Echocardiography (EchoCG). Left ventricular end-systolic size

Echocardiography (EchoCG) is a method for studying morphological and functional changes in the heart and its valve apparatus using ultrasound.

The echocardiographic research method allows:

• Quantitatively and qualitatively assess the functional state of the LV and RV.
• Assess regional LV contractility (for example, in patients with coronary artery disease).
• Assess LVMM and identify ultrasound signs of symmetric and asymmetric hypertrophy and dilatation of the ventricles and atria.
• Assess the condition of the valve apparatus (stenosis, insufficiency, valve prolapse, presence of vegetations on the valve leaflets, etc.).
• Assess the level of pressure in the PA and identify signs of pulmonary hypertension.
• Identify morphological changes in the pericardium and the presence of fluid in the pericardial cavity.
• Identify intracardiac formations (thrombi, tumors, additional chords, etc.).
• Assess morphological and functional changes in main and peripheral arteries and veins.

Indications for echocardiography:

• suspicion of acquired or congenital heart defects;
• auscultation of heart murmurs;
• febrile states of unknown cause;
• ECG changes;
• previous myocardial infarction;
• increased blood pressure;
• regular sports training;
• suspicion of a heart tumor;
• suspected thoracic aortic aneurysm.

Left ventricle

The main causes of local disturbances in LV myocardial contractility:

• Acute myocardial infarction (MI).
• Post-infarction cardiosclerosis.
• Transient painful and silent myocardial ischemia, including ischemia induced by functional stress tests.
• Constant ischemia of the myocardium, which has still retained its viability (the so-called “hibernating myocardium”).
• Dilated and hypertrophic cardiomyopathies, which are often also accompanied by uneven damage to the LV myocardium.
• Local disturbances of intraventricular conduction (blockade, WPW syndrome, etc.).
• Paradoxical movements of the IVS, for example, with volume overload of the RV or bundle branch blocks.

Right ventricle

The most common causes of impaired RV systolic function:

• Tricuspid valve insufficiency.
• Pulmonary heart.
• Stenosis of the left atrioventricular orifice (mitral stenosis).
• Atrial septal defects.
• Congenital heart defects accompanied by severe pulmonary arterial hydrangea (for example, VSD).
• PA valve insufficiency.
• Primary pulmonary hypertension.
• Acute right ventricular myocardial infarction.
• Arrhythmogenic pancreatic dysplasia, etc.

Interventricular septum

An increase in normal values ​​is observed, for example, with some heart defects.

Right atrium

Only the value of the VDV is determined - the volume at rest. A value of less than 20 ml indicates a decrease in EDV, a value of more than 100 ml indicates its increase, and an EDV of more than 300 ml occurs with a very significant increase in the right atrium.

Heart valves

Echocardiographic examination of the valve apparatus reveals:

• fusion of valve leaflets;
• insufficiency of one or another valve (including signs of regurgitation);
• dysfunction of the valve apparatus, in particular the papillary muscles, leading to the development of prolapse of the valves;
• the presence of vegetation on the valve flaps and other signs of damage.

The presence of 100 ml of fluid in the pericardial cavity indicates a small accumulation, and over 500 - a significant accumulation of fluid, which can lead to compression of the heart.

Norms

Left ventricular parameters:

• Left ventricular myocardial mass: men - 135-182 g, women - 95-141 g.
• Left ventricular myocardial mass index (often referred to as LVMI on the form): men 71-94 g/m2, women 71-89 g/m2.
• End-diastolic volume (EDV) of the left ventricle (the volume of the ventricle that it has at rest): men - 112±27 (65-193) ml, women 89±20 (59-136) ml.
• End-diastolic dimension (EDD) of the left ventricle (the size of the ventricle in centimeters that it has at rest): 4.6-5.7 cm.
• End systolic dimension (ESD) of the left ventricle (the size of the ventricle it has during contraction): 3.1-4.3 cm.
• Wall thickness in diastole (outside of heart contractions): 1.1 cm. With hypertrophy - an increase in the thickness of the ventricular wall due to too much load on the heart - this figure increases. Figures of 1.2-1.4 cm indicate slight hypertrophy, 1.4-1.6 indicate moderate hypertrophy, 1.6-2.0 indicate significant hypertrophy, and a value of more than 2 cm indicates high degree hypertrophy.
• Ejection fraction (EF): 55-60%. The ejection fraction shows how much blood relative to the total amount the heart ejects with each contraction; normally it is slightly more than half. When the ejection fraction decreases, heart failure is indicated.
• Stroke volume (SV) is the amount of blood that is ejected by the left ventricle in one contraction: 60-100 ml.

Right ventricle parameters:

• Wall thickness: 5 ml.
• Size index 0.75-1.25 cm/m2.
• Diastolic size (size at rest) 0.95-2.05 cm.

Parameters of the interventricular septum:

• Resting thickness (diastolic thickness): 0.75-1.1 cm. Excursion (moving from side to side during heart contractions): 0.5-0.95 cm.

Left atrium parameters:

• Size: 1.85-3.3 cm.
• Size index: 1.45-2.9 cm/m2.

Standards for heart valves:

• There is no pathology.

Norms for the pericardium:

• The pericardial cavity normally contains no more than 10-30 ml of fluid.

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Formula

The mass of the left ventricular myocardium (calculation) is determined by the following formula:

0.8*(1.04*(MZhP+KDR+ZSLZh)*3-KDR*3)+0.6, where

• IVS – value (in cm) equal to the thickness of the interventricular septum in diastole;
• EDR is a value equal to the end-diastolic size of the left ventricle;
• LVSP is a value (in cm) equal to the thickness of the posterior wall of the left ventricle in diastole.

MI – myocardial mass index is determined by the formula:

MI=M/H2.7 or MI=M/S, where

• M – mass of the left ventricular myocardium (in g);
• H – height (in m);
• ​ S – body surface area (in m2).

Reasons

The reasons leading to left ventricular hypertrophy include:

• arterial hypertension;
• various heart defects;
• cardiomyopathy and cardiomegaly.

The mass of the left ventricular myocardium in 90% of patients with arterial hypertension exceeds the norm. Often hypertrophy develops with mitral valve insufficiency or with aortic defects.

The reasons why myocardial mass may exceed the norm are divided into:

• genetic;
• biochemical;
• demographic.

Scientists have found that cardiac hypertrophy can be promoted by the presence or absence of several fragments in human DNA. Among the biochemical factors leading to myocardial hypertrophy, an excess of norepinephrine and angiotensin can be identified. Demographic factors for the development of cardiac hypertrophy include race, age, gender, physical activity, a tendency to obesity and alcoholism, and the body's sensitivity to salt. For example, men have higher myocardial mass than normal more often than women. In addition, the number of people with a hypertrophied heart increases with age.

Stages and symptoms

In the process of increasing myocardial mass, three stages are distinguished:

• compensation period;
• subcompensation period;
• period of decompensation.

Symptoms of left ventricular hypertrophy begin to manifest themselves noticeably only at the stage of decompensation. When decompensated, the patient experiences shortness of breath, fatigue, palpitations, drowsiness and other symptoms of heart failure. Specific signs of myocardial hypertrophy include a dry cough and facial swelling that appears during the day or in the evening.

Consequences of left ventricular myocardial hypertrophy

High blood pressure not only worsens well-being, but also provokes the onset of pathological processes that affect target organs, including the heart: with arterial hypertension, hypertrophy of the left ventricular myocardium occurs. This is explained by an increase in collagen content in the myocardium and its fibrosis. An increase in myocardial mass entails an increase in myocardial oxygen demand. Which, in turn, leads to ischemia, arrhythmia and cardiac dysfunction.

Cardiac hypertrophy (increased left ventricular myocardial mass) increases the risk of developing cardiovascular disease and can lead to premature death.

However, myocardial hypertrophy is not a death sentence: people with a hypertrophied heart can live for decades. You just need to monitor your blood pressure and regularly undergo ultrasound of the heart to monitor hypertrophy over time.

Treatment

The method of treating left ventricular myocardial hypertrophy depends on the cause that caused the development of this pathology. If necessary, surgery may be prescribed.

Heart surgery for myocardial hypertrophy can be aimed at eliminating ischemia - coronary artery stenting and angioplasty. In case of myocardial hypertrophy due to heart disease, valve replacement or dissection of adhesions is performed if necessary.

Slowing down the processes of hypertrophy (if it is caused by a sedentary lifestyle) in some cases can be achieved by using moderate physical activity, such as swimming or running. The cause of left ventricular myocardial hypertrophy may be obesity: normalizing weight while switching to a balanced diet will reduce the load on the heart. If hypertrophy is caused by increased loads (for example, during professional sports), then you need to gradually reduce them to an acceptable level.

Medicines prescribed by doctors for left ventricular hypertrophy are aimed at improving myocardial nutrition and normalizing heart rhythm. When treating myocardial hypertrophy, you should stop smoking (nicotine reduces the supply of oxygen to the heart) and drinking alcohol (many medications used for myocardial hypertrophy are not compatible with alcohol).

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How does the muscular system of the heart work?

The myocardium is the thickest layer of the heart, located midway between the endocardium (inner layer) and the epicardium on the outside. A feature of the heart is the ability of the atria and ventricles to contract independently, independently of each other, even to “work” autonomously.

Contractility is provided by special fibers (myofibrils). They combine the characteristics of skeletal and smooth muscle tissue. That's why:

• distribute the load evenly across all departments;
• have striations;
• ensure non-stop work of the heart throughout a person’s life;
• are reduced regardless of the influence of consciousness.

Each cell has an elongated nucleus with a large number of chromosomes. Thanks to this, myocytes are more “tenacious” compared to cells of other tissues and are able to withstand significant loads.

The atria and ventricles have different myocardial densities:

1. In the atria, it consists of two layers (superficial and deep), which differ in the direction of the fibers; transverse or circular myofibrils are located on the outside, and longitudinal ones on the inside.
2. The ventricles are provided with an additional third layer, lying between the first two, with a horizontal direction of the fibers. This mechanism strengthens and maintains the force of contraction.

What does myocardial mass indicate?

The total weight of the heart in an adult is about 300 g. The development of ultrasound diagnostic methods has made it possible to calculate the part related to the myocardium from this weight. The average myocardial mass for men is 135 g, for women - 141 g. The exact mass is determined by the formula. It depends on:

• size of the left ventricle in the diastole phase;
• thickness of the interventricular septum and posterior wall.

An even more specific indicator for diagnosis is the myocardial mass index. For the left ventricle, the norm for men is 71 g/m2, for women - 62. This value is calculated automatically by a computer when entering data on a person’s height and body surface area.

Mechanism of heart contraction

Thanks to the development of electron microscopy, the internal structure of the myocardium, the structure of the myocyte, which provides the property of contractility, has been established. Thin and thick protein chains called “actin” and “myosin” have been identified. When actin fibers slide over myosin fibers, muscle contraction occurs (systole phase).

The biochemical mechanism of contraction is the formation of the common substance “actomyosin”. In this case, potassium plays an important role. Leaving the cell, it promotes the connection of actin and myosin and their absorption of energy.

The energy balance in myocytes is maintained by replenishment during the relaxation phase (diastole). Biochemical components involved in this process:

• oxygen,
• hormones,
• enzymes and coenzymes (B vitamins are especially important in their role),
• glucose,
• lactic and pyruvic acids,
• ketone bodies.
• amino acids.

What influences the process of contractility?

Any diastolic dysfunction disrupts energy production, the heart loses “recharge” and does not rest. Myocyte metabolism is influenced by:

• nerve impulses coming from the brain and spinal cord;
• lack or excess of “components” for a biochemical reaction;
• disruption of the flow of necessary substances through the coronary vessels.

Blood supply to the myocardium is carried out through the coronary arteries, extending from the base of the aorta. They are sent to different parts of the ventricles and atria, breaking up into small branches that feed the deep layers. An important adaptive mechanism is the system of collateral (auxiliary) vessels. These are reserved arteries that are normally in a collapsed state. For them to be included in the blood circulation, the main vessels must fail (spasm, thrombosis, atherosclerotic damage). It is this reserve that can limit the infarction zone and provides nutritional compensation in the event of myocardial thickening during hypertrophy.

Maintaining satisfactory contractility is essential to prevent heart failure.

Properties of the heart muscle

In addition to contractility, the myocardium has other exceptional properties that are inherent only to the muscle tissue of the heart:

1. Conductivity - equates myocytes to nerve fibers, since they are also capable of conducting impulses, transmitting them from one area to another.
2. Excitability - in 0.4 seconds. The entire muscular structure of the heart becomes excited and ensures a complete release of blood. The correct rhythm of the heart depends on the occurrence of excitation in the sinus node, located deep in the right atrium and the further passage of the impulse along the fibers to the ventricles.
3. Automatism is the ability to independently form a focus of excitation, bypassing the established direction. This mechanism causes a disruption in the correct rhythm, as other areas take on the role of driver.

Various myocardial diseases are accompanied by minor or severe impairments of the listed functions. They determine the clinical features of the course and require a special approach to treatment.

Let us consider pathological changes in the myocardium and their role in the occurrence of certain diseases of the heart muscle.

Types of myocardial damage

All myocardial damage is divided into:

1. Non-coronary myocardial diseases are characterized by the absence of a connection between the causes and damage to the coronary arteries. These include inflammatory diseases or myocarditis, dystrophic and nonspecific changes in the myocardium.
2. Coronarogenic - consequences of impaired patency of the coronary vessels (foci of ischemia, necrosis, focal or diffuse cardiosclerosis, cicatricial changes).

Features of myocarditis

Myocarditis often occurs in men, women and children. Most often they are associated with inflammation of individual areas (focal) or the entire muscular layer of the heart (diffuse). The causes are infectious diseases (influenza, rickettsiosis, diphtheria, scarlet fever, measles, typhus, sepsis, polio, tuberculosis).

Carrying out preventive work to form a sufficient protective reaction through vaccinations made it possible to limit the disease. However, serious problems remain in the heart after diseases of the nasopharynx, due to the development of a chronic rheumatic process. Non-rheumatic myocarditis is associated with a severe stage of uremic coma and acute nephritis. The inflammatory reaction may be autoimmune, occurring as an allergy.

Histological examination reveals among muscle cells:

• granulomas of a typical structure in rheumatism;
• edema with accumulation of basophils and eosinophils;
• death of muscle cells with proliferation of connective tissue;
• accumulation of fluid between cells (serous, fibrinous);
• areas of dystrophy.

The result in all cases is impaired myocardial contractility.

The clinical picture is varied. It consists of symptoms of cardiac and vascular failure, rhythm disturbances. Sometimes the endocardium and pericardium are simultaneously affected.

Typically, failure of the right ventricular type develops more often, since the myocardium of the right ventricle is weaker and is the first to fail.

Patients complain of shortness of breath, palpitations, and a feeling of irregularities due to an acute illness or after an infection.

Rheumatic inflammation is always accompanied by endocarditis, and the process necessarily spreads to the valve apparatus. If treatment is delayed, a defect is formed. For a good response to therapy, temporary disturbances in rhythm and conduction without consequences are typical.

Myocardial metabolic disorders

Metabolic disorders often accompany myocarditis and coronary heart disease. It is not possible to find out what is primary, this pathology is so connected. Due to the lack of substances for energy production in cells, lack of oxygen in the blood during thyrotoxicosis, anemia, and vitamin deficiencies, myofibrils are replaced by scar tissue.

The heart muscle begins to atrophy and weaken. This process is characteristic of old age. A special form is accompanied by the deposition of lipofuscin pigment in the cells, due to which, on histology, the heart muscle changes color to brown-red, and the process is called “brown myocardial atrophy.” At the same time, dystrophic changes are found in other organs.

When does myocardial hypertrophy occur?

The most common cause of hypertrophic changes in the heart muscle is hypertension. Increased vascular resistance forces the heart to work against a high load.

The development of concentric hypertrophy is characterized by: the volume of the left ventricular cavity remains unchanged with a general increase in size.

Symptomatic hypertension in kidney diseases and endocrine pathologies are less common. Moderate thickening of the ventricular wall makes it difficult for blood vessels to grow deeper into the mass, and is therefore accompanied by ischemia and a state of oxygen deficiency.

Cardiomyopathies are diseases with unclear causes that combine all possible mechanisms of myocardial damage from increasing dystrophy leading to an increase in the ventricular cavity (dilated form) to pronounced hypertrophy (restrictive, hypertrophic).

A special variant of cardiomyopathy - spongy or non-compact myocardium of the left ventricle is congenital in nature, often associated with other heart and vascular defects. Normally, non-compact myocardium makes up a certain proportion of the heart mass. It increases with hypertension and hypertrophic cardiomyopathy.

Pathology is detected only in adulthood by symptoms of heart failure, arrhythmia, and embolic complications. With color Doppler, images are obtained in multiple planes, and the thickness of non-compact areas is measured during systole rather than diastole.

Myocardial damage during ischemia

In 90% of cases, atherosclerotic plaques are found in the coronary vessels during coronary artery disease, blocking the diameter of the feeding artery. A certain role is played by metabolic changes under the influence of impaired nervous regulation - the accumulation of catecholamines.

With angina pectoris, the state of the myocardium can be characterized as forced “hibernation” (hibernation). The hibernating myocardium is an adaptive response to a deficiency of oxygen, adenosine triphosphate molecules, and potassium ions, the main suppliers of calories. Occurs in local areas with prolonged circulatory disorders.

A balance is maintained between a decrease in contractility in accordance with the impaired blood supply. At the same time, myocyte cells are quite viable and can fully recover with improved nutrition.

“Stunned myocardium” is a modern term that characterizes the state of the heart muscle after restoration of coronary circulation in the heart region. The cells accumulate energy for several more days; contractility is impaired during this period. It should be distinguished from the phrase "myocardial remodeling", which means actual changes in myocytes due to pathological causes.

How does the myocardium change during coronary artery thrombosis?

Prolonged spasm or blockage of the coronary arteries causes necrosis of the part of the muscle that they supply with blood. If this process is slow, the collateral vessels will take over the “work” and prevent necrosis.

The focus of the infarction is located in the apex, anterior, posterior and lateral walls of the left ventricle. Rarely involves the septum and right ventricle. Necrosis in the inferior wall occurs when the right coronary artery is blocked.

If the clinical manifestations and the ECG picture agree in confirming the form of the disease, then you can be confident in the diagnosis and use combined treatment. But there are cases that require confirmation of the doctor’s opinion, primarily with the help of accurate, indisputable markers of myocardial necrosis. As a rule, diagnosis is based on the quantitative determination of breakdown products and enzymes that are more or less specific to necrotic tissues.

Can necrosis be confirmed by laboratory methods?

The development of modern biochemical diagnostics of infarction has made it possible to identify standard markers of myocardial necrosis for early and late manifestations of infarction.

Early markers include:

• Myoglobin - increases in the first 2 hours; the optimal use of this indicator is to monitor the effectiveness of fibrinolytic therapy.
• Creatine phosphokinase (CPK), a fraction from cardiac muscle, makes up only 3% of the total mass, so if it is not possible to determine only this part of the enzyme, the test has no diagnostic value. With myocardial necrosis, it increases on the second or third day. An increase in the indicator is possible in case of renal failure, hypothyroidism, and cancer.
• A cardiac type of protein that binds fatty acids - in addition to the myocardium, it is found in the wall of the aorta and the diaphragm. Regarded as the most specific indicator.

Late markers are considered:

• Lactate dehydrogenase, the first isoenzyme, reaches its highest level by the sixth or seventh day, then decreases. The test is considered low specific.
• Aspartate aminotransferase reaches its maximum at the 36th hour. Due to low specificity, it is used only in combination with other tests.
• Cardiac troponins remain in the blood for up to two weeks. They are considered the most specific indicator of necrosis and are recommended by international diagnostic standards.

The presented data on changes in the myocardium are confirmed by anatomical, histological and functional studies of the heart. Their clinical significance makes it possible to timely identify and assess the degree of destruction of myocytes, the possibility of their restoration, and monitor the effectiveness of treatment.

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If you have already undergone an ultrasound examination of the kidneys or, for example, the abdominal organs, then you remember that in order to roughly interpret their results, you most often do not have to go to the doctor - you can find out the basic information before visiting the doctor, by reading the report yourself. The results of a heart ultrasound are not so easy to understand, so it can be difficult to decipher them, especially if you analyze each indicator by number.

You can, of course, just look at the last lines of the form, where a general summary of the research is written, but this also does not always clarify the situation. So that you can better understand the results obtained, we present the basic norms of cardiac ultrasound and possible pathological changes that can be determined by this method.

Ultrasound standards for heart chambers

To begin with, we will present a few numbers that are sure to appear in every Doppler echocardiography report. They reflect various parameters of the structure and functions of individual chambers of the heart. If you are a pedant and take a responsible approach to deciphering your data, pay maximum attention to this section. Perhaps, here you will find the most detailed information in comparison with other Internet sources intended for a wide range of readers. Data may vary slightly between sources; Here are the figures based on materials from the manual “Norms in Medicine” (Moscow, 2001).

Left ventricular parameters

Left ventricular myocardial mass: men – 135-182 g, women – 95-141 g.

Left ventricular myocardial mass index (often referred to as LVMI on the form): men 71-94 g/m2, women 71-89 g/m2.

End-diastolic volume (EDV) of the left ventricle (the volume of the ventricle that it has at rest): men – 112±27 (65-193) ml, women 89±20 (59-136) ml

End-diastolic dimension (EDV) of the left ventricle(size of the ventricle in centimeters, which it has at rest): 4.6 – 5.7 cm

End systolic dimension (ESD) of the left ventricle(size of the ventricle it has during contraction): 3.1 – 4.3 cm

Wall thickness in diastole(outside heartbeat): 1.1 cm

With hypertrophy - an increase in the thickness of the ventricular wall due to too much load on the heart - this figure increases. Figures of 1.2–1.4 cm indicate slight hypertrophy, 1.4–1.6 indicate moderate hypertrophy, 1.6–2.0 indicate significant hypertrophy, and a value of more than 2 cm indicates high degree hypertrophy.

Ejection fraction (EF): 55-60%.

At rest, the ventricles are filled with blood, which is not completely ejected from them during contractions (systole). The ejection fraction shows how much blood relative to the total amount the heart ejects with each contraction; normally it is slightly more than half. When the EF indicator decreases, they speak of heart failure, which means that the organ pumps blood ineffectively, and it can stagnate.

Stroke volume(the amount of blood that is ejected by the left ventricle in one contraction): 60-100 ml.

Right ventricular parameters

Wall thickness: 5 ml

Size index 0.75-1.25 cm/m2

Diastolic size (size at rest) 0.95-2.05 cm

Parameters of the interventricular septum

Resting thickness (diastolic thickness): 0.75-1.1 cm

Excursion (moving from side to side during heart contractions): 0.5-0.95 cm. An increase in this indicator is observed, for example, with certain heart defects.

Right atrium parameters

For this chamber of the heart, only the value of EDV is determined - the volume at rest. A value of less than 20 ml indicates a decrease in EDV, a value of more than 100 ml indicates its increase, and an EDV of more than 300 ml occurs with a very significant increase in the right atrium.

Left atrium parameters

Size: 1.85-3.3 cm

Size index: 1.45 – 2.9 cm/m2.

Most likely, even a very detailed study of the parameters of the heart chambers will not give you particularly clear answers to the question about the state of your health. You can simply compare your indicators with the optimal ones and on this basis draw preliminary conclusions about whether everything is generally normal for you. For more detailed information, contact a specialist; The volume of this article is too small for wider coverage.

Ultrasound standards for heart valves

As for deciphering the results of a valve examination, it should present a simpler task. It will be enough for you to look at the general conclusion about their condition. There are only two main, most common pathological processes: stenosis and valve insufficiency.

The term "stenosis" indicates a narrowing of the valve opening, in which the overlying chamber of the heart has difficulty pumping blood through it and may undergo hypertrophy, which we discussed in the previous section.

Failure– this is the opposite state. If the valve leaflets, which normally prevent the reverse flow of blood, for some reason cease to perform their functions, the blood that has passed from one chamber of the heart to another partially returns, reducing the efficiency of the organ.

Depending on the severity of the disorders, stenosis and insufficiency can be grade 1, 2 or 3. The higher the degree, the more serious the pathology.

Sometimes in the conclusion of a cardiac ultrasound you can find such a definition as “relative insufficiency”. In this condition, the valve itself remains normal, and blood flow disturbances occur due to the fact that pathological changes occur in the adjacent chambers of the heart.

Ultrasound standards for the pericardium

The pericardium, or pericardial sac, is the “bag” that surrounds the outside of the heart. It fuses with the organ in the area where the vessels originate, in its upper part, and between it and the heart itself there is a slit-like cavity.

The most common pathology of the pericardium is an inflammatory process, or pericarditis. With pericarditis, adhesions can form between the pericardial sac and the heart and fluid can accumulate. Normally, it is 10-30 ml, 100 ml indicates a slight accumulation, and over 500 indicates a significant accumulation of fluid, which can lead to difficulty in the full functioning of the heart and its compression...

To master the specialty of a cardiologist, a person must first study at the university for 6 years, and then study cardiology separately for at least a year. A qualified doctor has all the necessary knowledge, thanks to which he can not only easily decipher the conclusion to an ultrasound of the heart, but also make a diagnosis based on it and prescribe treatment. For this reason, deciphering the results of such a complex study as ECHO-cardiography should be provided to a specialized specialist, rather than trying to do it yourself, poking around for a long time and unsuccessfully with the numbers and trying to understand what certain indicators mean. This will save you a lot of time and nerves, since you will not have to worry about your probably disappointing and, even more likely, incorrect conclusions about your health.

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Source: serdce5.ru

Heart ultrasound is an informative and safe diagnostic method, another name for this procedure is echocardiography (EchoCG). What will this study show, what diseases does it detect and who needs to undergo it?

The value of this diagnostic method lies in the fact that it is able to identify pathologies of the heart muscle at the earliest stages, when the patient does not yet experience any symptoms of heart disease. The simplicity and safety of the method allows it to be used in children and adults.

In case of serious indications, echocardiography can be used to determine pathologies of heart development in the fetus even before the birth of the child.

Why is echocardiography performed?

EchoCG is used to identify changes in the structure of cardiac muscle tissue, dystrophic processes, malformations and diseases of this organ.

A similar study is carried out on pregnant women if there is a suspicion of pathology of fetal development, signs of developmental delay, the presence of epilepsy, diabetes mellitus, or endocrine disorders in the woman.

Indications for echocardiography may be symptoms of heart defects, if myocardial infarction, aortic aneurysm, inflammatory diseases, neoplasms of any etiology are suspected.

must be carried out if the following symptoms are observed:

• chest pain;
• weakness during physical activity and regardless of it;
• rapid heartbeat:
• interruptions in heart rhythm;
• swelling of the arms and legs;
• complications after influenza, ARVI, sore throat, rheumatism;
• arterial hypertension.

The examination can be done at the direction of a cardiologist or at your own request. There are no contraindications to its implementation. There is no special preparation for a cardiac ultrasound; it is enough to calm down and try to maintain a balanced state.

Specialist During the study, the following parameters are assessed:

• the state of the myocardium in the phase of systole and diastole (contraction and relaxation);
• the size of the heart chambers, their structure and wall thickness;
• the condition of the pericardium and the presence of exudate in the cardiac sac;
• functioning and structure of arterial and venous valves;
• the presence of blood clots, neoplasms;
• the presence of consequences of infectious diseases, inflammation, heart murmurs.

The results are most often processed using a computer program.

More details about this research methodology are described in this video:

Normal values ​​in adults and newborns

It is impossible to determine uniform standards for the normal state of the heart muscle for men and women, for adults and children of different ages, for young and elderly patients. The figures below are average values, there may be slight differences in each case.

The aortic valve in adults should open 1.5 centimeters or more, the opening area of ​​the mitral valve in adults is 4 sq. cm. The volume of exudate (liquid) in the heart sac should not exceed 30 sq. ml.

Deviations from the norm and principles for interpreting results

As a result of echocardiography, it is possible to detect such pathologies of the development and functioning of the heart muscle and associated diseases:

• heart failure;
• slowing, accelerating or interrupting heart rhythm (tachycardia, bradycardia);
• pre-infarction condition, post-infarction;
• arterial hypertension;
• vegetative-vascular dystonia;
• inflammatory diseases: cardiac myocarditis, endocarditis, exudative or constrictive pericarditis;
• cardiomyopathy;
• signs of angina pectoris;
• heart defects.

The examination protocol is filled out by a specialist performing cardiac ultrasound. The parameters of the functioning of the heart muscle in this document are indicated in two values ​​- the norm and the indicators of the subject. The protocol may contain abbreviations that are incomprehensible to the patient:

• LVM– mass of the left ventricle;
• LVMI– mass index;
• CDR– end diastolic size;
• TO– long axis;
• KO– short axis;
• LP– left atrium;
• PP– right atrium;
• FV– ejection fraction;
• MK– mitral valve;
• AK– aortic valve;
• DM– myocardial movement;
• DR– diastolic size;
• UO– stroke volume (the amount of blood that is ejected by the left ventricle in one contraction;
• TMMZhPd– thickness of the myocardium of the interventricular septum in the diastole phase;
• TMMJPS- the same, in the systole phase.

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Left ventricular myocardial hypertrophy (LVH), as an element of its structural restructuring, is considered a sign of morphological deviation from the norm, a clear predictor of an unfavorable prognosis of the disease that caused it , as well as a criterion that determines the choice of active treatment tactics.

Over the past twenty years, clinical studies have been conducted that have proven the independent contribution of drug-induced reduction in LV myocardial mass (LVMM) in patients with arterial hypertension (AH), which makes it necessary to determine and control LVMM. Based on these ideas, recommendations in recent years for the diagnosis and treatment of hypertension include in the algorithm of antihypertensive tactics for patient management the measurement of LVMM in order to determine the presence of LVH.

But still, there is no unambiguous idea about the pathogenicity of LVH, which is associated with interrelated problems of both methodological and methodological nature: The first concerns the reliability of methods for determining LVH, the second concerns the assessment of the results obtained in terms of the presence or absence of LVH. In addition, there are many instrumental approaches to determining LVMM.

When measuring LVMM, researchers are faced with multifactorial factors that do not influence it. This is the dependence of LVMM on body size, and the possibility of only an adaptive increase in LVMM, for example, during physical activity. There is also a difference in sensitivity of instrumental methods for determining LVMM: some authors are inclined towards greater sensitivity of MRI measurements.

All echocardiographic calculations of LVMM, based on determining the difference in LV volumes between the epicardium and endocardium, multiplied by myocardial density, face the problems of determining tissue interfaces and assessing the shape of the left ventricle.

And many methods are based on linear measurements in M-mode under B-mode control, or directly in a two-dimensional image. The previously existing problem of identifying tissue interfaces, such as “pericardium-epicardium” and “blood-endocardium”, has generally been resolved in recent years, but requires a critical attitude to the studies of past years and does not relieve researchers from the need to use all the technical capabilities of ultrasound -scanners.

Individual differences in LV geometry prevent the creation of a universal mathematical model, even in the absence of local disturbances in the structure of the LV and the approximation of its shape to an ellipse, which has generated a large number of formulas, and, consequently, criteria for determining LVH, resulting in different conclusions about the presence of hypertrophy in one and the same person. the same patient.

In addition, several calculation formulas for determining LVMM are currently used. The formulas recommended by the American Society of Echocardiography (ASE) and the Penn Convention (PC) are more often used, using three measured parameters: the thickness of the myocardium of the interventricular septum (IVS), the posterior wall of the LV (PLV) at the end of diastole and its end-diastolic size (EDD) with including (ASE formula) or not including endocardial thickness (PC formula) in left ventricular diameter, depending on the formula used.

the results obtained when applying these formulas are not always comparable, therefore, to interpret the data obtained, it is necessary to clarify the method used for calculating the parameters of the left ventricle, which in practice is not always available or is neglected. The reason for the discrepancy lies in the following. The cubic formula, originally recommended by ASE, was proposed by B.L. Troy and co-authors in 1972 (LVMM, gr = [(EDR + LVSD + LVAD) 3 -EDR 3 ]×1.05), and then modified using the R.B. regression equation. Devereux and Reichek in 1977 (Penn Convention formula) by analyzing the relationship between echocardiographic LVMM and postmortem anatomical LV mass in 34 adults (r=0.96, p<0,001) (ММЛЖ, гр = 1,04×[(КДР+МЖП+ЗСЛЖ) 3 -КДР 3 ]-13,6) .

The discrepancies in the values ​​of calculated LVMM obtained using these two formulas (cubic, proposed by B.L. Troy, and the PC formula) were within 20% and in 1986 R.B. Devereux, D.R. Alonso at.all. Based on the autopsy of 52 patients, an adjusted equation was proposed (LVMM, gr = 0.8 × (1.04 × [(EDR + LVSD + LVAD) 3 -EDR 3 ]) + 0.6 - ASE formula). LVMM determined by the PC formula was closely correlated with LVMM at autopsy (r=0.92; p<0,001), переоценивала наличие ГЛЖ лишь на 6%, а чувствительность у пациентов с ГЛЖ (масса миокарда при аутопсии >215 g) was 100% with a specificity of 86% (in 29 of 34 patients). The cubic formula was similarly correlated with LVMM at autopsy (r=0.90; p<0,001), но систематически переоценивала наличие ГЛЖ (в среднем на 25%), что было устранено введением скорректированного уравнения (формула ASE): ММЛЖ=0,8×(ММЛЖ-кубическая формула)+0,6 гр. Однако, при её использовании наблюдалась недооценка ММЛЖ при аутопсии в пределах 30% .

Less popular, but sometimes the Teicholz formula is used (LVMM = 1.05 × ((7 × (EDR + LV TZL + TMZH) 3)/2.4 + EDD + LV TZL + TMZhP) - ((7 × LV TZH 3)/(2 ,4+KDR))) . According to L. Teicholz, the norm is LVMM<150 гр, 150-199 гр — умеренной, а >200 g - pronounced LVH. However, these parameters can only be guidelines when using the Teicholz formula and, in addition, they do not take into account the relationship of LVMM with body size.

Virtual calculation of LVMM using the three above-mentioned formulas with a stable value of one of the parameters (either the sum of the thickness of the IVS and the LVSD, or EDR) and an increase in the other (either the EDR, or the sum of the thickness of the IVS and LVSD, respectively) by a stable arbitrary value, showed different sensitivity of the formulas to changing linear indicator. It turned out that the ASE formula is more sensitive to an increase in the thickness of the myocardial walls, the Teicholz formula is more sensitive to an increase in the LV cavity, and the PC formula parity takes into account changes in the linear dimensions and thickness of the myocardium and cavity. Thus, it is better to assess LVMM due to changes in myocardial thickness using formulas that are more sensitive in this regard - ASE and PC.

The second problem, in addition to determining LVMM, is the lack of unified criteria for its indexing, and, consequently, the formation of criteria for LVH. Determining the size of organs through their allometric dependence on body weight, accepted in comparative morphology, is unacceptable in the human population due to the variability of an individual’s body weight, which depends on many factors, in particular on constitutional characteristics, physical development, as well as possible changes in organ size as a result of disease .

The presence of a direct dependence of LVMM on body size requires its indexation. In this regard, left ventricular myocardial mass index (LVMI) is more often calculated when standardized to body surface area (BSA). There are several more ways to calculate myocardial mass index: by height, height 2.0, height 2.13, height 2.7, height 3.0; correction using a regression model of LVMM depending on age, body mass index and BSA.

Studies from past years prove the influence of various factors on myocardial mass in different age groups. Thus, in early childhood, the weight of the LV myocardium is mainly determined by the number of cardiomyocytes (CMC), which reach a maximum number during the first year of life; subsequently, the growth of the LV depends on the increase in the size of the CMC (physiological hypertrophy) and this physiological process is influenced by many factors - body size, blood pressure, blood volume, genetic factors, salt intake, blood viscosity, which determine the phenotypic growth of LV mass.

After puberty, other factors determine the degree of physiological hypertrophy, while in adults there is a correlation between LVMM and age. The effect of height on the variability of LVMM was studied by de G. Simone et al. and in 1995 on 611 normotensive individuals with normal body weight aged from 4 months to 70 years (of which 383 were children and 228 adult patients). LVMM was normalized to body weight, height, and BSA. Height-indexed 2.7 LVMM increased with height and age in children but not in adults, suggesting that other variables influence LV mass in adulthood.

Thus, the influence of different factors on the variability of LVMM in children and adults does not allow the use of the same approaches to the assessment and diagnosis of LVMH. At the same time, indexation to height 2.7 is more justified in children than in adults, who may have an overestimation of this criterion.

The correction of LVMM to BSA, calculated using the Du Bois formula, is more often used, but this standardization is imperfect, because it underestimates LVMM in individuals with obesity.

Analyzing data from the Framingham Heart Study and using the Penn Convention formula when indexing to height D. Levy, R.J. Garrison, D.D. Savage et al. LVH was defined as the deviation of LVMM values ​​from the mean ± 2SD in the control group, i.e. 143 g/m for men and 102 g/m for women. Over four years of follow-up, cardiovascular morbidity (CVD) was higher in individuals with greater LVMI: in men with LVMI<90 гр/м она составила 4,7% против 12,2% при ИММЛЖ ≥140 гр/м, у женщин — 4,1% и 16,1% соответственно . Наблюдался рост ССЗ при более высокой ММЛЖ у мужчин в 2,6, а у женщин — в 3,9 раза, что доказывает прогностическую значимость и важность правильной оценки массы миокарда, поиска более точных диагностических критериев ГМЛЖ для раннего её выявления.

In the domestic recommendations DAG-1, the criterion for diagnosing LVMH is the highest level of normal - a LVMI value of more than 110 g/m2 in women and 134 g/m2 in men, although a value of more than 125 g is prognostically unfavorable in men with arterial hypertension (AH). /m2.

The detection rate of LVMH in both obesity and CVD increases when indexed to height (growth 2.7), however, there is not yet enough data to judge the additional predictive value of this approach.

A comparison of different LVMM indexes for predicting mortality risk was studied by Y. Liao, R.S. Cooper, R. Durazo-Arvizu et al. (1997) in 998 patients with cardiac pathology during a 7-year follow-up. A high correlation of various indexes with each other was found (r=0.90-0.99). Moreover, an increase in any of the indices was associated with a threefold risk of death from all causes and heart disease. 12% of those with height-indexed LVMH had a modest increase in LVMM with no increase in risk, although overweight was common in this group, indicating that height-indexing is justified in the presence of obesity. Thus, myocardial hypertrophy, identified using various indexes, equally retains prognostic significance regarding the risk of death.

P. Gosse, V. Jullien, P. Jarnier et al. investigated the relationship between LVMI and mean daytime systolic blood pressure (SBP) according to 24-hour blood pressure monitoring (ABPM) data in 363 hypertensive patients not treated with antihypertensive drugs. Indexation of LVMM was carried out by BSA, height, height 2.7 and the obtained data were analyzed taking into account gender. LVMM corresponding to SBP >135 mm Hg. Art., was considered as a criterion for LVMH. A higher percentage of detection of LVH was found when indexing LVMH by height 2.7 (50.4%) and height (50.1%), and detection of LVH when indexing by PPT was 48.2% due to its decrease in obese individuals, therefore scientists conclude that the criterion for LVMH is more sensitive when indexed by height 2.7 and propose that cut-off points be considered a value exceeding 47 g/m 2.7 in women and 53 g/m 2.7 in men.

The above-mentioned controversial ideas about normal values ​​of LVMM, LVMI and LVH criteria are presented in Table 1.

Table 1

LVMI as a criterion for LVMH with and without gender

Indicator	Indexing		LVMI value
LVMI, g/m2 LVMI, g/m		D. Levy, Framingham Research, 1987
LVMI, g/m2		J.K. Galy, 1992
LVMI, g/m2		I.W. Hammond, 1986
LVMI, g/m		E. Aberget, 1995
LVMI, g/m2
LVMI, g/m 2.7		De G. Simone, 1994
LVMI, g/m 2.7		J.J. Mahn, 2014
LVMI, g/m2 LVMI, g/m LVMI, g/m 2.7		Recommendations for chamber quantification: Guidelines, 2005
Gender-neutral
LVMI, g/m2		M.J. Koren, 1981
LVMI, g/m 2.7		De G. Simone, 1995

A large range of scattering of LVMI standards within one indexation is obvious, and, consequently, uncertainty in conclusions about the presence of myocardial hypertrophy. Indexing LVMM by BSA gives a range of criteria from 116 to 150 g/m2 in men and 96 to 120 g/m2 in women; indexation to height 2.7 - 48 - 50 for men and 45 - 47 g/m 2.7 for women; indexation to height - 77.7 - 163 in men and 69.8 - 121 g/m. Consequently, it is impossible to confidently judge the presence or absence of LVMH if the LVMI value falls within the range of normal criteria. In addition, it is important that this indefinite interval will include a considerable proportion of patients with slight or moderate LVMH, which is characteristic of a huge group of people with mild hypertension.

The definition of LVMM is also important for characterizing a disproportionately high LVMM (LVMM), since the absolute values ​​of the actual mass are included in the formula for calculating the disproportionality coefficient, which determines the presence and severity of LVMM. An increase in LVMM to a greater extent than required by the hemodynamic load was detected in individuals both with and without LVH and is associated with an increased risk of cardiovascular complications, regardless of the presence of LVH.

So, despite the 30-year use of echo-kg as a criterion for determining LVMH, there remains inconsistency in various studies, there is no presentation of a universal standardization method, although each listed criterion is based on fairly large studies, a number of which are supported by autopsy data. The optimal method for normalizing LV mass remains controversial, and the use of different indexes causes confusion in threshold values, disorienting the work of scientists and practitioners in choosing the best indexing and interpretation of results, while maintaining the relevance of choosing a method for calculating LVMI. The controversial nature of examination methods has also been stated by other authors, who believe that studies of large population cohorts are needed to compare heart sizes measured by different methods, develop more accurate standards, select the best indexing methods, and identify factors influencing LVMM, many of which remain undisclosed.

It is possible that before searching for optimal algorithms for determining LVMM and its standardization in hypertension, it is necessary to clarify which of the above methods is most comparable with the others in assessing LVH. The discriminant analysis we carried out for this purpose, in which the criterion for group formation was one of the methods for diagnosing LVH, and all other methods in the aggregate were predictors, revealed that such a method was the PC formula with standardization by PPT (Table 2).

Table 2

Correspondence of the frequencies of cases of LVH according to different methods of its determination

(performance ratio (EFR) in %; p<0,001)

	All methods except dependent

Note: PCppt, PCgrowth, PCgrowth 2.7 - PC formula, indexing to PPP, growth and growth 2.7, respectively; ASEppt, ASEgrowth, ASEgrowth 2.7 - ASE formula, indexing to PPT, growth and growth 2.7, respectively.

On the other hand, the greatest predictiveness of the combination of ABPM indicators, integral structural and functional parameters of the LV and a number of regulatory peptides, revealed by discriminant analysis in relation to LVH (IFR = 95.7%) only in the case of using the RS technique with standardization to PPT, also testified in favor of its greatest adequacy for the diagnosis of LVH.

Reviewers:

Onishchenko Alexander Leonidovich, Doctor of Medical Sciences, Professor, Vice-Rector for Scientific Work, State Budgetary Educational Institution of Further Professional Education, NSIUV, Ministry of Health of Russia, Novokuznetsk;

Filimonov Sergey Nikolaevich, Doctor of Medical Sciences, Professor, Vice-Rector for Academic Affairs, State Budgetary Educational Institution of Further Professional Education, NSIUV, Ministry of Health of Russia, Novokuznetsk.

Bibliographic link

Zadorozhnaya M.P., Razumov V.V. CONTROVERSIAL ISSUES OF ECHOCARDIOGRAPHIC DETERMINATION OF MYOCARDIAL MASS OF THE LEFT VENTRICLE AND ITS HYPERTROPHY (ANALYTICAL REVIEW AND OWN OBSERVATIONS) // Modern problems of science and education. – 2015. – No. 6.;
URL: https://science-education.ru/ru/article/view?id=23603 (date of access: December 28, 2017).

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What allows examination (EchoCG)

Ultrasound of the heart allows the doctor to determine many parameters, norms and abnormalities in the functioning of the cardiovascular system, assess the size of the heart, the volume of the heart cavities, the thickness of the walls, the frequency of strokes, the presence or absence of blood clots and scars.

This examination also shows the condition of the myocardium, pericardium, large vessels, the mitral valve, the size and thickness of the walls of the ventricles, determines the condition of the valve structures and other parameters of the heart muscle.

After the examination (Echo CG), the doctor records the results of the examination in a special protocol, the decoding of which allows one to detect cardiac diseases, deviations from the norm, anomalies, pathologies, also make a diagnosis and prescribe appropriate treatment.

When should it be performed (Echo CG)

The earlier pathologies or diseases of the heart muscle are diagnosed, the greater the chance of a positive prognosis after treatment. An ultrasound should be performed for the following symptoms:

• periodic or frequent pain in the heart;
• rhythm disturbances: arrhythmia, tachycardia;
• dyspnea;
• increased blood pressure;
• signs of heart failure;
• previous myocardial infarction;
• if there is a history of heart disease;

You can undergo this examination not only with the direction of a cardiologist, but also with other doctors: endocrinologist, gynecologist, neurologist, pulmonologist.

What diseases can be diagnosed by cardiac ultrasound?

There are a large number of diseases and pathologies that are diagnosed by echocardiography:

1. ischemic disease;
2. myocardial infarction or pre-infarction condition;
3. arterial hypertension and hypotension;
4. congenital and acquired heart defects;
5. heart failure;
6. rhythm disturbances;
7. rheumatism;
8. myocarditis, pericarditis, cardiomyopathy;
9. vegetative – vascular dystonia.

Ultrasound examination can detect other disorders or diseases of the heart muscle. In the protocol of diagnostic results, the doctor makes a conclusion, which displays the information received from the ultrasound machine.

These examination results are reviewed by the attending cardiologist and, if any deviations are present, he prescribes treatment measures.

Decoding a heart ultrasound consists of multiple points and abbreviations that are difficult for a person who does not have a special medical education to understand, so we will try to briefly describe the normal indicators obtained by a person who does not have abnormalities or diseases of the cardiovascular system.

Decoding echocardiography

Below is a list of abbreviations that are recorded in the protocol after the examination. These indicators are considered the norm.

1. Left ventricular myocardial mass (LVMM):
2. Left ventricular myocardial mass index (LVMI): 71-94 g/m2;
3. Left ventricular end-diastolic volume (EDV): 112±27 (65-193) ml;
4. End-diastolic size (EDD): 4.6 – 5.7 cm;
5. End systolic size (ESR): 3.1 – 4.3 cm;
6. Wall thickness in diastole: 1.1 cm
7. Long axis (LO);
8. Short axis (KO);
9. Aorta (AO): 2.1 – 4.1;
10. Aortic valve (AV): 1.5 – 2.6;
11. Left anterior (LA): 1.9 – 4.0;
12. Right atrium (RA); 2.7 – 4.5;
13. Diastological thickness of the myocardium of the interventricular septum (TMVSD): 0.4 – 0.7;
14. Thickness of the myocardium of the interventricular septum systological (TMVPS): 0.3 – 0.6;
15. Ejection fraction (EF): 55-60%;
16. Miltra valve (MK);
17. Myocardial movement (MM);
18. Pulmonary artery (PA): 0.75;
19. Stroke volume (SV) is the amount of blood volume ejected by the left ventricle in one contraction: 60-100 ml.
20. Diastolic size (DS): 0.95-2.05 cm;
21. Wall thickness (diastolic): 0.75-1.1 cm;

After the results of the examination, at the end of the protocol, the doctor makes a conclusion in which he reports on the deviations or norms of the examination, and also notes the expected or exact diagnosis of the patient. Depending on the purpose of the examination, the person’s health status, age and gender of the patient, the examination may show slightly different results.

A complete interpretation of echocardiography is assessed by a cardiologist. Independent study of cardiac parameters will not give a person complete information on assessing the health of the cardiovascular system if he does not have special education. Only an experienced doctor in the field of cardiology will be able to interpret echocardiography and answer the patient’s questions.

Some indicators may deviate slightly from the norm or be recorded in the examination protocol under other points. It depends on the quality of the device. If the clinic uses modern equipment in 3D, 4D images, then more accurate results can be obtained, on which the patient will be diagnosed and treated.

Ultrasound of the heart is considered a necessary procedure that should be performed once or twice a year for prevention, or after the first ailments from the cardiovascular system. The results of this examination allow a medical specialist to detect cardiac diseases, disorders and pathologies in the early stages, as well as carry out treatment, give useful recommendations and return a person to a full life.

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When is it necessary to do an ultrasound of the heart?

The clinical picture of many diseases (gastrointestinal tract, nervous system, respiratory organs) is similar to that of cardiac pathologies. To correctly make a diagnosis, it is necessary to do an ultrasound of the heart when the following symptoms occur:

• nausea accompanied by surges in blood pressure;
• persistent headaches; dizziness up to loss of consciousness;
• weakness;
• persistent cough;
• dyspnea;
• swelling (legs, torso);
• cardiac arrhythmias;
• palpitations or a feeling of freezing of the heart muscle;
• pain of different localization: in the upper half of the abdomen, in the right hypochondrium, in the chest, under the shoulder blade on the left, behind the sternum;
• enlarged liver;
• cold extremities;
• pale, bluish-tinged skin;
• hyperthermia due to shortness of breath, chest pain and cyanosis, as well as the appearance of these symptoms after drinking alcohol;
• Noises are heard during auscultation.

It is this study that allows you to confirm or exclude heart damage.

Indications

There are a number of diseases in which the heart “suffers”. These include:

• scleroderma;
• angina pectoris;
• rheumatism;
• myocardial dystrophy;
• congenital anomalies and acquired defects;
• systemic pathologies (lupus erythematosus, etc.);
• history of myocardial infarction;
• arrhythmias;
• vascular aneurysm;
• tumor formations;
• arterial hypertension (including hypertension);
• heart murmurs of unknown etiology.

In the presence of these pathologies, ultrasound makes it possible to promptly notice the appearance of any abnormalities (both anatomical and functional) and take adequate measures.

Ultrasound of the heart is performed in cases where it is necessary to establish the cause of changes in the ECG, the type of heart failure, as well as to assess the functional state of the organ in athletes and in people who have undergone heart surgery.

The procedure is safe and can be performed on patients of any age. No referral required. If the doctor recommends it, where to do an ultrasound of the heart, the patient himself must decide, based on his financial capabilities. The cost of a cardiac ultrasound varies from 1,200 to 4,500 rubles (depending on the level of the medical institution, the qualifications of the specialist and the scope of the required examination).

When should you do an ultrasound for your child?

An ultrasound of the child’s heart should be done when the following disorders occur:

• causeless loss of consciousness;
• deviations in the cardiogram;
• the presence of a heart murmur;
• frequent colds;
• hereditary burden (close relatives had cardiac pathologies);
• baby has difficulty sucking a bottle (or breast);
• the child talks about unpleasant and painful sensations in the chest area;
• in the baby (even at rest), the color of the skin around the mouth, as well as on the arms and legs, changes;
• With little physical activity, the child sweats a lot and gets tired quickly.

If parents want to know whether their baby's heart is healthy, it is necessary to examine the organ. Your doctor will tell you where you can do an ultrasound of the heart. Information about how much a heart ultrasound costs can be clarified by calling the medical registrar or on the website of the medical institution. Prices for this service range from 1200-2500 rubles.

Ultrasound of the fetus

For early diagnosis of diseases of the cardiovascular system, ultrasound of the fetal heart is performed already in the early stages of embryonic development.

A woman comes for her first ultrasound examination when she is 6-8 weeks pregnant. When recording ultrasound readings of the fetal heart during pregnancy at this stage, the doctor pays attention to the heart rate. Normally, this indicator is in the range of 110-130 beats/min. If the heart rate is higher than the indicated figures, this indicates insufficient oxygen supply to the organs and tissues of the embryo. At low heart rates, some pathologies of the heart muscle are possible.

In the early stages, an ultrasound of the fetal heart can tell you how many babies a woman is carrying.

When an expectant mother comes for a heart ultrasound later in pregnancy, the doctor evaluates not only the number of heartbeats per minute, but also the correct development of the organ and the presence (or absence) of defects.

At week 20, the cardiac chambers and their structures are clearly visualized. And it is not difficult for an experienced specialist to see any deviations. If a heart pathology is detected in the unborn baby, treatment can begin immediately after birth.

What information does ultrasound provide?

When resorting to this diagnostic method, the patient is interested in the question: what does an ultrasound of the heart show? The first thing the doctor pays attention to is the morphological parameters. These include: the size of the organ and its parameters, the volume and thickness of the walls of its chambers, the condition of the valve apparatus, blood vessels, the presence of scar changes or blood clots (if any). The functional activity of the heart is also assessed: contraction frequency, rhythm of work, etc. The condition of the pericardium and myocardium is assessed.

Interpretation of the results of ultrasound examination of the heart

At the end of the ultrasound, the doctor fills out an examination protocol with (decoding of the ultrasound of the heart and a conclusion). In the protocol, opposite each parameter, the indicators of the normal ultrasound of the heart are indicated, with which the data of the subject are compared.

Normal values ​​for the left ventricle

Normal cardiac ultrasound findings may vary depending on the gender of the patient.

Myocardial mass – 95-141g (for women), 135-182g (for men).

Myocardial mass index (LVMI) – 71-89 g/m2 (for women), 71-94 g/m2 (for men).

The end diastolic size is from 4.6 to 5.7 cm.

The end-systolic size is from 3.1 to 4.3 cm.

The thickness of the wall outside the heart contraction (in the diastole phase) is about 1.1 cm. If this indicator is increased, this is referred to as “hypertrophy”. This change is most often associated with increased load on the heart muscle.

The ejection fraction is 55-60%. Shows how much blood (in volume) the heart ejects at the time of the next contraction (in relation to the total amount of blood in the organ). Low numbers for this indicator indicate heart failure. Stroke volume (60-100 ml) - this is how much blood is normally ejected by the LV during systole.

Normal values ​​for the right ventricle

The pancreas size index is from 0.75 to 1.25 cm/m2.

The thickness of the pancreas wall is 4-5mm.

Size at rest (diastolic) – from 0.95 to 2.05 cm.

Normal indicators for the interventricular septum

The thickness in diastole is in the range of 0.75 - 1.1 cm.

The excursion indicator (or deviation in both directions during contraction) ranges from 0.5 to 0.95 cm. With heart defects it increases significantly.

Normal indicators for the right atrium

The main parameter for this camera is EDV (end-diastolic volume). The limits of its norm are quite wide - from 20 to 100 ml.

Normal indicators for the left atrium

LA size index – from 1.45 to 2.90 cm/m2.

Size – from 1.85 to 3.30 cm.

Deviations in valve operation (1-3 degrees)

Insufficiency is a pathological condition in which the valve leaflets are not able to close completely. This leads to partial return of blood in the opposite direction, which reduces the efficiency of the heart muscle.

Stenosis is the opposite of insufficiency. It is characterized by a narrowing of the opening of a certain heart valve, which creates an obstacle to the passage of blood from chamber to chamber or vascular bed. As a result, wall hypertrophy develops.

Relative insufficiency - the valve is normal, but there are pathological changes in the heart chambers into which blood passes through it.

Ultrasound normal for the pericardium

The pericardial sac is most often subject to an inflammatory process (pericarditis). As a result, liquid accumulates in its cavity and adhesions form on the walls. Normally, the volume of exudate does not exceed 30 ml. When it increases, additional pressure is placed on the organ, which significantly complicates its functioning.

Another indicator is the thickness of the aorta, which is normally 2.1-4.1 cm.

If the examination reveals small deviations from the normal parameters of cardiac ultrasound, you should not make a diagnosis yourself. You should consult your doctor. Gender, age, concomitant diseases are all things that can affect the final result. Only a qualified cardiologist can decipher the norm of cardiac ultrasound, as well as any discrepancies that occur.

How is ultrasound examination performed?

No special preparation is required for cardiac ultrasound. All that is needed from the patient to obtain the most objective results: calm down and breathe evenly. Immediately before the examination, you should not overexert yourself physically, drink caffeine-containing drinks, or take medications (sedatives, etc.).

You can find out in detail how a heart ultrasound is performed on the Internet. On the websites of many medical centers, along with a description of the procedure itself and the price of cardiac ultrasound, visual materials are presented in the form of photographs and videos of cardiac ultrasound.

Before the heart examination, the patient undresses to the waist and lies down on the couch. All jewelry from the exposed area (chains, etc.) must be removed. The procedure is non-invasive. First, the subject lies on his back, then on his right side. The chest area is treated with gel. Afterwards, moving the sensor along the surface of the skin in the area of ​​projection of the organ, the heart is examined. The whole procedure takes no more than 20 minutes. The monitor displays the heart and adjacent structures, which is made possible thanks to the property of ultrasound. It is reflected from the fabric, and, depending on their density, gives the corresponding picture.

Heart ultrasound allows you to diagnose pathologies that have not yet begun to manifest symptoms.

Echocardiography (EchoCG) is a method for studying morphological and functional changes in the heart and its valvular apparatus using ultrasound.

The echocardiographic research method allows:

• Quantitatively and qualitatively assess the functional state of the LV and RV.
• Assess regional LV contractility (for example, in patients with coronary artery disease).
• Assess LVMM and identify ultrasound signs of symmetric and asymmetric hypertrophy and dilatation of the ventricles and atria.
• Assess the condition of the valve apparatus (stenosis, insufficiency, valve prolapse, presence of vegetations on the valve leaflets, etc.).
• Assess the level of pressure in the PA and identify signs of pulmonary hypertension.
• Identify morphological changes in the pericardium and the presence of fluid in the pericardial cavity.
• Identify intracardiac formations (thrombi, tumors, additional chords, etc.).
• Assess morphological and functional changes in main and peripheral arteries and veins.

Indications for echocardiography:

• suspicion of acquired or congenital heart defects;
• auscultation of heart murmurs;
• febrile states of unknown cause;
• ECG changes;
• previous myocardial infarction;
• increased blood pressure;
• regular sports training;
• suspicion of a heart tumor;
• suspected thoracic aortic aneurysm.

Left ventricle

The main causes of local disturbances in LV myocardial contractility:

• Acute myocardial infarction (MI).
• Post-infarction cardiosclerosis.
• Transient painful and silent myocardial ischemia, including ischemia induced by functional stress tests.
• Constant ischemia of the myocardium, which has still retained its viability (the so-called “hibernating myocardium”).
• Dilated and hypertrophic cardiomyopathies, which are often also accompanied by uneven damage to the LV myocardium.
• Local disturbances of intraventricular conduction (blockade, WPW syndrome, etc.).
• Paradoxical movements of the IVS, for example, with volume overload of the RV or bundle branch blocks.

Right ventricle

The most common causes of impaired RV systolic function:

• Tricuspid valve insufficiency.
• Pulmonary heart.
• Stenosis of the left atrioventricular orifice (mitral stenosis).
• Atrial septal defects.
• Congenital heart defects accompanied by severe pulmonary arterial hydrangea (for example, VSD).
• PA valve insufficiency.
• Primary pulmonary hypertension.
• Acute right ventricular myocardial infarction.
• Arrhythmogenic pancreatic dysplasia, etc.

Interventricular septum

An increase in normal values ​​is observed, for example, with some heart defects.

Right atrium

Only the value of the volumetric volume at rest is determined. A value of less than 20 ml indicates a decrease in EDV, a value of more than 100 ml indicates its increase, and an EDV of more than 300 ml occurs with a very significant increase in the right atrium.

Heart valves

Echocardiographic examination of the valve apparatus reveals:

• fusion of valve leaflets;
• insufficiency of one or another valve (including signs of regurgitation);
• dysfunction of the valve apparatus, in particular the papillary muscles, leading to the development of prolapse of the valves;
• the presence of vegetation on the valve flaps and other signs of damage.

The presence of 100 ml of fluid in the pericardial cavity indicates a small accumulation, and over 500 - a significant accumulation of fluid, which can lead to compression of the heart.

Norms

Left ventricular parameters:

• Left ventricular myocardial mass: men - 135-182 g, women - 95-141 g.
• Left ventricular myocardial mass index (often referred to as LVMI on the form): men 71-94 g/m2, women 71-89 g/m2.
• End-diastolic volume (EDV) of the left ventricle (the volume of the ventricle that it has at rest): men - 112±27 (65-193) ml, women 89±20 (59-136) ml.
• End-diastolic dimension (EDD) of the left ventricle (the size of the ventricle in centimeters that it has at rest): 4.6-5.7 cm.
• End systolic dimension (ESD) of the left ventricle (the size of the ventricle it has during contraction): 3.1-4.3 cm.
• Wall thickness in diastole (outside of heart contractions): 1.1 cm. With hypertrophy - an increase in the thickness of the ventricular wall due to too much load on the heart - this figure increases. Figures of 1.2-1.4 cm indicate slight hypertrophy, 1.4-1.6 indicate moderate hypertrophy, 1.6-2.0 indicate significant hypertrophy, and a value of more than 2 cm indicates high degree hypertrophy.


• Ejection fraction (EF): 55-60%. The ejection fraction shows how much blood relative to the total amount the heart ejects with each contraction; normally it is slightly more than half. When the ejection fraction decreases, heart failure is indicated.
• Stroke volume (SV) is the amount of blood that is ejected by the left ventricle in one contraction: 60-100 ml.

Right ventricle parameters:

• Wall thickness: 5 ml.
• Size index 0.75-1.25 cm/m2.
• Diastolic size (size at rest) 0.95-2.05 cm.

Parameters of the interventricular septum:

• Resting thickness (diastolic thickness): 0.75-1.1 cm. Excursion (moving from side to side during heart contractions): 0.5-0.95 cm.

Left atrium parameters:

• Size: 1.85-3.3 cm.
• Size index: 1.45-2.9 cm/m2.

Standards for heart valves:

• There is no pathology.

Norms for the pericardium:

• The pericardial cavity normally contains no more than 10-30 ml of fluid.

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Formula

The mass of the left ventricular myocardium (calculation) is determined by the following formula:

0.8*(1.04*(MZhP+KDR+ZSLZh)*3-KDR*3)+0.6, where

• IVS – value (in cm) equal to the thickness of the interventricular septum in diastole;
• EDR is a value equal to the end-diastolic size of the left ventricle;
• LVSP is a value (in cm) equal to the thickness of the posterior wall of the left ventricle in diastole.

MI – myocardial mass index is determined by the formula:

MI=M/H2.7 or MI=M/S, where

• M – mass of the left ventricular myocardium (in g);
• H – height (in m);
• ​ S – body surface area (in m2).

Reasons

The reasons leading to left ventricular hypertrophy include:

• arterial hypertension;
• various heart defects;
• cardiomyopathy and cardiomegaly.

The mass of the left ventricular myocardium in 90% of patients with arterial hypertension exceeds the norm. Often hypertrophy develops with mitral valve insufficiency or with aortic defects.

The reasons why myocardial mass may exceed the norm are divided into:

• genetic;
• biochemical;
• demographic.

Scientists have found that cardiac hypertrophy can be promoted by the presence or absence of several fragments in human DNA.

biochemical factors leading to myocardial hypertrophy can be identified as an excess of norepinephrine and angiotensin. Demographic factors for the development of cardiac hypertrophy include race, age, gender, physical activity, a tendency to obesity and alcoholism, and the body's sensitivity to salt. For example, men have higher myocardial mass than normal more often than women. In addition, the number of people with a hypertrophied heart increases with age.

Stages and symptoms

In the process of increasing myocardial mass, three stages are distinguished:

• compensation period;
• subcompensation period;
• period of decompensation.

Symptoms of left ventricular hypertrophy begin to manifest themselves noticeably only at the stage of decompensation. When decompensated, the patient experiences shortness of breath, fatigue, palpitations, drowsiness and other symptoms of heart failure. Specific signs of myocardial hypertrophy include a dry cough and facial swelling that appears during the day or in the evening.

Consequences of left ventricular myocardial hypertrophy

High blood pressure not only worsens well-being, but also provokes the onset of pathological processes that affect target organs, including the heart: with arterial hypertension, hypertrophy of the left ventricular myocardium occurs. This is explained by an increase in collagen content in the myocardium and its fibrosis. An increase in myocardial mass entails an increase in myocardial oxygen demand. Which, in turn, leads to ischemia, arrhythmia and cardiac dysfunction.

Cardiac hypertrophy (increased left ventricular myocardial mass) increases the risk of developing cardiovascular disease and can lead to premature death.

However, myocardial hypertrophy is not a death sentence: people with a hypertrophied heart can live for decades. You just need to monitor your blood pressure and regularly undergo ultrasound of the heart to monitor hypertrophy over time.

Treatment

The method of treating left ventricular myocardial hypertrophy depends on the cause that caused the development of this pathology. If necessary, surgery may be prescribed.

Heart surgery for myocardial hypertrophy can be aimed at eliminating ischemia - coronary artery stenting and angioplasty. In case of myocardial hypertrophy due to heart disease, valve replacement or dissection of adhesions is performed if necessary.

Slowing down the processes of hypertrophy (if it is caused by a sedentary lifestyle) in some cases can be achieved by using moderate physical activity, such as swimming or running. The cause of left ventricular myocardial hypertrophy may be obesity: normalizing weight while switching to a balanced diet will reduce the load on the heart. If hypertrophy is caused by increased loads (for example, during professional sports), then you need to gradually reduce them to an acceptable level.

Medicines prescribed by doctors for left ventricular hypertrophy are aimed at improving myocardial nutrition and normalizing heart rhythm. When treating myocardial hypertrophy, you should stop smoking (nicotine reduces the supply of oxygen to the heart) and drinking alcohol (many medications used for myocardial hypertrophy are not compatible with alcohol).

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How does the muscular system of the heart work?

The myocardium is the thickest layer of the heart, located midway between the endocardium (inner layer) and the epicardium on the outside. A feature of the heart is the ability of the atria and ventricles to contract independently, independently of each other, even to “work” autonomously.

Contractility is provided by special fibers (myofibrils). They combine the characteristics of skeletal and smooth muscle tissue. That's why:

• distribute the load evenly across all departments;
• have striations;
• ensure non-stop work of the heart throughout a person’s life;
• are reduced regardless of the influence of consciousness.

Each cell has an elongated nucleus with a large number of chromosomes. Thanks to this, myocytes are more “tenacious” compared to cells of other tissues and are able to withstand significant loads.

The atria and ventricles have different myocardial densities:

1. In the atria, it consists of two layers (superficial and deep), which differ in the direction of the fibers; transverse or circular myofibrils are located on the outside, and longitudinal ones on the inside.
2. The ventricles are provided with an additional third layer, lying between the first two, with a horizontal direction of the fibers. This mechanism strengthens and maintains the force of contraction.

What does myocardial mass indicate?

The total weight of the heart in an adult is about 300 g. The development of ultrasound diagnostic methods has made it possible to calculate the part related to the myocardium from this weight. The average myocardial mass for men is 135 g, for women - 141 g. The exact mass is determined by the formula. It depends on:

• size of the left ventricle in the diastole phase;
• thickness of the interventricular septum and posterior wall.

An even more specific indicator for diagnosis is the myocardial mass index. For the left ventricle, the norm for men is 71 g/m2, for women - 62. This value is calculated automatically by a computer when entering data on a person’s height and body surface area.

Mechanism of heart contraction

Thanks to the development of electron microscopy, the internal structure of the myocardium, the structure of the myocyte, which provides the property of contractility, has been established. Thin and thick protein chains called “actin” and “myosin” have been identified. When actin fibers slide over myosin fibers, muscle contraction occurs (systole phase).

The biochemical mechanism of contraction is the formation of the common substance “actomyosin”. In this case, potassium plays an important role. Leaving the cell, it promotes the connection of actin and myosin and their absorption of energy.

The energy balance in myocytes is maintained by replenishment during the relaxation phase (diastole). Biochemical components involved in this process:

• oxygen,
• hormones,
• enzymes and coenzymes (B vitamins are especially important in their role),
• glucose,
• lactic and pyruvic acids,
• ketone bodies.
• amino acids.

What influences the process of contractility?

Any diastolic dysfunction disrupts energy production, the heart loses “recharge” and does not rest. Myocyte metabolism is influenced by:

• nerve impulses coming from the brain and spinal cord;
• lack or excess of “components” for a biochemical reaction;
• disruption of the flow of necessary substances through the coronary vessels.

Blood supply to the myocardium is carried out through the coronary arteries, extending from the base of the aorta. They are sent to different parts of the ventricles and atria, breaking up into small branches that feed the deep layers. An important adaptive mechanism is the system of collateral (auxiliary) vessels. These are reserved arteries that are normally in a collapsed state. For them to be included in the blood circulation, the main vessels must fail (spasm, thrombosis, atherosclerotic damage). It is this reserve that can limit the infarction zone and provides nutritional compensation in the event of myocardial thickening during hypertrophy.

Maintaining satisfactory contractility is essential to prevent heart failure.

Properties of the heart muscle

In addition to contractility, the myocardium has other exceptional properties that are inherent only to the muscle tissue of the heart:

1. Conductivity - equates myocytes to nerve fibers, since they are also capable of conducting impulses, transmitting them from one area to another.
2. Excitability - in 0.4 seconds. The entire muscular structure of the heart becomes excited and ensures a complete release of blood. The correct rhythm of the heart depends on the occurrence of excitation in the sinus node, located deep in the right atrium and the further passage of the impulse along the fibers to the ventricles.
3. Automatism is the ability to independently form a focus of excitation, bypassing the established direction. This mechanism causes a disruption in the correct rhythm, as other areas take on the role of driver.

Various myocardial diseases are accompanied by minor or severe impairments of the listed functions. They determine the clinical features of the course and require a special approach to treatment.

Let us consider pathological changes in the myocardium and their role in the occurrence of certain diseases of the heart muscle.

Types of myocardial damage

All myocardial damage is divided into:

1. Non-coronary myocardial diseases are characterized by the absence of a connection between the causes and damage to the coronary arteries. These include inflammatory diseases or myocarditis, dystrophic and nonspecific changes in the myocardium.
2. Coronarogenic - consequences of impaired patency of the coronary vessels (foci of ischemia, necrosis, focal or diffuse cardiosclerosis, cicatricial changes).

Features of myocarditis

Myocarditis often occurs in men, women and children. Most often they are associated with inflammation of individual areas (focal) or the entire muscular layer of the heart (diffuse). The causes are infectious diseases (influenza, rickettsiosis, diphtheria, scarlet fever, measles, typhus, sepsis, polio, tuberculosis).

Carrying out preventive work to form a sufficient protective reaction through vaccinations made it possible to limit the disease. However, serious problems remain in the heart after diseases of the nasopharynx, due to the development of a chronic rheumatic process. Non-rheumatic myocarditis is associated with a severe stage of uremic coma and acute nephritis. The inflammatory reaction may be autoimmune, occurring as an allergy.

Histological examination reveals among muscle cells:

• granulomas of a typical structure in rheumatism;
• edema with accumulation of basophils and eosinophils;
• death of muscle cells with proliferation of connective tissue;
• accumulation of fluid between cells (serous, fibrinous);
• areas of dystrophy.

The result in all cases is impaired myocardial contractility.

The clinical picture is varied. It consists of symptoms of cardiac and vascular failure, rhythm disturbances. Sometimes the endocardium and pericardium are simultaneously affected.

Typically, failure of the right ventricular type develops more often, since the myocardium of the right ventricle is weaker and is the first to fail.

Patients complain of shortness of breath, palpitations, and a feeling of irregularities due to an acute illness or after an infection.

Rheumatic inflammation is always accompanied by endocarditis, and the process necessarily spreads to the valve apparatus. If treatment is delayed, a defect is formed. For a good response to therapy, temporary disturbances in rhythm and conduction without consequences are typical.

Myocardial metabolic disorders

Metabolic disorders often accompany myocarditis and coronary heart disease. It is not possible to find out what is primary, this pathology is so connected. Due to the lack of substances for energy production in cells, lack of oxygen in the blood during thyrotoxicosis, anemia, and vitamin deficiencies, myofibrils are replaced by scar tissue.

The heart muscle begins to atrophy and weaken. This process is characteristic of old age. A special form is accompanied by the deposition of lipofuscin pigment in the cells, due to which, on histology, the heart muscle changes color to brown-red, and the process is called “brown myocardial atrophy.” At the same time, dystrophic changes are found in other organs.

When does myocardial hypertrophy occur?

The most common cause of hypertrophic changes in the heart muscle is hypertension. Increased vascular resistance forces the heart to work against a high load.

The development of concentric hypertrophy is characterized by: the volume of the left ventricular cavity remains unchanged with a general increase in size.

Symptomatic hypertension in kidney diseases and endocrine pathologies are less common. Moderate thickening of the ventricular wall makes it difficult for blood vessels to grow deeper into the mass, and is therefore accompanied by ischemia and a state of oxygen deficiency.

Cardiomyopathies are diseases with unclear causes that combine all possible mechanisms of myocardial damage from increasing dystrophy leading to an increase in the ventricular cavity (dilated form) to pronounced hypertrophy (restrictive, hypertrophic).

A special variant of cardiomyopathy - spongy or non-compact myocardium of the left ventricle is congenital in nature, often associated with other heart and vascular defects. Normally, non-compact myocardium makes up a certain proportion of the heart mass. It increases with hypertension and hypertrophic cardiomyopathy.

Pathology is detected only in adulthood by symptoms of heart failure, arrhythmia, and embolic complications. With color Doppler, images are obtained in multiple planes, and the thickness of non-compact areas is measured during systole rather than diastole.

Myocardial damage during ischemia

In 90% of cases, atherosclerotic plaques are found in the coronary vessels during coronary artery disease, blocking the diameter of the feeding artery. A certain role is played by metabolic changes under the influence of impaired nervous regulation - the accumulation of catecholamines.

With angina pectoris, the state of the myocardium can be characterized as forced “hibernation” (hibernation). The hibernating myocardium is an adaptive response to a deficiency of oxygen, adenosine triphosphate molecules, and potassium ions, the main suppliers of calories. Occurs in local areas with prolonged circulatory disorders.

A balance is maintained between a decrease in contractility in accordance with the impaired blood supply. At the same time, myocyte cells are quite viable and can fully recover with improved nutrition.

“Stunned myocardium” is a modern term that characterizes the state of the heart muscle after restoration of coronary circulation in the heart region. The cells accumulate energy for several more days; contractility is impaired during this period. It should be distinguished from the phrase "myocardial remodeling", which means actual changes in myocytes due to pathological causes.

How does the myocardium change during coronary artery thrombosis?

Prolonged spasm or blockage of the coronary arteries causes necrosis of the part of the muscle that they supply with blood. If this process is slow, the collateral vessels will take over the “work” and prevent necrosis.

The focus of the infarction is located in the apex, anterior, posterior and lateral walls of the left ventricle. Rarely involves the septum and right ventricle. Necrosis in the inferior wall occurs when the right coronary artery is blocked.

If the clinical manifestations and the ECG picture agree in confirming the form of the disease, then you can be confident in the diagnosis and use combined treatment. But there are cases that require confirmation of the doctor’s opinion, primarily with the help of accurate, indisputable markers of myocardial necrosis. As a rule, diagnosis is based on the quantitative determination of breakdown products and enzymes that are more or less specific to necrotic tissues.

Can necrosis be confirmed by laboratory methods?

The development of modern biochemical diagnostics of infarction has made it possible to identify standard markers of myocardial necrosis for early and late manifestations of infarction.

Early markers include:

• Myoglobin - increases in the first 2 hours; the optimal use of this indicator is to monitor the effectiveness of fibrinolytic therapy.
• Creatine phosphokinase (CPK), a fraction from cardiac muscle, makes up only 3% of the total mass, so if it is not possible to determine only this part of the enzyme, the test has no diagnostic value. With myocardial necrosis, it increases on the second or third day. An increase in the indicator is possible in case of renal failure, hypothyroidism, and cancer.
• A cardiac type of protein that binds fatty acids - in addition to the myocardium, it is found in the wall of the aorta and the diaphragm. Regarded as the most specific indicator.

Late markers are considered:

• Lactate dehydrogenase, the first isoenzyme, reaches its highest level by the sixth or seventh day, then decreases. The test is considered low specific.
• Aspartate aminotransferase reaches its maximum at the 36th hour. Due to low specificity, it is used only in combination with other tests.
• Cardiac troponins remain in the blood for up to two weeks. They are considered the most specific indicator of necrosis and are recommended by international diagnostic standards.

The presented data on changes in the myocardium are confirmed by anatomical, histological and functional studies of the heart. Their clinical significance makes it possible to timely identify and assess the degree of destruction of myocytes, the possibility of their restoration, and monitor the effectiveness of treatment.

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If you have already undergone an ultrasound examination of the kidneys or, for example, the abdominal organs, then you remember that in order to roughly interpret their results, you most often do not have to go to the doctor - you can find out the basic information before visiting the doctor, by reading the report yourself. The results of a heart ultrasound are not so easy to understand, so it can be difficult to decipher them, especially if you analyze each indicator by number.

You can, of course, just look at the last lines of the form, where a general summary of the research is written, but this also does not always clarify the situation. So that you can better understand the results obtained, we present the basic norms of cardiac ultrasound and possible pathological changes that can be determined by this method.

Ultrasound standards for heart chambers

To begin with, we will present a few numbers that are sure to appear in every Doppler echocardiography report. They reflect various parameters of the structure and functions of individual chambers of the heart. If you are a pedant and take a responsible approach to deciphering your data, pay maximum attention to this section. Perhaps, here you will find the most detailed information in comparison with other Internet sources intended for a wide range of readers. Data may vary slightly between sources; Here are the figures based on materials from the manual “Norms in Medicine” (Moscow, 2001).

Left ventricular parameters

Left ventricular myocardial mass: men – 135-182 g, women – 95-141 g.

Left ventricular myocardial mass index (often referred to as LVMI on the form): men 71-94 g/m2, women 71-89 g/m2.

End-diastolic volume (EDV) of the left ventricle (the volume of the ventricle that it has at rest): men – 112±27 (65-193) ml, women 89±20 (59-136) ml

End-diastolic dimension (EDV) of the left ventricle(size of the ventricle in centimeters, which it has at rest): 4.6 – 5.7 cm

End systolic dimension (ESD) of the left ventricle(size of the ventricle it has during contraction): 3.1 – 4.3 cm

Wall thickness in diastole(outside heartbeat): 1.1 cm

With hypertrophy - an increase in the thickness of the ventricular wall due to too much load on the heart - this figure increases. Figures of 1.2–1.4 cm indicate slight hypertrophy, 1.4–1.6 indicate moderate hypertrophy, 1.6–2.0 indicate significant hypertrophy, and a value of more than 2 cm indicates high degree hypertrophy.

Ejection fraction (EF): 55-60%.

At rest, the ventricles are filled with blood, which is not completely ejected from them during contractions (systole). The ejection fraction shows how much blood relative to the total amount the heart ejects with each contraction; normally it is slightly more than half. When the EF indicator decreases, they speak of heart failure, which means that the organ pumps blood ineffectively, and it can stagnate.

Stroke volume(the amount of blood that is ejected by the left ventricle in one contraction): 60-100 ml.

Right ventricular parameters

Wall thickness: 5 ml

Size index 0.75-1.25 cm/m2

Diastolic size (size at rest) 0.95-2.05 cm

Parameters of the interventricular septum

Resting thickness (diastolic thickness): 0.75-1.1 cm

Excursion (moving from side to side during heart contractions): 0.5-0.95 cm. An increase in this indicator is observed, for example, with certain heart defects.

Right atrium parameters

For this chamber of the heart, only the value of EDV is determined - the volume at rest. A value of less than 20 ml indicates a decrease in EDV, a value of more than 100 ml indicates its increase, and an EDV of more than 300 ml occurs with a very significant increase in the right atrium.

Left atrium parameters

Size: 1.85-3.3 cm

Size index: 1.45 – 2.9 cm/m2.

Most likely, even a very detailed study of the parameters of the heart chambers will not give you particularly clear answers to the question about the state of your health. You can simply compare your indicators with the optimal ones and on this basis draw preliminary conclusions about whether everything is generally normal for you. For more detailed information, contact a specialist; The volume of this article is too small for wider coverage.

Ultrasound standards for heart valves

As for deciphering the results of a valve examination, it should present a simpler task. It will be enough for you to look at the general conclusion about their condition. There are only two main, most common pathological processes: stenosis and valve insufficiency.

The term "stenosis" indicates a narrowing of the valve opening, in which the overlying chamber of the heart has difficulty pumping blood through it and may undergo hypertrophy, which we discussed in the previous section.

Failure– this is the opposite state. If the valve leaflets, which normally prevent the reverse flow of blood, for some reason cease to perform their functions, the blood that has passed from one chamber of the heart to another partially returns, reducing the efficiency of the organ.

Depending on the severity of the disorders, stenosis and insufficiency can be grade 1, 2 or 3. The higher the degree, the more serious the pathology.

Sometimes in the conclusion of a cardiac ultrasound you can find such a definition as “relative insufficiency”. In this condition, the valve itself remains normal, and blood flow disturbances occur due to the fact that pathological changes occur in the adjacent chambers of the heart.

Ultrasound standards for the pericardium

The pericardium, or pericardial sac, is the “bag” that surrounds the outside of the heart. It fuses with the organ in the area where the vessels originate, in its upper part, and between it and the heart itself there is a slit-like cavity.

The most common pathology of the pericardium is an inflammatory process, or pericarditis. With pericarditis, adhesions can form between the pericardial sac and the heart and fluid can accumulate. Normally, it is 10-30 ml, 100 ml indicates a slight accumulation, and over 500 indicates a significant accumulation of fluid, which can lead to difficulty in the full functioning of the heart and its compression...

To master the specialty of a cardiologist, a person must first study at the university for 6 years, and then study cardiology separately for at least a year. A qualified doctor has all the necessary knowledge, thanks to which he can not only easily decipher the conclusion to an ultrasound of the heart, but also make a diagnosis based on it and prescribe treatment. For this reason, deciphering the results of such a complex study as ECHO-cardiography should be provided to a specialized specialist, rather than trying to do it yourself, poking around for a long time and unsuccessfully with the numbers and trying to understand what certain indicators mean. This will save you a lot of time and nerves, since you will not have to worry about your probably disappointing and, even more likely, incorrect conclusions about your health.

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Echocardiography (EchoCG) is a method for studying morphological and functional changes in the heart and its valve apparatus using ultrasound.

The echocardiographic research method allows:

• Quantitatively and qualitatively assess the functional state of the LV and RV.
• Assess regional LV contractility (for example, in patients with coronary artery disease).
• Assess LVMM and identify ultrasound signs of symmetric and asymmetric hypertrophy and dilatation of the ventricles and atria.
• Assess the condition of the valve apparatus (stenosis, insufficiency, valve prolapse, presence of vegetations on the valve leaflets, etc.).
• Assess the level of pressure in the PA and identify signs of pulmonary hypertension.
• Identify morphological changes in the pericardium and the presence of fluid in the pericardial cavity.
• Identify intracardiac formations (thrombi, tumors, additional chords, etc.).
• Assess morphological and functional changes in main and peripheral arteries and veins.

Indications for echocardiography:

• suspicion of acquired or congenital heart defects;
• auscultation of heart murmurs;
• febrile states of unknown cause;
• ECG changes;
• previous myocardial infarction;
• increased blood pressure;
• regular sports training;
• suspicion of a heart tumor;
• suspected thoracic aortic aneurysm.

Left ventricle

The main causes of local disturbances in LV myocardial contractility:

• Acute myocardial infarction (MI).
• Post-infarction cardiosclerosis.
• Transient painful and silent myocardial ischemia, including ischemia induced by functional stress tests.
• Constant ischemia of the myocardium, which has still retained its viability (the so-called “hibernating myocardium”).
• Dilated and hypertrophic cardiomyopathies, which are often also accompanied by uneven damage to the LV myocardium.
• Local disturbances of intraventricular conduction (blockade, WPW syndrome, etc.).
• Paradoxical movements of the IVS, for example, with volume overload of the RV or bundle branch blocks.

Right ventricle

For shortness of breath, swelling of the extremities.

When fainting.

In the event that a person is often bothered by dizziness.

If there is a suspicion of a heart tumor.

For angina pectoris.

After a heart attack, etc.

Research in relation to pregnant women

A safe and universal method for detecting heart problems is called echocardiography. What does it mean? There is only one thing - it can be carried out in relation to all categories of the population, both adults and children. This study is even prescribed to pregnant women. And it is done in order to detect cardiac pathology in the fetus and take the necessary measures to save the baby. EchoCG is absolutely harmless for both mother and baby.

Pregnant women must undergo this research method in the following situations:

If the woman in labor had a history of heart defects.

The previous pregnancy ended in miscarriage.

If a woman has diabetes.

During pregnancy, the expectant mother contracted rubella.

If a woman took antibiotics or antiepileptic drugs in the 1st or 2nd trimester.

Differences between ECG and EchoCG

The first is like electrocardiography.

Echocardiography means nothing more than echocardiography. What is this procedure and how is it different from the first? It is also called ultrasound of the heart. The differences are as follows:

Similarities of EchoCG and ECG

Both research methods can assess the size. For example, enlargement of the right or left atrium can be detected using these diagnostic methods.

Also, both methods can detect the abnormal location of the body’s “engine”.

Swelling of the heart muscle and inflammation of surrounding tissues can also be detected using these diagnostic methods.

Advantages and disadvantages of each method

ECG is an affordable research option. However, it cannot always show a clear picture of the problem, unlike heart ultrasound. What EchoCG will clearly show are structural abnormalities. This research method ensures the accuracy of the image; this method is more reliable in determining the health of this internal organ. The advantage of cardiac ultrasound is that the specialist can visually observe its chambers. However, this diagnostic method has one drawback: it is performed only in private clinics, and the cost is several times more expensive than an ECG.

Boundary parameters of cardiac echocardiography

After an ultrasound of this organ is performed, the specialist who conducted the study will definitely refer the person to a cardiologist so that he can interpret the results. In order not to worry once again, not to stress yourself out, in the table below you can familiarize yourself with the borderline permissible values:

These are the main values ​​that the doctor pays attention to when viewing an ultrasound.

Echocardiography: interpretation of results

Only a cardiologist can correctly read, understand and explain to the patient the results of this diagnostic method. Independent study of the basic parameters of cardiac indicators does not provide a person with complete information on assessing the state of his health. But for peace of mind, the patient can familiarize himself with those described above. Only an experienced doctor in the field of cardiology can correctly decipher the result of the device’s operation, as well as answer the patient’s questions.

It also happens that some indicators deviate from the norm and are recorded in the examination protocol under other points. This suggests that the quality of the device is not very good. If a medical institution uses modern equipment, then the echocardiography doctor will receive more accurate results, on the basis of which the patient will be diagnosed and treated.

What diseases can be diagnosed using echocardiography?

Thanks to this method, many problems can be identified. This:

Heart failure.

Rheumatism.

Ischemic disease.

Heart tumor.

Vegetovascular dystonia.

Myocarditis.

Myocardial infarction.

Arterial hypertension.

Hypotension.

Congenital or acquired heart defects.

Heart tumor.

Methods of performing ultrasound

Echocardiography diagnostic methods have the following:

Transthoracic technique.

Transesophageal ultrasound.

The first diagnostic method is the most common because it has been used for a long time. The transthoracic technique for detecting cardiac problems is carried out through the chest using a sensor that is pressed against the patient's body in the area of ​​the heart. During the procedure, the patient is on the couch in a position lying on his side or back.

Transesophageal echocardiography - what is this research method and how is it performed? This is also a method of ultrasound diagnosis of the heart. However, it is carried out not from the surface of the chest, as with the transthoracic technique, but from the esophagus. The sensor is located exactly there; thanks to this method, the doctor can get as close to the heart as possible, and also see those parts of it that are not visible with a standard ultrasound.

Cost of the procedure

Not all public clinics and hospitals can boast that they can offer a heart examination method such as echocardiography. Prices for this procedure in private clinics range from 2200-3000 rubles. It all depends on the prestige of the hospital, the qualifications of the doctor, the availability of modern equipment, and the location of the medical institution that provides paid services. In Moscow, for example, it will be more expensive to do an echocardiography than in Voronezh.

If we compare the price of an ultrasound and an ECG, then in the latter case a person will have to pay up to 700 rubles. Moreover, electrocardiograms are often performed free of charge in public hospitals.

Preparing for a transesophageal examination

Echocardiography is done on an outpatient basis. Several hours before the procedure, the patient should abstain from water and food. Also, a person should not drink coffee or consume other products containing caffeine the day before the ultrasound (chocolate, strong tea). It is also necessary to stop taking medications that contain a component such as nitroglycerin. Even before the procedure, the specialist should ask if the patient has dentures. They must be removed before echocardiography.

Performing transesophageal ultrasound of the heart

Preparation and performance of transthoracic ultrasound

In this case, no planned actions are necessary. The procedure is performed in this order:

1. The patient undresses to the waist and lies down on the couch.

2. The specialist applies a special gel to the left side of the chest. This is necessary so that ultrasonic waves are better transmitted.

3. Then the healthcare worker places the sensor on the chest area and notes all the data.

4. After the procedure, the specialist processes all the information received and after a few minutes gives a written conclusion to the patient. On the document, a person can read about what tentative diagnosis the doctor gave him. But this does not mean that we can put an end to this. With the result of the ultrasound, the patient must consult a cardiologist.

Contraindications

In general, cardiac echocardiography is a completely harmless procedure. But due to some anatomical features of patients, problems may arise due to insufficient penetration of ultrasound by the transesophageal method. This can happen, for example, with chest deformation, the presence of pronounced hair in men, obesity, or large breast size in women.

In the following situations, performing an ultrasound of the heart is unacceptable:

If a person has a stomach ulcer or acute gastritis.

The patient has a tumor of any severity.

In this case, transesophageal ultrasound of the heart is not performed. Only transthoracic echocardiography is allowed.

Conclusion

From the article you understood that a synonym for the concept of echocardiography is ultrasound. Both words refer to the same process. Cardiac echocardiography is an accurate research method that allows us to identify various diseases of this organ even in the initial stages. Transthoracic ultrasound can be performed on absolutely all patients. While transesophageal echocardiography is used infrequently, since in this case a camera with an endoscope is inserted through the esophagus.

Almost all organs in the human body are paired. But there is only one heart and it begins to work long before we are born.

Life goes on, the heart beats, and at some point - an ambulance, flashing lights, a cardiology hospital and a disappointing diagnosis. Or maybe there is no person! It's sad, but many heart diseases can be diagnosed early. An accurate, painless examination is ultrasound diagnostics of the heart and blood vessels.

Carrying out echocardiography

Echocardiography with Dopplerography, as this procedure is correctly called, is used in the diagnosis and treatment of various diseases.

Who is indicated for cardiac ultrasound?

The study is carried out for all age categories of patients - from newborn toddlers to adult patients and pregnant women. If there is a suspicion of any pathology of the heart muscles or blood vessels, then you can undergo this study without waiting for an emergency.

• Planned events:
  • infants - if the expectant mother did not undergo a routine ultrasound or if congenital malformations are suspected;
  • teenagers – during a period of intensive growth;
  • pregnant women - to resolve the issue of independent delivery in case of chronic heart disease;
  • athletes – to assess the state of the cardiovascular system.
• Diagnosis of pathologies of the endocardium and valve apparatus:
  • arrhythmias – tachycardia, bradycardia;
  • threatening or existing heart attack;
  • ischemic disease;
  • oncopathology of the heart;
  • disturbances of cardiac activity due to alcoholic, toxic, endocrine intoxication.

Angina attack

• Pericarditis of various origins;
• Hypertension;
• Heart failure;
• Dynamic observation during the treatment of heart diseases or organ surgery.

• history of diabetes mellitus;
• heart defects in the patient and immediate family;
• rubella during pregnancy or high levels of antibodies in the test for TORCH infections;
• miscarriage of unknown origin;
• taking anticonvulsants during pregnancy in the 1st and 2nd trimesters;
• before planning a pregnancy after suffering from influenza, sore throat, or cardiac diseases.

Pregnant woman consulting with a cardiologist

Many clinics do not require a doctor's referral to undergo the procedure. It is enough to be mentally prepared and you can contact ultrasound diagnostic specialists through a family doctor, therapist or cardiologist.

There is no special preparation for cardiac ultrasound. Before the procedure, the patient is allowed to eat, walk, and drink his favorite drinks. You should only give up alcohol, coffee, and strong tea. The active substances in these products may cause vasospasm.

If you are taking any cardiac medications, please notify your doctor before the procedure. This will distort the results of the study.

Echocardiography technique

Ultrasound of the heart makes it possible to evaluate:

• linear dimensions of the organ and its parts;
• the thickness of the walls of the organ, its components and the integrity of the external areas;
• gives a clear picture of the tissue structure, the presence of perforations in different areas;
• condition of the valves, their contractility;
• blood flow in the aorta and other vessels;
• integrity of the walls of the aorta and other vessels;
• blood pressure, direction of its movement in the heart;
• assess the functioning of the pericardium.

The manipulation takes place in a lying position on your back or on your left side in front of the doctor. The study lasts no more than 20 minutes. Before manipulation, be sure to remove all jewelry - chains, crosses, earrings from the area being examined.

The patient's position during echocardiography is on the left side

There are no strict regulations on the frequency of ultrasound examinations. During the procedure, there is no radiation or other load on the organ. Therefore, you can undergo the study as needed and even several times a week.

Ultrasound of the heart during pregnancy is performed for the mother at any stage according to indications. This procedure will not harm the unborn child. If it is necessary to conduct a study of the fetal heart, it is better to do this at 18 weeks. It is not worth doing a special ultrasound for the future toddler, since examination of the organ and its components is included in the mandatory examination protocol for a woman at 18–19 weeks.

For each subsequent ultrasound, you must take a transcript of the previous study. This will allow the doctor to see the process over time and draw correct conclusions about the results of treatment.

Ultrasound of the heart - how to decipher the results?

Based on the study, the doctor draws up a conclusion. Results may depend on the patient's gender and age.

Decoding the data obtained is not the final diagnosis! The ultrasound diagnostic doctor transmits the conclusion to the cardiologist. And only he, based on complaints, transcripts of tests, and electrocardiogram data, can draw accurate conclusions!

The final diagnosis is made by a cardiologist

Normal indicators for an adult are presented in the table:

Pieces of the heart	Indicator name	Normal values
Left ventricle	Weight of the heart muscle - myocardium	Men – from 135 to 182 g Women – from 95 to 141 g
	Myocardial weight index	Men - from 71 to 94 g/m2 Women – from 71 to 89 g/m2
	End diastolic size	46–57.1 mm
	End systolic size	31–43 mm
	Wall thickness in the diastolic phase - at the moment of relaxation	Within 11mm
	Ejection fraction - the ratio of the volume of blood pushed into the vessels at the time of contraction to the total volume in the heart	From 55 to 60%
	Stroke volume - shows how much blood is pushed into the vessels at the moment of muscle contraction	From 60 to 100 ml
Right ventricle	From 9 mm
	Normally, there should be no vegetations or neoplasms on the valves

The interpretation of these parameters indicates the amount of sagging of the valve during the closing of its valves. Only ultrasound gives these values. Valve prolapse cannot be diagnosed using other methods!

Interpretation of indicators for the pericardium is the absence of fluid. The thickness of the wall of the aorta - the vessel leaving the heart - ranges from 2.1 to 4.1 mm.

The doctor must make a conclusion on 2 sheets. In part 1, a visual picture with the presumed diagnosis is described. Part 2 of the conclusion describes the decoding of all parameters of the human heart. Without the latter, the study can be considered invalid!

Ultrasound of the heart is a procedure that it is advisable for every person to undergo at least once in their life. Love your flame motor and it will serve you for a lifetime!

(Ultrasound) helps to identify myocardial diseases at an early stage of development and confirm the expected diagnosis, identify existing complications, and evaluate the results of the course of treatment. This diagnostic method allows you to most accurately assess the condition of the heart and its structures. The main indications for ultrasound of the heart are: rapid heartbeat, difficulty breathing, heart pain, increased blood pressure, edema. This study is also prescribed for listening to heart murmurs, suspicions of cardiovascular diseases, cardiac tumors, for pathologies identified by ECG, after heart surgery, and heart attacks.

Ultrasound of the heart in early pregnancy helps determine the viability of the embryo, and after the sixth week helps determine the frequency of fetal heart contractions. Interpretation of ultrasound of the myocardium is needed to assess contractility and determine its resistance to increased loads. Using cardiac ultrasound, you can find out the volume of myocardial cavities, muscle mass, wall thickness, the presence of scars, blood clots, and heart rate.

Normal cardiac ultrasound findings

Each myocardial ultrasound report contains data on the following indicators. The normal weight of the left ventricle in men should be 135-182 grams, in women - 95-141 grams. The normal left ventricular mass index is 71-94 g/m2 in men and 71-89 g/m2 in women. Normally, the end-diastolic volume of the left ventricle in men is 112±27 (65-193) milliliters, in women 89±20 (59-136) milliliters. In the left ventricle, the normal end-diastolic size should be 4.6-5.7 centimeters, and the normal end-systolic size is 3.1-4.3 centimeters, and the wall thickness in diastole should be 1.1 centimeters.

The normal ejection fraction is 55-60 percent, and the volume of blood ejected per contraction by the left ventricle (stroke volume) is 60-100 milliliters. In the absence of pathologies, the dimensions of the right ventricle should be as follows: wall thickness - 3-5 mm, size index - 0.75-1.25, diastolic size - 0.95-2.05 centimeters. The interventricular septum should normally be as follows: its thickness at rest is 0.75-1.1 centimeters, movement from side to side during contractions (excursion) is 0.5-0.95 centimeters.

To determine the condition of the right atrium, only the EDV value is determined - the volume at rest, its normal value is 110-145 ml. The normal parameters of the left atrium are 1.85-3.3 centimeters, the size index should be 1.45-2.9. Deviations from these indicators indicate any pathological conditions or functional disorders of the heart.

Ultrasound of the heart, in other words, echocardiography, is carried out to identify abnormalities in the development of the organ and its organ. Periodic pain in the left hypochondrium requires an immediate visit to a cardiologist, who will prescribe an ultrasound of the heart and interpret it. The procedure itself is completely safe.

How is an ultrasound of the heart done?

To perform a cardiac ultrasound procedure, you can go to a medical facility yourself. A doctor's referral is not required for this diagnosis. Before starting the procedure, the specialist will ask you to undress to the waist and lie on your left side. The diagnostician will first apply a special conductive gel to the body, and then use a sensor to record the data necessary to interpret the ultrasound of the heart.

What does an ultrasound of the heart show?

Ultrasound of the heart is considered the most informative and safe method for determining the condition of the main human organ. This procedure will help determine in a person:

• organ size;
• absence or presence of scars;
• condition of all valves;
• thickness of external walls;
• stroke volume of the heart chambers;
• frequency of contractions;
• aortic diameter;
• percentage of blood ejection fraction.

Interpretation of cardiac ultrasound results

Upon completion of the cardiac ultrasound, the doctor who conducted the examination will provide a transcript in the form of a conclusion. If there are deviations from the norm, then after an ultrasound of the heart you need to visit a specialist to prescribe treatment.

Having the conclusion of the study in hand, you can independently decipher an ultrasound of the heart in an adult. But without medical education, this information can only be used to understand the general picture of the condition of the organ. The data specified in the protocol must be compared with normal cardiac ultrasound indicators:

If a slight deviation from the norm is detected according to the results of a cardiac ultrasound, then you need to understand that the outcome of the examination can be influenced by gender, age, and general health. Only a cardiologist can make an accurate diagnosis. An emergency visit to a specialist will help solve problems and begin treatment if necessary.

A distinctive feature is that with this hypertrophy the size of the ventricular cavity remains unchanged (OTS 45 mm). This disease is a consequence of other pathologies in the human body.

The main causes and symptoms of the disease

Reasons for the development of concentric hypertrophy of the left ventricle:

• high blood pressure;
• high peripheral resistance;
• increase in afterload.

Arterial hypertension most often causes concentric hypertrophy of the left ventricle. An increase in the mass and size of the left ventricular myocardium, which was formed as a result of high blood pressure, occurs in 65-70% of cases of all hypertrophies.

Most often this develops in athletes. The increase in size occurs due to an increase in myofibrils and mitochondria in the heart muscle.

What the disease threatens

Angina occurs due to the fact that the myocardium of the heart increases in size, and, as a rule, this happens unevenly. Coronary vessels often undergo compression. Angina pectoris is characterized by chest pain of a squeezing or pressing nature, irregular and rapid pulse, and increased blood pressure. You can relieve pain from angina pectoris with the help of nitrates. Short-acting nitroglycerin eliminates pain within a few minutes.

Atrial fibrillation is a disorder of the rhythm and frequency of the heart. Concentric myocardial hypertrophy develops with atrial fibrillation due to compression of the nerve fibers conducting the impulse by the enlarged heart muscle. Atrial fibrillation has very terrible consequences. So, during this rhythm disturbance, an increase in heart rate up to 200 beats per minute or more is observed. The heart does not have time to fill with blood in full. The blood is not enriched with oxygen, and an insufficient amount of it enters the myocardium through the coronary vessels. Oxygen starvation of cardiomyocytes occurs, which threatens dystrophic cardiomyopathy. There is no treatment for such heart dystrophy, only organ transplantation.

Thrombosis is another of the unpleasant complications of atrial fibrillation. Due to insufficient blood pumping, blood clots often form on the valves, as well as on the walls of the heart chambers. They arise as a result of damage, and subsequently the adhesion of red blood cells. A blood clot can break away from its attachment point in any situation and clog any vessel in the human body. Most often these are cerebral vessels - and this is a stroke - or pulmonary artery vessels (PE), which is practically a fatal diagnosis.

Ventricular fibrillation is a disturbance in the frequency and rhythm of heart contractions that threatens human life. The impulses entering the heart become unstable and intermittent, and then the ventricular myocardium, under their influence, begins to contract unevenly and, most importantly, ineffectively at tremendous speed.

This condition is acute and must be treated urgently. So, after a few seconds of fibrillation, a person loses consciousness, and if he is not helped within 5 minutes, this will lead to irreversible conditions in the brain due to damage to neurons due to oxygen starvation. Therapy can only be carried out by a specialist. This requires a defibrillator and some knowledge. Using a defibrillator, a huge shock is applied to the heart muscle, which changes the pathological charge of impulses to normal.

Unstable blood pressure - changes in blood pressure readings. This symptom develops due to compression of nerve fibers by hypertrophied myocardium. Instability of pressure leads to poor health, headaches, and sometimes loss of consciousness.

Dyspnea is a violation of the frequency and depth of breathing during physical activity, and with the progression of left ventricular myocardial hypertrophy at rest, “lack of air” occurs. A person cannot breathe, leans against the back of a chair or bed to facilitate the work of the pectoral muscles, and very often shortness of breath during hypertrophy is secondary, because it is not directly related to lung disease.

Due to disruption of the heart muscle (increased frequency, rhythm disturbance), blood that is not sufficiently saturated with oxygen enters the brain. There are sections called the respiratory center that respond to decreased oxygen levels by sending nerve impulses to the lungs and pulmonary muscles, causing them to breathe more.

However, an increase in breathing frequency leads to the fact that the lungs do not have time to fill with air, and breathing becomes shallow and ineffective. All this only makes the situation worse. Treatment consists of oxygen administration and fluid resuscitation.

Correct treatment of LVH

Treatment of concentric hypertrophy of the left ventricle should be complex and quite long in time.

Firstly, therapy should be aimed at eliminating the causes that provoked this pathology. Treatment of hypertrophy in arterial hypertension involves stabilizing blood pressure at normal values ​​through the constant use of antihypertensive drugs. Therapy for high peripheral vascular resistance is aimed at eliminating this pathology with medications.

Secondly, treatment of LVH is to slow down the processes of ventricular myocardial hypertrophy. This can be achieved by organizing the right lifestyle.

The right lifestyle consists of proper nutrition, adherence to its regimen, as well as sleep and rest patterns. It is necessary to add moderate physical activity every day.

Nutrition, of course, plays a special role in treatment. Products should be rich in polyunsaturated fats, which reduce the risk of developing atherosclerosis, and rich in vitamins and microelements. You should definitely lose weight, especially if you are obese. Thus, obesity itself is one of the mechanisms in the development of concentric hypertrophy of the left ventricular myocardium. There is more blood in the body of a fat person, and it should be pumped more often and faster, and this is an additional load on the heart muscle.

Among physical activities, it would be better to give preference to swimming or aerobics.

In any case, you can engage in physical activity only after consulting your doctor. And giving up bad habits has a significant positive effect on the entire body as a whole.

Thirdly, drug therapy. Concentric hypertrophy of the left ventricle, like other pathologies, cannot but have drugs in its treatment regimen. First of all, it is necessary to remember that if, after all the examinations, a diagnosis of GHL is made and pharmacological treatment is prescribed, then the therapy should continue for life! Most often, cardiologists use antiarrhythmic drugs (verapamil) and beta-blockers (enalapril) in their prescriptions.

If all of the above measures do not bring results, then in some cases doctors recommend surgical treatment. The operation involves removing a hypertrophied area of ​​the heart muscle. This surgical intervention is quite complex and risky, so it is used only in exceptional cases.

• Arrhythmia
• Heart disease
• Bradycardia
• Hypertension
• Hypertension
• Pressure and pulse
• Diagnostics
• Other
• Heart attack
• Ischemic disease
• Traditional medicine
• Heart defect
• Prevention
• Heart failure
• Angina pectoris
• Tachycardia

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Left ventricular myocardial mass is increased

The human body is characterized by the ability to quickly adapt to various changes in the functioning of the circulatory system. In most hypertensive patients, due to a persistent increase in blood pressure, a compensatory increase in the left ventricle occurs, which is fraught with loss of tissue elasticity with weakening of the cardiac septum. Myocardial hypertrophy is not a separate diagnosis, since it is only a general symptom of cardiac pathologies that require the body to constantly activate compensatory mechanisms.

Causes and pathogenesis

Regular physical and hemodynamic stress, forcing the heart to work harder than usual, over time leads to an increase in the mass of the myocardium, in particular the left ventricle. With arterial hypertension, muscle fibers are forced to contract harder to counteract the pressure in the circulatory system. Heart defects, as well as excessive physical activity, have a similar effect.

The following factors can lead to left ventricular hypertrophy:

• hypertension with persistent increase in blood pressure;
• endocrine pathologies (diabetes mellitus, obesity);
• conduction and heart rhythm disturbances;
• atherosclerotic changes in blood vessels;

Left ventricular myocardial hypertrophy is the growth and increase in muscle mass of this wall of the heart, which leads to a change in the shape and size of the entire organ.

• coronary heart disease;
• aortic stenosis;
• chronic stress;
• physical inactivity;
• prolonged overexertion, lack of proper rest;
• peripheral circulatory disorders;
• intense physical training;
• systemic diseases of connective and muscle tissue;
• presence of bad habits (smoking, alcohol).

Benign LVMH is common to many athletes who intensively train endurance. Less common is idiopathic cardiomyopathy, which is caused by a genetic predisposition.

People who have experienced myocardial infarction are more likely to experience hypertension with subsequent compensation of cardiac activity due to an increase in healthy muscle fibers of the heart.

Signs of left ventricular myocardial hypertrophy

Slow and uneven enlargement of the heart muscle, which can develop over years, is often characterized by a blurred clinical picture. Many people first learn about the presence of LVH only during a routine examination with detailed visualization of the chambers of the heart. Other variants of moderate myocardial hypertrophy are accompanied by pronounced symptoms, presented in the form of arrhythmia, angina pectoris, shortness of breath, and cyanosis.

Severe left ventricular hypertrophy is accompanied by shortness of breath and chest pain, as well as a feeling of palpitations and interruptions in heart function.

The most common signs indicating compensatory enlargement of the left ventricle include:

• chest pain, the pathogenesis of which is associated with compression of the coronary vessels that provide oxygen to the myocardium;
• a violation of the heart rhythm, which, due to its nature, can vary greatly in different patients: some patients experience severe tachycardia, others note interruptions in the functioning of the heart or atrial fibrillation;
• a feeling of lack of oxygen and rapid fatigue become frequent companions of left ventricular hypertrophy, since increased myocardial contractions due to increased muscle fibers lead to chronic fatigue due to overstrain of the circulatory system;
• changes in blood pressure, which most often consist of persistent hypertension, can be both a consequence of left ventricular hypertrophy and its true cause;
• a pressing headache that occurs against the background of spasm of cerebral vessels significantly affects the general well-being of the patient, and ischemia of brain tissue over time contributes to the development of chronic dizziness and impaired visual acuity.

The clinical picture of the disease largely depends on the cause that caused myocardial hypertrophy. If we are talking about renal hypertension, then the above symptoms are added to frequent urination and pain in the lumbar region. In case of myocardial infarction, which has caused a compensatory increase in healthy areas of the heart, cardiac arrhythmias and signs of tissue ischemia will predominate.

Also, in the stage of decompensation, the patient may experience episodes of cardiac asthma, since the myocardium of the left ventricle is not able to pump the required amount of blood

Treatment and diagnosis

Since myocardial enlargement is not an independent disease, its manifestations must be combated solely by eliminating the real cause of hypertrophy. To reduce the load on an overstrained heart, drugs of various pharmacological groups, including vitamin complexes, are used.

Before starting treatment, you need to undergo a thorough diagnosis, which includes: a series of laboratory tests, research on biochemical markers of a heart attack, electrocardiography, ultrasound of the heart.

Groups of drugs for the correction of cardiac activity in case of left ventricular myocardial hypertrophy:

• beta-blockers (“Atenolol”, “Propranolol”) – inhibit the effect of catecholamines on the myocardium, resulting in a decrease in blood pressure and a decrease in heart rate;
• ACE inhibitors – block the activity of angiotensin-converting enzyme, helping to correct blood pressure in arterial hypertension of renal origin (Captopril, Enalapril);
• blockers of slow calcium channels - inhibit the penetration of Calcium ions from the intercellular space into the heart cells, thereby significantly reducing the load on the myocardium (Verapamil);
• cardiac glycosides (preparations of digitalis, adonis, lily of the valley) and cardiotonics (“Dopamine”, “Dobutamine”) - help normalize heart contractions, relieve muscle tension, remove spasm of coronary vessels, equalize the frequency and rhythm of heart contractions;
• angioprotectors (“Rutin”, “Troxerutin”, vitamin C) – protect blood vessels from the pathogenic effects of free radicals, make them more resistant to ischemia, and help improve trophism with further restoration of the weakened vascular wall.

Depending on the presence and area of ​​affected areas on the heart, blood pressure levels and the general condition of the body, adequate treatment is selected. In some cases, taking medications may be sufficient to reduce the load on the myocardium and normalize pressure. Severe lesions of the heart and coronary vessels are corrected surgically. To prevent left ventricular myocardial hypertrophy, you need to carefully monitor your blood pressure, regularly visit a cardiologist and resort to appropriate medical tests.

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We were diagnosed with a weakened heart septum, while blood pressure and general body condition were normal. We don’t know what to do, maybe the child will become too tired...

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Myocardial hypertension

Causes and methods of treatment of myocardial hypertrophy

Left ventricular myocardial hypertrophy is a disease that means that the mass of the heart muscle has increased. It is often a consequence of hypertension, so it manifests itself in almost all patients who suffer from hypertension. At the initial stage, this is how the body reacts to increased pressure. Is an increase in myocardial mass so bad?

If we talk about the muscles of the legs and arms, for them this thickening during increased load is a completely positive phenomenon. With the heart muscle, the situation is completely different: the vessels that nourish the heart cannot grow as quickly as muscle mass. For this reason, his nutrition suffers, especially when the load on him increases. It is also worth considering the fact that there is a conducting system in the heart, which, one might say, does not grow. Because of this, zones of abnormal activity and conductivity develop. The consequence of this is numerous arrhythmias.

Concentric hypertrophy often results in an increased myocardial oxygen demand. A number of factors come into play here.

Focal necrosis and ischemia develop due to a failure of blood flow in the capillaries, which occurs due to the fact that the size of the muscle fibers reaches a critical level. It is believed that the weight of the heart in this case is twice the normal value. The following situation is observed: in relation to the volume of the myocardium, the surface area of ​​the capillaries decreases, but the distance between the capillaries and the muscle cell increases. In this regard, the myocardium requires 50 percent more oxygen than usual. This means that any deficiency in its supply makes the situation even worse. Patients live with this heart condition for decades. Therefore, it may seem that there is nothing to be afraid of. Despite this, it is worth recognizing the fact that the risk of consequences and complications in those who have hypertrophy is much higher compared to those who do not have such a diagnosis. Therefore, if this particular disease does not cause any particular inconvenience, then it can easily arise due to complications arising as a result of it. In addition to hypertension, there are other causes of this disease. Let's look at them below.

Causes and symptoms

One of the causes of the disease may be renal pressure

Hypertrophy may occur due to renal hypertension. In this case, the left ventricle is often affected. This can be considered an occupational disease of athletes. Sometimes they may develop right ventricular hypertrophy. There may be other reasons for the development of the disease. Depending on which part of the heart is affected by hypertrophy, the reasons may be different:

• cardiomyopathy; hypertrophic cardiomyopathy is characterized by the fact that the ventricles of the heart thicken unnaturally, causing the heart to be subject to additional stress; This is mainly a hereditary disease;
• excess weight, since this factor has become increasingly evident in children, this makes them prone to such heart pathology;
• mitral valve stenosis or insufficiency;
• aortic stenosis;
• stress;
• pulmonary diseases; they reduce kidney function, which especially affects the left atrium;
• congenital heart defects; this is when the heart does not develop as it should during nine months of pregnancy; dysfunction is often associated with the mitral valve, pulmonary valve and tricuspid valve;
• ventricular septal defect; because of this, the blood of the two sections is mixed; there is not enough oxygen in such mixed blood that goes to tissues and organs; in order to restore good nutrition to the body, the two parts of the heart begin to work more intensely, and this is an additional burden.

Symptoms of cardiac hypertrophy depend on the cause that caused it. A common symptom is irregular heart rhythm. In addition, you may experience:

• difficulty breathing;
• chest pain;
• increased fatigue;
• difficulty performing physical exercises;
• dyspnea;
• dizziness;
• fainting;
• swelling of the lower extremities.

Diagnosis and treatment

Doctor performing echocardiography

Only a doctor can diagnose this disease. In addition to talking with the patient, he will prescribe additional examination, which may include echocardiography and ECG. After the examination, he will prescribe the necessary medications. In addition, treatment includes the following:

• getting rid of excess body weight. it helps lower blood pressure;
• quitting smoking;
• reducing salt consumption, which also helps reduce blood pressure;
• increasing physical activity, but only after discussing with your doctor;
• diet.

Yes, you shouldn’t be too afraid of hypertension, but you shouldn’t take this disease lightly either. If you keep everything under control, your health will not fail!

Left ventricular myocardial hypertrophy, what is it and how dangerous is it?

Left ventricular myocardial hypertrophy is an increase in the mass of the heart muscle. which eventually occurs in almost all patients with hypertension. It is detected mainly during an ultrasound of the heart, less often with an ECG. At the initial stage, this is an adaptive reaction of the body to high blood pressure.

Here we can draw an analogy with the muscles of the arms and legs, which thicken under increased load. However, if this is good for these muscle groups, then for the heart muscle not everything is so simple. Unlike biceps, the vessels supplying the heart do not grow as quickly as muscle mass, as a result of which the nutrition of the heart may suffer, especially under the existing increased load. In addition, there is a complex conduction system in the heart that cannot “grow” at all, as a result of which conditions are created for the development of zones of abnormal activity and conduction, which is manifested by numerous arrhythmias.

Regarding the issue of danger to life, it is certainly better not to have hypertrophy; numerous studies have shown that the risk of complications in patients with hypertrophy is much higher than in those without it. But on the other hand, this is not some kind of acute situation that urgently needs to be corrected; patients live with hypertrophy for decades, and statistics may well distort the real situation. You must do what depends on you - this is monitoring blood pressure, doing an ultrasound once or twice a year to monitor this situation over time. So myocardial hypertrophy is not a death sentence - it is a hypertensive heart.

Left ventricular myocardial hypertrophy

Myocardial hypertrophy is characterized by an increase in muscle mass in the heart and requires medical treatment, as well as changes in the usual way of life. Otherwise, this pathology can cause a stroke or myocardial infarction.

Against the background of hypertension, most patients experience an uncontrolled increase in the mass of cardiac muscle tissue. The resulting pathology is called myocardial hypertrophy and can be detected in its different parts. As you know, the organ has two atria, into which blood flows from the circulatory system, and two ventricles, designed to push blood into the vessels. Hypertrophy of each part of the heart has its own specific causes, characteristic symptoms and treatment.

The disease can be of two forms:

The second type is more common (more than 50%), having hypertrophy of the lower, middle or upper part of the left ventricle and interventricular septum (IVS). In this case, the thickening of the myocardial muscles in some areas can reach 50–60 mm.

Concentric hypertrophy is somewhat less common and accounts for about 30% of the total number of people suffering from this disease. Primary myocardial damage can be characterized by pronounced hypertrophy of the muscle of the left ventricle and, less commonly, the right. There is also a decrease in the size of the cavities, and the diastolic function of the ventricle is significantly impaired with frequent disturbances in heart rhythm.

As for right ventricular myocardial hypertrophy, this pathology is a fairly rare disease. Since the right side of the heart is very dependent on the functioning of the lungs, the reasons why it occurs must be sought in violations of the respiratory function. Therefore, treatment should include measures to normalize lung function, as well as eliminate pulmonary valve stenosis.

Left ventricular myocardial hypertrophy

Myocardial hypertrophy leads to modification of the walls of the left ventricle. As previously noted, the disease occurs against a background of persistently high blood pressure, which forces the left ventricle to work more intensively. Taking into account heavy loads, the wall of the left ventricular chamber and the interventricular septum gradually increase in volume, thereby losing their elasticity. Ultimately, they slow down blood circulation and the heart loses its ability to function normally.

In this case, there is a danger of sudden and intense stress that myocardial tissue can receive if a person leads a sedentary lifestyle or abuses bad habits.

Of course, myocardial hypertrophy is not fatal and people live with this pathology for decades, but in any case this does not make it a safe disease. Without paying attention to the symptoms that arise from time to time and ignoring the necessary treatment, the modified condition of the left ventricle can cause a stroke or myocardial infarction.

Symptoms

Moderate hypertrophy of the myocardial tissue of the left ventricle and interventricular septum is characterized by heterogeneity of manifestations. In some cases, the disease may not manifest itself in any way for many years, and the patient may not realize that he has a pathology in the heart. However, we cannot exclude the possibility that the patient’s well-being for unknown reasons begins to deteriorate. In this case, treatment must be started immediately.

The most common symptom of left ventricular hypertrophy is angina, which occurs due to compression of the heart muscle vessels. As a result, it increases and the need for more oxygen and nutrients increases. In addition to this symptom, against the background of emerging heart pathology, atrial fibrillation, atrial fibrillation, and myocardial starvation occur.

Symptoms accompanying left ventricular hypertrophy:

1. Periodic pain in the chest and heart area.
2. Higher than normal blood pressure.
3. Pressure surges.
4. Arrhythmia.
5. Headaches.
6. Dyspnea.
7. Sleep disturbance.
8. Weakness and poor health.

As practice shows, moderate left ventricular hypertrophy can become a symptom indicating and characterizing the course of the following diseases:

• Heart failure.
• Congenital heart defect.
• Atherosclerosis.
• Pulmonary edema.
• Acute glomerulonephritis.
• Myocardial infarction.

Treatment

Treatment of a modified condition of the left ventricular myocardial tissue and interventricular septum should be carried out under constant medical supervision. It will also be necessary to eliminate the causes that provoke the deterioration of the patient’s condition. The main task with this diagnosis is to reduce the size of the left ventricle of the heart to its natural volume. In this case, treatment should have an integrated approach.

In addition to drug therapy, the patient must change his usual lifestyle, which will allow for more successful treatment. First of all, in the patient’s diet it is necessary to reduce salt intake, alcohol consumption, eliminate foods and dishes high in fat, as well as smoked and fried foods.

Unfortunately, in some cases, drug treatment may not produce positive results, then surgery is prescribed, during which a section of the heart muscle of the left ventricle or the interventricular septum is removed.

Left ventricular myocardial hypertrophy

Left ventricular myocardial hypertrophy is the growth and increase in muscle mass of this wall of the heart, which leads to a change in the shape and size of the entire organ or thickening of the interventricular septum. This pathology is usually detected accidentally during an Echo-CG or ECG. This symptom of many diseases can go completely unnoticed for a long time and be a harbinger of serious diseases or pathologies of the heart. Also, such a dangerous condition of the myocardium, in the absence of adequate and timely treatment, can lead to an increased risk of myocardial infarction or stroke, and therefore to death. According to statistics, deaths due to left ventricular hypertrophy are observed in 4% of cases.

Reasons

In most cases, left ventricular hypertrophy is a consequence of hypertension or long-term arterial hypertension caused by other diseases. It can occur in two forms:

• asymmetric hypertrophy: observed more often (in almost 50% of cases) and is characterized by thickening of the myocardium in the lower, upper or middle part of the left ventricle and the septum between the right and left ventricles, while the thickness of the myocardium in some areas can reach 60 mm;
• concentric (or symmetric) hypertrophy: observed in approximately 30% of patients with this pathology and is characterized by a pronounced change in the left ventricle, accompanied by a decrease in its volume, disturbances in heart rhythm and ventricular diastolic function.

Predisposing factors for an increase in the size and mass of the left ventricle may be:

• congenital heart defects: stenosis or coartication of the aorta, pulmonary artesia or hypoplasia of the left ventricle, lack of communication between the right atrium and the ventricle, single ventricle of the heart, common aortic trunk;
• acquired heart defects: mitral regurgitation, narrowing (stenosis) of the aortic valve;
• cardiomyopathy;
• intense and prolonged physical activity (among athletes or people whose profession involves intense physical activity);
• Fabry disease;
• atherosclerosis;
• obesity;
• diabetes mellitus;
• adynamia;
• sudden intense physical activity;
• sleep apnea (often observed in postmenopausal women and men);
• smoking, alcoholism, etc.

The formation of left ventricular hypertrophy is caused by difficult or impaired outflow of blood from the heart into the systemic circulation. As a result, the walls of the left ventricle are constantly under additional stress, and the adapting heart begins to “increase its mass” due to the growth of cardiomyocytes. The coronary vessels “do not have time” to grow as quickly as the myocardium, and the nutrition of the heart becomes insufficient. Also, due to an increase in the mass of the myocardium, zones of abnormal conductivity and activity can form in its thickness, which in turn leads to the development of arrhythmias.

In some cases, myocardial hypertrophy is also observed in absolutely healthy people (athletes or people engaged in heavy physical labor). It is caused by significant physical activity, which leads to intense work of the heart. In such cases, physiological hypertrophy of the left ventricle, subject to a rational exercise regime, as a rule, does not progress to the pathological stage, but the risk of developing various cardiovascular pathologies still increases.

Stages and clinical signs

The development of left ventricular muscle mass goes through three stages:

The most common symptom of left ventricular hypertrophy is:

• heart failure;
• congenital heart defects;
• atherosclerosis of coronary vessels;
• acute glomerulonephritis.

In the compensation stage, the left ventricle performs its functions well, and the patient does not feel myocardial hypertrophy at all. In such cases, hypertrophy of the heart wall may be accidentally detected during an ECG or Echo-CG.

When subcompensation occurs, the reason for contacting a cardiologist may be the following that appear after physical activity:

• increased fatigue;
• darkening of the eyes;
• muscle weakness;
• dyspnea;
• minor interruptions in heart function.

In some cases, the above-described signs of the subcompensation stage do not appear in healthy people, but develop only in people with existing heart defects or pathologies.

The symptoms of myocardial hypertrophy are most pronounced at the onset of the decompensation stage. They may manifest themselves with the following nonspecific signs:

• frequent drowsiness and increased fatigue;
• general weakness;
• sleep disorders;
• headaches;
• rapid heartbeat;
• instability of blood pressure;
• heart rhythm disturbances;
• cardialgia, reminiscent of angina attacks;
• pain in the chest area;
• dyspnea;
• muscle weakness.

More specific manifestations of left ventricular hypertrophy may include the following symptoms:

• swelling on the face in the evenings;
• decrease in pulse tension;
• atrial fibrillation;
• dry cough.

Also, in the stage of decompensation, the patient may experience episodes of cardiac asthma, since the myocardium of the left ventricle is not able to pump the required amount of blood, and blood stagnation forms in the pulmonary circulation.

Possible complications

Left ventricular hypertrophy can be complicated by the following serious consequences:

• myocardial infarction, angina pectoris;
• arrhythmia with ventricular fibrillation;
• heart failure;
• stroke;
• sudden cardiac arrest.

Diagnostics

To detect left ventricular hypertrophy, the following diagnostic examination methods are used:

• collection of medical history and analysis of patient complaints;
• percussion examination of the borders of the heart;
• chest x-ray;
• ECG with index calculation to determine the degree of hypertrophy;
• two-dimensional and Doppler Echo-CG;
• MRI of the heart;

With hypertrophic changes in the myocardium of the left ventricle, the following abnormalities may be detected on the electrocardiogram:

• increase in teeth SI, V6 and Rv I and III;
• the average QRS vector deviates to the right and forward;
• the time of internal deviations increases;
• deviation of the electrical axis to the left ventricle;
• myocardial conduction disorders;
• incomplete block of the His bundle;
• modifications of the electrical position;
• displacement in the transition zone.

Treatment

The main goal of treatment for left ventricular hypertrophy is aimed at eliminating the causes that cause it and reducing the size of the heart chamber. To do this, the patient is recommended to change his lifestyle and eliminate risk factors, drug therapy and, if necessary, surgical treatment.

Changing your lifestyle and eliminating risk factors

1. Blood pressure control. The patient is advised to regularly measure blood pressure.
2. Elimination of psycho-emotional tension and stressful situations.
3. Rational physical activity.
4. Quitting smoking and drinking alcohol.
5. Losing excess weight and preventing obesity.
6. Regular exercise and walks in the fresh air.
7. Reducing the amount of salt consumed, foods high in animal fats and fried, smoked, fatty and starchy foods.

Drug therapy

To correct arterial hypertension, the patient can be prescribed calcium channel blockers (Verapamil, Procardia, Diltiazem, etc.) in combination with beta-blockers (Carvedilol, Tenormin, Metopropol, etc.).

The complex of drug treatment may also include the following drugs:

• thiazide diuretics: Dichlorothiazide, Navidrex, Indal, Hypothiazide, etc.;
• ACE inhibitors: Capoten, Zestril, Enalapril, etc.;
• sartans: Valsartan, Teveten, Lorista, Mikardis, etc.

Surgical treatment

If drug therapy is ineffective, the patient may be indicated for the following types of surgical treatment:

• coronary stenting and angioplasty: used to eliminate the causes of myocardial ischemia;
• valve replacement: such operations are performed for valvular heart defects that have led to the formation of left ventricular hypertrophy;
• commissurotomy: performed when it is necessary to eliminate and dissect adhesions formed due to stenosis of the aortic mouth.

Left ventricular myocardial mass index is normal

General description

Echocardiography (EchoCG) is a method for studying morphological and functional changes in the heart and its valve apparatus using ultrasound.

The echocardiographic research method allows:

• Quantitatively and qualitatively assess the functional state of the LV and RV.
• Assess regional LV contractility (for example, in patients with coronary artery disease).
• Assess LVMM and identify ultrasound signs of symmetric and asymmetric hypertrophy and dilatation of the ventricles and atria.
• Assess the condition of the valve apparatus (stenosis, insufficiency, valve prolapse, presence of vegetations on the valve leaflets, etc.).
• Assess the level of pressure in the PA and identify signs of pulmonary hypertension.
• Identify morphological changes in the pericardium and the presence of fluid in the pericardial cavity.
• Identify intracardiac formations (thrombi, tumors, additional chords, etc.).
• Assess morphological and functional changes in main and peripheral arteries and veins.

Indications for echocardiography:

• suspicion of acquired or congenital heart defects;
• auscultation of heart murmurs;
• febrile states of unknown cause;
• ECG changes;
• previous myocardial infarction;
• increased blood pressure;
• regular sports training;
• suspicion of a heart tumor;
• suspected thoracic aortic aneurysm.

Left ventricle

The main causes of local disturbances in LV myocardial contractility:

• Acute myocardial infarction (MI).
• Post-infarction cardiosclerosis.
• Transient painful and silent myocardial ischemia, including ischemia induced by functional stress tests.
• Constant ischemia of the myocardium, which has still retained its viability (the so-called “hibernating myocardium”).
• Dilated and hypertrophic cardiomyopathies, which are often also accompanied by uneven damage to the LV myocardium.
• Local disturbances of intraventricular conduction (blockade, WPW syndrome, etc.).
• Paradoxical movements of the IVS, for example, with volume overload of the RV or bundle branch blocks.

Right ventricle

The most common causes of impaired RV systolic function:

• Tricuspid valve insufficiency.
• Pulmonary heart.
• Stenosis of the left atrioventricular orifice (mitral stenosis).
• Atrial septal defects.
• Congenital heart defects accompanied by severe pulmonary arterial hydrangea (for example, VSD).
• PA valve insufficiency.
• Primary pulmonary hypertension.
• Acute right ventricular myocardial infarction.
• Arrhythmogenic pancreatic dysplasia, etc.

Interventricular septum

An increase in normal values ​​is observed, for example, with some heart defects.

Right atrium

Only the value of the VDV is determined - the volume at rest. A value of less than 20 ml indicates a decrease in EDV, a value of more than 100 ml indicates its increase, and an EDV of more than 300 ml occurs with a very significant increase in the right atrium.

Heart valves

Echocardiographic examination of the valve apparatus reveals:

• fusion of valve leaflets;
• insufficiency of one or another valve (including signs of regurgitation);
• dysfunction of the valve apparatus, in particular the papillary muscles, leading to the development of prolapse of the valves;
• the presence of vegetation on the valve flaps and other signs of damage.

The presence of 100 ml of fluid in the pericardial cavity indicates a small accumulation, and over 500 - a significant accumulation of fluid, which can lead to compression of the heart.

Norms

Left ventricular parameters:

• Left ventricular myocardial mass: men -g, women -g.
• Left ventricular myocardial mass index (often referred to as LVMI on the form): men g/m2, women g/m2.
• End-diastolic volume (EDV) of the left ventricle (the volume of the ventricle that it has at rest): men - 112±27 (65-193) ml, women 89±20 (59-136) ml.
• End-diastolic dimension (EDD) of the left ventricle (the size of the ventricle in centimeters that it has at rest): 4.6-5.7 cm.
• End systolic dimension (ESD) of the left ventricle (the size of the ventricle it has during contraction): 3.1-4.3 cm.
• Wall thickness in diastole (outside of heart contractions): 1.1 cm. With hypertrophy - an increase in the thickness of the ventricular wall due to too much load on the heart - this figure increases. Figures of 1.2-1.4 cm indicate slight hypertrophy, 1.4-1.6 indicate moderate hypertrophy, 1.6-2.0 indicate significant hypertrophy, and a value of more than 2 cm indicates high degree hypertrophy.
• Ejection fraction (EF): 55-60%. The ejection fraction shows how much blood relative to the total amount the heart ejects with each contraction; normally it is slightly more than half. When the ejection fraction decreases, heart failure is indicated.
• Stroke volume (SV) is the amount of blood that is ejected by the left ventricle in one contraction: ml.

Right ventricle parameters:

• Wall thickness: 5 ml.
• Size index 0.75-1.25 cm/m2.
• Diastolic size (size at rest) 0.95-2.05 cm.

Parameters of the interventricular septum:

• Resting thickness (diastolic thickness): 0.75-1.1 cm. Excursion (moving from side to side during heart contractions): 0.5-0.95 cm.

Left atrium parameters:

Standards for heart valves:

Norms for the pericardium:

• There is normally no fluid in the pericardial cavity.

Formula

The mass of the left ventricular myocardium (calculation) is determined by the following formula:

• IVS – value (in cm) equal to the thickness of the interventricular septum in diastole;
• EDR is a value equal to the end-diastolic size of the left ventricle;
• LVSP is a value (in cm) equal to the thickness of the posterior wall of the left ventricle in diastole.

MI – myocardial mass index is determined by the formula:

MI=M/H2.7 or MI=M/S, where

• M – mass of the left ventricular myocardium (in g);
• H – height (in m);
• ​ S – body surface area (in m2).

Reasons

The reasons leading to left ventricular hypertrophy include:

• arterial hypertension;
• various heart defects;
• cardiomyopathy and cardiomegaly.

The mass of the left ventricular myocardium in 90% of patients with arterial hypertension exceeds the norm. Often hypertrophy develops with mitral valve insufficiency or with aortic defects.

The reasons why myocardial mass may exceed the norm are divided into:

Scientists have found that cardiac hypertrophy can be promoted by the presence or absence of several fragments in human DNA. Among the biochemical factors leading to myocardial hypertrophy, an excess of norepinephrine and angiotensin can be identified. Demographic factors for the development of cardiac hypertrophy include race, age, gender, physical activity, a tendency to obesity and alcoholism, and the body's sensitivity to salt. For example, men have higher myocardial mass than normal more often than women. In addition, the number of people with a hypertrophied heart increases with age.

Stages and symptoms

In the process of increasing myocardial mass, three stages are distinguished:

• compensation period;
• subcompensation period;
• period of decompensation.

Symptoms of left ventricular hypertrophy begin to manifest themselves noticeably only at the stage of decompensation. When decompensated, the patient experiences shortness of breath, fatigue, palpitations, drowsiness and other symptoms of heart failure. Specific signs of myocardial hypertrophy include a dry cough and facial swelling that appears during the day or in the evening.

Consequences of left ventricular myocardial hypertrophy

High blood pressure not only worsens well-being, but also provokes the onset of pathological processes that affect target organs, including the heart: with arterial hypertension, hypertrophy of the left ventricular myocardium occurs. This is explained by an increase in collagen content in the myocardium and its fibrosis. An increase in myocardial mass entails an increase in myocardial oxygen demand. Which, in turn, leads to ischemia, arrhythmia and cardiac dysfunction.

Cardiac hypertrophy (increased left ventricular myocardial mass) increases the risk of developing cardiovascular disease and can lead to premature death.

However, myocardial hypertrophy is not a death sentence: people with a hypertrophied heart can live for decades. You just need to monitor your blood pressure and regularly undergo ultrasound of the heart to monitor hypertrophy over time.

Treatment

The method of treating left ventricular myocardial hypertrophy depends on the cause that caused the development of this pathology. If necessary, surgery may be prescribed.

Heart surgery for myocardial hypertrophy can be aimed at eliminating ischemia - coronary artery stenting and angioplasty. In case of myocardial hypertrophy due to heart disease, valve replacement or dissection of adhesions is performed if necessary.

Slowing down the processes of hypertrophy (if it is caused by a sedentary lifestyle) in some cases can be achieved by using moderate physical activity, such as swimming or running. The cause of left ventricular myocardial hypertrophy may be obesity: normalizing weight while switching to a balanced diet will reduce the load on the heart. If hypertrophy is caused by increased loads (for example, during professional sports), then you need to gradually reduce them to an acceptable level.

Medicines prescribed by doctors for left ventricular hypertrophy are aimed at improving myocardial nutrition and normalizing heart rhythm. When treating myocardial hypertrophy, you should stop smoking (nicotine reduces the supply of oxygen to the heart) and drinking alcohol (many medications used for myocardial hypertrophy are not compatible with alcohol).

How does the muscular system of the heart work?

The myocardium is the thickest layer of the heart, located midway between the endocardium (inner layer) and the epicardium on the outside. A feature of the heart is the ability of the atria and ventricles to contract independently, independently of each other, even to “work” autonomously.

Contractility is provided by special fibers (myofibrils). They combine the characteristics of skeletal and smooth muscle tissue. That's why:

• distribute the load evenly across all departments;
• have striations;
• ensure non-stop work of the heart throughout a person’s life;
• are reduced regardless of the influence of consciousness.

Each cell has an elongated nucleus with a large number of chromosomes. Thanks to this, myocytes are more “tenacious” compared to cells of other tissues and are able to withstand significant loads.

The atria and ventricles have different myocardial densities:

1. In the atria, it consists of two layers (superficial and deep), which differ in the direction of the fibers; transverse or circular myofibrils are located on the outside, and longitudinal ones on the inside.
2. The ventricles are provided with an additional third layer, lying between the first two, with a horizontal direction of the fibers. This mechanism strengthens and maintains the force of contraction.

What does myocardial mass indicate?

The total weight of the heart in an adult is about 300 g. The development of ultrasound diagnostic methods has made it possible to calculate the part related to the myocardium from this weight. The average myocardial mass for men is 135 g, for women - 141 g. The exact mass is determined by the formula. It depends on:

• size of the left ventricle in the diastole phase;
• thickness of the interventricular septum and posterior wall.

An even more specific indicator for diagnosis is the myocardial mass index. For the left ventricle, the norm for men is 71 g/m2, for women - 62. This value is calculated automatically by a computer when entering data on a person’s height and body surface area.

Mechanism of heart contraction

Thanks to the development of electron microscopy, the internal structure of the myocardium, the structure of the myocyte, which provides the property of contractility, has been established. Thin and thick protein chains called “actin” and “myosin” have been identified. When actin fibers slide over myosin fibers, muscle contraction occurs (systole phase).

The biochemical mechanism of contraction is the formation of the common substance “actomyosin”. In this case, potassium plays an important role. Leaving the cell, it promotes the connection of actin and myosin and their absorption of energy.

The energy balance in myocytes is maintained by replenishment during the relaxation phase (diastole). Biochemical components involved in this process:

• oxygen,
• hormones,
• enzymes and coenzymes (B vitamins are especially important in their role),
• glucose,
• lactic and pyruvic acids,
• ketone bodies.
• amino acids.

What influences the process of contractility?

Any diastolic dysfunction disrupts energy production, the heart loses “recharge” and does not rest. Myocyte metabolism is influenced by:

• nerve impulses coming from the brain and spinal cord;
• lack or excess of “components” for a biochemical reaction;
• disruption of the flow of necessary substances through the coronary vessels.

Blood supply to the myocardium is carried out through the coronary arteries, extending from the base of the aorta. They are sent to different parts of the ventricles and atria, breaking up into small branches that feed the deep layers. An important adaptive mechanism is the system of collateral (auxiliary) vessels. These are reserved arteries that are normally in a collapsed state. For them to be included in the blood circulation, the main vessels must fail (spasm, thrombosis, atherosclerotic damage). It is this reserve that can limit the infarction zone and provides nutritional compensation in the event of myocardial thickening during hypertrophy.

Maintaining satisfactory contractility is essential to prevent heart failure.

Properties of the heart muscle

In addition to contractility, the myocardium has other exceptional properties that are inherent only to the muscle tissue of the heart:

1. Conductivity - equates myocytes to nerve fibers, since they are also capable of conducting impulses, transmitting them from one area to another.
2. Excitability - in 0.4 seconds. The entire muscular structure of the heart becomes excited and ensures a complete release of blood. The correct rhythm of the heart depends on the occurrence of excitation in the sinus node, located deep in the right atrium and the further passage of the impulse along the fibers to the ventricles.
3. Automatism is the ability to independently form a focus of excitation, bypassing the established direction. This mechanism causes a disruption in the correct rhythm, as other areas take on the role of driver.

Various myocardial diseases are accompanied by minor or severe impairments of the listed functions. They determine the clinical features of the course and require a special approach to treatment.

Let us consider pathological changes in the myocardium and their role in the occurrence of certain diseases of the heart muscle.

Types of myocardial damage

All myocardial damage is divided into:

1. Non-coronary myocardial diseases are characterized by the absence of a connection between the causes and damage to the coronary arteries. These include inflammatory diseases or myocarditis, dystrophic and nonspecific changes in the myocardium.
2. Coronarogenic - consequences of impaired patency of the coronary vessels (foci of ischemia, necrosis, focal or diffuse cardiosclerosis, cicatricial changes).

Features of myocarditis

Myocarditis often occurs in men, women and children. Most often they are associated with inflammation of individual areas (focal) or the entire muscular layer of the heart (diffuse). The causes are infectious diseases (influenza, rickettsiosis, diphtheria, scarlet fever, measles, typhus, sepsis, polio, tuberculosis).

Carrying out preventive work to form a sufficient protective reaction through vaccinations made it possible to limit the disease. However, serious problems remain in the heart after diseases of the nasopharynx, due to the development of a chronic rheumatic process. Non-rheumatic myocarditis is associated with a severe stage of uremic coma and acute nephritis. The inflammatory reaction may be autoimmune, occurring as an allergy.

Histological examination reveals among muscle cells:

• granulomas of a typical structure in rheumatism;
• edema with accumulation of basophils and eosinophils;
• death of muscle cells with proliferation of connective tissue;
• accumulation of fluid between cells (serous, fibrinous);
• areas of dystrophy.

The result in all cases is impaired myocardial contractility.

The clinical picture is varied. It consists of symptoms of cardiac and vascular failure, rhythm disturbances. Sometimes the endocardium and pericardium are simultaneously affected.

Typically, failure of the right ventricular type develops more often, since the myocardium of the right ventricle is weaker and is the first to fail.

Patients complain of shortness of breath, palpitations, and a feeling of irregularities due to an acute illness or after an infection.

Rheumatic inflammation is always accompanied by endocarditis, and the process necessarily spreads to the valve apparatus. If treatment is delayed, a defect is formed. For a good response to therapy, temporary disturbances in rhythm and conduction without consequences are typical.

Myocardial metabolic disorders

Metabolic disorders often accompany myocarditis and coronary heart disease. It is not possible to find out what is primary, this pathology is so connected. Due to the lack of substances for energy production in cells, lack of oxygen in the blood during thyrotoxicosis, anemia, and vitamin deficiencies, myofibrils are replaced by scar tissue.

The heart muscle begins to atrophy and weaken. This process is characteristic of old age. A special form is accompanied by the deposition of lipofuscin pigment in the cells, due to which, on histology, the heart muscle changes color to brown-red, and the process is called “brown myocardial atrophy.” At the same time, dystrophic changes are found in other organs.

When does myocardial hypertrophy occur?

The most common cause of hypertrophic changes in the heart muscle is hypertension. Increased vascular resistance forces the heart to work against a high load.

The development of concentric hypertrophy is characterized by: the volume of the left ventricular cavity remains unchanged with a general increase in size.

Symptomatic hypertension in kidney diseases and endocrine pathologies are less common. Moderate thickening of the ventricular wall makes it difficult for blood vessels to grow deeper into the mass, and is therefore accompanied by ischemia and a state of oxygen deficiency.

Cardiomyopathies are diseases with unclear causes that combine all possible mechanisms of myocardial damage from increasing dystrophy leading to an increase in the ventricular cavity (dilated form) to pronounced hypertrophy (restrictive, hypertrophic).

A special variant of cardiomyopathy - spongy or non-compact myocardium of the left ventricle is congenital in nature, often associated with other heart and vascular defects. Normally, non-compact myocardium makes up a certain proportion of the heart mass. It increases with hypertension and hypertrophic cardiomyopathy.

Pathology is detected only in adulthood by symptoms of heart failure, arrhythmia, and embolic complications. With color Doppler, images are obtained in multiple planes, and the thickness of non-compact areas is measured during systole rather than diastole.

Myocardial damage during ischemia

In 90% of cases, atherosclerotic plaques are found in the coronary vessels during coronary artery disease, blocking the diameter of the feeding artery. A certain role is played by metabolic changes under the influence of impaired nervous regulation - the accumulation of catecholamines.

With angina pectoris, the state of the myocardium can be characterized as forced “hibernation” (hibernation). The hibernating myocardium is an adaptive response to a deficiency of oxygen, adenosine triphosphate molecules, and potassium ions, the main suppliers of calories. Occurs in local areas with prolonged circulatory disorders.

A balance is maintained between a decrease in contractility in accordance with the impaired blood supply. At the same time, myocyte cells are quite viable and can fully recover with improved nutrition.

“Stunned myocardium” is a modern term that characterizes the state of the heart muscle after restoration of coronary circulation in the heart region. The cells accumulate energy for several more days; contractility is impaired during this period. It should be distinguished from the phrase "myocardial remodeling", which means actual changes in myocytes due to pathological causes.

How does the myocardium change during coronary artery thrombosis?

Prolonged spasm or blockage of the coronary arteries causes necrosis of the part of the muscle that they supply with blood. If this process is slow, the collateral vessels will take over the “work” and prevent necrosis.

The focus of the infarction is located in the apex, anterior, posterior and lateral walls of the left ventricle. Rarely involves the septum and right ventricle. Necrosis in the inferior wall occurs when the right coronary artery is blocked.

If the clinical manifestations and the ECG picture agree in confirming the form of the disease, then you can be confident in the diagnosis and use combined treatment. But there are cases that require confirmation of the doctor’s opinion, primarily with the help of accurate, indisputable markers of myocardial necrosis. As a rule, diagnosis is based on the quantitative determination of breakdown products and enzymes that are more or less specific to necrotic tissues.

Can necrosis be confirmed by laboratory methods?

The development of modern biochemical diagnostics of infarction has made it possible to identify standard markers of myocardial necrosis for early and late manifestations of infarction.

Early markers include:

• Myoglobin - increases in the first 2 hours; the optimal use of this indicator is to monitor the effectiveness of fibrinolytic therapy.
• Creatine phosphokinase (CPK), a fraction from cardiac muscle, makes up only 3% of the total mass, so if it is not possible to determine only this part of the enzyme, the test has no diagnostic value. With myocardial necrosis, it increases on the second or third day. An increase in the indicator is possible in case of renal failure, hypothyroidism, and cancer.
• A cardiac type of protein that binds fatty acids - in addition to the myocardium, it is found in the wall of the aorta and the diaphragm. Regarded as the most specific indicator.

Late markers are considered:

• Lactate dehydrogenase, the first isoenzyme, reaches its highest level by the sixth or seventh day, then decreases. The test is considered low specific.
• Aspartate aminotransferase reaches its maximum at the 36th hour. Due to low specificity, it is used only in combination with other tests.
• Cardiac troponins remain in the blood for up to two weeks. They are considered the most specific indicator of necrosis and are recommended by international diagnostic standards.

The presented data on changes in the myocardium are confirmed by anatomical, histological and functional studies of the heart. Their clinical significance makes it possible to timely identify and assess the degree of destruction of myocytes, the possibility of their restoration, and monitor the effectiveness of treatment.

If you have already undergone an ultrasound examination of the kidneys or, for example, the abdominal organs, then you remember that in order to roughly interpret their results, you most often do not have to go to the doctor - you can find out the basic information before visiting the doctor, by reading the report yourself. The results of a heart ultrasound are not so easy to understand, so it can be difficult to decipher them, especially if you analyze each indicator by number.

You can, of course, just look at the last lines of the form, where a general summary of the research is written, but this also does not always clarify the situation. So that you can better understand the results obtained, we present the basic norms of cardiac ultrasound and possible pathological changes that can be determined by this method.

Ultrasound standards for heart chambers

To begin with, we will present a few numbers that are sure to appear in every Doppler echocardiography report. They reflect various parameters of the structure and functions of individual chambers of the heart. If you are a pedant and take a responsible approach to deciphering your data, pay maximum attention to this section. Perhaps, here you will find the most detailed information in comparison with other Internet sources intended for a wide range of readers. Data may vary slightly between sources; Here are the figures based on materials from the manual “Norms in Medicine” (Moscow, 2001).

Left ventricular myocardial mass: men – g, women – g.

Left ventricular myocardial mass index (often referred to as LVMI on the form): men g/m2, women g/m2.

End-diastolic volume (EDV) of the left ventricle (volume of the ventricle that it has at rest): men – 112±27 (65-193) ml, women 89±20 (59-136) ml

End-diastolic dimension (EDD) of the left ventricle (the size of the ventricle in centimeters that it has at rest): 4.6 – 5.7 cm

End systolic dimension (ESR) of the left ventricle (the size of the ventricle it has during contraction): 3.1 – 4.3 cm

Wall thickness in diastole (outside of heart contractions): 1.1 cm

With hypertrophy - an increase in the thickness of the ventricular wall due to too much load on the heart - this figure increases. Figures of 1.2–1.4 cm indicate slight hypertrophy, 1.4–1.6 indicate moderate hypertrophy, 1.6–2.0 indicate significant hypertrophy, and a value of more than 2 cm indicates high degree hypertrophy.

At rest, the ventricles are filled with blood, which is not completely ejected from them during contractions (systole). The ejection fraction shows how much blood relative to the total amount the heart ejects with each contraction; normally it is slightly more than half. When the EF indicator decreases, they speak of heart failure, which means that the organ pumps blood ineffectively, and it can stagnate.

Stroke volume (the amount of blood that is ejected by the left ventricle in one contraction): ml.

Wall thickness: 5 ml

Size index 0.75-1.25 cm/m2

Diastolic size (size at rest) 0.95-2.05 cm

Parameters of the interventricular septum

Resting thickness (diastolic thickness): 0.75-1.1 cm

Excursion (moving from side to side during heart contractions): 0.5-0.95 cm. An increase in this indicator is observed, for example, with certain heart defects.

For this chamber of the heart, only the value of EDV is determined - the volume at rest. A value of less than 20 ml indicates a decrease in EDV, a value of more than 100 ml indicates its increase, and an EDV of more than 300 ml occurs with a very significant increase in the right atrium.

Size: 1.85-3.3 cm

Size index: 1.45 – 2.9 cm/m2.

Most likely, even a very detailed study of the parameters of the heart chambers will not give you particularly clear answers to the question about the state of your health. You can simply compare your indicators with the optimal ones and on this basis draw preliminary conclusions about whether everything is generally normal for you. For more detailed information, contact a specialist; The volume of this article is too small for wider coverage.

Ultrasound standards for heart valves

As for deciphering the results of a valve examination, it should present a simpler task. It will be enough for you to look at the general conclusion about their condition. There are only two main, most common pathological processes: stenosis and valve insufficiency.

The term “stenosis” refers to a narrowing of the valve opening, in which the overlying chamber of the heart has difficulty pumping blood through it and may undergo hypertrophy, which we discussed in the previous section.

Insufficiency is the opposite condition. If the valve leaflets, which normally prevent the reverse flow of blood, for some reason cease to perform their functions, the blood that has passed from one chamber of the heart to another partially returns, reducing the efficiency of the organ.

Depending on the severity of the disorders, stenosis and insufficiency can be grade 1, 2 or 3. The higher the degree, the more serious the pathology.

Sometimes in the conclusion of a cardiac ultrasound you can find such a definition as “relative insufficiency”. In this condition, the valve itself remains normal, and blood flow disturbances occur due to the fact that pathological changes occur in the adjacent chambers of the heart.

Ultrasound standards for the pericardium

The pericardium, or pericardial sac, is the “bag” that surrounds the outside of the heart. It fuses with the organ in the area where the vessels originate, in its upper part, and between it and the heart itself there is a slit-like cavity.

The most common pathology of the pericardium is an inflammatory process, or pericarditis. With pericarditis, adhesions can form between the pericardial sac and the heart and fluid can accumulate. Normally, 100 ml indicates a small accumulation, and over 500 indicates a significant accumulation of fluid, which can lead to difficulty in the full functioning of the heart and its compression...

To master the specialty of a cardiologist, a person must first study at the university for 6 years, and then study cardiology separately for at least a year. A qualified doctor has all the necessary knowledge, thanks to which he can not only easily decipher the conclusion to an ultrasound of the heart, but also make a diagnosis based on it and prescribe treatment. For this reason, deciphering the results of such a complex study as ECHO-cardiography should be provided to a specialized specialist, rather than trying to do it yourself, poking around for a long time and unsuccessfully with the numbers and trying to understand what certain indicators mean. This will save you a lot of time and nerves, since you will not have to worry about your probably disappointing and, even more likely, incorrect conclusions about your health.