Myocardial mass: essence, norm, calculation and index, what it says. Left ventricular myocardial mass index: normal, increased Left ventricular myocardial mass normal

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.

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

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:

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

Diagnosis and treatment

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:

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!

The information on the site is provided for informational purposes only and does not constitute a guide to action. Do not self-medicate. Consult your healthcare provider.

How is the mass of the left ventricular myocardium determined?

In men, the average mass of the left ventricular myocardium (normal) is 135 g, and in women 95 g. At the same time, the upper limit, the excess of which is considered to be exceeding the norm for men is 183 g, and for women – 141 g.

The average value of the left ventricular myocardial mass index is 71 g/m2 in men and 62 g/m2 in women. The upper limit of this index is 94 and 89 g/m2, respectively.

The causes and mechanism of changes in left ventricular mass in various diseases are still poorly understood.

Myocardial hypertrophy is a fundamental mechanism of adaptation of the heart muscle to increased stress that occurs both during cardiovascular diseases and during physical exercise. The heart muscle, like any muscle, thickens when the load on it is increased.

The blood vessels supplying this organ cannot keep up with its growth, which is why heart tissue starves and various diseases develop. With myocardial hypertrophy, problems also arise in the conduction system of the heart, as a result of which zones of abnormal activity appear in it and arrhythmias appear.

The best method for studying the anatomy of the heart and its function is echocardiography. This method is superior to ECG in sensitivity to cardiac hypertrophy. Myocardial hypertrophy can also be detected using cardiac ultrasound.

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).

Causes

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. Hypertrophy often 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).

What is myocardial hypertrophy of the left ventricle of the heart, characteristic signs and treatment

Often, during instrumental examination (ECG or ultrasound of the heart), myocardial hypertrophy is detected. This condition is characterized by an increase in the volume of several chambers of the heart. Most often the left ventricle is enlarged. A disease in which ventricular hypertrophy occurs is called hypertrophic cardiomyopathy.

The human heart consists of 3 layers: epicardium, endocardium and myocardium. The latter is represented by muscle tissue. It is she who contracts and ensures the movement of blood through the vessels. The muscular layer is present in both ventricles and atria. Each chamber of the heart has a cavity. With hypertrophy, its volume may decrease or remain unchanged.

Left ventricular myocardial hypertrophy is detected most often. This is due to its size and function. The systemic circulation begins from the left ventricle. This pathology is a consequence of heart disease or defects. The degree of hypertrophy is determined by the thickness of the left ventricular wall. Moderate changes in the myocardium of the left ventricle are present if the thickness of its wall does not exceed 21 mm.

With an average degree, this figure ranges from 21 to 25 mm. Severe hypertrophy of the left ventricular myocardium is characterized by a wall thickness of more than 25 mm. A moderate degree of increase does not pose a threat to the sick person. There are 3 types of hypertrophy: concentric, eccentric and obstructive. Concentric hypertrophy of the left ventricle develops due to excess pressure in this chamber of the heart.

This is most often observed with narrowing and insufficiency of the aortic valve. Eccentric ventricular hypertrophy is characterized by the fact that a lot of blood enters it. This leads to its stretching. An increase in its volume is a compensatory reaction of the body aimed at increasing cardiac output.

The reasons for the increase in myocardial volume and proliferation of muscle fibers are different. Hypertrophy of the left ventricle of the heart is due to the following reasons:

congenital heart defects;
genetic defects;
bicuspid valve insufficiency;
mitral stenosis;
narrowing of the aortic valve and its insufficiency;
primary arterial hypertension;
atherosclerotic lesions of the aorta and valves;
coronary heart disease.

Enlargement of the right ventricle of the heart is often observed. The cause may be narrowing of the aortic valve, pulmonary arterial hypertension, ventricular septal defect, tetralogy of Fallot (heart disease in young children). The reason may lie in lung diseases (emphysema, fibrosis, chronic bronchitis, asthma, sarcoidosis, pneumonia).

Against the background of ventricular hypertrophy, enlargement of the atria is often observed. The likelihood of developing this pathology increases with the following predisposing factors:

overweight;
smoking;
chronic stress;
alcoholism;
poor nutrition;
atherosclerosis;
diabetes mellitus;
insomnia;
hard physical work.

Hypertrophy is often detected in people involved in sports. The reason is a greater load and a higher tissue demand for oxygen.

Most often, eccentric hypertrophy of the left ventricle is detected during electrocardiography. This chamber of the heart has the largest mass. The thickness of the LV walls varies from 4 to 14 mm in different sections. When a large amount of blood enters this chamber and the pressure increases over time, the following changes are observed:

the muscle wall thickens;
muscle fibers lengthen;
myocardial mass increases;
the number of cells increases.

Hypertrophied myocardium needs more oxygen and often suffers from a lack of it. Ischemia develops, which causes impaired cardiac contractility. Often the muscle wall thickens and swells, which aggravates the situation. Hypertrophy of the left ventricle of the heart is dangerous because it disrupts the process of relaxation and contraction of the heart muscle.

In such people, the heart wears out faster. The most common cause of this disease is hypertension. Other factors include atherosclerosis, endocrine pathology, and heart defects. This pathology is more often detected in males over 50 years of age. Hypertrophy itself may not manifest itself in any way. Symptoms are due to the underlying disease and the consequences of left ventricular enlargement.

The most commonly observed symptoms are:

a feeling of interruptions in the work of the heart;
high blood pressure;
periodic attacks of suffocation;
shortness of breath on exertion;
acrocyanosis;
swelling in the upper and lower extremities;
pain in the heart area;
dizziness;
loss of consciousness.

Moderate hypertrophy in the absence of heart failure and pulmonary pathology is not dangerous.

Due to certain heart diseases, the right ventricle often suffers. The pulmonary circulation begins with it. There are moderate, moderate and severe degrees of pancreatic hypertrophy. In the first case, the weight of the left stomach exceeds the weight of the right, but the latter is enlarged. The average degree is characterized by a decrease in this difference. In severe cases, the pancreas becomes larger than the left.

In a healthy person, the weight of the left ventricle is almost 3 times greater than the weight of the right. HPG is a syndrome that develops primarily against the background of pulmonary pathology. In the early stages it does not manifest itself at all. Changes may be detected incidentally during preventative studies. HPG manifests itself with the following symptoms:

prolonged, intermittent chest pain;
shortness of breath;
fainting;
heart rhythm disturbances;
swelling of the limbs in the afternoon;
dizziness;
frequent heartbeat;
drop in blood pressure.

Hypotension and tachycardia are the most common symptoms.

Enlarged ventricles most often indicate the presence of hypertrophic cardiomyopathy in a person.

This is a disease that affects the myocardium. This pathology leads to impaired diastolic function, arrhythmia and heart failure. This disease affects 0.2-1% of the population. Mostly adults are affected. Middle-aged males are more often affected.

In the absence of proper treatment, this disease leads to paroxysmal ventricular tachycardia in every second patient. Possible consequences include the development of bacterial endocarditis with damage to the valve apparatus. The disease often runs in families. LV enlargement in this situation is not associated with heart defects, coronary artery disease and hypertension. The development of the disease is based on gene mutations. This pathology is often combined with atherosclerosis of the coronary arteries.

With cardiomyopathy, the following changes are observed:

left ventricular enlargement (less frequently right);
dilatation of the left atrium;
an increase in the size of the interventricular septum.

Hypertrophy can be moderate, moderate or severe. For years, this disease occurs in a latent (asymptomatic) form. The first symptoms most often appear at age. Hypertrophic cardiomyopathy is manifested by the following symptoms:

rapid breathing with difficulty inhaling;
loss of consciousness;
dizziness;
pain behind the sternum;
a feeling of interruptions in the work of the heart.

An early symptom is shortness of breath. At first its appearance is associated with stress, but then it appears at rest. Sometimes it intensifies when a person takes a standing position. A decrease in blood flowing into the aorta leads to dizziness and fainting. The heart itself suffers.

The volume of blood in the coronary arteries decreases, which causes chest pain. Unlike an attack of angina, the pain is not relieved by nitrates. The most dangerous consequences of cardiomyopathy and left ventricular hypertrophy include sudden cardiac death.

Concentric hypertrophy of the left ventricular myocardium can only be detected during instrumental examination. Ultrasound (EchoCG) allows you to accurately assess the condition of the heart and its chambers. It may reveal the following changes:

thickening of the apex and septum of the heart;
thickening of the anterior and posterior walls of the myocardium;
the presence of areas with reduced contractility.

Electrocardiography is of great value. This is a method for assessing the electrical potentials of the heart. The electrocardiogram reveals an increase in the R wave in the left precordial leads, as well as an increase in the amplitude of the S wave in the right leads. The electrical axis of the heart is shifted to the left. There is a change in the ST segment and deepening of the Q wave. Often left ventricular hypertrophy is combined with conduction disturbances.

In this case, signs of bundle branch block may be detected. Additional diagnostic methods include stress tests, laboratory tests, coronary angiography, and magnetic resonance imaging. An X-ray examination is required. The doctor measures blood pressure and listens to heart sounds. It is necessary to identify the cause of myocardial hypertrophy.

If hypertrophy of the left ventricular myocardium with pronounced clinical manifestations is detected, then treatment is required. It is aimed at the underlying disease. For cardiovascular diseases, the following groups of drugs are most often used:

ACE inhibitors (Captopril, Perindopril, Enalapril, Prestarium);
beta-blockers (Bisoprolol, Metoprolol, Recardium);
calcium channel blockers (Amlodipine, Verapamil);
combination drugs (Prestance);
statins (Lovastatin, Atorvastatin, Simvastatin);
sartans;
antiplatelet agents.

Beta blockers reduce myocardial oxygen demand and stop hypertrophy. Calcium blockers reduce heart rate and prevent further growth of muscle fibers and cells. If arrhythmia develops, antiarrhythmic drugs are prescribed. The treatment regimen for such patients often includes nitrates, anticoagulants, antioxidants, and diuretics. To strengthen the heart muscle and blood vessels, antioxidants (Actovegin, Coenzyme Q10) and vitamins are indicated.

If hypertrophic cardiomyopathy is detected, medications are initially prescribed at a low dose, then increased. For moderate hypertrophy, beta blockers, anticoagulants and calcium channel blockers are indicated. If there are signs of heart failure, then cardiac glycosides and diuretics are effective. In the presence of obstructive cardiomyopathy, antibiotics are often prescribed. They are necessary to prevent the development of bacterial endocarditis.

In case of defects of the mitral, aortic or tricuspid valve and high pressure inside the ventricles, surgical treatment (plasty or prosthetics) is indicated. In cases of severe cardiac conduction disturbance, the patient may need a pacemaker. In the absence of therapeutic measures, in 3-8% of cases, hypertrophic cardiomyopathy ends in death.

The lifestyle of patients with myocardial hypertrophy involves adherence to a therapeutic diet, cessation of smoking and alcohol, limitation of exercise, adherence to treatment prescribed by a doctor, and adherence to a work and rest regime. With total cardiac hypertrophy, sick people often become disabled. Thus, hypertrophy of the heart muscle is most often caused by cardiomyopathy and cardiac valve defects.

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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.

Causes

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;
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;
headache;
cardiopalmus;
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

Blood pressure control. The patient is advised to regularly measure blood pressure.
Elimination of psycho-emotional tension and stressful situations.
Rational physical activity.
Quitting smoking and drinking alcohol.
Losing excess weight and preventing obesity.
Regular exercise and walks in the fresh air.
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.

Surgery

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.

Calculation of left ventricular myocardial mass

Calculation of the mass of the left ventricular myocardium is carried out during a diagnostic examination of the heart. The resulting value characterizes the internal state of the cardiac chamber. These measurements are studied in order to identify pathological disorders in its structure and assess the ability to perform the main function. The task of the left ventricular myocardium is to perform rhythmic contractions that push blood under high pressure into the aorta. This is vital for continuous blood supply to the entire body.

Normal indicators

The weight of the heart muscle is measured in grams and calculated using a formula whose terms are obtained by echocardiography. Particular attention is focused on the condition of the left ventricle. This is due to its significant functional load and greater susceptibility to changes than the right one.

There is an established norm for the mass of the left ventricular myocardium. Its boundaries vary depending on the gender of the patient, as shown in the table:

The data obtained during an instrumental examination must be correlated with the weight, build and physical activity of a particular person.

This is necessary to explain possible deviations from the norm. The patient's characteristics, his occupation, age, previous operations or heart disease play a role in determining the cause of myocardial changes.

The cardiac muscle mass of a frail woman differs from the athletic physique of a man, and this constitutes a range of normative parameters.

Taking into account the patient’s height and weight characteristics, the mass index of the left ventricular myocardium is calculated; its norm is shown in the table:

Myocardial mass and index are two diagnostic parameters that reflect the internal state of the heart and indicate the risk of circulatory disorders.

Hypertrophy

The thickness of the left ventricular myocardium is normally measured when it relaxes and is 1.1 centimeters. This indicator does not always remain this way. If it is elevated, then myocardial hypertrophy is noted on the left. This indicates excessive work of the heart muscle and can be of two types:

Physiological (growth of muscle mass under the influence of intense training);
pathological (enlargement of the heart muscle as a result of the development of the disease).

If the thickness of the wall of the left ventricle is from 1.2 to 1.4 centimeters, slight hypertrophy is recorded. This condition does not yet indicate pathology and can be detected during a medical examination of athletes. With intense training, skeletal muscles and at the same time myocardial muscles build up. In this case, changes in cardiac muscle tissue should be monitored using regular echocardiography. The risk of physiological hypertrophy transforming into a pathological form is very high. Thus, sports can be harmful to health.

When the heart muscle changes up to two centimeters, states of moderate and significant hypertrophy are considered. They are characterized by the appearance of shortness of breath, a feeling of lack of air, pain in the heart area, disturbance of its rhythm and increased fatigue. If this change in the myocardium is detected in a timely manner, it can be corrected with medication.

An increase of more than 2 centimeters is diagnosed as high-grade hypertrophy.

This stage of myocardial pathology is life-threatening due to its complications. The treatment method is selected according to the individual situation.

Principle of determining mass

The determination of myocardial mass is calculated using numbers obtained during echocardiography. For accuracy and objectivity of measurement assessments, they are carried out in a combination of modes, comparing two- and three-dimensional images. The data is supplemented by the results of Doppler studies and indicators of ultrasound scanners, which are capable of displaying a projection of the heart in natural size on the monitor screen.

Calculation of myocardial mass can be done in several ways. Preference is given to two formulas ASE and PC, which use the following indicators:

the thickness of the muscular septum separating the cardiac ventricles;
directly the thickness of the posterior wall of the left chamber in a calm state, until the moment of its contraction;
full size of the relaxed left ventricle.

The interpretation of values obtained from echocardiography should be considered by an experienced specialist in functional diagnostics. When evaluating the results, he will note that the ASE formula represents the left ventricle along with the endocardium (the cardiac membrane lining the chambers). This may cause distortion in the measurement of its thickness.

Formula

All measurements are taken in centimeters. Each abbreviation means:

The myocardial index can be measured using one of the formulas:

The meanings of the accepted abbreviations mean:

In measurements, the area of the subject is used, because it is a more accurate value than body weight. This is due to limiting dependence on excess fat tissue. The surface area is calculated using a fixed formula, where the parameters change according to the patient’s age.

The myocardial index is most indicative in pediatrics. This is due to the fact that adult height remains unchanged when calculated over several survey years. The child’s growth is constantly changing, thanks to which pathologies in cardiac parameters can be accurately tracked.

The average value of the left ventricular myocardial mass index is 71 g/m2 in men and 62 g/m2 in women. The upper limit of this index is 94 and 89 g/m2, respectively.

The causes and mechanism of changes in left ventricular mass in various diseases are still poorly understood.

Formula

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

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).

Causes

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. Hypertrophy often develops with mitral valve insufficiency or with aortic defects.

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

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

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

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.

Myocardial mass index

<0,001) (ММЛЖ, гр = 1,04×[(КДР+МЖП+ЗСЛЖ) 3 -КДР 3 ]-13,6) .

<0,001), переоценивала наличие ГЛЖ лишь на 6%, а чувствительность у пациентов с ГЛЖ (масса миокарда при аутопсии ><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% .

<150 гр,гр - умеренной, а >

<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.

J.K. Galy, 1992

I.W. Hammond, 1986

E. Aberget, 1995

De G. Simone, 1994

Gender-neutral

M.J. Koren, 1981

De G. Simone, 1995

<0,001)

All methods except dependent

Bibliographic link

URL: http://science-education.ru/ru/article/view?id=23603 (access date: 03/10/2018).

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The magazine has been published since 2005. The journal publishes scientific reviews, articles of a problematic and scientific-practical nature. The journal is presented in the Scientific Electronic Library. The journal is registered with the Center International de l'ISSN. Journal numbers and publications are assigned a DOI (Digital object identifier).

Myocardial mass: essence, norm, calculation and index, what it says

What is myocardial mass and how to evaluate it correctly? This question is most often asked by patients who have undergone echocardiography and found, among other parameters, heart muscle mass and mass index.

Myocardial mass is the weight of the heart muscle, expressed in grams and calculated using ultrasound data. This value characterizes many pathological processes, and its change, usually upward, may indicate an unfavorable prognosis for the course of the pathology and an increased risk of serious complications.

The basis for the increase in myocardial mass is hypertrophy, that is, thickening, which characterizes structural changes in the heart muscle, which forces doctors not only to carry out dynamic observation, but also to switch to active treatment tactics.

Modern recommendations regarding the treatment and diagnosis of various heart pathologies indicate that the mass of the left ventricular (LV) myocardium is not only possible, but also necessary to be controlled, and for this, periodic ultrasound examinations of the heart are included in the protocols for the management of patients at risk of cardiac hypertrophy.

On average, the normal myocardial mass for men is considered to be in the range of g, for women - g.

Correct interpretation of echocardiography indicators still remains a serious problem, because it is necessary to correlate instrumentally obtained data with a specific patient and establish whether hypertrophy already exists or some deviation of the mass from the norm can be considered a physiological feature.

To a certain extent, myocardial mass can be considered a subjective indicator, because the same result for people of different height, weight and gender can be assessed differently. For example, the indicator of myocardial mass in a large man involved in weightlifting will normally be excessive for a fragile girl of short stature who is not keen on going to the gym.

It has been established that myocardial mass has a close relationship with the body size of the subject and the level of physical activity, which must be taken into account when interpreting the results, especially if the indicator differs very slightly from the norm.

How to calculate the mass of the left ventricular myocardium at home?

The left ventricular myocardial mass index is a figure that determines the exact weight of the patient’s heart muscle in grams, obtained by calculating specific data taken by an ultrasound machine during a heart scanning procedure. This index characterizes some cardiac pathologies associated with structural changes in the patient’s myocardium and shows the degree of their severity.

The principle of calculating the mass of the LV myocardium

The mass of the left ventricular myocardium has a certain norm, any deviations from which indicate a disease affecting the heart or myocardium. Often the data deviate upward, and there is only one reason for this phenomenon - hypertrophy of the heart muscle.

It is recommended to monitor LV mass on an ongoing basis in order to be able to prevent serious cardiac pathology in advance. This is especially true for those patients who have an increased risk of hypertrophy. The normal calculation result after echocardiography is considered to be a LV mass of 135 to 182 g if the patient is a man, and from 95 to 141 g in women.

However, we note that in some cases a slightly increased mass of the heart or myocardium is considered a physiological feature of a person that does not indicate the course of the disease in his body. To determine whether hypertrophy affects the heart or not, the doctor must compare the individual physical characteristics of the patient with the obtained size and weight of his myocardium. And only after the pathological nature of hypertrophy is confirmed, the doctor can make a rough diagnosis, which must be confirmed by a number of additional laboratory and instrumental studies.

Reasons influencing the deviation of the LV myocardial mass index from the norm

In most cases, the left ventricle and the myocardium as a whole enlarge under the influence of certain pathologies that provoke significant overload of the heart:

valve defects;
cardiomyopathy;
arterial hypertension;
myocardial dystrophy.

In some cases, the mass of the heart muscle and tissue increases without the impact of hypertrophic pathologies. For example, if a man or woman is actively involved in sports, the myocardium is enriched with oxygen more intensely, as a result of which the thickness of the walls of these organs, as well as weight, increases significantly.

However, we note that hypertrophy as a disease is considered common among athletes, because a normal increase in myocardial mass over time can become a pathological abnormality requiring medical intervention. Typically, this phenomenon is observed in cases where the thickness of the patient’s heart muscle significantly exceeds the size of his coronary arteries, as a result of which the left ventricle and the entire heart cease to receive a sufficient amount of blood. The result of such a deviation is heart failure, causing death.

Important! In any case, the increased mass of the myocardium indicates serious loads on the left ventricle and heart of a person, due to which their hypertrophy occurs. Therefore, even if such a deviation is, at first glance, normal, it is still recommended not to allow it.

Methods for calculating LV myocardial mass

In most cases, the determination of IMM is made using the echocardiography procedure, based on the results of scanning the heart and myocardium in different modes. However, to accurately calculate the mass of the left ventricular myocardium, echocardiography data alone is not enough, and the doctor will definitely need an additional image of the organs, in two- and three-dimensional projection.

You can scan the myocardium and left ventricle using a Doppler or a special ultrasound machine, which displays a projection of the organ on the screen in natural size. Many may ask why the mass of only one left ventricle is calculated? The answer is simple: the left ventricle, unlike the right, is subjected to much greater loads, due to which hypertrophy occurs more often in its cavity.

The rate of myocardial mass index itself is calculated in many ways, but today medicine uses only two of the most effective formulas: ASE and PC, which include the following data:

the thickness of the heart muscle between the right and left ventricles;
the thickness of the posterior cavity of the left ventricle (this indicator is measured in two stages: when the organ is completely filled with blood and when it is emptied);
end-diastolic dimensions of the LV.

If you calculate the myocardial mass using the ASE formula, then you should take into account that the thickness of the heart muscle also includes the thickness of the endocardium, which is not observed when calculating using the RS formula. Therefore, the name of the formula must be indicated in the protocol when calculating, since the initial mass according to them is slightly different.

So, to determine the mass index of the left ventricle, you initially need to scan the heart and myocardium, and substitute the resulting sizes of these organs into the following formula:

The abbreviations in this formula have the following designations:

IVS – width of the septum between the ventricles, expressed in cm;
EDR – left ventricular end-diastolic size;
LVSP is an indicator of the thickness of the posterior cavity of the left ventricle, expressed in cm.

Depending on who the patient is (male or female), the rate of myocardial mass index will be slightly different. This difference looks like this:

If the patient is a man, then the norm for him will be from 135 to 182 grams;
If the patient is a woman, then the norm for her ranges from 95 to 141 grams.

If the indicator is too high, it can be assumed that hypertrophy is rapidly developing in the patient’s body, requiring urgent medical intervention.

Calculation of myocardial mass depending on the patient’s weight and height

To determine the stage of development of hypertrophy at the time of its diagnosis and understand how dangerous it is for the patient’s health, the doctor compares the size and mass of the myocardium with the height and weight of the patient. However, during this procedure certain difficulties often arise.

If the patient is a man or woman over the age of 25, then his body is already fully formed, and the heart does not change its size in the future without the influence of negative factors such as hypertrophy. However, if the patient has not reached the above-mentioned age, then his myocardium is able to change its size and weight even without the occurrence of any pathology, which in turn will greatly complicate diagnosis.

As for calculating the ratio of myocardial mass to body height and weight, it is performed strictly according to the following formula:

The abbreviation of this formula is deciphered as follows:

M – muscle weight, expressed in grams;
P – patient’s height;
P is the area of the patient’s body, expressed in square meters.

Having calculated the above-mentioned parameters and established the connection between them, the doctor determines whether the LV is hypertrophied or not, at what stage of development the pathology is at the time of the examination. However, this is not enough to make an accurate diagnosis; the patient will still have to undergo a number of additional laboratory and instrumental studies.

Calculation of left ventricular myocardial mass

Normal indicators

There is an established norm for the mass of the left ventricular myocardium. Its boundaries vary depending on the gender of the patient, as shown in the table:

The data obtained during an instrumental examination must be correlated with the weight, build and physical activity of a particular person.

The cardiac muscle mass of a frail woman differs from the athletic physique of a man, and this constitutes a range of normative parameters.

Taking into account the patient’s height and weight characteristics, the mass index of the left ventricular myocardium is calculated; its norm is shown in the table:

Myocardial mass and index are two diagnostic parameters that reflect the internal state of the heart and indicate the risk of circulatory disorders.

Hypertrophy

Physiological (growth of muscle mass under the influence of intense training);
pathological (enlargement of the heart muscle as a result of the development of the disease).

An increase of more than 2 centimeters is diagnosed as high-grade hypertrophy.

This stage of myocardial pathology is life-threatening due to its complications. The treatment method is selected according to the individual situation.

Principle of determining mass

Calculation of myocardial mass can be done in several ways. Preference is given to two formulas ASE and PC, which use the following indicators:

the thickness of the muscular septum separating the cardiac ventricles;
directly the thickness of the posterior wall of the left chamber in a calm state, until the moment of its contraction;
full size of the relaxed left ventricle.

Formula

All measurements are taken in centimeters. Each abbreviation means:

The myocardial index can be measured using one of the formulas:

The meanings of the accepted abbreviations mean:

Myocardial mass index

Sinus bradyarrhythmia
Diastolic dysfunction
Atrial fibrillation
Hypertension syndrome
Myocardial infarction

Reasons for deviation of heart mass and mass index from normal figures

Myocardial mass is increased due to pathological processes leading to its overload:

Arterial hypertension;
Valve defects;
Cardiomyopathy and myocardial dystrophy.

An increase in the mass of muscle tissue also occurs normally - with intense physical training, when intense sports activities cause the growth of not only skeletal muscles, but also the myocardium, which supplies the organs and tissues of the trainee with oxygen-rich blood.

Athletes, however, risk over time becoming people with myocardial hypertrophy, which under certain conditions can become pathological. When the thickness of the heart muscle becomes greater than the coronary arteries can supply with blood, there is a risk of heart failure. It is this phenomenon that is most often associated with sudden death in well-trained and apparently healthy people.

Thus, an increase in myocardial mass, as a rule, indicates a high load on the heart, whether during sports training or pathological conditions, but regardless of the cause, hypertrophy of the heart muscle deserves close attention.

Methods for calculating myocardial mass and mass index

The calculation of myocardial mass and its index is made based on echocardiography data in different modes, and the doctor must use all the possibilities of instrumental examination, correlating two- and three-dimensional images with Doppler data and using additional capabilities of ultrasound scanners.

Since from a practical point of view, the greatest role is played by the large mass of the left ventricle, as the most functionally loaded and susceptible to hypertrophy, below we will discuss the calculation of the mass and mass index specifically for this chamber of the heart.

The calculation of the myocardial mass index and the mass itself in different years was carried out using a variety of formulas due to the individual characteristics of the geometry of the heart chambers of the subjects, which make it difficult to create a standard calculation system. On the other hand, a large number of formulas complicated the formulation of criteria for hypertrophy of a specific part of the heart, so conclusions regarding its presence in the same patient could differ with different methods of assessing echocardiography data.

Today the situation has improved somewhat, largely thanks to more modern ultrasound diagnostic devices, which allow only minor errors, but there are still few calculation formulas for determining the mass of the left ventricular (LV) myocardium. The most accurate of them are the two proposed by the American Society of Echocardiography (ASE) and the Penn Convention (PC), which take into account:

The thickness of the heart muscle in the septum between the ventricles;
The thickness of the posterior wall of the LV at the end of the period of filling with blood and before the next contraction;
End-diastolic size (EDV) of the left ventricle.

In the first formula (ASE), the thickness of the left ventricle includes the thickness of the endocardium, in the second similar calculation system (PC) it is not taken into account, therefore the formula used must be indicated as a result of the study, since the interpretation of the data may be erroneous.

Both calculation formulas are not absolutely reliable and the results obtained from them often differ from those at autopsy, however, of all those proposed, they are the most accurate.

The formula for determining myocardial mass looks like this:

0.8 x (1.04 x (IVS + ESD + LVSD) x 3 - ESD x 3) + 0.6, where IVS is the width of the interventricular septum in centimeters, ESD is the end-diastolic size, LVSD is the thickness of the posterior wall of the LV in centimeters.

The norm for this indicator differs depending on gender. Among men, the normal range will be g, for women - g.

In addition to the objectivity of assessing myocardial mass, there is another problem: the need to identify clear indexing criteria to determine the presence and degree of hypertrophy, because mass has a direct relationship with the body size of the subject.

Myocardial mass index is a value that takes into account the patient’s height and weight parameters, correlating myocardial mass to body surface area or height. It is worth noting that the mass index, which takes into account height, is more applicable in pediatric practice. In adults, growth is constant and therefore does not have such an impact on the calculation of cardiac muscle parameters, and perhaps even leads to erroneous conclusions.

The mass index is calculated as follows:

MI=M/H2.7 or M/P, where M is muscle mass in grams, P is the height of the subject, P is body surface area, m2.

Domestic experts adhere to a single accepted figure for the maximum left ventricular myocardial mass index - 110 g/m2 for women and 134 g/m2 for the male population. With diagnosed hypertension, this parameter is reduced in men to 125. If the index exceeds the specified maximum permissible values, then we are talking about the presence of hypertrophy.

The echocardiographic study form usually indicates lower average mass index standards relative to the body surface: g/m2 for men and g/m2 for women (different formulas are used, so the indicators may differ). These limits characterize the norm.

If the mass of the myocardium is correlated with the length and area of the body, then the range of variation in the norm of the indicator will be quite high: in men and in women when taking into account body area, in men and in women when indexing by height.

Taking into account the above-described features of the calculations and the obtained figures, it is impossible to accurately exclude left ventricular hypertrophy, even if the mass index falls within the range of normal values. Moreover, many people have a normal index, while they have already been diagnosed with initial or moderate cardiac hypertrophy.

Thus, myocardial mass and mass index are parameters that allow us to judge the risk or presence of cardiac muscle hypertrophy. Interpretation of echocardiography results is a complex task that can only be accomplished by a specialist with sufficient knowledge in the field of functional diagnostics. In this regard, patients’ independent conclusions are far from always correct, so it is better to go to a doctor to decipher the result in order to exclude false conclusions.

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 determining 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, recent recommendations for the diagnosis and treatment of hypertension include the measurement of LVMM in the algorithm of antihypertensive tactics for patient management 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. However, 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. But 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 between the calculated LVMM values obtained using these two formulas (the cubic formula 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 × + 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,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 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 were 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. Moreover, 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.

LVMI as a criterion for LVMH with and without gender

D. Levy, Framingham Research, 1987

J.K. Galy, 1992

I.W. Hammond, 1986

E. Aberget, 1995

De G. Simone, 1994

J.J. Mahn, 2014

Recommendations for chamber quantification: Guidelines, 2005

Gender-neutral

M.J. Koren, 1981

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 m2 in women; indexation to height 2.0 for men games/m 2.7 for women; indexation to height - 77 for men and 69 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 indexations 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 controversy 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 forming a group 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).

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.

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 (access date: 09/02/2017).

Field of activity (technology) to which the described invention relates

The development know-how, namely this invention of the author, relates to the field of medicine and can be used to diagnose left ventricular myocardial hypertrophy.

DETAILED DESCRIPTION OF THE INVENTION

In cardiological practice, special attention should be paid to the diagnosis of left ventricular hypertrophy. This is due to the fact that, as numerous studies show, left ventricular myocardial hypertrophy is a more strict predictor of cardiovascular complications and mortality than blood pressure levels and other risk factors [Florya V.G. The role of left ventricular remodeling in the pathogenesis of chronic circulatory failure. // Cardiology, 1997, No. 5, pp. 63-69; Yurenev A.P., Gerashchenko Yu.S., Dubov P.B. On the prognosis of the course of the disease in patients with hypertension and coronary insufficiency. // Ter. arch. 1994; 66:4:9-11; Bikkina M., Levy D., Evans J.S et al. Left ventricular mass and risk of stroke in an elderly cohort: the Framingham Heart Study. JAMA, 1994; 272; 33-36; Devereux R.B. Left ventricular geometry, pathophysiology and prognosis. J Am Coll Cardiol 1995; 25:]. Even a small change in left ventricular mass within the normal range can be a predictor of increased cardiovascular risk.

An increase in left ventricular mass is a common final pathway for many adverse cardiovascular outcomes [Florya V.G. The role of left ventricular remodeling in the pathogenesis of chronic circulatory failure. // Cardiology, 1997, No. 5, pp. 63-69; Devereux R.B. Left ventricular geometry, pathophysiology and prognosis. J Am Coil Cardiol 1995; 25:].

According to the Framingham Study, individuals aged 35 to 64 years with electrocardiographic evidence of LVH have a 3- to 6-fold higher risk of developing cardiovascular disease than individuals without LVH. After the appearance of ECG signs of LVH, 35% of men and 20% of women die within 5 years; in older age groups, 5-year mortality among men and women reaches 50 and 35%, respectively.

Due to its important prognostic value, clear criteria are needed to diagnose LVH as early as possible and conduct dynamic monitoring of the process of cardiac remodeling. Currently, there are several methods for diagnosing left ventricular myocardial hypertrophy.

The simplest and most accessible method is electrocardiography. There are the following ECG criteria for left ventricular hypertrophy:

Sokolov-Lyon index (SV1+RV5/RV6>35 mm) (sensitivity 22%, specificity 100%)

Cornell voltage index RaVL+SV3>28 mm in men and >20 mm in women (sensitivity 42%, specificity 96%)

RaVL>11 mm (sensitivity 11%, specificity 96%). [Prevention, diagnosis and treatment of primary arterial hypertension in the Russian Federation. // Clinical pharmacology and therapy 2000, No. 9 (3), pp. 5-30].

Despite the high specificity of the electrocardiographic method (96-100%), it has low sensitivity (22-42%), which does not allow it to be used effectively to solve the assigned problems.

Another method for diagnosing ventricular myocardial hypertrophy is known from the patent literature (automatic certificate No. class A 61 B 5/02), including an electrocardiographic examination of the patient in conventional leads, characterized in that in order to increase the accuracy of determining the predominance of myocardial hypertrophy of the right or left ventricle hearts with their combined hypertrophy, additionally determine the ratio of the amplitude of the R wave to the sum of the amplitudes of the Q, R, S waves in standard leads, the ratio of the amplitude of the R wave to the sum of the amplitudes of the R and S waves in the chest leads V1 and V2, V4 and V5, sum up the obtained values in pairs taking into account their direction and value in leads III, V1, V2, V4 with the sign /+/, and in leads I, V5 - with the sign /-/ and the hypertrophy index (HI) is determined using the formula: HIG=(R/(Q +R+S)III-R/(Q+R+S)I)+(R/(R+S)V1+R/(R+S)V2)+(R/(R+S)V4-R /(R+S)V5), where Q, R, S are the amplitudes of the waves of the QRS ECG complex in leads I, III, V1, V2, V4, V5, mm, and with values of IG = 0.43 or less - the predominance of hypertrophy left ventricle with combined ventricular hypertrophy of the heart. This method only allows one to determine the predominance of hypertrophy of one of the ventricles and cannot be used for its early diagnosis. The method is based on electrocardiographic criteria and, therefore, its sensitivity is insufficient.

The diagnosis of LVH can be established as a result of a pathological examination (normal myocardial mass is 1/215 of body weight in men and 1/250 of body weight in women [Human Anatomy. Gain M.G., N.K. Lysenkov, V. I. Bushkovich. St. Petersburg, “Hippocrates”, 1997]), but it can only be performed posthumously, which significantly limits the possibilities of its use.

Currently, echocardiographic criteria are most often used to diagnose myocardial hypertrophy. The echocardiographic research method allows you to obtain clear data on the basis of which changes in the structure and function of the heart are assessed. In diagnosing LVH, this method is more sensitive than electrocardiography. Left ventricular myocardial mass, which can be calculated from echocardiographic studies, is a more reliable predictor of morbidity and mortality.

Typically, echocardiography determines:

Thickness of the interventricular septum (IVS)

Thickness of the posterior wall of the left ventricle (PLW),

Hypertrophy is spoken of in cases where the IVS exceeds 10 mm, and the LVSD exceeds 11 mm [Strutynsky A.V. Echocardiogram: analysis and interpretation. // M., 2001], however, left ventricular hypertrophy can be observed even with normal values of the IVS and LVSD due to its dilatation.

A more accurate echocardiographic sign of LVH is an increase in the mass of the left ventricular myocardium, which is calculated using the formula proposed by R. Devereux and N. Reichek:

where LVMM is the mass of the left ventricular myocardium;

IVS - thickness of the interventricular septum in diastole;

LVDS - thickness of the posterior wall of the left ventricle in diastole;

The myocardial mass calculated in this way is not related to the constitutional characteristics of the patient. That is why there is still no unity in understanding at what values of the mass of the left ventricular myocardium we can talk about LVH [Sidorenko B.A., Preobrazhensky D.V. Left ventricular hypertrophy: pathogenesis, diagnosis and the possibility of reverse development under the influence of antihypertensive therapy. // Cardiology.; 5:80-85]. This drawback, on the one hand, significantly limits the use of the Devereux and Reichek formula in diagnosing myocardial hypertrophy itself in a given patient, and on the other, does not allow the use of this indicator for epidemiological studies.

Myocardial mass largely depends on gender and anthropometric parameters of the human body [Human Anatomy. Gain M.G., N.K. Lysenkov, V.I. Bushkovich. St. Petersburg, “Hippocrates”, 1997], therefore, as a criterion for diagnosing LVH, the left ventricular myocardial mass index is used, calculated by the formula:

where IMI is the left ventricular myocardial mass index;

LVMM - left ventricular myocardial mass;

S is the surface area of the body.

Body surface area is calculated using the Dubois formula [Human Physiology in 2 volumes, ed. V.M.Pokrovsky and G.F.Korotko, M., Medicine, 2001 // T.2, p.119]:

S-m 0.425 h 0.725 71.84,

where m is body weight;

The normal proportions of the human body, its organs and tissues, which form the basis for calculating the myocardial mass index, can vary significantly under various pathological conditions. This is confirmed by the fact that different authors cite unequal values of the left ventricular myocardial mass index as the lower limit for LVH in men and women [Sidorenko B.A., Preobrazhensky D.V. Left ventricular hypertrophy: pathogenesis, diagnosis and the possibility of reverse development under the influence of antihypertensive therapy // Cardiology.; 5:80-85].

Calculations of myocardial mass index are given in Tables 1-8.

When calculating body surface area using the Dubois formula, with an increase in body weight (with edema, obesity) by 25%, the body surface area will increase by approximately 10%, and with an increase in body weight by 50%, by approximately 19%. Accordingly, a decrease in the myocardial mass index (MIM), calculated using this formula, will occur without changing the value of its real mass and morphological properties. Similarly, there is a formal increase in the myocardial mass index with a decrease in body weight (weight loss, dehydration due to vomiting, diarrhea, prescription of diuretics, etc.). In addition, one cannot focus on this indicator in persons who have lost limbs or with developmental anomalies, due to the fact that body surface area, body weight and height in such people are related by other ratios.

With age, a person's height decreases by 5-7 cm due to an increase in the curvature of the spine and a decrease in the thickness of the intervertebral discs [Textbook of anatomy for students of medical institutes, ed. prof. Sapina M.R. in 2 vols., M., Medicine, 1987, T.1], which leads to the inadequacy of the use of this method for diagnosing myocardial hypertrophy in elderly and senile people. In addition, a person’s height changes even during the day by 2-4 cm [Zhigulev N.M., Badzgaradze Yu.D., Zhigulev S.N. Osteochondrosis of the spine: a guide for doctors. - St. Petersburg.. - Publishing house "Lan", 592 p.].

In connection with the above, myocardial mass index calculated on the basis of body surface area is a very unstable indicator, the use of which for the diagnosis of myocardial hypertrophy in a number of cases gives false positive and false negative results. This makes it impossible to use the myocardial mass index for dynamic monitoring of patients, when it is necessary to assess, for example, the effectiveness of therapy or the degree of prognostic risk in a given patient with myocardial hypertrophy.

The objective of the present invention is to achieve an objective criterion that allows diagnosing left ventricular myocardial hypertrophy, which could be used with equal success both for one-time use and for dynamic monitoring of a specific patient, as well as during epidemiological studies.

The solution to this problem is achieved by calculating the myocardial mass index based on the results of echocardiographic studies and anthropometric measurements. The method is carried out as follows.

The patient undergoes an echocardiographic study to determine the thickness of the interventricular septum, the thickness of the posterior wall of the left ventricle and the end-diastolic size. After this, the mass of the left ventricular myocardium is calculated using the formula:

where IVS is the thickness of the interventricular septum in diastole;

ZS - thickness of the posterior wall of the left ventricle in diastole;

EDD - end diastolic size of the left ventricle.

Then the patient undergoes anthropometric measurements (in cm):

a) width of the forearm at the level of the styloid process of the ulna, d;

b) circumference of the forearm at the level of the styloid process of the ulna, p;

c) the distance from the styloid process of the ulna to the apex of the olecranon process of the ulna, L.

After this, the bone coefficient k is calculated using the formula:

It closely correlates (correlation coefficient r = 0.91) with body surface area in healthy people with normal body weight, and does not change with a decrease or increase in unstable indicators that determine body surface area. Then the left ventricular myocardial mass index (H i) is calculated using the formula:

The criterion for the presence of left ventricular myocardial hypertrophy is an H i value of more than 0.6.

We propose an indicator that links myocardial mass to the size of the forearm bones, which are more stable than height and weight, which determine the body surface area.

The formation of the skeleton of the forearm ends by the age of 25, and the established proportions are maintained without significant changes until the end of a person’s life [Textbook of anatomy for students of medical institutes, ed. prof. Sapina M.R. in 2 vols., M., Medicine, 1987, T.1]. Pathological changes in soft tissues (edema, dehydration, excessive development of subcutaneous fat, weight loss) do not have a noticeable effect on bone size.

Using the ratio of myocardial mass to an indicator associated with the size of the skeletal bones makes it possible to exclude incorrect changes in the myocardial mass index that occur in the conditions described above. This makes it possible to monitor the dynamics of myocardial hypertrophy, for example, during therapeutic measures accompanied by changes in body weight. In addition, this makes it possible to adequately diagnose myocardial hypertrophy in patients without limbs (provided they have at least one forearm), with developmental anomalies, etc.

The method can also be used to monitor myocardial hypertrophy in patients in cases where it is difficult to determine their height and weight (for example, in unconscious patients who are in skeletal traction, in a plaster cast, etc.).

Another advantage of our method is that the dynamics of myocardial mass can be assessed throughout the patient's life and, therefore, used in epidemiological studies. This is possible due to the fact that the value of the proposed bone coefficient k and the associated myocardial mass index will practically not change with age, while the body surface area can vary and lead to an incorrect change in the generally accepted left ventricular myocardial mass index.

Patient S, 55 years old, diagnosis: Art. II hypertension. IBS. Angina pectoris II FC. CHF stage I

Upon admission to the hospital, the patient underwent electrocardiographic, echocardiographic and anthropometric studies.

The results of electrocardiography do not provide grounds to diagnose myocardial hypertrophy in the patient. When using the proposed H i index, the diagnosis of hypertrophy is obvious.

Patient A, 78 years old, diagnosis: IHD. Angina pectoris III FC. Hypertension, stage II. CHF II B. Diabetes mellitus type II, moderate to severe. Obesity III degree. Upon admission to the hospital, an echocardiographic examination and anthropometric measurements were performed, the following results were obtained:

From the tables it is clear that using the generally accepted IMM, we cannot diagnose myocardial hypertrophy, because this patient is overweight and we get a deliberately false result (BMI = 129.62) - absence of hypertrophy. Using the new H i criterion (H i >0.6), we diagnose myocardial hypertrophy.

After the therapy, the patient’s body weight changed (due to the disappearance of edema and a decrease in subcutaneous fatty tissue), after repeated examination the following results were obtained:

Thus, based on the IMM, one can draw a false conclusion that during the therapy the patient developed myocardial hypertrophy. (IMI increased from 129.62 to 140.59). If the H i criterion is used as a criterion for left ventricular myocardial hypertrophy, it becomes obvious that the patient’s actual myocardial hypertrophy has not undergone any changes (H i remained equal to 0.62).

Patient B., 55 years old, both lower limbs are missing, diagnosis: diabetes mellitus type II, severe. Diabetic angiopathy of the extremities. Stumps of both thighs. When carrying out the studies described above, the following was obtained:

Using IMM in this case is impossible, because the calculated surface area does not reflect the normal proportions of the body and we get an incorrect result (MMI = 204.80), and therefore, we diagnose left ventricular myocardial hypertrophy even in its absence; using our method, we reject the diagnosis of hypertrophy.

Thus, our proposed method for diagnosing left ventricular myocardial hypertrophy using bone coefficient k and myocardial mass index H i allows us to adequately assess the presence or absence of left ventricular myocardial hypertrophy, conduct dynamic monitoring of a specific patient, and also makes it possible to use the obtained data in epidemiological studies .

Claim

A method for diagnosing left ventricular myocardial hypertrophy, which consists in the fact that the patient undergoes an echocardiographic study with determination of the end-diastolic size, the myocardial thickness of the posterior wall of the left ventricle in diastole, the myocardial thickness of the interventricular septum in diastole, the mass of the left ventricular myocardium using the Devereaux formula with the calculation of the myocardial mass index of the left ventricle, characterized in that the patient is additionally measured the width of the forearm between its lateral surfaces at the level of the styloid process of the ulna, the circumference of the forearm at the level of the styloid process of the ulna, the length of the ulna from the styloid process to the apex of the ulnar process of the ulna, and based on the data obtained calculate the bone coefficient k:

where d is the width of the forearm at the level of the styloid process of the ulna;

p - circumference of the forearm at the level of the styloid process of the ulna;

L is the length of the ulna from the styloid process to the apex of the olecranon process of the ulna,

then the myocardial mass index is calculated taking into account the bone coefficient H i using the formula:

with values greater than 0.6, left ventricular myocardial hypertrophy is diagnosed.

Inventor's name:

Patent owner's name: Kivva Vladimir Nikolaevich (RU); Maklyakov Yuri Stepanovich (RU); Pshenichkin Konstantin Ivanovich (RU); Slavskaya Natalya Aleksandrovna (RU); Morozova Elena Aleksandrovna (RU); Ryabov Andrey Anatolyevich (RU); Abramova Tatyana Nikolaevna (RU)

Postal address for correspondence:, Rostov-on-Don, st. Taganrog highway, 126/1, apt. 22, V.N. Kivwe

Patent start date: 2004.12.23

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 begins, under their influence, 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 an obese person, and it must 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.

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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.

cardiac ischemia;
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 an increase in muscle fibers leads 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.

1 Comment on “Left ventricular myocardial hypertrophy - what is it?”

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?

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

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:

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

Diagnosis and treatment

Doctor performing echocardiography

getting rid of excess body weight. it helps lower blood pressure;
to give up 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:

Periodic pain in the chest and heart area.
Higher than normal blood pressure.
Pressure surges.
Arrhythmia.
Headache.
Dyspnea.
Sleep disturbance.
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 consumption, 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

Causes

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;
adynamia;
sudden intense physical activity;
sleep apnea (often observed in postmenopausal women and men);
smoking, alcoholism, etc.

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.

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;
headache;
cardiopalmus;
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.

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

Changing your lifestyle and eliminating risk factors

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

Drug therapy

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.

Surgery

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 - moderate, 1.6-2.0 - significant, and a value of more than 2 cm indicates high 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).

Causes

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. Hypertrophy often develops with mitral valve insufficiency or with aortic defects.

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

Stages and symptoms

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

compensation period;
subcompensation period;
period of decompensation.

Consequences of left ventricular myocardial hypertrophy

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

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.

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” in autonomous mode.

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:

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.
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:

Conductivity - equates myocytes to nerve fibers, since they are also capable of conducting impulses, transmitting them from one area to another.
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.
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:

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.
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 heart 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 related. 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 contact a doctor - the basic information can be found out before visiting the doctor, by reading the report yourself. The results of cardiac 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 (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.

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.

The principle of calculating the mass of the LV myocardium

Left ventricle of the myocardium in normal condition and with hypertrophy

Reasons influencing the deviation of the LV myocardial mass index from the norm

In most cases, the left ventricle and the myocardium as a whole enlarge under the influence of certain pathologies that provoke significant overload of the heart:

valve defects;
cardiomyopathy;
arterial hypertension;
myocardial dystrophy.

Sport as a cause of increased LV myocardial mass

Important! In any case, the increased mass of the myocardium indicates serious loads on the left ventricle and heart of a person, due to which their hypertrophy occurs. Therefore, even if such a deviation is, at first glance, normal, it is still recommended not to allow it.

Methods for calculating LV myocardial mass

The rate of myocardial mass index itself is calculated in many ways, but today medicine uses only two of the most effective formulas: ASE and PC, which include the following data:

the thickness of the heart muscle between the right and left ventricles;
the thickness of the posterior cavity of the left ventricle (this indicator is measured in two stages: when the organ is completely filled with blood and when it is emptied);
end-diastolic dimensions of the LV.

So, to determine the mass index of the left ventricle, you initially need to scan the heart and myocardium, and substitute the resulting sizes of these organs into the following formula:

0.8 * (1.04 * (MZhP + KDR + ZSLZH) * 3 – KDR * 3) + 0.6

The abbreviations in this formula have the following designations:

IVS – width of the septum between the ventricles, expressed in cm;
EDR – left ventricular end-diastolic size;
LVSP is an indicator of the thickness of the posterior cavity of the left ventricle, expressed in cm.

Depending on who the patient is (male or female), the rate of myocardial mass index will be slightly different. This difference looks like this:

If the patient is a man, then the norm for him will be from 135 to 182 grams;
If the patient is a woman, then the norm for her ranges from 95 to 141 grams.

If the indicator is too high, it can be assumed that hypertrophy is rapidly developing in the patient’s body, requiring urgent medical intervention.

Calculation of myocardial mass depending on the patient’s weight and height

Establishing a relationship between LV myocardial mass and patient body size

As for calculating the ratio of myocardial mass to body height and weight, it is performed strictly according to the following formula:

MI = M/N2.7

The abbreviation of this formula is deciphered as follows:

M – muscle weight, expressed in grams;
P – patient’s height;
P is the area of the patient’s body, expressed in square meters.

What is associated with the formation of left ventricular diastolic dysfunction? Prevention measures

The heart is an organ located in the mediastinum. It consists of the atrium and the left ventricle. The atria receive arterial blood coming from the lungs through the left side. Mitral and aortic valves are the area of formation of cardiopathy (mitral stenosis and aortic insufficiency).

Anatomical features

The right region consists of the right atrium and ventricle and receives venous blood from the systemic circulation through the superior and inferior vena cava.

The right atrioventricular valve has a tricuspid valve that closes during systole and opens during diastole.

The right side of the heart is responsible for the pulmonary circulation. Consequently, there is a large or systemic circle of blood circulation and a small circle.

With the rhythmic contractions of the first two atria and two ventricles, the same amount of blood is synchronously displaced. The atrium (atrium) pushes venous blood throughout the body through the vena cava. Passing through the lungs, the blood reaches the left atrium, from where it passes into the left ventricle and from here through the aortic artery it is distributed to all tissues and organs. The heart consists of three components:

The endocardium, or inner lining, lines the inside of the heart, and its folds form the valves.
The myocardium or cardiac muscle is the middle layer, consisting of the myocardium itself, as well as specific tissue. The myocardium has different thicknesses in the two ventricles. Thus, the left ventricle, in order to push blood, has a much thicker wall than the right one, which pushes blood only to the two lungs. The atria have a thinner wall than the ventricles.
The pericardium is the outer layer of the heart. This is a serous membrane containing, like the pleura, two layers.

The specific tissue consists of embryonic-like muscle, very rich in nerve cells and includes:

The sinoatrial node is located in the right atrial wall, next to the superior vena cava.
The atrioventricular node, consisting of the ventricular node, located in the posterior inferior septum, and the bundle of His, which runs from the previous Aschoff-Tawar node, down the wall between the ventricles, and is divided into two branches (right and left), ending at the level of the Purkinje network.

In a pathological condition, all three layers may be affected separately (myocarditis, endocarditis or pericarditis) or simultaneously (pancarditis).

The heart is vascularized through two coronary arteries. The coronary arteries empty into the coronary sinus, which opens into the right atrium.

The heart is innervated by nerve cells of the sympathetic and parasympathetic systems.

The heart is a kind of pump organ. Blood circulation is possible thanks to its rhythmic contractions. Heart contractions begin with the filling of the atria during diastole, when there is an influx of venous blood.

Description of myocardial mass

The most important question that experts ask is the myocardial mass index of the left ventricle and right heart. This indicator must be accurately assessed. In addition, this parameter is often of interest to people who have undergone echocardiography and found the heart muscle mass index among the key parameters. The normal myocardial mass is 135-182 g in men and 95-141 g in women.

This is the average. In general, this parameter indicates the weight of the heart muscle, which is calculated after an ultrasound examination. The unit of measurement is gram. Many pathological processes are characterized by this value. If upward changes occur, then the mass of the left ventricular myocardium in this case indicates the likelihood of complications. Accordingly, the prognosis is unfavorable.

When myocardial mass increases, they speak of the presence of hypertrophy. In fact, this is a thickening of the muscle structure, which indicates a structural restructuring within the heart. In this case, doctors are forced to carry out dynamic monitoring, and in certain cases, also take active therapeutic actions. The mass index of the left ventricular myocardium in a healthy person and a patient differs.

Modern therapeutic options dictate the need to monitor such an important indicator as the mass of the left ventricular myocardium. This must be done in people with a potential risk of cardiac hypertrophy. Cardiac ultrasound and echocardiography should be prescribed. But it is even more important to be able to correctly interpret the data obtained. This remains a serious problem today, since not everyone can relate this information to individual patients. It is important to correctly establish whether a certain left ventricular myocardial mass index is a physiological feature or whether there are deviations from the norm.

The left ventricular myocardial mass index is to some extent a subjective parameter, since it is impossible to identify the same result for people of different gender, height and weight. Take, for example, a large man who periodically lifts weights. Its physiological norm will be excessive for a short girl with a fragile build who rarely visits the gym.

Myocardial mass is closely related to body size. How often a person exercises is also important.

When interpreting the results, you should take this into account. If the indicator differs only slightly from the acceptable norm, this does not always indicate pathology.

Reasons for rejection

Myocardial mass can be increased if any disease occurs. This contributes to overloading the muscle tissue. What pathologies contribute to this:

valve defect;
arterial hypertension;
myocardial dystrophy and cardiomyopathy.

If a person exercises vigorously, muscle tissue grows. This is considered the norm. After all, not only skeletal muscles are built up during sports. Corresponding changes also occur in the myocardium, as it has to better saturate the organs and tissues with blood. True, athletes have a certain risk. They may fall into the category of people with myocardial hypertrophy. Under certain conditions, this situation threatens the emergence of pathology. If the thickness of the muscular tissue of the heart is greater than the coronary vessels can pump blood through, heart failure occurs. That is why attacks occur in well-trained and apparently absolutely healthy people.

It turns out that an increase in myocardial mass in any case indicates an increase in the load on the heart. It doesn’t matter whether we are talking about pathology or sports training. Regardless of the cause, hypertrophy requires special attention.

How to count

The myocardial mass index is calculated in accordance with echocardiography data. Various regimes are possible here. In this case, the doctor needs to use the capabilities of instrumental methods, comparing two- and three-dimensional images, including Doppler readings and ultrasound scanners. From a practical point of view, the large mass of the left ventricle plays the greatest role, since it is this section that has the greatest importance and is considered to be the most overloaded. This chamber of the heart is considered first.

The myocardial mass index is calculated using various formulas. The fact is that the examined patients always have their own individual characteristics of the geometry of the organ cavities. Accordingly, it is quite difficult to derive a certain standard formula. On the other hand, the formulation is complicated by the large number of possible formulas and criteria for hypertrophy of a particular section; it turns out that in the same patient, when using certain methods of assessing echocardiography data, differences are found.

Today, it is a pleasure to improve the situation thanks to advanced technologies. The latest ultrasound diagnostic devices have appeared. They allow minimal errors. And yet, there are several formulas for determining the mass of the left ventricular myocardium. The American Society of Echocardiography has proposed the main one. This is what is considered the most reliable. This takes into account:

thickness of muscle tissue in the interventricular septum;
thickness of the posterior wall of the left ventricle after filling with blood and before the next contraction;
the final size of the left ventricle in diastole.

The formula itself looks like this:

0.8 x (1.04 x (IVS + ESD + LVSD) x 3 - ESD x 3) + 0.6, where IVS is the width of the interventricular septum in cm, ESD is the end-diastolic size, LVSD is the thickness of the posterior wall of the LV in cm

In addition to an objective assessment of this indicator, another problem arises. But today it is necessary to find clear indexing criteria to identify hypertrophy and its degree. After all, as was said earlier, this index is directly related to the size of the human body. This is a value that takes into account the parameters of height and weight, correlating the mass of muscle tissue with the body surface area or height of a person. However, in adults, growth is constant, so it does not have a significant impact on the calculation of parameters. It is possible that in the future it will be recognized as superfluous, since it can lead to erroneous conclusions.

Acute myocardial infarction (AMI) or heart attack - acute coronary syndrome. It is the most severe ischemic heart disease (IBS).

Acute coronary syndromes and acute forms of coronary heart disease are divided into:

unstable angina;
myocardial infarction without ST elevation on the ECG and myocardial infarction with ST elevation.

A common feature between all acute coronary syndromes resulting from pathophysiological processes is atherosclerosis and blockage (complete or incomplete) of the vessels that supply blood to the heart (coronary arteries) and an acute imbalance between the need for oxygen and its supply to the area of vascularization from the affected blood vessel.

Unstable angina or the so-called pre-infarction state is associated with incomplete occlusion of the coronary artery. There is no necrosis of the heart muscle, so there are no signs of a heart attack.

This video talks about the pre-infarction state.

Acute myocardial infarction is accompanied by necrosis (death) of myocardial cells, which develop under the influence of various causes that trigger acute myocardial ischemia. This most often occurs when atherosclerosis affects one or more coronary arteries with the development of intracoronary thrombosis after detachment of the atherosclerotic plaque from the wall, which leads to temporary or permanent occlusion of one or more vessels. Depending on the thickness of the myocardial wall, heart attacks are divided into two groups (based on ECG changes):

Non-transmural infarction - most often occurs due to incomplete occlusion of the coronary artery, but in this case there is myocardial necrosis, which does not affect the entire thickness of the heart muscle. The difference between the key forms is detected in laboratory tests that report myocardial necrosis (specific marker - Troponin) - in this form it is higher.
Transmural infarction - occurs due to complete occlusion of the coronary artery, which leads to complete disruption of the oxygen supply and necrosis of muscle cells in the area of the blood supply to the affected artery. The death of the first myocardial cells is achieved after 15 minutes of artery blockage.

The determining factors for the development of both types are early spontaneous reperfusion and the presence of a developed collateral network of vessels in the ischemic zone.

What are the heart attack statistics?

Statistics from coronary artery disease and myocardial infarction indicate that they are the leading cause of disability worldwide.

Coronary artery disease (CHD) is a major health problem and is the leading cause of hospitalizations each year. Coronary heart disease and myocardial infarction are the leading causes of disability, according to the World Health Organization (WHO).

Causes

Atherosclerosis of the coronary arteries underlies ischemic heart disease. Risk factors for the development of atherosclerosis:

hypertension;
diabetes;
dyslipidemia;
smoking;
decreased physical activity.

These factors lead to dysfunction of the endothelium (the inner lining of blood vessels). Areas of endothelial dysfunction created conditions for the formation of atherosclerotic plaques, i.e. to the accumulation of cholesterol with subsequent inflammation and fibrosis of the vascular wall. This causes a narrowing of the lumen of the arteries. Atherosclerotic plaques can increase over a period of months, days, or even hours.

Atherosclerotic plaques are divided into stable and unstable. A stable plaque is characteristic of stable angina. An unstable plaque is found in acute coronary syndromes. The stability of plaque does not depend on its size, but on the degree of inflammation in it, the thickness of the fibrous layer and the size of its lipid core.

Small, thin-walled plaques are more likely to rupture and this leads to acute thrombosis due to rapid aggregation of platelets around the rupture. The growth of the plate over several days or months is associated with damage to the plaques, over which there is a thrombus covered with fibrous tissue.

Risk factors for atherosclerosis and coronary heart disease, respectively, are divided into reversible and non-correctable.

Unadjustable risk factors include:

age;
family history.

Adjustable risk factors:

Smoking. Active and passive smoking damages the vascular endothelium and thus contributes to the occurrence of atherosclerosis. Smoking also increases blood clotting. Tobacco doubles the risk of atherosclerosis. Quitting smoking partially restores the adverse effects on the vessel wall caused by it. When smoking stops, lipid levels improve.
High levels of cholesterol and triglycerides (dyslipidemia). Cholesterol is the main part of atherosclerotic plaques. High levels of so-called LDL, as well as triglycerides, underlie atherosclerosis. Their growth is caused by an unhealthy diet consisting of sources of animal fats, cholesterol and carbohydrates. Typically, total cholesterol levels are<5,0 ммоль / л, триглицеридов <1,7 ммоль / л. С другой стороны, высокий уровень «хорошего» холестерина - ЛПВП (>1.3 mmol/L) may help eliminate excess cholesterol from the bloodstream and thereby reduce the risk of heart attack.
High blood pressure. Hypertension damages arteries, especially the coronary arteries. Therefore, risk factors for high blood pressure are also risk factors for coronary heart disease.
Decreased physical activity. Immobilization leads to obesity and, accordingly, an increase in cholesterol levels. People who maintain regular aerobic physical activity have a lower risk of heart attack. Physical activity is necessary to lower blood pressure.
Diabetes. Diabetes is one of the most serious risk factors for atherosclerosis and coronary heart disease. About 60% of patients with myocardial infarction have diabetes or impaired glucose tolerance. About 40% of patients with diabetes have had acute coronary artery disease during their lifetime. Good diabetes control leads to a reduction in cardiovascular risk in diabetics.
Alcohol. Moderate alcohol consumption increases HDL cholesterol (good cholesterol) and thus has a protective effect on myocardial infarction. Men should not exceed the amount of 75 ml per day, and women should not take more than 50 ml. Increased consumption of alcoholic beverages leads to hypertension and increased triglycerides, which in turn increases the risk of heart attack. Polyphenols, substances found in wine, have proven antioxidant effects, reduce the risk of cardiovascular disease and improve endothelial dysfunction.

What are the symptoms of a heart attack?

The main symptom of acute myocardial infarction is chest pain (angina). This is caused by irritation of the nerve endings in the area of the heart attack. Chest pain during a heart attack can begin at rest or with minimal physical effort, as well as due to psycho-emotional stress. The pain is severe, prolonged, widespread and intractable with nitroglycerin. Patients often describe severe cutting pain behind the sternum, lasting from 20 minutes to several hours.

Typical chest pain during a heart attack includes:

hands;
jaw;
back or epigastrium;
stomach.

Some patients only report strange pressure in the chest.

Sometimes chest pain is accompanied by restlessness, sweating, shortness of breath, weakness and palpitations. Pain in myocardial infarction is not affected by nitroglycerin. Myocardial infarction may also be asymptomatic (10-30%), especially in older diabetics or after coronary artery bypass grafting. Sometimes a heart attack manifests itself in its complications - acute heart failure or peripheral embolism.

The differential diagnosis for chest pain is broad. Non-cardiac causes should be considered:

Aortic dissection is acute pain in the joints that lasts for several hours. The pain often radiates to the back or lower extremities. As a rule, a pulse may not be felt in a single large artery of the extremities.
Acute pericarditis - pain in the pericardium is also acute and is often accompanied by cough and shortness of breath. The localization of pain is in the shoulders, neck and extends to the collarbone area.
Pleural pain is a sharp, cutting pain that occurs with every breath. When breathing stops, the pain disappears.
Pulmonary embolism - the patient is predominantly suffocating. The pain is pleural in nature and localized in the chest. The history of predisposing factors points towards this diagnosis.
Costal chondritis (Tietze syndrome) - it is characteristic that the pain is located in one point (the patient points to it with a finger), it increases with pressure and depends on movements of the chest wall. The damaged area may be red.
Shingles - Pain is often detected before the typical rash occurs, making diagnosis difficult. The typical disease of herpes zoster is its relation to a specific site (the area of the skin innervated by the sensory nerve).
Pneumothorax - the main symptom is the sudden onset of shortness of breath and an irritating cough.
Reflux esophagitis is typically a burning pain that gets worse when lying down.
Esophageal rupture - no characteristic ECG changes, pain associated with swallowing, may be hydropneumothorax, subcutaneous emphysema and medial skeletal lesions.
Depression - patients feel constant pressure in the chest, which is felt at rest and disappears with effort.

How is myocardial infarction diagnosed?

The diagnosis of myocardial infarction is based on clinical, instrumental and laboratory data.

Of the instrumental studies, electrocardiography and echocardiography are of greatest importance.

Laboratory tests are very useful in confirming myocardial infarction and are an important prognostic indicator. They also provide useful information about the patient's general condition.

Coronary angiography provides the most accurate diagnosis and establishes the cause of a heart attack. You can switch from a diagnostic procedure to treating a heart attack by loosening a blocked artery.

Electrocardiogram (ECG)

An electrocardiogram is the main method for diagnosing myocardial infarction. Acute ECG changes in transmural infarction include: abnormal position of the Q wave, accompanied by characteristic changes in the ST segment and T wave.

During myocardial infarction there are several stages of electrocardiography. Of particular note are the increase in the location of the ST segment in more than one ECG section, deep symmetrical T-waves with restoration of the ST segment, and a pathological Q wave (indicating the presence of necrosis). The changes are fully visible on the ECG after acute myocardial infarction and gradually disappear within 3-6 months after the peak manifestation of the disease. The ST segment gradually returns to the baseline and becomes isoelectric. The negative T-wave gradually decreases in amplitude and may even disappear completely, and in some cases becomes positive.

The Q wave must be 25% larger than the R wave to be considered abnormal. ST height is adopted to identify pathology. In differential diagnosis, the phenomenon of ST segment elevation can be seen in Prinzmetal syndrome, left ventricular aneurysm, pericarditis, and less commonly in early repolarization syndrome.

Nontransmural infarction is associated with ST depression accompanied by a negative T-wave.

Using an ECG, you can also determine the location of myocardial infarction - on the front, bottom or side wall.

Echocardiography is one of the main methods for research. Echocardiography can determine infarct size, complications, and provide valuable prognostic information. The mobility (kinetics) of sections of the left ventricle is assessed as normokinesia, hypokinesia, akinesia and dyskinesia.

In addition to segmental kinetics, echocardiography also determines left ventricular filling function and ejection fraction. Its normal rate is >55%. Reduced ejection fraction is a poor prognostic feature.

Echocardiography is an indispensable method for diagnosing mechanical complications of myocardial infarction.

These are rupture of the papillary muscle with subsequent dysfunction of the mitral valve, damage to the interventricular septum, rupture of the free wall of the LV, the occurrence of aneurysm and pseudoaneurysm of the LV, thrombosis, pericarditis.

Laboratory tests

Laboratory tests play an important role in the diagnosis of myocardial infarction. With the development of acute mycardial infarction, the presence of increased troponin was found to indicate necrosis. Its level also allows one to judge the degree of necrosis, the presence of reperfusion and damage.

The most important indicator of myocardial damage is cardiac troponin (Troponin T and Troponin I).

Cardiac troponins are highly specific for the myocardium and are not found in the blood under normal conditions. That's why finding them in the blood is a sure sign of a heart attack. Troponin increases 3-4 hours after a heart attack, and the maximum is reached after 12-36 hours. With a mini-heart attack, troponins are detected in the blood for only 2-3 days. Normal troponin values 12 hours after the onset of chest pain exclude the diagnosis of myocardial infarction.

Troponin, creatinine phosphokinase and, in particular, its CPK-MB fraction are used to diagnose myocardial infarction. Levels of these two enzymes increase with a heart attack, with CPK-MB being more than 6% of the normal value. Increased levels of the enzyme are also observed in conditions associated with muscle trauma (including muscle injections), muscle diseases, intoxications, necrosis of the pancreas and liver, hyperthyroidism, etc.

Other abnormalities in laboratory tests for myocardial infarction:

increased blood sugar levels (hyperglycemia);
leukocytosis;
increase in sedimentation, etc.

Higher C-reactive protein values in myocardial infarction indicate a poor prognosis.

Natriuretic peptide testing also has prognostic value.

Coronary angiography

Coronary angiography is an invasive method for visualizing the coronary arteries. This is the gold standard in the etiological diagnosis of coronary heart disease and myocardial infarction. Access is through an artery in the leg or arm. Using special catheters, the doctor reaches the heart and injects contrast material. An X-ray device monitors the filling of the arteries with this material.

From a diagnostic procedure, in the presence of significant (narrow) narrowed or blocked arteries, it becomes a therapeutic procedure - percutaneous coronary intervention (PCI).

CT scan

Computed tomography is primarily used in the differential diagnosis of chest pain. This makes it possible to distinguish between aortic aneurysms, acute pulmonary embolism and other pathologies. The most modern computed tomographs can judge the patency of the coronary arteries.

Scintigraphy and positron emission tomography (PET)

Scintigraphy and positron emission tomography (PET) are used in patients after myocardial infarction before revascularization to recognize viable areas of myocardium.

Treatment of myocardial infarction

Acute myocardial infarction is a serious condition that requires treatment in the intensive care unit and a precise medical approach. Specialized medical care guarantees survival. Everyone should know that sudden, severe chest pain lasting more than 5 minutes requires immediate medical attention. When treating myocardial infarction, three phases are considered:

pre-hospital;
sick leave;
post-infarction (after a heart attack).

Pre-hospital phase

At the first suspicion of acute myocardial infarction, the doctor should give acetylsalicylic acid 325-500 mg and clopidogrel 300 mg. It is very important to overcome the pain - with opiates (morphine or fentanyl). Patients with a heart rate greater than 60 beats per minute who have no contraindications should be given a beta blocker.

For bradycardia, atropine is given in a dose of 0.5 mg several times. Gradually this amount is increased to 3 mg. It is also important to supply the patient with an oxygen mask at a dosage of 10 l/min. Beta blockers and nitrates are given for high blood pressure, and vasopressors are required for hypotension. In case of low blood pressure, acute myocardial infarction with right ventricular defect, sufficient fluid infusion is required.

If necessary, cardiopulmonary resuscitation begins.

The doctor must make the right decision for further behavior and aim to stabilize the patient’s health. If a diagnosis of myocardial infarction is made, reperfusion therapy (treatment to eliminate the cause of the myocardial infarction) is given.

Hospital phase

Patients with acute myocardial infarction are placed in an intensive cardiology department. After administration, it is necessary to monitor the patient’s hemodynamic parameters - heart rate, pulse and blood pressure. Respiratory rate, diuresis and body temperature are also examined. Pain relief and oxygen supply continue. Electrocardiographic, echocardiographic and laboratory tests are performed.

Drug treatment of myocardial infarction

In the treatment of myocardial infarction, various drugs are used, which are selected individually depending on the patient’s condition.

Anticoagulants and antiplatelet agents

Antiplatelet agents and anticoagulants are given in the prehospital setting. It is recommended that acetylsalicylic acid be taken continuously after myocardial infarction along with clopidogrel for 12 months in patients after percutaneous coronary intervention. This reduces the risk of stent thrombosis and also reduces the risk of recurrent incidents.

Beta blockers

Beta blockers reduce heart rate, blood pressure, and contractility. This leads to improved coronary blood flow and reduced oxygen consumption by myocardial cells. In the acute phase of myocardial infarction, beta blockers are seen in patients with accelerated cardiac output (>80 mcg/min) along with high blood pressure with preserved left ventricular systolic function.

The goal of beta blocker treatment is to achieve a heart rate of 50-70 mcg/min.

and systolic blood pressure at 120 mm Hg. For patients with mild symptoms, they are prescribed within the first 24 hours. Treatment begins with low doses.

Statins

Statins are drugs that lower blood lipid levels and also have many different effects that lead to the stabilization of atherosclerotic plaques. Statin therapy is indicated in all patients with acute myocardial infarction.

The goal is to lower cholesterol levels (LDL<2,5 ммоль / л). Их дают в первые часы.

The drugs are contraindicated in people with liver dysfunction. All patients with AMI should be monitored for lipid profiles within the first 24 hours.

ACE inhibitors

ACE inhibitors are prescribed to all patients with stable pain and hemodynamic parameters in acute myocardial infarction. They are given in the first hours, and then this treatment is continued. The greatest benefit of ACE inhibitor therapy is observed in patients with heart failure and left ventricular dysfunction, as well as normal or high blood pressure. In hemodynamically unstable patients, administration of an ACE inhibitor is required to stabilize the condition. In case of intolerance to ACE inhibitors, angiotensin II receptor blockers are given.

Nitrates

Intravenous nitrates are recommended in all patients with myocardial infarction who have persistent signs of angina in combination with elevated blood pressure and heart failure. They are contraindicated if the patient has taken a phosphodiesterase type 5 inhibitor, sildenafil (Viagra), within the last 24 hours.

Calcium antagonists

Calcium antagonists have no place in the routine treatment of myocardial infarction. An exception is verapamil, which can be given to people intolerant to beta blockers to lower their heart rate. Verapamil is not required in patients with reduced left ventricular systolic function or heart failure. It is not combined with a beta blocker.

Antiarrhythmic drugs

Prophylactic administration of antiarrhythmic drugs in patients with acute myocardial infarction is not practiced. It is important to periodically monitor potassium levels in the blood. When tachyarrhythmia (ventricular tachycardia and atrial fibrillation) occurs during a heart attack, amiodarone is the most appropriate antiarrhythmic drug. In cases of severe, sustained arrhythmias, magnesium is also administered slowly. In cases of rapid atrial fibrillation, it is advisable to use beta blockers and Amiodarone.

The goal of treatment is to slow the heart rate and therefore reduce myocardial oxygen consumption.

Patients with sinus bradycardia and 2nd and 3rd degree AV node block are prescribed atropine.

Thus, the myocardial mass index is an indicator that allows us to judge the likely risks of hypertrophy of cardiac tissue or its presence in the present. Only a specialist can correctly interpret the results of echocardiography. He must be a true professional in the field of functional diagnostics.

Video “Hypertrophy of the left ventricle of the heart”

This video talks about left ventricular hypertrophy, since this disease is directly related to the mass of the mocardium.

And a little about secrets...

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Education: Federal State Budgetary Institution Clinical Hospital, Moscow. Field of activity: general surgery...