Mitral valve prolapse (MVP) occupies a leading place in the structure of cardiovascular diseases in childhood. This term means deflection, protrusion of the valve leaflets into the cavity of the left atrium during left ventricular systole. The introduction of echocardiography in the examination of children contributed to the identification of the phenomenon of prolapse even in cases of the absence of characteristic auscultatory changes (the so-called “pseudo” MVP, “silent” MVP).

All variants of MVP are divided into primary (idiopathic) and secondary:

1. Primary MVP refers to a condition of the mitral valve apparatus in which the sagging of the leaflets into the left atrium is not associated with any systemic connective tissue disease, or with heart diseases leading to a decrease in the cavity of the left ventricle.

2. Secondary MVP can be caused by a variety of reasons: connective tissue diseases (Marfan syndrome, Ehlers-Danlos syndrome, elastic pseudoxanthoma, etc.), in which accumulation of acidic mucopolysaccharides occurs in the valve stroma, myxomatous transformation of the leaflets, chords, dilatation of the atrioventricular ring; heart diseases (congenital defects, anomalies of coronary circulation, myocardial diseases, arrhythmias, etc.), in which prolapse of the valves is caused by a violation of sequential contraction and (or) relaxation of the walls of the left ventricle or the occurrence of valvular-ventricular disproportion, neuroendocrine, psychoemotional and metabolic disorders (migraine , thyrotoxicosis, vegetative-vascular dystonia, neuroses, hysteria, fears, anorexia nervosa, etc.). Of primary importance in this case are disorders of the autonomic innervation of the mitral valve leaflets and the subvalvular apparatus.

Frequency.

The frequency of MVP in children ranges from 2 to 16% and depends on the method of its detection (auscultation, phonocardiography, echocardiography).

The frequency of detection of MVP increases with age. Most often it is detected at the age of 7-15 years.

In newborns, MVP syndrome is casuistically rare.

In children with various cardiac pathologies, MVP is detected in 10-23% of cases, reaching high values ​​in hereditary connective tissue diseases.

In children under 10 years of age, mitral valve prolapse occurs approximately equally often in boys and girls; over 10 years of age, it is found much more often in girls in a ratio of 2:1.

Etiology.

Congenital anomalies (including microanomalies) of valve development. The theory of congenital microanomalies of the architecture of the valves, chords and atrioventricular ring, which over time, due to repeated microtrauma against the background of hemodynamic influences, become more pronounced, accompanied by excess production of collagen in the stroma of the valve predominantly III type.

The theory of the primary defect in the development of the connective tissue apparatus of the mitral valve. The latter is combined with an increase in the number of stigmas of disembryogenesis. Confirmation of the theory of congenital microanomalies of the mitral valve is the high frequency of detection of impaired distribution of chordae tendineae to the mitral valves and abnormal chordae in the left ventricle.

Some congenital anomalies lead to prolapse of the mitral leaflets, accompanied by mitral regurgitation. For example, severe mitral valve prolapse with holosystolic murmur and mitral regurgitation occurs in the absence of mitral valve commissural tendon filaments.

Myxomatous transformation of valve leaflets: myxomatous transformation is associated with a nonspecific reaction of the connective tissue structures of the valve to any pathological process. Myxomatosis may be the result of incomplete differentiation of valve tissue, when at the early embryonic stage the influence of factors stimulating its development weakens. Myxomatosis can be hereditarily determined.

"Myocardial" theory the occurrence of MVP is based on the fact that in patients with leaflet prolapse, angiographic studies reveal changes in left ventricular contraction and relaxation of the following types:

"Hourglass".

Inferior basal hypokinesia.

Inappropriate shortening of the long axis of the left ventricle.

Abnormal contraction of the left ventricle like a “ballerina’s leg.”

Hyperkinetic contraction.

Premature relaxation of the anterior wall of the left ventricle.

The occurrence of secondary mitral valve prolapse is associated with the following pathological conditions:

Hereditary pathology of connective tissue (Marfan syndrome, Ehlers-Danlos syndrome, elastic pseudoxanthoma, etc.). Genetically determined defect in the synthesis of collagen and elastic structures.

Deposition of glycosaminoglycans in the stroma of the valve.

Valve-ventricular disproportion.

Conditions when the mitral valve is too large for the ventricle or the ventricle is too small for the valve.

Congenital heart defects accompanied by “underload” of the left heart: Ebstein’s anomaly, atrioventricular communication, atrial septal defect, abnormal drainage of the pulmonary veins, etc.

Neuroendocrine abnormalities (hyperthyroidism).

Pathogenesis of MVP.

Transformation of the mitral valve leaflets, normally rigid, into loose myxomatous tissue and a decrease in the content of collagen structures leads to the fact that during systole, under the influence of intraventricular pressure, the leaflets bend towards the left atrium. With a large deflection of the valves, mitral regurgitation develops, which, however, is not as pronounced as with organic mitral insufficiency.

The normal functioning of the mitral valve apparatus depends on the correct interaction between its various elements, which include the valve leaflets, tendon filaments, papillary muscles, annulus fibrosus, as well as on the synchrony of contractions of the left atrium and left ventricle. An important pathogenetic factor that determines the occurrence and also determines the degree of mitral valve prolapse is the shape of the valve leaflets. With MVP, the total valve area significantly exceeds normal values. At the same time, the larger the area the valve occupies, the weaker it resists the forces of intraventricular pressure.

The mitral valves normally touch their surfaces so that one valve overlaps the other, which is not observed in semilunar valves. Prolapse is usually observed in the free part of the leaflet, and as long as the leaflets touch each other, mitral regurgitation is not observed. This causes the auscultatory phenomenon of isolated clicks in the heart. If prolapse occurs in the area of ​​​​the contacting surfaces of the leaflets, then even with a small amount of deflection, mitral regurgitation can occur, the volume of which is determined by the amount of divergence of the leaflets in systole and the degree of expansion of the atrioventricular opening.

The subvalvular apparatus plays a major role in the genesis of leaflet prolapse and mitral insufficiency. With lengthening of the chord or weak contractility of the papillary muscle, the valve leaflets may prolapse to a greater extent, and the degree of regurgitation will also increase.

The volume of the left ventricle in systole and diastole, as well as heart rate, have a great influence on the amount of leaflet prolapse and can significantly change the auscultatory and echocardiographic manifestations of MVP.

The degree of prolapse is inversely related to the value of the end-diastolic volume of the left ventricle. Weak chordal tension with a decrease in the end-diastolic volume of the left ventricle contributes to a greater degree of valve prolapse. Physiological and pathological conditions that cause a decrease in the end-diastolic volume of the left ventricle (tachycardia, hypovolemia, decreased venous return of blood) increase the degree of MVP. Various factors causing an increase in the volume of the left ventricle (bradycardia, hypervolemia, increased venous return of blood) with MVP can be compensatory in nature, because contribute to the tension of the chordae tendineae and, accordingly, reduce the protrusion of the mitral valve leaflets into the cavity of the left atrium.

Clinical picture of MVP.

Clinical manifestations of mitral valve prolapse in children vary from minimal to significant and are determined by the degree of connective tissue dysplasia of the heart, autonomic and neuropsychiatric abnormalities.

Most children have a history of indications of an unfavorable course of the antenatal period. Complicated pregnancy in mothers is most often observed in the first 3 months (toxicosis, threat of miscarriage, ARVI). It is during this critical period of intrauterine development that intensive tissue differentiation and the formation of organs, including the mitral valve, occur.

In approximately 1/3 of cases there are indications of an unfavorable course of labor (quick, rapid labor, vacuum extraction, cesarean section during labor). Subsequently, children with birth trauma develop minimal brain dysfunction, intracranial hypertension, and psychoneurological abnormalities (asthenoneurotic syndrome, logoneurosis, enuresis).

From an early age, signs (or indications in history) of dysplastic development of connective tissue structures of the musculoskeletal and ligamentous apparatus (hip dysplasia, inguinal and umbilical hernias) can be detected. Determining the presence of these anomalies in the anamnesis is important for the correct assessment of connective tissue disorders, since the latter may not be detected during examination (spontaneous disappearance, surgical treatment).

Most children with MVP have a history of predisposition to colds, early onset of tonsillitis, and chronic tonsillitis.

Most children, usually over 11 years of age, have numerous and varied complaints of chest pain, palpitations, shortness of breath, a feeling of heart failure, dizziness, weakness, and headaches. Children characterize pain in the heart as “stabbing”, “pressing”, “aching” and feel it in the left half of the chest without any irradiation. In most children, they last for 5-20 minutes, arise in connection with emotional stress and are usually accompanied by vegetative disorders: unstable mood, cold extremities, “chilliness”, palpitations, sweating, pass spontaneously or after taking tincture of valerian, valocordin .

Cardialgia with MVP may be associated with regional ischemia of the papillary muscles when they are excessively tense. Neurovegetative disorders are manifested by palpitations, a feeling of “interruptions” in the work of the heart, “tingling”, “fading” of the heart.

Headaches often occur during overwork, anxiety, in the morning before school starts and are combined with irritability, sleep disturbance, anxiety, and dizziness.

Shortness of breath, fatigue, and weakness usually do not correlate with the severity of hemodynamic disorders, as well as with exercise tolerance, are not associated with skeletal deformities and have a psychoneurotic origin.

Shortness of breath can be iatrogenic and is explained by detraining, because Doctors and parents often limit children’s physical activity for no reason. Along with this, shortness of breath can be caused by hyperventilation syndrome (deep sighs, periods of fast and deep breathing movements in the absence of changes in the lungs). This syndrome in children is based on neurosis of the respiratory center or is a manifestation of masked depression (DeGuire S. et al., 1992).

Physical data: n During clinical examination, most children show dysplastic developmental features (minor anomalies) of connective tissue:

Flat feet.

Asthenic physique.

Tallness.

Reduced nutrition.

Poor muscle development.

Increased extension of small joints.

Poor posture (scoliosis, straight back syndrome).

Gothic sky.

- “Tower Skull”.

Muscular hypotonia.

Prognathism.

Hypotelorism of the eyes.

Low location and flattening of the ears.

Arachnodactyly.

Typical auscultatory signs of mitral valve prolapse are:

Isolated clicks (clicks).

Combination of clicks with late systolic murmur.

Isolated late systolic murmur (LPS).

State of the autonomic nervous system:

Since the first description of the MVP syndrome, it has been known that such patients are characterized by psycho-emotional lability and vegetative-vascular disorders, especially pronounced in young women and adolescents.

According to H. Boudoulas, patients with MVP exhibit increased excretion of catecholamines during the day, and it decreases at night and has peak-like increases during the day. Increased excretion of catecholamines correlates with the severity of clinical manifestations in MVP. In patients with MVP, high catecholaminemia is detected due to both adrenaline and norepinephrine fractions. Using a pharmacological test with isoproterenol, H. Boudoulas et al. showed that hypersympathicotonia is associated primarily with a decrease in the number of α-adrenergic receptors; the number of active β-adrenergic receptors remains unchanged. Other authors have suggested β-adrenergic hyperactivity, both central and peripheral. Using the method of occlusion plethysmography and a pharmacological test with phenylephrine, F. Gaffhey et al. found autonomic dysfunction in MVP syndrome, which is characterized by a decrease in parasympathetic, an increase in α-adrenergic and normal β-adrenergic tone. Sympathoadrenal disorders may be based on abnormal synthesis of a regulatory protein that stimulates the production of guanine nucleotides (Davies A.O. et al., 1991).

Detectable autonomic disorders, predominantly of the sympathicotonic type, according to most authors, are responsible for many clinical manifestations of MVP syndrome: palpitations, shortness of breath, heart pain, morning fatigue, fainting are directly associated with increased sympathicoadrenergic activity. The listed symptoms, as a rule, disappear while taking β-blockers, sedatives, drugs that reduce sympathetic and increase vagal tone, and during acupuncture. Individuals with hypersympathicotonia are characterized by decreased body weight, asthenic physique, and asthenoneurotic reactions, which is also often found in MVP syndrome.

Psycho-emotional disorders. Many children with MVP, mainly in adolescence, exhibit psychoemotional disorders, represented by depressive and asthenic symptom complexes.

Depressive conditions are the most frequently identified, accounting for more than half of the calls. The psychopathological picture of these conditions corresponds to the structure of “masked”, erased depressions (subdepressions), in which vegetative and affective disorders appear in one complex, and if the former immediately attract the attention of the doctor and the patient, the latter can be seen not only by the doctor and the patient’s immediate environment, but they are often not realized by the patient themselves, coming to light only with in-depth questioning.

Asthenic symptoms can be observed both as part of an independent (asthenic) syndrome and as part of the structure of more complex neurotic and neurosis-like, psychopathic and psychopath-like syndromes. The latter are more common than neurotic level syndromes.

It should be noted that the identification of prolonged and progressive true asthenic symptoms should alert the clinician to undetected somatoneurological organic pathology.

Instrumental diagnostics.

Electrocardiography: The main electrocardiographic abnormalities found in MVP in children include changes in the terminal part of the ventricular complex, cardiac rhythm and conduction disturbances.

Disorders of the repolarization process. Changes in the repolarization process on a standard ECG are recorded in various leads, and 4 typical options can be distinguished:

Isolated T-wave inversion in the limb leads; II, III , avF without ST segment displacement.

Inversion of T waves in the limb leads and left chest leads (mainly in V5-V6) in combination with a slight shift of the ST segment below the isoline.

T wave inversion combined with ST segment elevation.

Prolongation of the QT interval.

Various types of resting ECG arrhythmias are recorded in isolated cases, the frequency of their detection increases by 2-3 times against the background of physical activity and by 5-6 times during daily ECG monitoring. Among the wide variety of arrhythmias in children with primary MVP, sinus tachycardia, supraventricular and ventricular extrasystoles, supraventricular forms of tachycardia (paroxysmal, non-paroxysmal) are most often found, less often - sinus bradycardia, parasystole, atrial fibrillation and flutter, WPW syndrome.

Electrophysiological study. Patients with MVP often exhibit various electrophysiological abnormalities (Gil R., 1991):

Violation of sinus node automaticity - 32.5%.

Additional atrioventricular pathways - 32.5%.

Slowing of conduction through the atrioventricular node - 20%.

Violation of intraventricular conduction: in the proximal segments - 15%; in the distal segments - 7.5%.

Radiography. In the absence of mitral regurgitation, expansion of the shadow of the heart and its individual chambers is not observed. In most children, the heart shadow is located in the middle and is disproportionately reduced compared to the width of the chest (Fig. 1).

Small heart sizes in 60% are combined with bulging of the pulmonary artery arch. It is known that a small heart, as a variant of hypoevolutionary development, is found in 8-17% of healthy children 14-17 years old. Children with small hearts often exhibit high stature, asthenic physique, chronic foci of infection, signs of vegetative dystonia with a decrease in the level of cholinergic regulation and a significant increase in sympathetic effects on the body. This hypoevolution of the heart is probably associated with the phenomenon of acceleration of development, accompanied by asynchrony in the development of internal organs, in particular the cardiovascular system and its regulatory mechanisms (R.A. Kalyuzhnaya). Detectable bulging of the pulmonary artery arch is a confirmation of the inferiority of connective tissue in the structure of the vascular wall of the pulmonary artery, and borderline pulmonary hypertension and “physiological” pulmonary regurgitation are quite often determined.

Objective assessment of the functional state of the cardiovascular system;

Detection of changes in the cardiovascular system in the form of latent coronary insufficiency, vascular hyperreactivity, heart rhythm disturbances (including life-threatening arrhythmias), conduction and repolarization process;

Determining the effectiveness of therapy with antiarrhythmic, antihypertensive and other drugs;

Predicting the course and complications;

Development of a rehabilitation program and evaluation of its effectiveness;

Assessment of physical performance and features of adaptation of the cardiorespiratory system to muscle load.

In children with primary MVP without mitral regurgitation, physical performance indicators correspond to age standards; in cases of mitral insufficiency, they are reduced according to the magnitude of the regurgitant discharge. Most children have low tolerance to physical activity and a predominance of chronotropic regulatory mechanisms over inotropic ones, which indicates a maladaptive circulatory response to stress and is associated with excessive involvement of sympathetic-adrenal mechanisms.

The bicycle ergometry method has an important prognostic significance in identifying persons at risk of sudden arrhythmogenic death. The appearance of ventricular arrhythmias during exercise, especially in cases of asymptomatic long QT syndrome with MVP, indicates an unfavorable prognosis and dictates the need to prescribe β-blockers. Normalization of the QT interval during physical activity and the absence of ventricular arrhythmias indicate a favorable course of the syndrome.

Echocardiography. One-dimensional echocardiography in 80% of cases in patients with typical auscultatory (phonocardiographic) signs confirms the diagnosis of mitral valve prolapse. However, with M-echocardiography, false-positive and false-negative examination results are possible. Unreliable diagnosis is usually associated with non-compliance with the research technique. If the sensor is placed above the standard position or the beam is directed at a downward angle, false holosystolic flexion of the leaflets can be detected in 60% of healthy people. In this regard, one-dimensional echocardiography cannot be used when prolapse is suspected, since the rate of false-positive cases is very high. In patients with auscultatory manifestations of MVP, one-dimensional echocardiography is used to determine the type of prolapse, the depth of leaflet sagging, associated anomalies and complications (mitral insufficiency, bacterial endocarditis, etc.). For children with MVP, according to one-dimensional echocardiography, late systolic (in the form of a “question mark”) (Fig. 2) or holosystolic (in the form of a “trough”) flexion of the leaflets in systole is characteristic.

The criteria for mitral valve prolapse according to one-dimensional echocardiography are as follows:

2. Multiple echoes from the valve leaflets.

3. Thickening, “shaggy” cusps of the mitral valve.

4. Diastolic flutter of the mitral valve leaflets.

5. Increased diastolic excursion of the anterior mitral leaflet.

6. Increased speed of early diastolic closure of the anterior mitral leaflet.

7. Increased systolic excursion of the interventricular septum.

8. Increased systolic excursion of the posterior wall of the left ventricle.

9. Increased systolic excursion of the aortic root; moderate dilatation of the root is possible.

The criteria for mitral valve prolapse according to two-dimensional echocardiography are (Fig. 3):

1. Bending of one or both leaflets beyond the line of coaptation (projection of the mitral orifice) in the parasternal long-axis view of the left ventricle or the projection of the 4 chambers from the apex.

2. Thickness and redundancy of the valves.

3. Excessive excursion of the left atrioventricular ring.

4. Increase in the area of ​​the mitral orifice (more than 4 cm2).

Along with this, two-dimensional echocardiography makes it possible to detect morphological microanomalies in the structure of the valve apparatus that underlie the occurrence of mitral valve prolapse:

Ectopic attachment or impaired distribution of tendon filaments to the valves (their predominant attachment at the base and in the body).

Changes in the configuration and position of the papillary muscles.

Lengthening tendon threads.

Enlargement (redundancy) of valves.

If the diagnosis of MVP is difficult during standard echocardiography, the patient must be re-examined in a standing position, in which case the visualization of the prolapsed valve becomes more clear.

The disadvantage of echocardiography is the impossibility of reliable diagnosis of bacterial vegetations in MVP. This fact is explained by the fact that the valves with prolapse on the echogram look thickened and shaggy due to their scalloping. False-positive results of studies of bacterial vegetations on the valve in patients with MVP using one-dimensional echocardiography are 40%. A more reliable diagnosis of bacterial vegetations in MVP is possible using transesophageal echocardiography, but this method is not yet widely used in pediatric practice.

Dopplerography. Doppler echocardiography allows quantitative assessment of transmitral blood flow and valve function (Vmax - maximum diastolic flow through the mitral valve). Mitral valve regurgitation is diagnosed by the presence of turbulent systolic flow behind the mitral valve leaflets in the left atrium.

Typically, mitral regurgitation with mitral valve prolapse is observed with isolated late systolic and holosystolic murmur. The magnitude of regurgitation does not exceed 1-2 degrees and reaches large values ​​when the depth of cusp of the valves is more than 10 mm, separation of the chords or pronounced dilatation of the atrioventricular ring.

Diagnostic criteria for primary MVP.

Correct diagnosis of primary MVP is important. In 1986, based on the ongoing Framingham study, diagnostic criteria for primary MVP were proposed, which were divided into main, additional and nonspecific.

Main :

A) auscultatory - mid- and late-systolic clicks in combination with late-systolic murmur, mid- and late-systolic clicks at the apex, isolated late-systolic murmur at the apex;

b) auscultation in combination with echocardiography - holosystolic murmur of mitral regurgitation and corresponding echocardiographic criterion;

V) echocardiographic:

Displacement of the septal leaflets in systole beyond the coaptation point, in the projection of the long axis of the left ventricle and in the four-chamber projection with apical access;

Late systolic prolapse more than 3 mm. Additional:

A) anamnestic - neurotic manifestations, psycho-emotional instability, the presence of mitral valve prolapse in persons of the 1st degree of kinship;

b) auscultatory - intermittent mid-late systolic clicks at the apex;

V) clinical - low body weight, asthenic physique, low blood pressure, signs of dysplastic development;

G) radiographic - small heart size, bulging pulmonary artery arch;

d) echocardiographic:

Systolic deflection of the leaflets beyond the coaptation line in a four-chamber projection.

Non-specific:

A) clinical - chest pain, weakness, dizziness, shortness of breath, palpitations, attacks of fear;

b) electrocardiographic - isolated inversion of T waves in leads II, III , aVF, or in combination with inversion in the left precordial leads;

V) echocardiographic - isolated moderate systolic deflection of the mitral leaflets in a four-chamber projection;

G) Holter monitoring - atrial and ventricular (single, group) extrasystoles.

Thus:

1. The presence of two main criteria, i.e. a combination of auscultatory and echocardiographic signs, allows us to speak convincingly about primary mitral valve prolapse.

2. The diagnosis of mitral valve prolapse can be made in the presence of one main and several additional criteria: “silent” MVP (one main criterion on two-dimensional echocardiography) in the presence of 2-3 additional criteria represent a clinical type of primary mitral valve prolapse.

3. The presence of only additional criteria gives the right to assume a diagnosis of mitral valve prolapse.

4. Nonspecific criteria are not decisive when making a diagnosis, since the latter can occur in the absence of the phenomenon of prolapse.

Correct diagnosis of primary MVP should include determining the state of the morphological structures of the valve (for example, dilatation of the left atrioventricular orifice, lengthening of the chords, increased area of ​​the leaflets, abnormal attachment of the chords, abnormalities of the papillary muscles, etc.), as well as information about the presence or absence of mitral regurgitation. For example, primary mitral valve prolapse, abnormal attachment of the chordae to the anterior mitral leaflet, without mitral regurgitation.

Clinical variants of primary mitral valve prolapse.

A comparison of the results of clinical and instrumental examinations for each individual child allows us to identify four variants of MVP, which reflect the severity of the disease and have varying degrees of severity of interrelated signs.

First clinical variant characterized by a minimal degree of severity of clinical symptoms of the disease. There are no complaints or they are characteristically related to autonomic disorders (mild cardialgia). In children of this group, the level of external minor developmental anomalies does not exceed the conditionally threshold level. Auscultation of the heart reveals isolated clicks that are permanent or heard during provocative tests (after physical exertion, in orthostasis). On the ECG at rest there are no changes in the repolarization process or there is a slight decrease in the T wave in the left precordial leads. In the orthostatic position and when performing an electrocardiographic test with isadrin, disruption of the repolarization process does not occur. X-rays reveal normal or reduced sizes of the heart shadow. Echocardiographic examination reveals moderate holo- or late-systolic flexion of the mitral leaflets, not exceeding 5 mm. According to Doppler ultrasound, there is no mitral regurgitation. The vegetative status (according to the initial autonomic tone and cardiointervalography) is characterized as sympathicotonic; in most cases, normal autonomic reactivity and excessive autonomic support of activity are determined. Physical performance (according to bicycle ergometry data) corresponds to the indicators of healthy children.

Second clinical option is characterized by typical manifestations of MVP syndrome. Children are characterized by such psycho-emotional traits as emotional instability, tearfulness, shyness, and self-doubt. Clinical examination reveals characteristic external features: asthenic physique, decreased body weight, poor muscle development, etc. Auscultation reveals a combination of clicks with late systolic murmur. An ECG at rest reveals a decrease in the repolarization process in the myocardium in the form of an isoelectric or smoothed T wave in the left precordial leads. In the orthoposition and during the ST-T test with isadrin, the changes intensify, but T wave inversion is not observed. A chest x-ray reveals a small heart shadow and moderate bulging of the pulmonary artery arch. Doppler echocardiography reveals late systolic leaflet prolapse, the depth of which does not exceed 7 mm, regurgitation is absent or does not exceed 1 grade. In the vegetative status, sympathicotonic disorders predominate or VSD of a mixed type occurs. Bicycle ergometry reveals a moderate decrease in physical performance indicators and a decrease in adaptation of the cardiovascular system to stress, associated with an excessive chronotropic response.

At third variant of MVP syndrome Clinical and instrumental indicators have the most pronounced deviations. When determining signs of connective tissue disorders in these children, a high level of minor developmental anomalies is revealed: tall stature, asthenic physique, often chest deformities (scoliosis, kyphosis, funnel deformity, etc.), elongation of the limbs, loose joints, myopia, etc. Orthostatic hypotension can be determined. , which causes dizziness, weakness, and syncope. On auscultation, an isolated late-systolic murmur is typical; a holosystolic murmur may be heard. The ECG shows pronounced ST-T changes that intensify (up to T wave inversion) in the orthostatic position. Doppler echocardiography reveals large late systolic or holosystolic leaflet prolapse with mitral regurgitation grades 1-3. In the vegetative status, signs of VSD of a mixed type or a predominance of the parasympathetic division of the autonomic nervous system are revealed. Children have low levels of physical performance and a maladaptive response from the cardiovascular system to physical activity.

The fourth (“silent”) version of the secondary gun in children it is characterized by the absence of classical auscultatory (phonocardiographic) manifestations of the syndrome and is detected by two-dimensional echocardiographic examination (one main sign). Often this variant of MVP is detected during clinical examination of healthy children with features of an asthenic constitution. Sometimes a “silent” MVP is detected during examination for cardialgia, arrhythmias, and repolarization changes on the ECG.

Complications.

In most cases, MVP proceeds favorably and only in 2-4% leads to serious complications. The main complications of primary MVP are:

Acute or chronic mitral insufficiency;

Bacterial endocarditis;

Thromboembolism;

Life-threatening arrhythmias;

Sudden death.

Acute mitral regurgitation occurs due to the separation of tendon threads from the cusps of the mitral valve, is observed casuistically rarely in childhood and is mainly associated with chest trauma in patients against the background of myxomatous degeneration of the chordae.

Chronic mitral insufficiency in patients with MVP syndrome, it is an age-dependent phenomenon and develops after 40 years of age. It has been shown that in adult patients, mitral valve prolapse is the basis of mitral regurgitation in 60% of cases (Luxereau P. et al., 1991). In children, mitral regurgitation with MVP is most often asymptomatic and is diagnosed by Doppler echocardiography. To determine the severity of mitral regurgitation, a complex of clinical and instrumental indicators is used.

Mild mitral regurgitation is characterized by:

Shortness of breath only during physical activity.

The third tone is missing.

Short early and late systolic murmur.

Sinus rhythm.

Moderate dilatation of the left atrium.

Regurgitation according to Doppler + or ++.

Severe mitral regurgitation is characterized by:

Orthopnea.

Atrial fibrillation.

Pronounced dilatation of the left atrium and left ventricle, the appearance of dilatation of the right sections.

Venous congestion in the lungs.

Doppler regurgitation +++ or ++++.

Characteristic complications of mitral regurgitation in MVP are:

Congestive heart failure.

Pulmonary hypertension.

Arterial thromboembolism.

Risk factors for the development of “pure” (non-inflammatory) mitral regurgitation in prolapse syndrome according to two-dimensional echocardiography are:

Dilation of the left atrioventricular orifice.

Prolapse of predominantly the posterior mitral leaflet.

Thickening of the posterior mitral leaflet.

Infectious endocarditis. The significance of MVP in the occurrence of infective endocarditis has not been fully determined. Mitral valve prolapse is a high risk factor for infective endocarditis. The absolute risk of the disease is 4.4 times higher than in the population. The frequency of infective endocarditis in patients with MVP increases with age, so in children this syndrome is rarely the cause of infective endocarditis and occurs with a frequency of 1 case in 500 patients.

Sudden death. The incidence of sudden death in MVP syndrome depends on many factors, the main ones being electrical instability of the myocardium in the presence of long QT interval syndrome, ventricular arrhythmias, concomitant mitral insufficiency, neurohumoral imbalance and other factors. The risk of sudden death in the absence of mitral regurgitation is low and does not exceed 2:10,000 per year, while with concomitant mitral regurgitation it increases 50-100 times.

In most cases, sudden death in patients with MVP is of arrhythmogenic origin and is caused by the sudden onset of idiopathic ventricular tachycardia (fibrillation) or against the background of long QT interval syndrome.

In rare cases, sudden cardiac death in patients with MVP may be due to a congenital anomaly of the coronary arteries (abnormal origin of the right or left coronary artery), leading to acute myocardial ischemia and necrosis.

Thus, the main risk factors for sudden death in children with MVP syndrome are:

1. ventricular arrhythmias grade III-V according to Lown;

2. prolongation of the corrected QT interval by more than 440 ms;

3. the appearance of ischemic changes on the ECG during physical activity;

4. history of cardiogenic syncope.

Treatment.

The management tactics for children with primary MVP vary depending on the severity of leaflet prolapse and the nature of autonomic and cardiovascular changes.

The main principles of treatment are:

1) complexity;

2) duration;

3) taking into account the direction of functioning of the autonomic nervous system.

It is mandatory to normalize work, rest, daily routine, adherence to the correct regime with sufficient sleep. The issue of physical education and sports is decided individually after the doctor evaluates the indicators of physical performance and adaptability to physical activity. Most children, in the absence of mitral regurgitation, severe disturbances in the repolarization process and ventricular arrhythmias, tolerate physical activity satisfactorily. If they have medical supervision, they can lead an active lifestyle without any restrictions on physical activity. Children can be recommended swimming, skiing, skating, and cycling. Sports activities associated with jerky movements (jumping, karate wrestling, etc.) are not recommended.

The detection of mitral regurgitation, ventricular arrhythmias, changes in metabolic processes in the myocardium, and prolongation of the QT interval on the electrocardiogram in a child dictates the need to limit physical activity and sports. These children are allowed to engage in physical therapy under the supervision of a doctor.

Based on the fact that mitral valve prolapse is a particular manifestation of vegetative-vascular dystonia in combination with connective tissue disorders, treatment is based on the principle of restorative and vegetotropic therapy.

The entire complex of therapeutic measures should be built taking into account the individual characteristics of the patient and the functional state of the autonomic nervous system.

An important part of the comprehensive treatment of children with MVP is non-drug therapy. For this purpose, psychotherapy, auto-training, physiotherapy (electrophoresis with magnesium, bromine in the upper cervical spine), water treatments, acupuncture, and spinal massage are prescribed. Much attention should be paid to the treatment of chronic foci of infection; tonsillectomy is performed if indicated.

Drug therapy should be aimed at:

1) treatment of vegetative-vascular dystonia;

2) prevention of the occurrence of myocardial neurodystrophy;

3) psychotherapy;

4) antibacterial prophylaxis of infective endocarditis.

For moderate manifestations of sympathicotonia, herbal medicine with sedative herbs is prescribed: tincture of valerian, motherwort, herbal collection (sage, wild rosemary, St. John's wort, motherwort, valerian, hawthorn), which simultaneously has a slight dehydration effect.

If there are changes in the repolarization process on the ECG, courses of treatment are carried out with drugs that improve metabolic processes in the myocardium (panangin, riboxin, vitamin therapy, carnitine). A beneficial effect has been noted from the use of the drug coenzyme Q-10, which significantly improves bioenergetic processes in the myocardium and is especially effective in secondary mitochondrial failure.

Indications for the use of β-blockers are frequent, group, early (type R on T) ventricular extrasystoles, especially against the background of prolongation of the QT interval and persistent repolarization disorders; The daily dose of obzidan is 0.5-1.0 mg/kg body weight, treatment is carried out for 2-3 months or more, after which the drug is gradually withdrawn. Rare supraventricular and ventricular extrasystoles, if not combined with long QT interval syndrome, as a rule, do not require any drug interventions.

Psychotherapy. Treatment of children and adolescents with MVP should include psychopharmacotherapy with explanatory and rational psychotherapy aimed at developing an adequate attitude towards the condition and treatment.

If the autonomic tone is sympathicotonic, certain dietary activities- limiting sodium salts, increasing the intake of potassium and magnesium salts (buckwheat, oatmeal, millet porridge, soybeans, beans, peas, apricots, peaches, rose hips, dried apricots, raisins, zucchini; from medications - panangin). Shown vitamin therapy (multivitamins, B1), the collection of sedative herbs. To improve microcirculation, vinkopan, cavinton, trental are prescribed.

Psychopharmacotherapy is carried out according to well-known principles and is based on an analysis of the structure and daily dynamics of psychopathological disorders. Patients are usually treated with a combination of psychotropic drugs. Of the antidepressants, drugs with a balanced or sedative effect are most often used (azafen - 25-75 mg per day, pyrazidol - 25-37.5 mg per day, anafranil, tryptisol, amitriptyline - 6.25-25 mg per day). Less commonly used are antidepressants with a stimulating effect (melipramine -12.5-25 mg per day, ludiomil, etc.). Of the neuroleptics, preference is given to sonapax with its thymoleptic effect and phenothiazine drugs (triftazine - 5-10 mg per day, etapazine - 10-15 mg per day), given their activating effect with a selective effect on thinking disorders. Of the nootropic drugs, piracetam (nootropil) is preferred, and in the presence of epileptoid signs on the electroencephalogram - phenibut, pantogam.

There are known observations where only one psychopharmacological correction of depressive states and panic attacks in patients with MVP contributed to its complete disappearance.

Treatment of mitral insufficiency. With the development of mitral regurgitation, traditional treatment is carried out with cardiac glycosides, diuretics, potassium preparations, and vasodilators. In children with isolated late- or holosystolic murmur, mitral regurgitation is in a state of compensation for a long time, however, in the presence of functional (borderline) pulmonary hypertension and myocardial instability, phenomena of circulatory failure may occur, usually against the background of intercurrent diseases, less often after prolonged psycho-emotional stress ( exams, conflict situations). Such children can be prescribed a course of treatment with maintenance doses of cardiac glycosides (digoxin 1/5 of the saturation dose - 0.03-0.05 mg/kg, depending on age, 2 times a day) and non-hypotensive doses of angiotensin-converting enzyme inhibitors (captopril).

Surgery: In case of severe mitral regurgitation, refractory to drug therapy, surgical correction of the defect is performed. Clinical indications for surgical treatment of MVP complicated by severe mitral regurgitation are:

Circulatory failure II B, refractory to therapy with cardiac glycosides, diuretics and vasodilators;

Addition of atrial fibrillation;

Addition of pulmonary hypertension (no more than stage 2);

Attachment of bacterial endocarditis, incurable with antibacterial drugs.

Hemodynamic indications for surgical treatment of mitral regurgitation are:

Increased pressure in the pulmonary artery (more than 25 mm Hg);

Reduced ejection fraction (less than 40%);

Regurgitation fraction more than 50%;

Exceeding the end-diastolic volume of the left ventricle by 2 times.

Radical surgical correction of MVP syndrome is used, including the following surgical options depending on the prevailing morphological abnormalities:

Plication of the mitral leaflet;

Creation of artificial chords using polytetrafluoroethylene sutures;

Shortening of the chordae tendineae;

Suturing of commissures;

It is advisable to supplement reconstructive operations on the mitral valve by suturing the Carpanier support ring.

If it is impossible to carry out a reconstructive operation, the valve is replaced with an artificial prosthesis.

Outpatient observation.

Since the possibility of progression of changes in the mitral valve with age cannot be excluded, as well as the high probability of severe complications, the need for clinical monitoring of children with MVP is dictated. They must be re-examined by a pediatrician, cardiologist and undergo follow-up studies at least 2 times a year.

In a clinic, during medical examination, anamnesis is collected: the course of pregnancy and childbirth, the presence of psychosomatic diseases in the family, the presence of signs of dysplastic development in the first years of life is established (congenital dislocation and subluxation of the hip joints, hernia), the reasons for observation by a psychoneurologist are determined, the age of onset and frequency sore throat Complaints are detected, including those of an asthenoneurotic nature: headaches, cardialgia, palpitations, etc.

The child is examined with an assessment of constitutional features and minor developmental anomalies, auscultation in the supine position, left side, sitting, standing, after jumping and when straining, an electrocardiogram is recorded in the supine and standing position, it is advisable to do echocardiography (if this is not possible, the study is carried out in diagnostic and cardiology centers).

If necessary, consultation with an otolaryngologist, psychoneurologist, or geneticist is carried out. During the clinical examination, a conversation is held with parents, who are explained the essence of this condition and the peculiarities of the course of MVP in a particular child.

The follow-up notes the dynamics of auscultatory manifestations, electrocardiogram and echocardiogram indicators, and monitors the implementation of the prescribed recommendations.

Secondary mitral valve prolapse.

Secondary MVP can be caused by a wide variety of reasons, which are conventionally divided into:

1. Hereditary diseases of connective tissue, in which accumulation of acidic mucopolysaccharides in the valve stroma, myxomatous transformation of the leaflets, chords, and dilatation of the atrioventricular ring occur.

2. Caused by heart diseases (congenital defects - atrial septal defect, Ebstein's disease, bicuspid aortic valve, coronary fistula, tetralogy of Fallot, hypertrophic cardiomyopathy, coronary circulation anomalies, etc.).

3. ECG abnormalities - atrioventricular dissociation, CLC, WPW syndromes, in which prolapse of the leaflets is caused by a violation of the sequential contraction and relaxation of the walls of the left ventricle or the occurrence of valvular-ventricular disproportion.

4. Arise from neuroendocrine and psychoemotional disorders (thyrotoxicosis, migraine, neurosis, hysteria, anorexia nervosa), in which disorders of the autonomic innervation of the valves and subvalvular apparatus are of primary importance.

In a number of conditions, mitral valve prolapse can significantly affect the course of the underlying disease.

MVP and atrial septal defect.

A frequent combination of ASD and mitral valve prolapse has been noted, reaching 50-70% with a secondary defect. MVP and ASD have common mechanisms of occurrence - connective tissue dysplasia. Along with this, with large defects, volume overload of the right parts occurs and a decrease in blood flow through the left ventricle. MVP with ASD in most cases is accompanied by auscultatory changes (clicks, late noise) and is rarely “silent” (detected by echocardiography). In approximately 30% of patients with ASD, leaflet prolapse is accompanied by cardialgia and inversion of T waves in the left precordial leads.

Mitral valve prolapse due to ASD increases the risk of infective endocarditis. Considering the high incidence of mitral valve prolapse with interatrial defects and the possible long-term asymptomatic course of the defect, all children with diagnosed MVP should undergo a thorough examination of the septum to exclude hidden heart defects.

MVP and Ebstein's anomaly.

MVP with Ebstein's anomaly is observed in 30-40% of cases and occurs due to connective tissue dysplasia, valvular-ventricular disproportion, and abnormal course of the excitation wave along the additional atrion-doventricular pathways.

When Ebstein's anomaly is combined with MVP, children more often develop pulmonary hypertension, right ventricular failure, and the risk of infective endocarditis increases.

MVP and anomalous origin of the left coronary artery from the pulmonary artery (Blunt-White-Garland syndrome).

Although this congenital anomaly is accompanied by left-sided cardiomegaly, patients with Blunt-White-Garland syndrome may have mitral valve prolapse. The high incidence of MVP with this anomaly can contribute to the correct diagnosis, since in dilated cardiomyopathies accompanied by coronary circulatory failure, mitral valve prolapse is practically not observed.

MVP and hypertrophic cardiomyopathy.

With hypertrophic cardiomyopathy, MVP syndrome is found in 3-8% of patients and has an adverse effect on the course of the underlying disease and significantly increases the risk of sudden death. Thus, with a combination of MVP and hypertrophic cardiomyopathy, atrial fibrillation and mitral regurgitation are observed much more often (3 times).

MVP and rheumatism.

Previously, there was a position that mitral valve prolapse and rheumatism in children are rarely combined, and in the presence of clinical manifestations of MVP, the diagnosis of rheumatism can be practically excluded. On the contrary, the presence of the classical Kissel-Jones-Nesterov criteria for rheumatism excluded prolapse syndrome. This misconception has led to a large number of diagnostic errors, on the one hand, overdiagnosis of rheumatic valvulitis in children with harmless prolapse, and on the other, underestimation of rheumatic valvulitis in the presence of a murmur of mitral regurgitation in the phenomenon of prolapse.

It is known that rheumatism is a disease with a hereditary predisposition. Numerous studies indicate a tendency of children suffering from rheumatic disease to connective tissue dysplasia. Acquired mitral valve disease is formed mainly in patients with external anomalies (stigmas) of connective tissue. On the other hand, the predisposition of children with primary MVP to chronic foci of infection (repeated tonsillitis, chronic tonsillitis) allows them to be classified as a risk group for the development of rheumatic disease.

It has been shown that in the acute phase of a rheumatic attack, the phenomenon of prolapse of the mitral valves (according to two-dimensional echocardiography) is observed in 30-46.8% of children. The occurrence of MVP in rheumatic valvulitis is caused by mucoid swelling and softening of the valves; with adequate (prednisolone, penicillin) therapy, valve prolapse decreases. Thus, MVP syndrome does not exclude rheumatic disease and is even a provoking factor for the disease. It can be assumed that children with MVP syndrome who have suffered a rheumatic attack are much more likely to develop mitral regurgitation due to connective tissue dysplasia of the valve leaflets.

MVP and juvenile hyperthyroidism.

Hyperthyroidism is caused by an increase in the level of circulating thyroid hormone when it is overproduced by the thyroid gland and much less often when there is an excess of thyroid-stimulating hormone.

Clinical symptoms of hyperthyroidism include neuropsychiatric abnormalities, anxiety, emotional lability, depression, and in severe cases, psychosis. Characterized by weight loss, muscle weakness, and diarrhea. On examination, moist skin, tremor of the fingers, exophthalmos, and weakness of the thigh muscles are revealed.

Cardiovascular disorders in hyperthyroidism are manifested by systolic arterial hypertension, mitral valve prolapse, hyperkinetic cardiac syndrome and tachysystolic forms of cardiac arrhythmias.

Systolic arterial hypertension is labile in nature, increases with psycho-emotional stress, and rarely reaches crisis levels.

MVP is found in most patients with thyrotoxicosis and is caused by valvular-ventricular disproportion, when the small size of the left ventricular cavity against the background of tachycardia does not correspond to the size of the left atrioventricular opening. Prolapse may be accompanied by auscultatory symptoms (clicks, late systolic murmur) or detected during two-dimensional echocardiographic examination (“silent” prolapse). Typically, such prolapse does not lead to mitral regurgitation and therefore has no hemodynamic significance. However, its diagnosis is important in terms of preventing infective endocarditis, especially in patients with concomitant supraventricular arrhythmias (atrial fibrillation).

In the development of thyrotoxicosis, a significant role is played by factors of hereditary predisposition. As a rule, a high frequency of thyroid metabolism disorders is determined in families of patients with thyrotoxicosis.

MVP for hypertensive type NCD usually not accompanied by typical auscultatory manifestations of the syndrome (“silent” prolapse) and is detected only during echocardiographic examination.

With NPD of the hypotensive type low blood pressure is accompanied by cephalgia, emotional lability, excitability or apathy, decreased physical performance, dizziness, irritability, and decreased mental performance.

Prolapse of the valves can occur due to an increase in the interval between contraction of the left atrium and the ventricle (due to a delay in atrioventricular conduction), as well as due to the increased force of blood expulsion from the left ventricle with preserved contractility and a rare rhythm. As a rule, there is a “silent” prolapse, detected by echocardiography.

1. Educational and methodological material:

Fig.1. X-ray of mitral valve prolapse: the heart shadow is located in the middle, the arch of the pulmonary artery protrudes.

Rice. 2. One-dimensional echocardiogram with mitral valve prolapse: bowing of the valve leaflets in the shape of a “question mark” (indicated by an arrow).

Rice. 3. Two-dimensional echocardiogram for mitral valve prolapse: bowing of the leaflets into the cavity of the left atrium.

Table 1.

Hereditary syndromes accompanied by mitral valve prolapse

1. Test tasks:

Patients with mitral valve prolapse may have:

A) circulatory failure;

B) infective endocarditis;

B) heart rhythm disturbance;

D) myocardial infarction;

D) all of the above.

Mitral valve prolapse in children over 10 years of age is more often detected:

A) in boys;

B) in girls;

C) equally often in both sexes.

the occurrence of secondary mitral valve prolapse may be associated with:

A) hereditary pathology of connective tissue;

B) arterial hypertension;

B) atrial septal defect;

D) congenital hypothyroidism;

D) valvular-ventricular disproportion.

Features of the medical history of children with mitral valve prolapse are:

A) suffered rickets at an early age;

B) toxicosis of the 1st trimester of pregnancy in the mother;

C) unfavorable course of labor (caesarean section, vacuum extraction);

D) frequent colds;

D) the presence of MVP in close relatives.

The most common complaints with mitral valve prolapse are:

A) cardialgia;

B) swelling in the lower extremities;

B) “flickering of flies” before the eyes;

D) interruptions in heart function;

D) general weakness.

Typical auscultatory signs of mitral valve prolapse are:

A) “quail” rhythm;

B) isolated clicks;

B) late systolic murmur;

In children with primary MVP, the following heart rhythm disturbances are most often found:

A) WPW syndrome;

B) sinus tachycardia;

B) AV blockade;

D) supraventricular extrasystole;

D) atrial febrilation.

Based on the Framingham study, the presence of primary MVP can be convincingly stated if the patient has:

A) 3 additional criteria + 1 nonspecific;

B) more than 2 additional criteria;

B) 1 main criterion + 1 additional;

D) 2 main criteria.

Drug therapy for MVP should be aimed at:

A) treatment of vegetative-vascular disorders;

B) prevention of myocardial neurodystrophy;

B) psychotherapy;

D) correction of metabolic disorders;

D) prevention of infective endocarditis.

surgical treatment of mitral valve prolapse:

A) is carried out;

B) is not carried out.

Sample test answers: