Hypertrophic cardiomyopathy. Myocardial hypertrophy - signs and symptoms. Treatment of hypertrophic cardiomyopathy of the left ventricle of the heart

Frequency of sudden death in young people working population is growing catastrophically. One of the honorable leading positions among the causes of death is occupied by hypertrophic cardiomyopathy - excess myocardial mass without an increase in the volume of the cavities of the heart. Is it enough to stop smoking and exercise to prevent death?

The essence of the disease is a violation of the normal contraction and relaxation of the heart muscle. With a decrease in contractility, little blood flows to the periphery, and circulatory failure develops. In the absence of relaxation in diastole, the heart is poorly filled with blood. The pumping function suffers, it has to contract more often to supply the body. This is the mechanism for the appearance of an accelerated pulse.

Hypertrophic cardiomyopathy, what is it? The diagnosis is valid if there is:

• widespread or limited increase in myocardial thickness up to 1.5 cm or more;
• decrease in ventricular capacity;
• violation of their diastole;
• chest pain;
• dizziness;
• fainting not associated with neurological diseases.

Myocardial hypertrophy

Types and variants of the course of the disease

There are 4 types of hypertrophic cardiomyopathy:

1. With increase upper sections septa between the ventricles.
2. Hypertrophy of the entire septum.
3. Concentric expansion of the wall and narrowing of the left ventricle.
4. Isolated apical enlargement.

Main hemodynamic types:

• obstruction is permanent;
• obstruction is periodic, only during physical activity;
• hidden or labile, develops from time to time, for example, with a decrease in pressure.

Causes of hypertrophic cardiomyopathy

Symptoms appear without previous inflammatory phenomena or provoking factors. The cause is a genetic defect that is hereditary, family character.

1. As a result of gene mutation, the synthesis of myocardial contractile proteins is disrupted.
2. Muscle fibers have an irregular structure and location, and in places are replaced by connective tissue.
3. The altered cardiomyocytes contract uncoordinatedly, the load on them increases, the fibers thicken, and the entire thickness of the myocardium hypertrophies.

The disease is congenital, the first manifestations begin in childhood and go unnoticed. It is important to carry out a preventive examination.

Symptoms of the disease

Depending on the thickness of the myocardium, 3 degrees of the disease are distinguished:

• moderate hypertrophy;
• moderate;
• pronounced hypertrophy.

Hypertrophic cardiomyopathy, symptoms, and the danger of this pathology lie in the fact that the problems are not limited to the myocardium:

• hypertrophy of the papillary muscles and fibrous part develops interventricular septum, endocardium;
• thickening of the mitral valve walls impedes blood flow;

All of the above factors lead to changes in the structure of the walls of the vessels that supply the myocardium; their lumen narrows by more than 50%. This is a direct road to a heart attack.

Irradiation of pain during myocardial infarction

In the initial stages, the disease is uncharacteristic, the symptoms are very numerous and nonspecific. The following modifications of the course of the disease are distinguished:

• asymptomatic;
• according to the type of vegetative-vascular dystonia;
• in the form of a heart attack;
• cardialgia;
• decompensation;

Each option has its own symptoms. Complaints of varying severity are typical:

• chest pain;
• increased breathing rate;
• rhythm disturbance;
• dizziness;
• fainting;
• may appear for the first time and immediately end in sudden death.

Obstructive hypertrophic cardiomyopathy is characterized by a classic triad of symptoms:

• chest pain;
• rhythm disturbance;
• episodes of loss of consciousness.

Loss of consciousness or a near-syncope state is explained by a lack of blood supply to the brain.

The most serious symptom of hypertrophic cardiomyopathy is arrhythmia, which determines the prognosis of the disease.

Patients note the appearance of attacks of interruptions in the work of the heart, alternating with tachycardia. The attacks are accompanied unpleasant sensations behind the sternum, a feeling of fear of death. How to provide emergency assistance if symptoms of arrhythmia occur, read.

Hypertrophic obstructive cardiomyopathy, what is it? This is a disease, the inevitable end of which is characterized by difficulty breathing, a feeling of lack of air.

At visual inspection In patients, an abnormal, multicomponent cardiac impulse is detected, followed by a second, less strong contraction of the left ventricle when the blood has passed through the narrowed area. Normally, there is no second impulse, but patients may have 2, 3, or 4 such impulses. The size of the heart is increased to the left.

Hypertrophic cardiomyopathy according to ICD 10 is divided into:

• dilatational I42.0;
• obstructive I42.1;
• another I42.2.

At the same time, when considering the disease, situations that complicate the course of pregnancy are excluded, postpartum period. These are independent diseases.

Additional examination methods

When performing an ECG, specific signs of hypertrophic cardiomyopathy cannot be found. Most often there is hypertrophy of the left ventricle, left atrium, and myocardial ischemia.

All of the above changes on the ECG in combination with reduced voltage and scar changes in the myocardium indicate hypertrophic cardiomyopathy.

Echocardiography is more informative, because it allows you to see:

• enlargement of the interventricular septum;
• decreased septal mobility during systole;
• decrease in left ventricular volume;
• enlargement of the left atrium cavity;
• increase in contractility of the left ventricle.
• abnormal movement of the mitral valve leaflets.

The gold standard for early and successful detection of hypertrophic cardiomyopathy is electrocardiography, ECHO-CG, ultrasound.

MRI, positron emission tomography allow you to clearly see where and what changes have occurred.

Treatment

The choice of treatment tactics depends on the characteristics of the course of the disease and the age at which the disease manifested.

Hypertrophic cardiomyopathy with outflow tract obstruction is treated with primary emphasis on restoring left ventricular outlet diameter.

It is mandatory to use anti-arrhythmia drugs that reduce oxygen consumption and improve the absorption of available oxygen and nutrients. You can learn more about the causes of arrhythmia in this.

Various representatives of beta-blockers are the drugs of choice. The effect of these drugs is antiarrhythmic. They normalize the rhythm, reduce the frequency of episodes of loss of consciousness, slow down the pulse, and reduce myocardial contractility. The main mechanism of their action is aimed at ensuring that the heart has time to relax and the left ventricle is filled with blood for further work.

Selective and non-selective drugs are known. Currently, the list of beta blockers has expanded. New modern drugs have appeared that have the property of normalizing vascular tone that nourishes the myocardium:

• Carvedilol;
• Celipres;
• Bucindolol.

Most effective means Bisaprolol remains for the treatment of tachycardia.

These medications should not be prescribed for bronchial asthma, low blood pressure, bradycardia, or atherosclerosis of peripheral arteries.

The daily dose of the drug is selected individually by gradually increasing the amount of the blocker used.

Hypertrophic cardiomyopathy (ICD code 10 - I42) is a contraindication to the use of drugs, cardiac glycosides, nitrites, because they increase obstruction.

If blockers are ineffective, treatment of hypertrophic cardiomyopathy is permanent - Cordarone, . If necessary, Novocaine, Nicotinamide, Quinine are added.

Surgery

The ineffectiveness of conservative therapy requires surgical intervention. All operations are performed under artificial cardiopulmonary bypass with artificial hypothermia up to 32°C. Types of operations used:

1. Removal of overgrown muscle tissue in the interatrial septum. The risk of fatal postoperative complications is 9–10%.
2. Percutaneous injection of 96% alcohol into the left coronary artery causes necrosis of the wall as in an infarction in the anterior septal region.
3. Placement of pacemakers.
4. Implantation of defibrillators.

Prevention of heart failure

Considering that the annual mortality rate for the initial diagnosis of heart failure is 33%, much attention is paid to preventive measures. The main methods of prevention include:

• avoid stress, think about positive things, listen to classical music;
• relax more, spend time outdoors;
• avoid smoking and alcohol;
• cure kidney disease, anemia, diabetes, sleep apnea– snoring, bronchitis, tonsillitis, teeth and other sources of infection in the body;
• dosed physical activity, provided that it is permitted by the attending physician;
• proper nutrition using fish, herbs, dairy products and avoiding fatty, fried, smoked, salty foods;
• cholesterol control;
• prevention of thrombosis, increased blood clotting;
• regular examinations: ECG, ECHO-CG, ergometry, MRI with angiography, Doppler examination.

Possible complications

If patients live to be 40–50 years old, bacterial endocarditis, strokes, arterial hypertension, heart attacks, pulmonary embolism, and fatal intestinal vascular thrombosis occur.

Forecast

Average duration life expectancy with hypertrophic cardiomyopathy is low. The course and prognosis are considered unfavorable, because the mortality rate reaches 7-8% annually, especially if left untreated. Half of these patients die young due to exercise physical exercise, sex.

Effects aggravating the course of hypertrophic cardiomyopathy:

• ventricular arrhythmia;
• the younger the disease manifests itself, the more serious its prognosis;
• significant increase in heart muscle mass;
• attacks of loss of consciousness;
• the presence of sudden death in relatives.

Useful video

You can learn more about hypertrophic cardiomyopathy, causes, symptoms from the following video:

Conclusion

1. Hypertrophic cardiomyopathy cannot be cured.
2. Efforts should be aimed at slowing the development of symptoms, preventing and treating complications, and increasing the length and quality of life of the patient.
3. The patient is required to exercise discipline medicines, follow the doctor’s recommendations, conduct healthy image life.

Hypertrophy of the left or right parts of the heart occurs due to damage to the muscles, valves of the organ, due to disruption of blood flow. This often happens when congenital anomalies development, due to increased blood pressure, lung diseases, and significant physical activity. Most often, hypertrophy of the left ventricle of the heart is detected. This is due to the greater functional load in this area.

Reasons for appearance

The disease occurs as a result of various disorders that interfere with the normal functioning of the organ. The myocardium begins to contract with increased load, its metabolism increases, tissue volume and cell mass increase.

At the initial stage of the disease, the heart maintains normal blood flow due to an increase in its mass. But later the myocardium is depleted, and hypertrophy gives way to atrophy - the cells significantly decrease in size.

There are two types of pathology: concentric - the heart enlarges, its walls thicken, the atria/ventricles decrease, and eccentric (the organ is enlarged, but the cavities are expanded).

Cardiac hypertrophy can affect healthy people involved in physical labor and athletes. Against the background of such changes, acute heart failure may occur. When engaging in bodybuilding, hockey, or heavy physical labor, you need to monitor the condition of the myocardium.

Due to its occurrence, ventricular hypertrophy is divided into 2 types:

• working – due to increased load on a healthy body;
• substitution is the result of adaptation to work with another disease.

Causes of left ventricular damage

Most often, the muscle of the left ventricle undergoes changes. If its thickness is more than 1.2 cm, this violation occurs. In this case, hypertrophy of the IVS (interventricular septum) of the heart is also observed. In severe cases, the thickness can reach 3 cm and the weight can reach 1 kg.

Poor blood pumping into the aorta is provoked, therefore blood supply throughout the body is disrupted. Weight gain leads to a lack of oxygen and nutrients. As a result, hypoxia and sclerosis occurs.

Causes of changes in the left ventricle: arterial hypertension; cardiomyopathy; narrowing (stenosis) of the aortic valve; increased physical activity; hormonal disorders; obesity; kidney disease with secondary hypertension.

Causes of left atrium damage:

• Arterial hypertension;
• Hypertrophic cardiomyopathy;
• Congenital pathologies of the heart/aorta;
• General obesity, especially in children and adolescents;
• Stenosis/insufficiency of the aortic or mitral valve.

Causes of right ventricular damage

Changes in the right atrium are usually associated with pulmonary pathologies and disturbances in the pulmonary circulation of blood flow. Blood enters the right atrium through the vena cava from tissues and organs. From there it enters the ventricle through the tricuspid valve and further into the pulmonary artery and lungs.

In the latter, gas exchange occurs. It is for this reason that it disrupts the normal structure of the right sections due to various diseases of the respiratory system.

The main factors provoking atrial hypertrophy of right-sided localization:

• Congenital developmental pathologies (eg tetralogy of Fallot, IVS defect);
• Chronic obstructive pulmonary diseases, for example, emphysema, pneumosclerosis, bronchial asthma, bronchitis;
• Tricuspid valve stenosis/insufficiency, pulmonary valve changes, right ventricular enlargement.

Chronic lung pathology provokes damage to the vessels of the small circle, proliferation of connecting tissues, gas exchange and microcirculation decreases. As a result, blood pressure in the vessels of the lungs increases, so the myocardium begins to contract with greater force, which leads to hypertrophy.

Narrowing or incomplete closure of the tricuspid valve leads to the same disruption of blood flow as in a similar case with mitral pathology.

Causes of changes in the right ventricle: congenital malformations, chronic pulmonary hypertension, narrowing of the pulmonary valve, increased venous pressure with congestive insufficiency.

Hypertrophy of the right ventricle of the heart occurs if the thickness of its wall is more than 3 mm. It leads to the expansion of departments and poor circulation. As a result, venous return through the vena cava is disrupted, and stagnation occurs. Patients develop swelling, shortness of breath, bluish skin, and then complaints about work internal organs.

It should be noted that if the left ventricle is damaged, the left atrium will also be affected. Then the right sections are also subject to changes.

Symptoms of hypertrophy of the left and right ventricle of the heart

When the myocardium of the left half is damaged, the following occur: fainting, dizziness, shortness of breath, arrhythmias, pain in this area, weakness, and fatigue.

When the right half is affected, following symptoms: cough, shortness of breath, difficulty breathing; swelling; cyanosis, pale skin; rhythm disturbance.

How is hypertrophy of both ventricles of the heart diagnosed?

The simplest and at the same time effective methods are ultrasonography(ultrasound) and echocardiography (ECG). In the process, the thickness of the walls and the size of the organ are determined.

Indirect symptoms of changes detected on the ECG:

• When the right sections change, the electrical conductivity changes, the rhythm is disrupted, and a deviation of the electrical axis to the right is observed;
• Changes in the left sections are indicated by deviation of the axis to the left, respectively, and voltage signs are recorded.

It is also possible to confirm or refute the diagnosis based on the results of x-rays of organs chest.

Treatment of various forms of cardiac hypertrophy

All efforts to eliminate the disease are directed primarily at the cause that caused it.

For example, if a disorder occurs due to a respiratory disease, the course of treatment is aimed at compensating lung function. Anti-inflammatory therapy is prescribed. Bronchodilators and a number of others are used, depending on the underlying cause.

In case of damage to the left side caused by arterial hypertension, treatment only involves taking antihypertensive medications of different groups, as well as diuretics.

If severe valve defects are detected, they may resort to surgery and even prosthetics.

Treatment of hypertrophy of the left and right ventricle of the heart in all cases of the disease includes eliminating the symptoms of myocardial damage. For this purpose, antiarrhythmic therapy is used, as well as cardiac glycosides.

It is possible that drugs will be prescribed that improve the metabolic process in the heart muscle (eg riboxin, ATP, etc.). Patients are advised to adhere to a special diet, limit fluid and salt intake. In case of obesity, efforts are directed towards normalizing body weight.

At congenital defect heart pathology is eliminated surgically, if possible. In very severe cases, when the structure is severely damaged and hypertrophic cardiomyopathy develops, the only option is an organ transplant.

As can be judged from the above, the approach to patients is carried out purely individually. Doctors take into account all existing manifestations of organ dysfunction, general state patient, presence of concomitant diseases.

It should be noted that timely detected myocardial pathology can be corrected in the vast majority of cases. Feeling the first alarming symptoms You must immediately seek advice from a specialist - a cardiologist. After the examination, he will identify the cause of the disease and prescribe adequate treatment.

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Causes

The causes of hypertrophic cardiomyopathy were established after an ultrasound scan of the patients' relatives. It turned out that 65% of members of the same family have similar changes in the heart muscle.

There are 2 forms of the disease based on etiology.

Primary or idiopathic

Primary is the hereditary form of cardiomyopathy. The development of genetics has made it possible to establish the exact gene responsible for the development of the disease in half of the cases. In 50% of families, an exact indication of the altered genes has not been established.

The type of inheritance is autosomal dominant. This means that the disease necessarily manifests itself in the heirs, regardless of the gender of the child. Hypertrophic cardiomyopathy in children occurs with a 50% probability if one of the parents is healthy and the other is a carrier of the mutant gene. If both parents have genetic changes, then the probability reaches 100%.

Scientists believe that gene mutation can occur under the influence of unfavorable conditions in the external environment (smoking, past infections, radiation) affecting the expectant mother during pregnancy.

Secondary

Secondary changes form after the age of 60 in patients with hypertension who had changes in the structure of muscle tissue in the prenatal period.

It has been established that 1/5 of patients who survive to old age may develop systole weakness and dilation of the left ventricular cavity. In such cases, hypertrophic cardiomyopathy does not differ from the dilated type.

The mechanism of pathology development

As a result of genetic mutations, “wrong” main protein molecules that ensure the contraction process, actin and myosin, appear in muscle tissue. They don't produce enough calories due to sharp decline content of necessary enzymes. In 90% of patients, muscle cells lose their direction. In the myocardial tissue, areas incapable of contraction are formed.

In response, other fibers take over the work functions. Their muscle mass increases (hypertrophies) because they have to contract with increased load. The thickness of the left ventricle increases, although no data are available on congenital or acquired defects or hypertension. At the same time, thickening of the interventricular septum occurs. This leads to a narrowing of the blood ejection pathways into the aorta.

Areas of hypertrophy may be localized in patches (usually at the exit to the aorta) or affect a large part of the left ventricle. Less commonly, they spread to the right side of the heart muscle. Damage occurs to the valve leaflets (mitral and aortic), and to the vessels supplying the myocardium.

During diastole, the atria have to work harder to fill the ventricles, because the tissues become dense, hard, and lose elasticity. The pressure in the pulmonary circulation increases.

Increased muscle mass requires more oxygen. The discrepancy between the growth of myocardial demands and capabilities leads to the development of ischemia. This is also facilitated by mechanical compression of the mouth of the left coronary artery.

Types of heart damage

Due to the uniformity and symmetry of the development of areas of myocardial hypertrophy, the following forms are distinguished:

• symmetrical (concentric) - the thickness of the walls of the left ventricle increases to the same extent along the anterior, posterior surfaces and in the area of ​​the septum, less often hypertrophy of the right ventricle is added;
• asymmetrical - areas of thickening form in the upper or lower part of the interventricular septum, it becomes one and a half to three times thicker back wall left ventricle (in normal heart they are equal), in 2/3 of patients these changes are combined with hypertrophy of the region of the anterior, lateral walls of the left ventricle or apex, without changes in the posterior wall.

Based on the strength of the obstruction to the flow of blood from the left ventricle to the aorta, it is customary to distinguish:

• obstructive hypertrophic cardiomyopathy (subaortic or subvalvular) - changes in anatomical relationships create a barrier to blood exit;
• non-obstructive - there is no barrier.

Clinical picture

Symptoms of hypertrophic cardiomyopathy first appear between the ages of 20 and 25. The most typical are the following:

• Pain behind the sternum of a pressing nature, very similar to attacks of angina, have a similar irradiation in left shoulder, neck, shoulder blade. Unlike angina pectoris, they are not relieved by medications containing Nitroglycerin. There are atypical pains of aching or stabbing type.
• An important sign is increased shortness of breath with changes in horizontal position body to vertical. Over time, increased shortness of breath leads to cardiac asthma and pulmonary edema.
• Arrhythmias, increased heart rate.
• Dizziness to the point of fainting, is associated with a malnutrition of the brain. It intensifies during physical activity, straining, after a heavy meal, and when getting up quickly.

For hypertrophic cardiomyopathy, a characteristic manifestation is the sudden death of a person (the classification specifies that no more than 1 hour should pass from the moment of loss of consciousness, the case cannot have any signs of violence).

How to identify the disease

Diagnosis of the disease is very difficult. The doctor needs to know the family history (cases of confirmed disease in relatives or sudden death at a young age), the course of pregnancy in the mother, connections with industrial toxic substances, previous infectious diseases, stay in areas with high radiation.

During the examination, the doctor pays attention to the pallor of the skin, cyanosis of the lips and fingers. High or normal blood pressure is recorded.

On auscultation, a characteristic murmur is heard over the projection of the aorta.

For the purpose of exclusion possible pathology heart and blood vessels, a general blood test, urine test, biochemical tests for metabolic products, glucose, and the blood coagulation system are checked.

Additional examination methods

Hardware diagnostics allows you to accurately identify disease problems.

• An ECG study records information on disturbed rhythm, hypertrophy of the heart, and the development of blockades.
• The phonocardiogram records noise from certain points, which makes it possible to establish a connection between the audible noise and the aorta.
• An x-ray shows an increase in the contours of the cardiac shadow, but the size may be normal if hypertrophy develops inside the cavity.
• Ultrasound is the main method in making a diagnosis. The size of the heart chambers, wall thickness, condition of the valve apparatus, interventricular septum are assessed, and blood flow disturbances are observed.
• Magnetic resonance imaging allows you to obtain a three-dimensional image of the heart, identify obstruction, and the degree of wall thickness.
• Genetic research is a method of the future, but it is not yet developed enough.
• By inserting catheters into the cavities of the heart, the pressure in the atria and ventricles and the speed of blood flow are studied and measured. The technique allows you to take material for a biopsy.
• Coronary angiography of the heart vessels is performed in patients over 40 years of age for differential diagnosis With ischemic lesions heart vessels.

A biopsy is permissible only if all other diseases are excluded and there is no help from other diagnostic methods. Under a microscope, altered muscle fibers become visible.

Treatment

Specific elimination of gene mutations has not yet been achieved. Treatment of hypertrophic cardiomyopathy is carried out with medications that affect all aspects of the pathogenesis of the disease.

If signs of the disease are detected, it is necessary to limit physical activity and stop playing sports.

If the patient has any chronic infectious diseases, prophylactic antibiotics are prescribed.

Groups of medications that block adrenergic receptors, calcium antagonists are used, and agents that reduce thrombus formation in the cavities of the heart are added.

Surgical methods

The method of choice for open heart surgery is myotomy - removal of part of the interventricular septum from the inside or through the aorta. The mortality rate of these operations reaches 5%, which is comparable to the overall mortality rate.

A more gentle technique is carried out - concentrated alcohol is injected into the septal area through a puncture of the chest and heart under ultrasound control. Cell death and thinning of the septum are artificially caused. The obstacle to the passage of blood is reduced.

To treat the disturbed rhythm, an electrical stimulator or defibrillator is implanted (depending on the type of disorder).

Modern data suggest that survival after surgical treatment for 10 years is 84%, and with continuous conservative treatment - 67%.

In case of obstruction, an operation is used to replace the mitral valve with an artificial one, this eliminates its contact with the septum and “clears” the passage for blood flow.

Course of the disease

Hypertrophy is possible from the moment of birth. But in most patients it begins to appear during adolescence. Over three years, the thickness of the myocardial wall increases by 2 times. However, no symptoms of the disease are found in 70% of patients. By the age of 18 (less often until 40), the progression of thickening of the heart wall stops.

Further clinical manifestations are formed due to the obstructive variant of the pathology. In cases of non-obstructive forms, the course is favorable and is detected by chance during an ECG examination.

The annual incidence of sudden death from hypertrophic cardiomyopathy and its complications among adults is up to 3%, among children – from 4 to 6%. The main cause is considered to be ventricular fibrillation.

What are the possible complications?

Hypertrophic cardiomyopathy does not occur in isolation; the disease affects all aspects of the heart’s activity and causes serious complications.

• Arrhythmias and impaired conduction are observed in almost every patient. Depending on the severity, they may come out on top in terms of threat to the patient’s life. They are the direct cause of cardiac arrest or fibrillation.
• The addition of infection of the mitral and aortic valves leads to the development of endocarditis with subsequent insufficiency of the valve apparatus.
• Separation of a blood clot and introduction of an embolus into the vessels of the brain (up to 40% of cases), into internal organs, and into the arteries of the extremities occurs when atrial fibrillation, paroxysmal form.
• The development of chronic heart failure is possible during a long course of the disease, when part of the myocardial muscle fibers are replaced by scar tissue.

Forecast

Treatment can lead to temporary stabilization of hypertrophy. Average life expectancy does not directly depend on the form of the disease. The most favorable prognosis is considered to be with a long asymptomatic course, as well as with apical localization and the absence of cases of sudden death among relatives.

The main sign that aggravates the prognosis among patients from 15 to 50 years old is considered to be fainting, ischemia, and ventricular tachycardia detected on the ECG. The appearance of shortness of breath and chest pain in a patient sharply increases the risk of sudden death.

Statistical studies show, from the moment of detection, a five-year survival rate of 82 to 98%, a ten-year survival rate of 64 to 89%, with an average annual mortality rate of 1%.

Complexities in the etiological factors of the disease make any kind of prevention almost impossible. With this pathology, the main attention should be paid to identifying it, starting from adolescence, and carrying out symptomatic therapy.

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What is myocardial hypertrophy

This autosomal dominant disease is characterized by hereditary traits of gene mutation and affects the heart. It is characterized by an increase in the thickness of the walls of the ventricles. Hypertrophic cardiomyopathy (HCM) has a classification code according to ICD 10 No. 142. The disease is often asymmetric, with the left ventricle of the heart more susceptible to damage. This happens:

• chaotic arrangement of muscle fibers;
• damage to small coronary vessels;
• formation of areas of fibrosis;
• obstruction of blood flow - an obstacle to the ejection of blood from the atrium due to displacement of the mitral valve.

With heavy loads on the myocardium caused by diseases, sports, or bad habits, the body’s protective reaction begins. The heart needs to cope with increased work volumes without increasing the load per unit of mass. Compensation begins to occur:

• increased protein production;
• hyperplasia – increase in the number of cells;
• increase muscle mass myocardium;
• wall thickening.

Pathological myocardial hypertrophy

At long work myocardium under loads that are constantly increased, a pathological form of HCM occurs. A hypertrophied heart is forced to adapt to new conditions. Myocardial thickening occurs at a rapid pace. In this situation:

• growth of capillaries and nerves lags behind;
• blood supply is disrupted;
• the influence of nervous tissue on metabolic processes changes;
• myocardial structures wear out;
• the ratio of myocardial sizes changes;
• systolic and diastolic dysfunction occurs;
• repolarization is disrupted.

Myocardial hypertrophy in athletes

Abnormal development of the myocardium—hypertrophy—occurs unnoticed in athletes. During high physical activity, the heart pumps large volumes of blood, and the muscles, adapting to such conditions, increase in size. Hypertrophy becomes dangerous, causing stroke, heart attack, sudden cardiac arrest, in the absence of complaints and symptoms. You should not suddenly stop training to avoid complications.

Sports myocardial hypertrophy has 3 types:

• eccentric - muscles change proportionally - typical for dynamic activities - swimming, skiing, long-distance running;
• concentric hypertrophy - the ventricular cavity remains unchanged, the myocardium increases - observed in gaming and static types;
• mixed - inherent in activities with the simultaneous use of immobility and dynamics - rowing, cycling, skating.

Myocardial hypertrophy in a child

It is possible that myocardial pathologies may appear from the moment of birth. Diagnosis at this age is difficult. Hypertrophic changes in the myocardium are often observed during adolescence, when cardiomyocyte cells actively grow. Thickening of the anterior and posterior walls occurs until the age of 18, then stops. Ventricular hypertrophy in a child is not considered a separate disease - it is a manifestation of numerous ailments. Children with HCM often have:

• heart disease;
• myocardial dystrophy;
• hypertension;
• angina pectoris.

Causes of cardiomyopathy

It is customary to distinguish between primary and secondary causes hypertrophic development of the myocardium. The first ones are influenced by:

• viral infections;
• heredity;
• stress;
• alcohol consumption;
• physical overload;
• excess weight;
• toxic poisoning;
• changes in the body during pregnancy;
• drug use;
• lack of microelements in the body;
• autoimmune pathologies;
• malnutrition;
• smoking.

Secondary causes of myocardial hypertrophy are provoked by the following factors:

Left ventricular hypertrophy

More often, the walls of the left ventricle are susceptible to hypertrophy. One of the causes of LVH is high pressure, which forces the myocardium to work at an accelerated rhythm. Due to the resulting overloads, the left ventricular wall and IVS increase in size. In this situation:

• the elasticity of the myocardial muscles is lost;
• blood circulation slows down;
• violated normal operation hearts;
• there is a danger of a sudden load on it.

Left ventricular cardiomyopathy increases the heart's need for oxygen, nutrients. Changes in LVH can be noticed during instrumental examination. Low output syndrome appears - dizziness, fainting. Among the signs accompanying hypertrophy:

• angina pectoris;
• pressure changes;
• heartache;
• arrhythmia;
• weakness;
• high blood pressure;
• bad feeling;
• shortness of breath at rest;
• headache;
• fatigue;

Right atrial hypertrophy

Enlargement of the wall of the right ventricle is not a disease, but a pathology that appears when there is overload in this department. It occurs due to the receipt of a large amount of venous blood from large vessels. The cause of hypertrophy can be:

• birth defects;
• atrial septal defects, in which blood enters the left and right ventricles simultaneously;
• stenosis;
• obesity.

Right ventricular hypertrophy is accompanied by symptoms:

• hemoptysis;
• dizziness;
• night cough;
• fainting;
• chest pain;
• shortness of breath without exertion;
• bloating;
• arrhythmia;
• signs of heart failure - swelling of the legs, enlarged liver;
• malfunction of internal organs;
• cyanosis skin;
• heaviness in the hypochondrium;
• dilation of veins in the abdomen.

Hypertrophy of the interventricular septum

One of the signs of the development of the disease is hypertrophy of the IVS (interventricular septum). The main cause of this disorder is gene mutations. Hypertrophy of the septum provokes:

• ventricular fibrillation;
• atrial fibrillation;
• mitral valve problems;
• ventricular tachycardia;
• impaired blood flow;
• heart failure;
• cardiac arrest.

Dilation of the heart chambers

Hypertrophy of the interventricular septum can provoke an increase in the internal volume of the heart chambers. This expansion is called myocardial dilatation. In this position, the heart cannot perform the function of a pump, and symptoms of arrhythmia and heart failure occur:

• fast fatiguability;
• weakness;
• dyspnea;
• swelling of the legs and arms;
• rhythm disturbances;

Cardiac hypertrophy - symptoms

The danger of myocardial disease in asymptomatic progression for a long time. It is often diagnosed accidentally during medical examinations. As the disease progresses, signs of myocardial hypertrophy may be observed:

• chest pain;
• heart rhythm disturbance;
• shortness of breath at rest;
• fainting;
• fatigue;
• labored breathing;
• weakness;
• dizziness;
• drowsiness;
• swelling.

Forms of cardiomyopathy

It should be noted that the disease is characterized by three forms of hypertrophy, taking into account the systolic pressure gradient. All together the obstructive form of HCM corresponds. Stand out:

• basal obstruction – resting state or 30 mm Hg;
• latent – ​​calm state, less than 30 mm Hg – it characterizes the non-obstructive form of HCM;
• labile obstruction – spontaneous intraventricular gradient fluctuations.

Myocardial hypertrophy - classification

For convenience of work in medicine, it is customary to distinguish between the following types of myocardial hypertrophy:

• obstructive – at the top of the septum, over the entire area;
• non-obstructive – symptoms are mild, diagnosed by chance;
• symmetrical – all walls of the left ventricle are affected;
• apical - the heart muscles are enlarged only from above;
• asymmetrical - affects only one wall.

Eccentric hypertrophy

With this type of LVH, the ventricular cavity expands and at the same time a uniform, proportional compaction of the myocardial muscles occurs, caused by the growth of cardiomyocytes. With a general increase in heart mass, the relative thickness of the walls remains unchanged. Eccentric myocardial hypertrophy can affect:

• interventricular septum;
• top;
• side wall.

Concentric hypertrophy

The concentric type of disease is characterized by volume preservation internal cavity with an increase in heart mass due to a uniform increase in wall thickness. There is another name for this phenomenon - symmetrical myocardial hypertrophy. The disease occurs as a result of hyperplasia of myocardiocyte organelles, provoked by high blood pressure. This development of events is typical for arterial hypertension.

Myocardial hypertrophy – degrees

To correctly assess the patient’s condition with HCM, a special classification has been introduced that takes into account myocardial thickening. According to how much the size of the walls increases during heart contraction, cardiology distinguishes 3 degrees. Depending on the thickness of the myocardium, the stages are determined in millimeters:

• moderate – 11-21;
• average – 21-25;
• pronounced – over 25.

Diagnosis of hypertrophic cardiomyopathy

On initial stage, with a slight development of wall hypertrophy, identifying the disease is very difficult. The diagnostic process begins with interviewing the patient, finding out:

• presence of pathologies in relatives;
• the death of one of them at a young age;
• past diseases;
• fact of radiation exposure;
• external signs during visual inspection;
• blood pressure values;
• indicators in blood and urine tests.

A new direction is being used – genetic diagnosis of myocardial hypertrophy. The potential of hardware and radiological methods helps to establish the parameters of HCM:

• ECG - determines indirect signs - rhythm disturbances, hypertrophy of sections;
• X-ray - shows an increase in the contour;
• Ultrasound – assesses myocardial thickness, blood flow disturbances;
• echocardiography – records the location of hypertrophy, diastolic dysfunction;
• MRI – gives a three-dimensional image of the heart, determines the degree of myocardial thickness;
• ventriculography – examines contractile functions.

How to treat cardiomyopathy

The main goal of treatment is to return the myocardium to its optimal size. Activities aimed at this are carried out in a comprehensive manner. Hypertrophy can be cured when done early diagnosis. An important part in the system of myocardial health is played by lifestyle, which implies:

• diet;
• giving up alcohol;
• smoking cessation;
• weight loss;
• drug exclusion;
• limiting salt intake.

Drug treatment of hypertrophic cardiomyopathy includes the use of drugs that:

• reduce blood pressure - ACE inhibitors, angiotensin receptor antagonists;
• regulate heart rhythm disturbances - antiarrhythmics;
• drugs with a negative ionotropic effect relax the heart - beta blockers, calcium antagonists from the verapamil group;
• remove fluid - diuretics;
• improve muscle strength - ionotropes;
• when threatened infective endocarditis– antibiotic prophylaxis.

An effective method of treatment that changes the course of excitation and contraction of the ventricles is dual-chamber pacing with a shortened atrioventricular delay. More complex cases - severe asymmetric hypertrophy of the IVS, latent obstruction, lack of effect of the drug - require the participation of surgeons for regression. Help save a patient's life:

• installation of a defibrillator;
• pacemaker implantation;
• transaortic septal myectomy;
• excision of part of the interventricular septum;
• transcatheter septal alcohol ablation.

Cardiomyopathy - treatment with folk remedies

On the recommendation of the treating cardiologist, you can supplement the main course with herbal remedies. Traditional treatment for left ventricular hypertrophy involves the use of viburnum berries without heat treatment, 100 g per day. It is useful to consume flax seeds, which have a positive effect on heart cells. Recommend:

• take a spoonful of seeds;
• add boiling water - liter;
• hold in a water bath for 50 minutes;
• filter;
• drink per day - dose 100 g.

Oat infusion for regulating the functioning of the heart muscles has good reviews in the treatment of HCM. According to the healers' prescription, it is required:

• oats – 50 grams;
• water – 2 glasses;
• heat to 50 degrees;
• add 100 g of kefir;
• pour in radish juice - half a glass;
• stir, stand for 2 hours, strain;
• put 0.5 tbsp. honey;
• dosage – 100 g, three times a day before meals;
• course – 2 weeks.

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Definition. Left ventricular myocardium (LVMH) is an excess of the mass of the left ventricle relative to its proper value due to thickening (proliferation) of the myocardium (heart muscle).

Methods for diagnosing LVMH. Currently, 3 instrumental methods are used to diagnose LVMH:

— Standard ECG. When verifying LVMH, a conventional ECG is generally characterized by low sensitivity - no more than 30%. In other words, of the total number of patients who objectively have LVMH, an ECG allows it to be diagnosed in only a third. However, the more pronounced the hypertrophy, the higher the likelihood of recognizing it using a regular ECG. Severe hypertrophy almost always has ECG markers. Thus, if the ECG correctly diagnoses LVMH, this most likely indicates its severe degree. Unfortunately, in our medicine, the usual ECG is given too much great importance when diagnosing LVMH. Often, using low-specific ECG criteria for LVMH, doctors speak affirmatively about the phenomenon of hypertrophy where it actually does not exist. You should not expect more from a standard ECG than it actually shows.

— Ultrasound of the heart. It is the “gold standard” in the diagnosis of LVMH, as it allows real-time visualization of the walls of the heart and the necessary calculations. To assess myocardial hypertrophy, it is customary to calculate relative values ​​that reflect myocardial mass. However, for simplicity, it is permissible to know the value of only two parameters: the thickness of the anterior (interventricular septum) and posterior wall of the left ventricle, which makes it possible to diagnose hypertrophy and its degree.

— Magnetic resonance imaging (MRI)). An expensive method of layer-by-layer scanning of the “zone of interest”. To assess LVMH, it is used only if for some reason ultrasound of the heart is not feasible: for example, in a patient with obesity and pulmonary emphysema, the heart will be covered on all sides by lung tissue, which will make its ultrasound visualization impossible (extremely rare, but this does occur).

The thickness of the IVS and the left ventricular myocardium is directly related to left ventricular myocardial hypertrophy (the clinical significance of the EDR during hypertrophy will be discussed). If the normal value of even one of the two presented parameters is exceeded, we can speak of “hypertrophy”.

Causes and pathogenesis of LVMH. Clinical conditions that can lead to LVMH (in order of decreasing frequency):

1. Diseases leading to increased afterload on the heart:

— Arterial hypertension (hypertension, secondary hypertension)

— Heart defect (congenital or acquired) - aortic stenosis.

Afterload is understood as a set of physical and anatomical parameters of the cardiovascular body that create an obstacle to the passage of blood through the arteries. Afterload is determined mainly by the tone of the peripheral arteries. A certain basic value of arterial tone is the norm and one of the obligate manifestations of homeostasis, maintaining the level of blood pressure, according to the current needs of the body. An excessive increase in arterial tone will mark an increase in afterload, which is clinically manifested by an increase in blood pressure. So, with spasm of the peripheral arteries, the load on the left ventricle increases: it needs to contract more strongly in order to “push” blood through the narrowed arteries. This is one of the main links in pathogenesis in the formation of a “hypertensive” heart.

The second common cause that leads to an increase in afterload on the left ventricle, and therefore creates an obstacle to arterial blood flow, is aortic stenosis. With aortic stenosis, the aortic valve is affected: it shrinks, calcifies, and becomes deformed. As a result, the aortic opening becomes so small that the left ventricle must contract much more strongly to ensure that an adequate volume of blood passes through the critical bottleneck. Currently, the main cause of aortic stenosis is senile (senile) valve damage in the elderly.

Microscopic changes during myocardial hypertrophy include thickening of the cardiac fibers and some proliferation of connective tissue. At first, this is of a compensatory nature, but with a long-term increased afterload (for example, with long-term untreated hypertension), the hypertrophied fibers are subjected to dystrophic changes, the architectonics of the myocardial syncytium is disrupted, and sclerotic processes in the myocardium are predominant. As a result, hypertrophy turns from a compensation phenomenon into a mechanism for the manifestation of heart failure - the heart muscle cannot work under tension for an indefinitely long time without consequences.

2. Congenital cause LVMH: hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy is a genetically determined disease, which is characterized by the appearance of unmotivated LVMH. The manifestation of hypertrophy occurs after birth: as a rule, in childhood or adolescence, less often in adults, but in any case no later than 35-40 years. Thus, in hypertrophic cardiomyopathy, LVMH occurs against a background of complete well-being. This disease is not very rare: according to statistics, 1 person out of 500 suffers from it. In my clinical practice, I annually see 2-3 patients with hypertrophic cardiomyopathy.

Unlike a hypertensive heart, with hypertrophic cardiomyopathy, LVMH can be very pronounced (severe) and often asymmetrical (more on this in more detail). Only with hypertrophic cardiomyopathy does the thickness of the wall of the left ventricle sometimes reach “exorbitant” values ​​of 2.5-3 cm or more. Microscopically, the architecture of the cardiac fibers is grossly disrupted.

3. LVMH as a manifestation of systemic pathological processes.

— Obesity. Excess body weight is not exclusively cosmetic problem. This is a deep pathophysiological process affecting all organs and systems, during which biochemical processes, psychodynamics of thinking, human selfhood, etc. change. With obesity adipose tissue it is deposited in excess not only under the skin, but also in almost all organs. The heart is forced to provide blood to “the body with all its excess mass.” Such an increased load cannot but affect cardiac functionality - it certainly increases: the heart contracts more often and stronger. Thus, in obesity, LVMH can develop in the absence of persistent arterial hypertension.

In obesity, the myocardium thickens not only due to the proliferation of cardiac fibers and connective tissue, but also due to the deposition of excess fat.

— Amyloidosis(primary or secondary) - a pathology in which a special amyloid protein is deposited in the internal organs, leading to the development of diffuse sclerosis and organ failure. Despite the possibility of developing LVMH due to amyloidosis, it rarely comes to the fore in the clinical picture of the disease: other organs (for example, kidneys) are more significantly affected, which will determine the specific picture of the disease.

4. Regarding natural causes LVMH.

— Elderly age . Senile age is characterized by slow but steadily progressive degradation (dystrophy) of all organs and systems. The specific gravity of water and parenchymal components in organs decreases; on the contrary, sclerotic processes intensify. The heart of an old man is no exception: the muscle fibers become thinner and loosen, at the same time, the connective tissue develops powerfully, due to which LVMH primarily occurs in old age. What is important to know is that senile LVMH, in the absence of other causes, never reaches significant values. It does not exceed the degree of “insignificant” and is more often only an age-related phenomenon, without any special clinical significance.

— The heart of an athlete. We are talking about people who have been involved in professional sports for a long time. LVMH in such subjects can be called pure form compensatory (working), as well as concomitant hypertrophy skeletal muscles. After the end of a sports career, LVMH undergoes complete or partial regression.

The following diseases (conditions) lead to concentric LVMH:

S-hypertrophy has no particular clinical significance, being more often a marker of an “age-related” heart. Occasionally, this type of hypertrophy occurs in middle-aged people.

Clinical significance of LVMH. Diseases leading to the development of LVMH can be asymptomatic for a long time (years, decades) or have nonspecific manifestations: for example, headache due to arterial hypertension. The earliest symptom of LVH (which, by the way, can appear after years of hypertrophy) is dyspnea with usual physical activity: walking, climbing stairs. Mechanism of shortness of breath: диастолическая SЃРµСЂРґРµС‡РЅР°СЏ недостаточРШость. It is known that blood filling of the heart occurs during diastole (relaxation): blood moves along a concentration gradient from the atria to the ventricles. With hypertrophy, the left ventricle becomes thicker, stiffer, denser - this leads to the fact that the process of relaxation and stretching of the heart becomes more difficult and incomplete; Accordingly, the blood supply to such a ventricle is disrupted (decreased). Clinically, this phenomenon manifests itself as shortness of breath. Symptoms of diastolic heart failure in the form of shortness of breath and weakness may be the only manifestation of LVMH for many years. However, in the absence of adequate treatment of the underlying disease, the symptoms will gradually increase, leading to a progressive decrease in exercise tolerance. The final outcome of advanced diastolic heart failure will be the development of systolic heart failure, the treatment of which is even more difficult. So, LVMH is a direct path to heart failure, and therefore to high risk early cardiac death.

The next common complication of LVMH is development of paroxysmal atrial fibrillation (atrial fibrillation). Impaired relaxation (diastole) of the hypertrophied left ventricle inevitably entails an increase in blood pressure in it; this in turn causes the left atrium to contract more strongly in order to “push” the required volume of blood into the “container” with increased pressure. However, the left atrium is a thin-walled cardiac chamber that cannot operate in super mode for a long time; As a result, the left atrium dilates (widens) to accommodate the excess blood. Dilatation of the left atrium is one of the most important risk factors for the development of atrial fibrillation. As a rule, damage to the left atrium for a long time is manifested only by atrial extrasystole; subsequently, when the atrium “dilates sufficiently” to “maintain” fibrillation, atrial fibrillation occurs: first paroxysmal, then constant. The risks that atrial fibrillation brings into a patient’s life are described in detail in a separate chapter.

Obstructive syncope. A rare variant of the course of LVMH. It is almost always a complication of the asymmetric variant of hypertrophic cardiomyopathy, when the thickness of the interventricular septum is so great that there is a threat of transient obstruction (blocking) of blood flow in the area of ​​the outflow tract of the left ventricle. Paroxysmal obstruction (cessation) of blood flow in this “critical place” will inevitably lead to fainting. As a rule, the risk of developing obstruction occurs when the thickness of the interventricular septum exceeds 2 cm.

Ventricular extrasystole- another possible satellite for LVMH. It is known that any micro- and macroscopic changes in the heart muscle can theoretically be complicated by extrasystole. Hypertrophied myocardium is an ideal arrhythmogenic substrate. The clinical course of ventricular extrasystole against the background of LVMH is variable: more often, its role is limited to a “cosmetic arrhythmic defect”. However, if the disease leading to LVMH is not treated (ignored), and the regimen for limiting intense physical activity is not followed, life-threatening ventricular arrhythmias triggered by extrasystole may develop.

Sudden cardiac death. The most severe complication of LVMH. Most often, LVMH due to hypertrophic cardiomyopathy leads to this outcome. There are two reasons. Firstly, in this disease, LVMH can be particularly massive, which makes the myocardium extremely arrhythmogenic. Secondly, hypertrophic cardiomyopathy very often has an asymptomatic course, which does not allow patients to take preventive measures in the form of limiting intense physical activity. Sudden cardiac death in other nosologies complicated by LVMH is generally a rare phenomenon, if only because the manifestation of these diseases begins with symptoms of heart failure, which in itself forces the patient to see a doctor, which means there is a real opportunity to take the disease under control.

Possibility of regression of LVMH. The likelihood of a decrease in the mass (thickness) of the left ventricular myocardium during treatment depends on the cause of hypertrophy and its degree. Classic example is an athletic heart, the walls of which can decrease to normal thickness after the end of a sports career.

LVMH due to arterial hypertension or aortic stenosis can successfully regress with timely, complete and long-term control of these diseases. However, it is considered this way: only mild hypertrophy undergoes absolute regression; when treating moderate hypertrophy, there is a chance of reducing it to mild; and heavy can “become medium”. In other words, the more advanced the process, the less likely it is to return everything completely to its original state. However, any degree of regression of LVMH automatically means correctness in the treatment of the underlying disease, which in itself reduces the risks that hypertrophy introduces into the subject’s life.

With hypertrophic cardiomyopathy, any attempts at drug correction of the process are pointless. There are surgical approaches for the treatment of massive hypertrophy of the interventricular septum, which is complicated by obstruction of the left ventricular outflow tract.

The likelihood of regression of LVMH due to obesity, in older people, and with amyloidosis is practically absent.

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One of the characteristic symptoms of hypertrophic cardiomyopathy is hypertrophy of the IVS (interventricular septum). When this pathology occurs, thickening of the walls of the right or left ventricle of the heart and the interventricular septum occurs. This condition itself is a derivative of other diseases and is characterized by an increase in the thickness of the walls of the ventricles.

Despite its prevalence (IVS hypertrophy is observed in more than 70% of people), it is most often asymptomatic and is detected only during very intense physical activity. After all, hypertrophy of the interventricular septum itself is its thickening and the resulting reduction in the useful volume of the chambers of the heart. As the thickness of the cardiac walls of the ventricles increases, the volume of the heart chambers also decreases.

In practice, this all leads to a reduction in the volume of blood that is released by the heart into the vascular bed of the body. To provide the organs with a normal amount of blood under such conditions, the heart must contract stronger and more often. And this, in turn, leads to its early wear and tear and the occurrence of diseases of the cardiovascular system.

Symptoms and causes of hypertrophic cardiomyopathy

A large number of people around the world live with undiagnosed IVS hypertrophy, and only with increased physical activity does their existence become known. As long as the heart can ensure normal blood flow to organs and systems, everything proceeds hidden and the person will not experience any painful symptoms or other discomfort. But you should still pay attention to some symptoms and contact a cardiologist if they occur. These symptoms include:

• chest pain;
• shortness of breath with increased physical activity (for example, climbing stairs);
• dizziness and fainting;
• increased fatigue;
• tachyarrhythmia that occurs for short periods of time;
• heart murmur on auscultation;
• labored breathing.

It is important to remember that undiagnosed IVS hypertrophy can cause sudden death even in young and physically strong people. Therefore, a medical examination by a therapist and/or cardiologist should not be neglected.

The causes of this pathology lie not only in an incorrect lifestyle. Smoking, alcohol abuse, excess weight - all this becomes a factor contributing to the increase severe symptoms and the manifestation of negative processes in the body with an unpredictable course.

And doctors call gene mutations the reason for the development of IVS thickening. As a result of these changes at the level of the human genome, the heart muscle becomes abnormally thick in some areas.

The consequences of the development of such a deviation become dangerous.

After all, additional problems in such cases will be disturbances in the conduction system of the heart, as well as weakening of the myocardium and the associated decrease in the volume of blood ejected during cardiac contractions.

Possible complications of IVS hypertrophy

What complications are possible with the development of cardiopathy of the type under discussion? Everything will depend on the specific case and individual development of the person. After all, many will never know throughout their lives that they have this condition, and some may experience significant physical ailments. We list the most common consequences of thickening of the interventricular septum. So:

1. 1. Heart rhythm disturbances such as tachycardia. Common types such as atrial fibrillation, ventricular fibrillation and ventricular tachycardia directly related to IVS hypertrophy.
2. 2. Disorders of blood circulation in the myocardium. Symptoms that occur when the outflow of blood from the heart muscle is disrupted include chest pain, fainting and dizziness.
3. 3. Dilated cardiomyopathy and associated volume reduction cardiac output. The walls of the heart chambers, under conditions of pathologically high load, become thinner over time, which is the cause of the appearance of this condition.
4. 4. Heart failure. The complication is very life-threatening and in many cases ends in death.
5. 5. Sudden cardiac arrest and death.

Of course, the last two conditions are terrifying. But, nevertheless, with a timely visit to the doctor, if any symptom of cardiac dysfunction occurs, a timely visit to the doctor will help you live a long and happy life.

Myocardial hypertrophy (hypertrophic cardiomyopathy) is a significant thickening and enlargement of the walls of the left ventricle of the heart. Its cavity inside is not expanded. In most all cases, thickening of the interventricular septa is also possible.

Due to thickening, the heart muscle becomes less extensible. The myocardium can be thickened over the entire surface or in some areas, it all depends on the course of the disease:

• If the myocardium hypertrophies primarily under the aortic outlet, narrowing of the left ventricular outlet may occur. In this case, the inner lining of the heart thickens and the functioning of the valves is disrupted. In most cases, this occurs due to uneven thickening.
• Asymmetrical thickening of the septum is possible without disruption of the valve apparatus and a decrease in output from the left ventricle.
• Apical hypertrophic cardiomyopathy occurs as a result of enlargement of the muscle at the apex of the heart.
• Myocardial hypertrophy with symmetrical circular hypertrophy of the left ventricle.

Disease history

Hypertrophic cardiomyopathy has been known since the mid-19th century. It was described in detail only in 1958 by the English scientist R. Teare.

Significant progress in the study of the disease was the introduction of some non-invasive research methods, when they learned about the existence of obstructions of the outflow tract and disorders of dystolic function.

This is reflected in the corresponding names of the disease: “idiopathic hypertrophic subaortic stenosis”, “muscular subaortic stenosis”, “hypertrophic obstructive cardiomyopathy”. Today, the term “hypertrophic cardiomyopathy” is universal and generally accepted.

With the widespread introduction of echocardiography studies, it was revealed that the number of patients with myocardial hypertrophy is much greater than was thought in the 70s. Every year, 3-8% of patients with this disease die. And every year the mortality rate is growing.

Prevalence and significance

Most often, people aged 20-40 suffer from myocardial hypertrophy; men are about twice as likely. Although it has a very varied course and progresses, the disease does not always manifest itself immediately. IN in rare cases from the very beginning of the disease, the patient’s condition is serious and the risk of sudden death is quite high.

The incidence of hypertrophic cardiomyopathy is about 0.2%. The mortality rate ranges from 2 to 8%. The leading cause of death is sudden cardiac death and life-threatening cardiac arrhythmias. The main reason is hereditary predisposition. If relatives did not suffer from this disease, it is believed that a mutation of the heart muscle protein genes occurred.

The disease can be diagnosed at any age: from birth to old age, but most often patients are young people of working age. The prevalence of myocardial hypertrophy does not depend on gender or race.

In 5-10% of all registered patients, with a long course of the disease, a transition to heart failure is possible. In some cases, in the same number of patients, an independent regression of hypertrophy, a transition from the hypertrophic to the dilated form, is possible. The same number of cases occur due to complications arising in the form of infective endocarditis.

Without appropriate treatment, mortality is up to 8%. In half of the cases, death occurs as a result acute heart attack, ventricular fibrillation and complete atrioventricular heart block.

Classification

In accordance with the location of hypertrophy, myocardial hypertrophy is distinguished:

• left ventricle (asymmetric and symmetric hypertrophy);
• right ventricle.

Basically, asymmetric hypertrophy of the interventricular septum is detected on the entire surface or in some of its parts. Less commonly, hypertrophy of the apex of the heart, anterolateral or posterior wall can be found. In 30% of cases, the share is symmetrical hypertrophy.

Taking into account the systolic pressure gradient in the left ventricle, hypertrophic cardiomyopathy is distinguished:

• obstructive;
• non-obstructive.

The non-obstructive form of myocardial hypertrophy usually includes symmetrical hypertrophy of the left ventricle.

Asymmetric hypertrophy can refer to both obstructive and non-obstructive forms. Apical hypertrophy mainly refers to the non-obstructive variant.

Depending on the degree of thickening of the heart muscle, hypertrophy is distinguished:

• moderate (up to 20 mm);
• medium (21-25 mm);
• pronounced (more than 25 mm).

Based on clinical and physiological classifications, 4 stages of myocardial hypertrophy are distinguished:

• I - pressure gradient at the outlet of the left ventricle is not more than 25 mm Hg. Art. (no complaints);
• II - the gradient increases to 36 mm Hg. Art. (appearance of complaints during physical exertion);
• III - the gradient increases to 44 mm Hg. Art. (shortness of breath and angina pectoris appear);
• IV - gradient above 80 mm Hg. Art. (hemodynamic impairment, sudden death is possible).

Left atrial hypertrophy is a disease in which the left ventricle of the heart thickens, causing the surface to lose its elasticity.

If the compaction of the heart septum occurs unevenly, disturbances in the functioning of the aortic and mitral valves of the heart may additionally occur.

Today, the criterion for hypertrophy is myocardial thickening of 1.5 cm or more. This disease is currently the main cause early death young athletes.

External manifestations of the disease are usually preceded by a long asymptomatic period.
The first symptoms often occur at a young age (20-35 years).

• Dyspnea (rapid breathing), often accompanied by dissatisfaction with inhalation. Initially, shortness of breath appears with significant loads, then with light loads and at rest. In some patients, shortness of breath increases when moving to a vertical position, which is associated with a decrease in blood flow to the heart.
• Dizziness, fainting (loss of consciousness) are associated with deterioration of blood supply to the brain due to a decrease in the volume of blood ejected by the left ventricle into the aorta (the largest vessel of the human body). Dizziness and fainting are provoked by a rapid transition to a vertical position, physical activity, straining (for example, with constipation and lifting weights), and sometimes by eating.
• Pressing, squeezing pain behind the sternum (the central bone of the front part of the chest to which the ribs are attached) occurs due to reduced blood flow into the heart’s own arteries. The reasons for this are: insufficient relaxation of the heart muscle and an increased need for oxygen and nutrients due to the increased muscle mass of the heart. Taking drugs from the group of nitrates (salts of nitric acid that dilate the heart’s own vessels) does not relieve pain in such patients (unlike pain with coronary disease heart disease – a disease associated with obstruction of blood flow through the heart’s own arteries).
• A feeling of accelerated heartbeat and interruptions in heart function appear with the development of cardiac arrhythmias.
• Sudden cardiac death (non-violent death caused by heart disease, manifested sudden loss consciousness within 1 hour from the onset of acute symptoms) may be the first and only manifestation of the disease.

Forms

Depending on the symmetry of hypertrophy (increase in thickness), the heart muscles are divided into symmetrical And asymmetrical shape.

• Symmetrical form of hypertrophic cardiomyopathy – equal thickening of the anterior and posterior walls of the left ventricle, as well as the interventricular septum – concentric (that is, in a circle) hypertrophy (thickening). In some patients, the thickness of the right ventricular muscle simultaneously increases.
• Asymmetric form of hypertrophic cardiomyopathy – predominant hypertrophy of the upper, middle or lower third of the interventricular septum (the partition between the left and right ventricles of the heart), the thickness of which becomes 1.5-3.0 times greater than that of the posterior wall of the left ventricle (normally they are the same). In some patients, hypertrophy of the interventricular septum is combined with hypertrophy of the anterior, lateral or apical region of the left ventricle, but the thickness of the posterior wall never increases. This form occurs in approximately 2/3 of patients.

• Obstructive form of hypertrophic cardiomyopathy (thickened interventricular septal muscle obstructs blood flow). Another name for this form is subaortic (that is, under the aorta) subvalvular stenosis.
• Non-obstructive form of hypertrophic cardiomyopathy (there are no obstructions to blood flow).

• Idiopathic (that is, the cause of which is unknown), or primary hypertrophic cardiomyopathy. Associated with the inheritance of altered genes (carriers of hereditary information) or with spontaneous mutation (sudden persistent changes) of genes that control the structure and function of contractile proteins of the heart muscle.
• Secondary hypertrophic cardiomyopathy (develops in elderly patients with arterial hypertension (prolonged increase in blood pressure), if special changes in the structure of the heart occurred during their intrauterine development). Many doctors do not agree with the etiological classification and consider only idiopathic (primary) cases to be hypertrophic cardiomyopathy.

Causes

• Primary hypertrophic cardiomyopathy in half of the cases is familial, that is, the special structure of the contractile proteins of the heart is inherited, which promotes the rapid growth of individual muscle fibers.
• In cases where there is no hereditary nature of hypertrophic cardiomyopathy, the disease is associated with spontaneous mutation (sudden persistent changes) of genes that control the structure and function of contractile proteins of the heart muscle. The mutation probably occurs under the influence of unfavorable factors external environment(ionizing treatment, smoking, infections, etc.) during the mother’s pregnancy.
• The cause of secondary hypertrophic cardiomyopathy is a long-term persistent increase in blood pressure in elderly patients with specific changes in the structure of the heart that occurred during their prenatal period.
• Risk factors for hypertrophic cardiomyopathy include hereditary predisposition and age 20-40 years.
• A risk factor for the development of mutations that can lead to hypertrophic cardiomyopathy is the influence of ionizing treatment, smoking, infections, etc. on the body of a pregnant woman.

Diagnostics

• Analysis of the medical history and complaints (when (how long ago) shortness of breath, dizziness, fainting, feeling of irregular heartbeat appeared, with which the patient associates the appearance of complaints).
• Life history analysis. It is determined what the patient and his close relatives were ill with, whether hypertrophic cardiomyopathy was detected in the patient’s relatives, whether he had a persistent increase in blood pressure, whether he was in contact with toxic substances.
• Physical examination. The color of the skin is determined (with hypertrophic cardiomyopathy, pallor or cyanosis - blueness of the skin - may develop due to insufficient blood flow). Percussion (tapping) reveals an enlargement of the heart to the left. When auscultating (listening) to the heart, a systolic (that is, during ventricular contraction) murmur above the aorta may be heard due to narrowing of the cavity of the left ventricle under the aortic valve. Arterial pressure normal or increased.
• Blood and urine tests are performed to identify concomitant diseases.
• Blood chemistry. The level of cholesterol and other lipids (fat-like substances), blood sugar, creatinine (a protein breakdown product), uric acid (a breakdown product of substances from the cell nucleus) is determined to identify concomitant organ damage.
• A detailed coagulogram (determining indicators of the blood coagulation system) allows you to determine increased blood clotting, significant consumption of coagulation factors (substances used to build blood clots), and identify the appearance of blood clot breakdown products in the blood (normally, there should be no blood clots or their breakdown products).
• Electrocardiography (ECG). With hypertrophic cardiomyopathy, enlargement of the ventricles of the heart is detected. Heart rhythm disturbances and intracardiac blockades (impaired conduction of electrical impulses through the heart muscle) may occur.
• Daily monitoring of the electrocardiogram (CMECG) allows you to assess the frequency and severity of cardiac arrhythmias and intracardiac blockades, and evaluate the effectiveness of treatment for arrhythmias.
• Stress electrocardiographic studies are an ECG test with dosed physical activity using a bicycle ergometer (specialized bicycle) or treadmill (treadmill). These research methods make it possible to assess exercise tolerance and make recommendations for treatment.
• A phonocardiogram (a method for analyzing heart sounds) in hypertrophic cardiomyopathy demonstrates the presence of a systolic (that is, during ventricular contraction) murmur over the aorta due to narrowing of the left ventricular cavity under the aortic valve.
• A survey chest x-ray allows you to evaluate the size and configuration of the heart and determine the presence of blood stagnation in the vessels of the lungs. Hypertrophic cardiomyopathy is characterized by normal or slightly enlarged heart sizes, since the thickening of the heart muscle occurs predominantly inward.
• Echocardiography (ultrasound examination of the heart) allows you to evaluate the size of the cavities and the thickness of the heart muscle, and detect heart defects. In hypertrophic cardiomyopathy, echocardiography reveals a decrease in the cavity of the left, less often the right, ventricle with an increase in the thickness of the interventricular septum and (in every third patient) the free walls of the left ventricle. Doppler echocardiography (ultrasound examination of the movement of blood through the vessels and cavities of the heart) reveals disturbances in blood movement during the formation of heart defects (most often - insufficiency of the mitral and tricuspid valves).
• Spiral CT scan(SCT) – a method based on a series of x-rays at different depths – allows you to obtain an accurate image of the organs being examined (heart and lungs).
• Magnetic resonance imaging (MRI), a method based on the formation of chains of water when strong magnets are applied to the human body, allows you to obtain an accurate image of the organs being studied (heart and lungs).
• Genetic analysis to identify genes (carriers of hereditary information) responsible for the development of hereditary hypertrophic cardiomyopathy is carried out in close relatives of patients with this disease.
• Radionuclide ventriculography (a research method in which a radioactive drug - that is, emitting gamma rays - is injected into the patient’s blood, and then pictures of the radiation from the patient are taken and analyzed on a computer). It is carried out mainly in case of low information content of echocardiography (for example, in obese patients), as well as when preparing the patient for surgical treatment. Radionuclide ventriculography in hypertrophic cardiomyopathy demonstrates an increase in the thickness of the walls of the ventricles and interventricular septum, a decrease in the cavity of the left (less often the right) ventricle, normal contractility hearts.
• Cardiac catheterization (diagnostic method based on inserting catheters - medical instruments in the form of a tube - into the cavities of the heart and measuring pressure in the atria and ventricles). With hypertrophic cardiomyopathy, a slow flow of blood from the left ventricle to the aorta is determined, while the pressure in the cavity of the left ventricle becomes significantly higher than in the aorta (normally they are equal). This research method is used primarily to perform endomyocardial biopsy (see below) only if other research methods do not allow establishing a diagnosis.
• Endomyocardial biopsy (taking a piece of the heart muscle together with the inner lining of the heart for examination) is performed during cardiac catheterization only if other research methods do not allow establishing a diagnosis. A biopsy (studied material obtained during a biopsy) with hypertrophic cardiomyopathy is characterized by an increase in the thickness and length of individual muscle fibers, their chaotic arrangement, the presence of scar changes in the heart muscle, and thickening of the walls of the small native arteries of the heart.
• Coronary cardiography (CCG) is a method in which contrast (a dye) is injected into the own vessels of the heart and the heart cavity, which makes it possible to obtain an accurate image of them, as well as to evaluate the movement of blood flow. It is performed on patients over 40 years of age to identify the condition of the heart’s own vessels and determine the presence of coronary heart disease (a disease associated with insufficient blood flow to the heart muscle through the heart’s own vessels), as well as before planned surgical treatment.
• Consultation is also possible.
• A consultation with a cardiac surgeon is also possible.

Treatment of hypertrophic cardiomyopathy

Non-drug treatment is carried out according to general principles.

• Conservative (that is, without surgery) treatment. There is no specific treatment for hypertrophic cardiomyopathy.
  • For hypertrophic cardiomyopathy medicines start with the smallest dosages, followed by individual dose increases (to reduce the risk of deterioration of blood flow from the left ventricle to the aorta).
  • The effectiveness of drugs differs in different patients, which is associated with individual sensitivity, as well as varying severity of structural heart disorders.
  • Medicines used in the treatment of hypertrophic cardiomyopathy in pregnant women:
    • beta-blockers (drugs that block beta-adrenergic receptors of the heart, blood vessels and lungs) control blood pressure and heart rate, reduce cardiac arrhythmias. Beta blockers are used only in the third trimester of pregnancy. In rare cases, beta blockers can cause fetal growth restriction, fetal oxygen deprivation, low level glucose ( simple carbohydrate) in the baby’s blood immediately after birth;
    • Calcium antagonists (drugs that prevent the entry of calcium ions - a special metal - into the cell) of the verapamil group increase blood flow through the heart’s own arteries, help improve relaxation and reduce the stiffness of the heart. Calcium antagonists are approved for use in the second half of pregnancy;
    • calcium antagonists of the diltiazem group have positive effects similar to the verapamil group, but improve the performance of patients to a lesser extent;
    • treatment and prevention of thromboembolism (separation of blood clots from the place of their formation (in hypertrophic cardiomyopathy - mainly on the inner lining of the heart of the heart above the thickening zone of the heart muscle and their movement with the blood flow with subsequent closure of the lumen of any vessel) is carried out according to general principles.

• It is advisable to perform surgical treatment for patients with severe hypertrophy (increased muscle thickness) of the interventricular septum (the partition between the left and right ventricles) before pregnancy. Types of operations.
  • Myotomy (myectomy) – surgical removal the inner part of the interventricular septum. The operation is performed on an open heart.
  • Ethanol ablation is the introduction of a concentrated solution of medical alcohol into the thickened interventricular septum by puncturing the chest and heart under ultrasound guidance. Alcohol causes the death of living cells. After the dead cells are resorbed and a scar is formed in their place, the thickness of the interventricular septum becomes smaller, which reduces the obstruction to blood flow from the left ventricle to the aorta.
  • Resynchronization therapy is a treatment method that restores impaired intracardiac conduction. It is performed using the implantation of a three-chamber (with electrodes placed in the right atrium and both ventricles) electrical stimulator (a device that generates electrical impulses and transmits them to the heart). In patients with non-simultaneous contraction of the left and right ventricles of the heart or non-simultaneous contraction of individual muscle bundles of the ventricles (determined by electrocardiography), this treatment method can improve intracardiac blood flow and prevent the development of severe complications.
  • Implantation of a cardioverter-defibrillator: implantation under the skin or muscle of the abdomen or chest of a special device connected by electrodes (wires) to the heart and constantly recording an intracardiac electrocardiogram. If a life-threatening cardiac arrhythmia occurs, the cardioverter-defibrillator delivers an electrical shock to the heart through an electrode, causing the heart to return to rhythm.

Complications and consequences

Complications of hypertrophic cardiomyopathy (in descending order of frequency of occurrence).

• Rhythm and conduction disorders. According to 24-hour electrocardiogram monitoring, arrhythmias (heart rhythm disturbances) are observed in almost every patient with hypertrophic cardiomyopathy. In some cases, they significantly aggravate the course of the disease, leading to the development of severe heart failure, fainting, and thromboembolism. Heart blocks (impaired transmission of electrical impulses through the heart muscle) develop in approximately every third patient with hypertrophic cardiomyopathy and can cause fainting and cardiac arrest.
• Sudden cardiac death (non-violent death caused by heart disease, manifested by sudden loss of consciousness within 1 hour from the onset of acute symptoms) develops due to serious violations rhythm and conductivity of the heart.
• Infectious endocarditis (infectious (that is, arising as a result of the introduction and reproduction in the human body of pathogenic - that is, disease-causing microorganisms) damage to the endothelium (the inner lining of the heart) and valves by various pathogens) occurs in approximately every twentieth patient with hypertrophic cardiomyopathy. As a result infectious process heart valve insufficiency develops.
• Thromboembolism (closure of the lumen of a vessel by a blood clot formed elsewhere and transferred by the bloodstream) complicates the course of hypertrophic cardiomyopathy in approximately every thirtieth patient. Thromboembolism usually occurs in the vessels of the brain, and less commonly in the vessels of the extremities and internal organs. As a rule, they occur with atrial fibrillation (a heart rhythm disorder in which individual sections of the atria contract independently of each other, and only part of the electrical impulses are transmitted to the ventricles).
• Chronic heart failure is a disease with a complex of characteristic symptoms (shortness of breath, fatigue, decreased physical activity), which are associated with insufficient blood supply to organs at rest or during exercise, and are also often accompanied by fluid retention in the body. Chronic heart failure develops during a long course of hypertrophic cardiomyopathy with the replacement of a large number of muscle fibers with scar tissue.

Prevention of hypertrophic cardiomyopathy

• Methods for specific prevention of cardiomyopathies have not been developed.
• Examination of close relatives of a patient with hypertensive cardiomyopathy (including genetic analysis - determining the presence in the body of genes - carriers of hereditary information - responsible for the occurrence of hypertrophic cardiomyopathy) allows us to identify the disease in them early stage, begin full-fledged treatment and thereby prolong life. It is advisable to carry out echocardiography (ultrasound examination of the heart) for young relatives of a patient with hypertrophic cardiomyopathy (from birth to 40 years of age) repeatedly (for example, once a year).
• Annual clinical examination of the population (preferably with 24-hour electrocardiogram monitoring) can detect this disease at an early stage, which contributes to timely treatment and prolongation of the patient's life.

Additionally

• The incidence of hypertrophic cardiomyopathy is 2-5 people per 100,000 population per year.
• Men get sick more often than women.
• The disease usually first appears at a young age (20-35 years).
• The sudden death of athletes is in many cases associated with the development of cardiac arrhythmias due to hypertrophic cardiomyopathy.